LESSON 1

THEMES:

1. METHODS OF EXAMINATION OF PATIENTS WITH SKIN DISEASES. PRIMARY AND SECONDARY SKIN LESIONS. DESCRIPTION OF AFFECTED AREA. FILLING IN PATIENT’S CARD.

2. PSORIASIS VULGARIS. LICHEN PLANUS, TYPES. PITYRIASIS ROSEA.

3. SEBORRHEA OF THE SCALP. SEBORRHEIC DERMATITIS. ALOPECIA AREATA. ACNE VULGARIS. ACNE ROSACEA. HIDRADENITIS PURULENT. FOLLICULITIS. STAPHYLOCOCCAL FOLLICULITIS

 

EXAMINATION OF PATIENT WITH SKIN DISEASES

1. Skin exam is not separate from the rest of the physical examination

2. Examine the patient in good lighting

 

http://www.aad.org/skin-conditions/about-dermatology

1.     PATIENT’S PASSPORT.

2.     PATIENT’S COMPLAINTS:

    Skin rashes;

    Subjective sensation, which are connected with skin rashes:

v itch of the skin;

v burning;

v pain;

v skin weeping;

v dryness of the skin;

v feeling of a tense skin;

v weakness, weight loss, fever etc.

 

Symptoms	Itching	Pain
Diurnal variation
Nocturnal T	Scabies
Daytime t	Photodermatosis
Seasonal	(because of sun exposure)
Summer aggravation	Fungal infections
	Insect bites
	Polymorphic light eruption
Winter aggravation	Ichthyosis	Systemic sclerosis
	Psoriasis
	Scabies (because of crowding)
	Chilblains
Precipitated by
Exercise	Cholinergic urticaria	Intermittent claudication
Cold	Cold urticaria	Raynauds phenomenon
Associated features
Rash	Drug Rash	Herpes zoster
Wkmk	Urticaria
Cyanosis		Raynaud’s phenomenon
Gangrene		+
H\popigmented lesion

 

HISTORY OF PRESENT ILLNESS:

                Possible etiology of the disease ( according patient’s mind).

                Duration of the disease:

Acute (< 2 month)

Chronic (> 2 month):

v course of a disease;

v previous treatment and effect from it;

v family history:

Family history is vital in patients with:

v •        Genetic disorders like ichthyosis, neurofibromatosis and epidermolysis bullosa.

v Infections and infestations e.g., scabies.

v Families exposed to similar environmental influences may also develop same disease e.g.

 

LIFE HISTORY ( PAST HISTORY)

 

                Past medical history.

                Associated inner diseases.

                Harmful habit.

                Occupational hazards.

                Allergological history.

 

OBJECTIVE INVESTIGATION:

 

 

TECHNIQUES OF EXAMINATION

 

 

http://www.nlm.nih.gov/medlineplus/skinhairandnails.html

 

 

1.  Inspect and palpate

 

 

Inspect and palpate skin for the following:

Skin inspection

The only way to know if your skin is healthy and intact is to look at it regularly. In areas where sensation (feeling) is decreased, skin inspection is essential and should become a habit. Plan it as a part of your regular daily routine, during a time when you are undressed anyway — such as after a shower, before dressing in the morning or after undressing in the evening. Daily skin inspection is necessary.

If you are unable to see some parts of your body, use a mirror or teach another person to check your skin for you. Long handled mirrors and other specially designed mirrors are available. Check all of your bony prominences, or areas where the bones protrude slightly below the skin (see illustrations below for the locations and names of these areas).

http://sci.washington.edu/info/pamphlets/skin_2.asp

       Color: Contrast with color of mucous membrane.

       Texture

       Turgor: Lift a fold of skin and note the ease with which it moves (mobility) and the speed with which it returns into place

       Moisture

       Pigmentation

       Lesions

       Hair distribution

       Warmth: Feel with back of your hand.

COLOR

 

    Patients ofteotice change in color before physician

    Look for increased pigmentation, loss of pigmentation

    Look for redness, pallor, cyanosis, and yellowing:

v Red color of oxyhemoglobin best assessed at fingertips, lips, and mucous membranes in dark-skinned people, palms and soles.

v For central cyanosis, look in lips, oral mucosa, and tongue.

v Jaundice – sclera.

 

MOISTURE

 

Dryness, sweating, and oiliness

 

DRY SKIN is common. It can occur at any age and for many reasons. Using a moisturizer often helps repair dry skin.

http://www.aad.org/skin-conditions/dermatology-a-to-z/dry-skin

 

 

The signs (what you see) and symptoms (what you feel) of dry skin are:

                  Rough, scaly, or flaking skin

                  Itching

Itching  Itching is a tingling or irritation of the skin that makes you want to scratch the affected area. Itching may occur all over the whole body or only in one location.  

http://www.nlm.nih.gov/medlineplus/ency/article/003217.htm

Considerations

Itching may occur all over the whole body (generalized) or only in one location (localized).

Causes

There are many causes of itching, including:

       Aging skin

       Atopic dermatitis

       Contact dermatitis (poison ivy or poison oak)

       Contact irritants (such as soaps, chemicals, or wool)

       Dry skin

       Hives

       Insect bites and stings

       Parasites such as pinworm, body lice, head lice, and pubic lice

       Pityriasis rosea

       Psoriasis

       Rashes (may or may not itch)

       Seborrheic dermatitis

       Sunburn

       Superficial skin infections such as folliculitis and impetigo

Generalized itching may be caused by:

                  Allergic reactions

                  Childhood infections (such as chickenpox or measles)

                  Hepatitis

                  Iron deficiency anemia

                  Kidney disease

                  Liver disease with jaundice

                  Pregnancy

                  Reactions to medications and substances such as antibiotics (penicillin, sulfonamides), gold, griseofulvin, isoniazid, opiates, phenothiazines, or vitamin A

Home Care

For persistent or severe itching, see your health care provider for a diagnosis and treatment instructions.

In the meantime, you can take some steps to help deal with the itch:

                  Avoid scratching or rubbing the itchy areas. Keep fingernails short to avoid damaging the skin from scratching. Family members or friends may be able to help by calling attention to your scratching.

                  Wear cool, light, loose bedclothes. Avoid wearing rough clothing, particularly wool, over an itchy area.

                  Take lukewarm baths using little soap and rinsing thoroughly. Try a skin-soothing oatmeal or cornstarch bath.

                  Apply a soothing lotion after bathing to soften and cool the skin.

                  Use moisturizer on the skin, particularly in the dry winter months. Dry skin is a common cause of itching.

                  Apply cold compresses to an itchy area.

                  Avoid prolonged exposure to excessive heat and humidity.

                  Take part in activities that distract from the itching during the day and make you tired enough to sleep at night.

                  Try over-the-counter oral antihistamines such as diphenhydramine (Benadryl), but be aware of possible side effects such as drowsiness.

                  Try over-the-counter hydrocortisone cream on itchy areas.

                  Gray, ashy skin in people with dark skin

                  Cracks in the skin, which may bleed if severe

                  Chapped or cracked lips

When dry skin cracks, germs can get in through the skin. Once inside, germs can cause an infection. Red, sore spots on the skin may be an early sign of an infection.

 

TEMPERATURE

 

http://www.nlm.nih.gov/medlineplus/images/boydoctor.jpg

 

v    Use back of fingertips

v    Identify warmth or coolness of skin

 

 

 

TEXTURE

 

Roughness or smoothness

 

MOBILITY AND TURGOR

 

v Lift fold of skin

v Note ease with which it lifts up (mobility) and speed with which it returns to place (turgor)

Changes in face with age

http://www.nlm.nih.gov/medlineplus/ency/imagepages/8665.htm

Facial skin tends to wrinkle with age.

 

HAIR

 

http://www.nlm.nih.gov/medlineplus/ency/imagepages/8669.htm

 

v Inspect and palpate

 

v Note quantity, distribution, and texture

 

 

 

 

Hair color is caused by a pigment (melanin) that is produced by the hair follicle. With aging, the follicle produces less melanin.

 

 

 

 

Aged hair follicles are no longer as prepared for new hair growth.

 

Hair follicle

Each hair sits in a cavity in the skin called a follicle. Over time the follicle can shrink causing the hair to become shorter and finer. Ordinarily, the hair should grow back but in men who are balding the very small follicle ceases to grow any hair. The cause of baldness is not well understood, but is thought to be related to the genes and male sex hormones of the individual.

http://www.nlm.nih.gov/medlineplus/ency/imagepages/19647.htm

 

NAILS

Nail abnormalities

http://www.nlm.nih.gov/medlineplus/ency/article/003247.htm

Nail abnormalities are problems with the color, shape, texture, or thickness of the fingernails or toenails.

Just like the skin, the fingernails tell a lot about your health.

                  Beau’s lines are depressions across the fingernail. These lines can occur after illness, injury to the nail, and when you are malnourished.

                  Brittle nails are often a normal result of aging. However, they also may be due to certain diseases and conditions.

Brittle nails

 

Like the skin, the fingernails are a reflection of a person’s state of health. Low levels of zinc and iron as well as thyroid problems can cause brittle nails. However, brittle nails are often a normal result of aging.

http://www.nlm.nih.gov/medlineplus/ency/imagepages/9136.htm

                  Koilonychia is an abnormal shape of the fingernail. The nail has raised ridges and is thin and curved inward. This disorder is associated with iron deficiency anemia.

                  Leukonychia is white streaks or spots on the nails.

                  Pitting is the presence of small depressions on the nail surface. Sometimes the nail is also crumbling. The nail can become loose and sometimes falls off.

                  Ridges are tiny, raised lines that develop across or up and down the nail.

CAUSES

Injury:

                  Crushing the base of the nail or the nail bed may cause a permanent deformity.

                  Chronic picking or rubbing of the skin behind the nail can cause a washboard nail.

                  Long-term exposure to moisture or nail polish can cause nails to peel and become brittle.

Infection:

                  Fungus or yeast cause changes in the color, texture, and shape of the nails.

       Bacterial infection may cause a change iail color or painful areas of infection under the nail or in the surrounding skin. Severe infections may cause nail loss.

       Viral warts may cause a change in the shape of the nail or ingrown skin under the nail.

       Certain infections (especially of the heart valve) may cause red streaks in the nail bed ( splinter hemorrhages).

Diseases:

       Disorders that affect the amount of oxygen in the blood (such as abnormal heart anatomy and lung diseases including cancer or infection) may cause clubbing.

Clubbed fingers

 

Clubbed fingers is a symptom of disease, often of the heart or lungs which cause chronically low blood levels of oxygen. Diseases which cause malabsorption, such as cystic fibrosis or celiac disease can also cause clubbing.

 

http://www.nlm.nih.gov/medlineplus/ency/imagepages/18127.htm

 

       Kidney disease can cause a build-up of nitrogen waste products in the blood, which can damage nails.

       Liver disease can damage nails.

       Thyroid diseases such as hyperthyroidism or hypothyroidism may cause brittle nails or splitting of the nail bed from the nail plate (onycholysis).

       Severe illness or surgery may cause horizontal depressions in the nails (Beau’s lines).

       Psoriasis may cause pitting, splitting of the nail plate from the nail bed, and chronic destruction of the nail plate (nail dystrophy).

       Other conditions that can affect the appearance of the nails include systemic amyloidosis, malnutrition, vitamin deficiency, and lichen planus.

       Skin cancers near the nail and fingertip can distort the nail. Subungal melanoma is a potentially deadly cancer that will normally appear as a dark streak down the length of the nail.

       Darkening of the cuticle associated with a pigmented streak may a sign of an aggressive melanoma.

Prevention

                  Do not bite, pick, or tear at your nails (in severe cases, some people may need psychological help or encouragement to stop these behaviors).

       Keep hangnails clipped.

       Wear shoes that don’t squeeze the toes together, and always cut the nails straight across along the top.

       To prevent brittle nails, keep the nails short and avoid nail polish. Use an emollient (skin softening) cream after washing or bathing.

Alternative Names

Beau’s lines; Fingernail abnormalities; Spooails; Onycholysis; Leukonychia; Koilonychia; Brittle nails

Aging changes iails

http://www.nlm.nih.gov/medlineplus/ency/imagepages/8671.htm

 

 

The nails change with aging, growing more slowly, and becoming dull and brittle. The color may change from translucent to yellowed and opaque. Nails, especially toenails, may become hard and thick and ingrown toenails may be more common. The tips of the fingernails may fragment. Sometimes, lengthwise (longitudinal) ridges will develop in the fingernails and toenails. This can be a normal aging change. However, some nail changes can be caused by infections, nutritional problems, trauma, and other problems.

 

SKIN LESIONS

http://www.youtube.com/watch?v=Ap5fJ-A1bIY

PRIMARY MORPHOLOGY

Macules are flat, nonpalpable lesions usually < 10 mm in diameter. Macules represent a change in color and are not raised or depressed compared to the skin surface. A patch is a large macule. Examples include freckles, flat moles, tattoos, port-wine stains, and the rashes of rickettsial infections, rubella, measles, and some allergic drug eruptions.

                                                    

 

 

 

Papules are elevated lesions usually < 10 mm in diameter that can be felt or palpated. Examples include nevi, warts, lichen planus, insect bites, seborrheic and actinic keratoses, some lesions of acne, and skin cancers. The term “maculopapular” is often loosely and improperly used to describe many red skin rashes; because this term is nonspecific and easily misused, it should be avoided.

 

 

 

                                                           

 

 

 

Plaques are palpable lesions > 10 mm in diameter that are elevated or depressed compared to the skin surface. Plaques may be flat topped or rounded. Lesions of psoriasis and granuloma annulare commonly form plaques.

 

 

 

                                                                      

 

 

 

Nodules are firm papules or lesions that extend into the dermis or subcutaneous tissue. Examples include cysts, lipomas, and fibromas.

 

 

 

                                                             

 

 

 

Vesicles are small, clear, fluid-filled blisters < 10 mm in diameter. Vesicles are characteristic of herpes infections, acute allergic contact dermatitis, and some autoimmune blistering disorders (eg, dermatitis herpetiformis).

 

 

 

                                                                

 

 

 

Bullae are clear fluid-filled blisters > 10 mm in diameter. These may be caused by burns, bites, irritant or allergic contact dermatitis, and drug reactions. Classic autoimmune bullous diseases include pemphigus vulgaris and bullous pemphigoid. Bullae also may occur in inherited disorders of skin fragility.

 

 

 

                                                                      

 

 

 

Pustules are vesicles that contain pus. Pustules are common in bacterial infections, folliculitis, and may arise in some inflammatory diseases including pustular

 

 

 

                                                              

 

 

Wheal (hive) – a firm edematous plaque resulting from infiltration of the dermis with fluid; wheals are transient and may last only a few hours

 

 

                                         

 

 

SECONDARY MORPHOLOGY

 

Erosion – focal loss of epidermis; erosions do not penetrate below the dermoepidermal junction and therefore heal without scarring.

 

 

 

 

                                              

 

Fissure – a linear loss of epidermis and dermis with sharply defined, nearly vertical walls.

 

                                              

 

 

Atrophy – a depression in the skin resulting from thinning of the epidermis or dermis.

 

                                                     

 

Scar – an abnormal formation of connective tissue implying dermal damage; after injury or surgery scars are initially thick and pink but with time

become white and atrophic.

 

                                                          

 

 

  Excoriation– an injury to a surface of the body caused by trauma, such as scratching, abrasion, or a chemical or thermal burn.

 

                                                         

 

Crust – a collection of dried serum and cellular debris; a scab.

 

 

                                                    

 

 

 

 

 

Scales – ecess dead epidermal cells that are produced by abnormal keratinization and shedding The may be fine, as in pityriasis; white and silvery, as in psoriasis; or large and fish-like, as in ichthyosis.

 

 

 

 

 

                                                 

 

Lichenification – an area of thickened epidermis induced by scratching; the skin lines are accentuated so that the surface looks like a washboard

 

                                                  

 

 

Burrow – An arrow, elevated, tortuous channel produced by a parasite.

   

 

                                            

                        

 

 

 

Petechia   – Lat. petecchia (plural = petechiae) = spot on skin) is a small (< 3 mm) red or purple bruise. It does not blanch on applying the pressure.

 

 

PSORIASIS

 

1. http://www.medicinenet.com/psoriasis/article.htm#what_is_psoriasis

2. http://www.youtube.com/watch?v=WRS9UJFKHMk

 

Psoriasis is a chronic disorder of the skin characterized by reddish, scaly patches of inflammation, most commonly affecting the elbows, knees, scalp, and/or groin. Psoriasis can be mild or severe. When it is severe, it can adversely affect functions of daily living including work and social activities.

Psoriasis has been reported to affect approximately 2% of the world’s population.

The treatment of psoriasis depends on its severity and location. Treatments range from local (cortisone cream application, emollients, coal tar, anthralin preparations, and sun exposure) to systemic (internal medications, including methotrexateand cyclosporine).

Psoriasis facts

• Psoriasis is a chronic inflammatory skin disease.
• Psoriasis has no known cause.
• The tendency toward developing psoriasis is inherited in genes.
• Psoriasis is not contagious.
• Psoriasis gets better and worse spontaneously and can have periodic remissions (clear skin).
• Psoriasis is controllable with medication.
• Psoriasis is currently not curable.
• There are many promising therapies, including newer biologic drugs.
• Future research for psoriasis is promising.

What is psoriasis?

Psoriasis is a noncontagious skin condition that produces red, dry plaques of thickened skin. The dry flakes and skin scales are thought to result from the rapid proliferation of skin cells that is triggered by abnormal lymphocytes from the blood . Psoriasis commonly affects the skin of the elbows, knees, and scalp.

Some people have such mild psoriasis (small, faint dry skin patches) that they may not even suspect that they have a medical skin condition. Others have very severe psoriasis where virtually their entire body is fully covered with thick, red, scaly skin.

Psoriasis is considered a non-curable, long-term (chronic) skin condition. It has a variable course, periodically improving and worsening. It is not unusual for psoriasis to spontaneously clear for years and stay in remission. Many people note a worsening of their symptoms in the colder winter months.

Psoriasis is seen worldwide, in all races, and both sexes. Although psoriasis can be seen in people of any age, from babies to seniors, most commonly patients are first diagnosed in their early adult years.

Patients with more severe psoriasis may have social embarrassment, job stress, emotional distress, and other personal issues because of the appearance of their skin.

 

 

Pathophysiology

Psoriasis is a complex, multifactorial disease that appears to be influenced by genetic and immune-mediated components. This is supported by the successful treatment of psoriasis with immune-mediating, biologic medications.

The pathogenesis of this disease is not completely understood. Multiple theories exist regarding triggers of the disease process including an infectious episode, traumatic insult, and stressful life event. In many patients, no obvious trigger exists at all. However, once triggered, there appears to be substantial leukocyte recruitment to the dermis and epidermis resulting in the characteristic psoriatic plaques.

Specifically, the epidermis is infiltrated by a large number of activated T cells, which appear to be capable of inducing keratinocyte proliferation. This is supported by histological examination and immuno-histochemical staining of psoriatic plaques revealing large populations of T cells within the psoriasis lesions. One report calculated that a patient with 20% body surface area affected with psoriasis lesions has around 8 billion blood circulating T cells compared with approximately 20 billion T cells located in the dermis and epidermis of psoriasis plaques.

Ultimately, a ramped-up, deregulated inflammatory process ensues with a large production of various cytokines (eg, tumor necrosis factor-α [TNF-α], interferon-gamma, interleukin-12). Many of the clinical features of psoriasis are explained by the large production of such mediators. Interestingly, elevated levels of TNF-α specifically are found to correlate with flares of psoriasis.

One study adds further support that T-cell hyperactivity and the resulting proinflammatory mediators (in this case IL-17/23) play a major role in the pathogenesis of psoriasis.

Key findings in the affected skin of patients with psoriasis include vascular engorgement due to superficial blood vessel dilation and altered epidermal cell cycle. Epidermal hyperplasia leads to an accelerated cell turnover rate (from 23 d to 3-5 d), leading to improper cell maturation.

Cells that normally lose their nuclei in the stratum granulosum retain their nuclei, a condition known as parakeratosis. In addition to parakeratosis, affected epidermal cells fail to release adequate levels of lipids, which normally cement adhesions of corneocytes. Subsequently, poorly adherent stratum corneum is formed leading to the flaking, scaly presentation of psoriasis lesions, the surface of which often resembles silver scales.

Conjunctival impression cytology demonstrated a higher incidence of squamous metaplasia, neutrophil clumping, and nuclear chromatin changes in patients with psoriasis.

 

 

 

 

Etiology

Psoriasis involves hyperproliferation of the keratinocytes in the epidermis, with an increase in the epidermal cell turnover rate. (See Pathophysiology.) The cause of the loss of control of keratinocyte turnover is unknown. However, environmental, genetic, and immunologic factors appear to play a role.

Environmental factors

Many factors besides stress have also been observed to trigger exacerbations, including cold, trauma, infections (eg, streptococcal, staphylococcal, human immunodeficiency virus), alcohol, and drugs (eg, iodides, steroid withdrawal, aspirin, lithium, beta-blockers, botulinum A, antimalarials). One study showed an increased incidence of psoriasis in patients with chronic gingivitis. Satisfactory treatment of the gingivitis led to improved control of the psoriasis but did not influence long term incidence, highlighting the multifactor and genetic influences of this disease.

Hot weather, sunlight, and pregnancy may be beneficial, although the latter is not universal. Perceived stress can exacerbate psoriasis. Some authors suggest that psoriasis is a stress-related disease and offer findings of increased concentrations of neurotransmitters in psoriatic plaques.

Genetic factors

Patients with psoriasis have a genetic predisposition for the disease. The gene locus is determined. The triggering event may be unknown in most cases, but it is likely immunologic. The first lesion commonly appears after an upper respiratory infection.

Psoriasis is associated with certain human leukocyte antigen (HLA) alleles, particularly human leukocyte antigen Cw6 (HLA-Cw6). In some families, psoriasis is an autosomal dominant trait.

A multicenter meta-analysis confirmed that deletion of 2 late cornified envelope (LCE) genes, LCE3C and LCE3B, is a common genetic factor for susceptibility to psoriasis in different populations.^[9]

Obesity is another factor associated with psoriasis. Whether it is related to weight alone, genetic predisposition to obesity, or a combination of the 2 is not certain. Onset or worsening of psoriasis with weight gain and/or improvement with weight loss is observed.

Immunologic factors

Evidence suggests that psoriasis is an autoimmune disease. Studies show high levels of dermal and circulating TNF-α. Treatment with TNF-α inhibitors is often successful. Psoriatic lesions are associated with increased activity of T cells in the underlying skin.

Psoriasis is related to excess T-cell activity. Experimental models can be induced by stimulation with streptococcal super antigen, which cross-reacts with dermal collagen. This small peptide has been shown to cause increased activity among T cells in patients with psoriasis but not in control groups. Some of the newer drugs used to treat severe psoriasis directly modify the function of lymphocytes.

Also of significance is that 2.5% of those with HIV develop worsening psoriasis with decreasing CD4 counts. This is paradoxical; in that the leading hypothesis on the pathogenesis of psoriasis supports T-cell hyperactivity and treatments geared to reduce T-cell counts help reduce psoriasis severity. This finding is possibly explained by a decrease in CD4 T cells, which leads to overactivity of CD8 T cells, which drives the worsening psoriasis. The HIV genome may drive keratinocyte proliferation directly.

HIV associated with opportunistic infections may see increased frequency of superantigen exposure leading to similar cascades as above mentioned.

Guttate psoriasis often appears following certain immunologically active events, such as streptococcal pharyngitis, cessation of steroid therapy, and use of antimalarial drugs.

 

Symptoms of psoriasis may include the following:

• Worsening of a long-term erythematous scaly area
• Sudden onset of many small areas of scaly redness
• Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma
• Family history of similar skin condition
• Pain (especially in erythrodermic psoriasis and in some cases of traumatized plaques or in the joints affected by psoriatic arthritis)
• Pruritus (especially in eruptive, guttate psoriasis)
• Afebrile (except in pustular or erythrodermic psoriasis in which the patient may have high fever)
• Dystrophic nails
• Long-term rash with recent presentation of joint pain
• Joint pain without any visible skin findings

The skin almost always is affected before the eyes. Ocular findings occur in approximately 10% of patients. The most common ocular symptoms are redness and tearing due to conjunctivitis or blepharitis.

The non-ocular symptoms are related to rash and psoriatic arthritis. The rash can be uncomfortable or even painful. Psoriatic arthritis can cause stiffness, pain, throbbing, swelling, or tenderness of the joints. The distal joints, such as the fingers, toes, wrists, knees, and ankles, are most often affected.

 

 

 

 

 

 

 

PSORIASIS VULGARIS

 

Common 0.5-3% of population; single or multiple plaques; age 15-40 (mean age 28yrs); extensor surfaces, back, sacrum, hairline, knees, elbows.

 

 

 

 

 

 

GUTTATE PSORIASIS

 

Multiple small lesions post infection; often spontaneously resolve in 2-3/12; respond poorly to topical agents; differential with pityriasis; (scale confined to edge of esions)

 

 

 

 

 

FLEXURAL PSORIASIS

 

Typical eczema distribution; often associated with psoriasis in the hair; differential with intertrigo.

 

 

 

 

 

 

 

ERYTHRODERMIC PSORIASIS

 

Results when 90% of body affected; precipitated by withdraw of steroids; Consequences: infection; dehydration; high out-put cardiac failure

 

 

 

 

 

 

PALMOPLANTAR  PSORIASIS

 

Vesicles on soles of hands & feet; painful rather than itchy; chronic condition

 

 

 

 

 

 

PSORIATIC  ARTHRITIS

 

5 main clinical subtypes:

 

    symmetrical polyarthritis;

    asymmetrical oligoarthritis (large joint);

    spondylitic (sero-negative);

    distal-interphalangeal (nail);

    severe mutilans.

 

 

 

 

 

 

NAIL  PSORIASIS

 

50% of patients with skin involvement; 90% of psoriatic arthritis; pitting; onycholysis of distal nail bed; subungal hyperkeratosis

 

 

 

        

 

 

Complications

Complications of psoriasis may include the following:

• Secondary infections
• Possible increased risk of lymphoma
• Possible increased risk of cardiovascular and ischemic heart disease
• Psoriatic arthritis
• Mitral valve prolapse

Lab Studies

Laboratory studies and findings for patients with psoriasis may include the following:

• Test result for rheumatoid factor (RF) is negative.
• Erythrocyte sedimentation rate (ESR) is usually normal (except in pustular and erythrodermic psoriasis).
• Uric acid level may be elevated in psoriasis (especially in pustular psoriasis), causing confusion with gout in psoriatic arthritis.
• Fluid from pustules is sterile with neutrophilic infiltrate.
• Perform fungal studies. (This is especially important in cases of hand and foot psoriasis that seem to be worsening with the use of topical steroids.)

If starting systemic therapies such as immunological inhibitors, consider obtaining baseline laboratory studies (ie, complete blood count [CBC], blood urea nitrogen [BUN]/creatinine, liver function tests [LFTs], hepatitis panel, tuberculosis [TB] screening).

 

Treatment

http://www.oprah.com/health/Dr-Oz-Discusses-Possible-Treatments-for-Psoriasis-Video

Treatment of Skin Lesions

Patients with guttate, erythrodermic, or pustular psoriasis may present to the emergency department. In each of these cases, restoration of the barrier function of the skin is of prime concern. This can be performed with cleaning and bandaging.

Plaque and scalp lesions are frequently encountered in patients seeking care for other problems, and initial treatment of the lesions should be offered.

The simplest treatment of psoriasis is daily sun exposure, sea bathing, topical moisturizers, and relaxation. Moisturizers, such as petrolatum jelly, are helpful. Daily application of moisturizing cream to the affected area is inexpensive and successful adjunct to psoriasis treatment. Application immediately after a bath or shower helps to minimize itching and tenderness. Section 3 (2009) of the AAD guideline discusses topical agents and recommends their use adjunctively but not as monotherapy if the disease is extensive or recalcitrant.

Nonprescription tar preparations are available and have therapeutic success, especially when used in conjunction with topical corticosteroids; the newer foams are less messy preparations than some of the older ones. Anthralin, topical corticosteroids, salicylic acid, phenolic compounds, and calcipotriene (a vitamin D analog) also may be effective. Systemic corticosteroids are generally ineffective, and they can significantly exacerbate the disease upon withdrawal. Combination therapy with a vitamin D analog (calcipotriol and calcipotriene) or a retinoid such as tazarotene and a topical corticosteroid is more effective than therapy with either agent alone. Oatmeal baths may be helpful.

Solar or ultraviolet radiation may be helpful. Various ultraviolet light treatments are used—most commonly, psoralen-ultraviolet A (PUVA) therapy. Among phototherapy options, Section 5 (2010) of the AAD guideline gives the highest recommendation to oral PUVA or a combination of PUVA and topical agents.Psoralen is a photosensitizer that is ingested prior to light exposure. PUVA treatment results in conjunctival hyperemia and dry eye, particularly if sun protection is not used. With proper eye protection, there does not appear to be a risk of cataract. Psoralens for either topical (bath) or systemic use may occasionally be difficult to obtain because of stocking shortages.

According to the AAD guidelines, PUVA can result in long remissions, but long-term use of PUVA in Caucasians may increase the risk of squamous cell carcinoma (SCC) and possibly malignant melanoma. A prospective study of 1,380 patients found a strong correlation betweeumber of PUVA treatments and risk of developing one or more SCC. According to the study, exposure to more than 350 PUVA treatments greatly increases the risk of SCC.

Narrow-band ultraviolet B (UVB) therapy has always been accepted as a good treatment modality of psoriasis and the AAD guidelines recommend it over broad-band (UVA), although both are less effective than PUVA. As with PUVA, the guidelines also recommend treatment with combinations of UVB and topic or systemic agents.However, a study by Keaney and Kirsner gives objective reasoning for the benefit of narrow-band UV therapy by showing decreases in T cells, dendritic cells, and interleukins within responsive psoriatic plaques compared with plaques that did not respond to therapy. Gutate psoriasis may prove especially responsive to phototherapy. Therapies such as UVB and PUVA have low efficacy for the treatment of nail psoriasis because of the blockage of the UV radiation by the intervening nail plate.

Patients with psoriasis should avoid injury to skin, including sunburn and other physical trauma, as these areas may develop psoriasis. The appearance of psoriatic lesions in previously uninvolved areas after irritation or trauma is known as the Köbner phenomenon. Patients with psoriasis should also avoid drugs known to worsen the problem (eg, chloroquine, beta-blockers, aspirin or other NSAIDs).

In severe cases, retinoids (acitretin), methotrexate, cyclosporine, 6-thioguanine, azathioprine, a biologic, or hydroxyurea may be used. Retinoids have been reported to cause dry eye, blepharitis, corneal opacities, cataracts, and decreased night vision. All of these may be associated with gastrointestinal intolerance, hepatic damage (acitretin, 6-thioguanine, azathioprine, methotrexate), marrow suppression (6-thioguanine, methotrexate, azathioprine, hydroxyurea) or renal damage (cyclosporine). The use of these systemic medications, with appropriate safety considerations, is supported by Section 4 (2009) of the AAD guidelines.

In addition, systemic retinoids and hydroxyurea may interfere with proper wound healing and elective procedures, including dental surgery, which are best performed before the start of the medications. Acitretin appears more effective than isotretinoin in psoriasis and does not require enrollment in the IPledge program. On the other hand, there is a 3-year pregnancy prohibition after its use, and many will not use this medication in any patient capable of ever becoming pregnant. Combination therapies, such as a biologic plus another immunosuppressive medication, have been used with good effect but data detailing the safest way to do this are scant. All of the systemic medications except acitretin may increase the risk of infection.

Abruptly stopping steroid therapy in psoriasis or adding known irritant drugs can result in the sudden worsening of psoriasis or appearance of a new form. Commonly, this new form is guttate psoriasis, which is much more severe and cosmetically problematic than the preexisting plaque type. It may also present with a more threatening pustular or erythrodermic psoriatic flare.

The use of biologic agents (proteins with pharmacologic activity) is discussed in Section 1 (2008) and reviewed, with updated safety information, in Section 6 of the AAD guidelines. The AAD recommends a set of baseline laboratory studies before starting treatment with a biologic agent to ensure any underlying conditions or risk factors are understood.

Many of the therapies for psoriasis manipulate the function of the immune system and expose the patient to risk of severe infections while blunting the body’s response. In these patients, findings suggestive of minor infections must be taken seriously, and the risk versus the benefit of continuing the drug in the face of the infection must be weighed.

 

Treatment of Ocular Complications

Keratoconjunctivitis sicca can be treated with ocular lubricants and punctal occlusion. Trichiasis and cicatricial ectropion usually require surgical treatment. Conjunctival, corneal, and anterior chamber inflammation can be treated with topical corticosteroids. Nonsteroidal anti-inflammatory agents or oral corticosteroids are occasionally necessary. Whether systemic immunosuppression is effective for ocular disease is not clear.

Corneal melting, inflammation, and vascularization can be difficult to treat. A bandage contact lens may retard the melting. Topical corticosteroids can control the infiltration and delay the vascularization. In some cases, progression can occur in spite of these treatments and can lead to the need for lamellar or penetrating keratoplasty.

 

References

 1. Pietrzak AT, Zalewska A, Chodorowska G, Krasowska D, Michalak-Stoma A, Nockowski P, et al. Cytokines and anticytokines in psoriasis. Clin Chim Acta. Aug 2008;394(1-2):7-21. [Medline].

2. Keaney TC, Kirsner RS. New insights into the mechanism of narrow-band UVB therapy for psoriasis. J Invest Dermatol. Nov 2010;130(11):2534. [Medline].

3. Kurd SK, Troxel AB, Crits-Christoph P, Gelfand JM. The risk of depression, anxiety, and suicidality in patients with psoriasis: a population-based cohort study. Arch Dermatol. Aug 2010;146(8):891-5. [Medline]. [Full Text].

4. Riveira-Munoz E, He SM, Escaramís G, et al. Meta-Analysis Confirms the LCE3C_LCE3B Deletion as a Risk Factor for Psoriasis in Several Ethnic Groups and Finds Interaction with HLA-Cw6. J Invest Dermatol. May 2011;131(5):1105-9. [Medline].

5. Patel RV, Shelling ML, Prodanovich S, Federman DG, Kirsner RS. Psoriasis and vascular disease-risk factors and outcomes: a systematic review of the literature. J Gen Intern Med. Sep 2011;26(9):1036-49. [Medline].

6. Stern DK, Creasey AA, Quijije J, Lebwohl MG. UV-A and UV-B Penetration of Normal Human Cadaveric Fingernail Plate. Arch Dermatol. Apr 2011;147(4):439-41. [Medline].

7. Keller JJ, Lin HC. The Effects of Chronic Periodontitis and Its Treatment on the Subsequent Risk of Psoriasis. Br J Dermatol. Jul 3 2012;[Medline].  

8. Li WQ, Han JL, Manson JE, Rimm EB, Rexrode KM, Curhan GC, et al. Psoriasis and risk of nonfatal cardiovascular disease in U.S. women: a cohort study. Br J Dermatol. Apr 2012;166(4):811-8. [Medline].

9. Oostveen AM, de Jager ME, van de Kerkhof PC, Donders AR, de Jong EM, Seyger MM. The influence of treatments in daily clinical practice on the Children’s Dermatology Life Quality Index in juvenile psoriasis: a longitudinal study from the Child-CAPTURE patient registry. Br J Dermatol. May 23 2012;[Medline].

10. Lucka TC, Pathirana D, Sammain A, Bachmann F, Rosumeck S, Erdmann R, et al. Efficacy of systemic therapies for moderate-to-severe psoriasis: a systematic review and meta-analysis of long-term treatment. J Eur Acad Dermatol Venereol. Mar 9 2012;[Medline].

11. Stern RS. The risk of squamous cell and basal cell cancer associated with psoralen and ultraviolet A therapy: A 30-year prospective study. J Am Acad Dermatol. Jan 18 2012;[Medline].

 

LICHEN PLANUS

 

1. http://emedicine.medscape.com/article/1123213-medication#5

2. http://freevideolectures.com/Course/118/Oral-Pathology/14

3. http://www.youtube.com/watch?v=iioBR_XCpJo

 

 

Lichen planus (LP) is a pruritic eruption commonly associated with hepatitis C. Lesions are characteristically papular, purple (violaceous color), polygonal, and peripherally located (eg. on the distal extremities). LP may also affect the genitalia or mucous membranes. It is most likely an immunologically mediated reaction, though the pathophysiology in unclear. See Oral Lichen Planus for more information on this variant of lichen planus.

Pathophysiology

Lichen planus is a cell-mediated immune response of unknown origin. It may be found with other diseases of altered immunity; these conditions include ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis.

An association is noted between lichen planus and hepatitis C virus infection chronic active hepatitis, and primary biliary cirrhosis.In one meta-analysis, 16% of patients with LP had hepatitis C infection.This association has been shown to exist in all regions of the world, including North America.  A workup for hepatitis C should be considered in patients with widespread or unusual presentations of lichen planus. Onset or exacerbation of lichen planus has also been linked to stressful events.

Most cases of lichen planus (LP) are insidious.

• Lesions usually develop on flexural surfaces of the limbs, such as the wrists (see the image below). After a week or more, a generalized eruption develops with maximal spreading within 2-16 weeks.

 

• 

 

• Lichen planus on the flexor part of the wrist.
• Pruritus is common in lichen planus but varies in severity depending on the type of lesion and the extent of involvement. Hypertrophic lesions are extremely pruritic.
• Oral lesions may be asymptomatic or have a burning sensation, or they may even be painful if erosions are present.
• In more than 50% of patients with cutaneous disease, the lesions resolve within 6 months, and 85% of cases subside within 18 months. On the other hand, oral lichen planus had been reported to have a mean duration of 5 years. Large, annular, hypertrophic lesions and mucous membrane involvement are more likely to become chronic.

  In addition to the cutaneous eruption, lichen planus (LP) can involve the mucous membranes, the genitalia, the nails, and the scalp. The clinical presentation of lichen planus has several forms: actinic (in sun-exposed areas), annular, atrophic, erosive, follicular, hypertrophic, linear, pigmented, and vesicular/bullous. The papules are violaceous, shiny, and polygonal; varying in size from 1 mm to greater than 1 cm in diameter (see the image below). They can be discrete or arranged in groups of lines or circles. Characteristic fine, white lines, called Wickham stria, are often found on the papules (see the image below).

 

 

 

Lichen planus shows Wickham striae (white, fine, reticular scales).

Mucous membrane involvement is common and may be found in patients who do not have skin involvement. Lesions are most commonly found on the tongue and the buccal mucosa; they are characterized by white or gray streaks forming a linear or reticular pattern on a violaceous background (see the image below). Oral lesions are classified as reticular, plaquelike, atrophic, papular, erosive, and bullous. Ulcerated oral lesions may have a higher incidence of malignant transformation in men, but this observation may be confounded by other factors, such as smoking and chewing tobacco. Lesions may also be found on the conjunctivae, the larynx, the esophagus, the tonsils, the bladder, the vulva, and the vaginal vault; throughout the gastrointestinal tract; and around the anus.

    

 

 

Lichen planus on the oral mucosa with ulceration in the center of the lesion appears with whitish papules and plaques in the periphery.

Genital involvement is common in lichen planus. Typically, men develop annular lesions on the glans. Wickham striae may also be observed on these lesions. Vulvar involvement can range from reticulate papules to severe erosions. Dyspareunia, a burning sensation, and pruritus are common in women. Vulvar and urethral stenosis may be a complication. It is estimated that more than 50% of women with oral lichen planus also had undiagnosed vulvar lichen planus. (Also see the clinical guideline summa

Nail findings are found in roughly 10% of patients with lichen planus. Thes findings are most commonly longitudinal grooving and ridging. Hyperpigmentation, subungual hyperkeratosis, onycholysis, and longitudinal melanonychia can result from lichen planus. Rarely, inflammation may result in permanent destruction of the nail matrix with subsequent pterygium formation. Lichen planus has been linked to childhood idiopathic nail atrophy and may overlap with twenty-nail dystrophy of childhood.

Cutaneous lesions may be accompanied by follicular and perifollicular lesions on the scalp, which may be violaceous, scaly, and pruritic papules. These lesions can progress to atrophic cicatricial alopecia, known as lichen planopilaris. This can appear even many weeks after the skin lesions have disappeared. Pseudopelade can be a final endpoint.

Variations in lichen planus include the following:

       Hypertrophic lichen planus: These extremely pruritic lesions are most often found on the extensor surfaces of the lower extremities, especially around the ankles. Hypertrophic lesions are often chronic; residual pigmentation and scarring can occur when the lesions eventually clear.

       Atrophic lichen planus: Atrophic lichen planus is characterized by a few lesions, which are often the resolution of annular or hypertrophic lesions.

       Erosive/ulcerative lichen planus: These lesions are found on the mucosal surfaces and evolve from sites of previous lichen planus involvement.

       Follicular lichen planus (aka Lichen planopilaris): This is characterized by keratotic papules that may coalesce into plaques. This condition is more common in women than in men, and ungual and erosive mucosal involvement is more likely to be present. A scarring alopecia may result.

       Annular lichen planus: Lichen planus papules that are purely annular are rare. Annular lesions with an atrophic center can be found on the buccal mucosa and the male genitalia.

       Linear lichen planus: Isolated linear lesions may form a zosteriform lesion, or they may develop as a Köebner effect.

       Vesicular and bullous lichen planus: Most commonly, these lesions develop on the lower limbs or in the mouth from preexisting lichen planus lesions. A rare condition, lichen planus pemphigoides, is a combination of both lichen planus and bullous pemphigoid.

       Actinic lichen planus: Subtropic or actinic lichen planus occurs in regions, such as Africa, the Middle East, and India. This mildly pruritic eruption usually spares the nails, the scalp, the mucous membranes, and covered areas. Lesions are characterized by nummular patches with a hypopigmented zone surrounding a hyperpigmented center.

       Lichen planus pigmentosus: This is a rare variant of lichen planus but can be more common in persons with darker-pigmented skin, such as Latinos or Asians. It usually appears on face and neck. Some believe it is similar to or the same as erythema dyschromicum perstans (ie, ashy dermatosis).

       Lichen planus pemphigoides: This is a rare form of lichen planus. Blisters subsequently develop on lichen planus lesions. Clinically, histopathologically and immunopathologically, it has features of lichen planus and bullous pemphigoid, it but carries a better prognosis than pemphigoid.

 

References

 

1. Pavlotsky F, Nathansohn N, Kriger G, Shpiro D, Trau H. Ultraviolet-B treatment for cutaneous lichen planus: our experience with 50 patients. Photodermatol Photoimmunol Photomed. Apr 2008;24(2):83-6. [Medline].

2. [Guideline] American College of Obstetricians and Gynecologists. Diagnosis and management of vulvar skin disorders. National Guideline Clearinghouse. May 2008.

3. Raslan HM, Ezzat WM, Abd El Hamid MF, Emam H, Amre KS. Skin manifestations of chronic hepatitis C virus infection in Cairo, Egypt. East Mediterr Health J. May-Jun 2009;15(3):692-700. [Medline].

4. [Best Evidence] Shengyuan L, Songpo Y, Wen W, Wenjing T, Haitao Z, Binyou W. Hepatitis C virus and lichen planus: a reciprocal association determined by a meta–analysis. Arch Dermatol. Sep 2009;145(9):1040-7. [Medline].

5. Bigby M. The relationship between lichen planus and hepatitis C clarified. Arch Dermatol. Sep 2009;145(9):1048-50. [Medline].

6. Rasi A, Behzadi AH, Davoudi S, Rafizadeh P, Honarbakhsh Y, Mehran M, et al. Efficacy of oral metronidazole in treatment of cutaneous and mucosal lichen planus. J Drugs Dermatol. Oct 2010;9(10):1186-90. [Medline].

7. Arias-Santiago S, Buendia-Eisman A, Aneiros-Fernandez J, et al. Cardiovascular risk factors in patients with lichen planus. Am J Med. Jun 2011;124(6):543-8. [Medline].

 

ORAL  LICHEN  PLANUS

1. http://emedicine.medscape.com/article/1078327-followup#a2649

2. http://www.youtube.com/watch?v=VRTOA8KTLvE

Background

Oral lichen planus (OLP) is a chronic inflammatory disease that causes bilateral white striations, papules, or plaques on the buccal mucosa, tongue, and gingivae. Erythema, erosions, and blisters may or may not be present. Note the images below.

 

Pathophysiology

Current data suggest that oral lichen planus is a T-cell–mediated autoimmune disease in which autocytotoxic CD8⁺ T cells trigger apoptosis of oral epithelial cells.

The dense sub-epithelial mononuclear infiltrate in oral lichen planus is composed of T cells and macrophages, and there are increased numbers of intra-epithelial T cells. Most T cells in the epithelium and adjacent to the damaged basal keratinocytes are activated CD8⁺ lymphocytes. Therefore, early in the formation of oral lichen planus lesions, CD8⁺ T cells may recognize an antigen associated with the major histocompatibility complex (MHC) class I on keratinocytes. After antigen recognition and activation, CD8⁺ cytotoxic T cells may trigger keratinocyte apoptosis. Activated CD8⁺ T cells (and possibly keratinocytes) may release cytokines that attract additional lymphocytes into the developing lesion.

Oral lichen planus lesions contain increased levels of the cytokine tumor necrosis factor (TNF)–alpha.Basal keratinocytes and T cells in the subepithelial infiltrate express TNF in situ.Keratinocytes and lymphocytes in cutaneous lichen planus express elevated levels of the p55 TNF receptor, TNF-RI.T cells in oral lichen planus contain mRNA for TNF and secrete TNF in vitro.Serum and salivary TNF levels are elevated in oral lichen planus patients.TNF polymorphisms have been identified in patients with oral lichen planus, and they may contribute to the development of additional cutaneous lesions.Oral lichen planus has been treated successfully with thalidomide, while thalidomide is known to suppress TNF production.Together, these data implicate TNF in the pathogenesis of oral lichen planus.

The lichen planus antigen is unknown, although it may be a self-peptide (or altered self-peptide), in which case lichen planus would be a true autoimmune disease. The role of autoimmunity in the pathogenesis is supported by many autoimmune features of oral lichen planus, including its chronicity, onset in adults, predilection for females, association with other autoimmune diseases, occasional tissue-type associations, depressed immune suppressor activity in patients with oral lichen planus, and the presence of autocytotoxic T-cell clones in lichen planus lesions. The expression or unmasking of the lichen planus antigen may be induced by drugs (lichenoid drug reaction), contact allergens in dental restorative materials or toothpastes (contact hypersensitivity reaction), mechanical trauma (Koebner phenomenon), viral infection, or other unidentified agents.

Clinical Presentation

Lichen planus may arise in patients with other immunologically mediated disorders, including alopecia areata, dermatomyositis, lichen sclerosis et atrophicus, morphea, myasthenia gravis, primary biliary cirrhosis, ulcerative colitis, and vitiligo.

In many patients, the onset of oral lichen planus is insidious, and patients are unaware of their oral condition. In such instances, the referring medical or dental practitioner identifies the clinical changes in the oral mucosa.

Some patients report a roughness of the lining of the mouth, sensitivity of the oral mucosa to hot or spicy foods or oral hygiene products, painful oral mucosa, sore gums, red or white patches on the oral mucosa, red gums, or oral ulcerations.

Approximately two thirds of patients with oral lichen planus report oral discomfort, especially in association with atrophic and erosive lesions. Erythematous and erosive lesions are often sensitive or painful. Symptoms vary from mucosal sensitivity to continuous debilitating pain.

Oral mucosal lichenoid lesions may occur after the administration of systemic drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonylureas, antimalarials, beta-blockers, and some angiotensin-converting enzyme (ACE) inhibitors. The period between the commencement of the drug therapy and the clinical appearance of oral lichen planus–like disease varies.

In rare cases, oral mucosal lichenoid lesions occur after a dental restoration is performed or after the patient starts using a denture; the lag period varies. Patients with an associated allergy to metals or components of the appliance should be evaluated by means of patch testing.

Up to 44% of patients with oral lichen planus develop coincident skin lesions. Conversely, more that 70% of patients with cutaneous lichen planus develop coincident oral lichen planus.

The genitals are involved in as many as 25% of women with oral lichen planus, compared with only 2-4% of men with oral lichen planus. The features are similar to those of the oral lesions. Patients do not often complain of pain or pruritus, although on questioning, they may admit to such symptoms.

In patients with oral lichen planus, scalp involvement (lichen planopilaris) is rare.

Nail involvement in patients with oral lichen planus is uncommon.

In a small group of patients, lichen planus may involve the esophagus.

Differential Diagnoses

       Dermatitis Herpetiformis

       Graft Versus Host Disease

       Linear IgA Dermatosis

       Oral Manifestations of Autoimmune Blistering Diseases

       Pemphigus Vulgaris

       Squamous Cell Carcinoma

Laboratory Studies

The history, typical oral lesions, and skin involvement are usually sufficient to diagnose oral lichen planus (OLP), though laboratory studies and biopsy may be required (see Procedures).

Direct immunofluorescence testing can help in distinguishing erosive or the rare bullous oral lichen planus from pemphigus vulgaris, benign mucous membrane pemphigoid, dermatitis herpetiformis, and linear immunoglobulin A (IgA) disease. The most characteristic feature of oral lichen planus is shaggy linear fibrin distribution.

Some studies show an increased incidence of C albicans infection in patients with oral lichen planus. Periodic acid-Schiff (PAS) staining of biopsy specimens and candidal cultures or smears may be performed. However, these tests may be of limited clinical value because oral C albicans is present in more than 70% of the population. The presence of C albicans and the oral load of this organism do not aid either the diagnosis or the treatment of oral lichen planus.

Other Tests

Skin patch testing may be helpful in identifying a contact allergy in some patients with oral lichen planus. The current recommendation is to use a standard series; a dental prosthesis series; and a metal salt series that includes gold, mercury, and palladium salts as well as other salts of metals used in dental restorations. Late readings, or those obtained at 10 and 17 days after the application of the skin patch, may be required.

The most common allergy is related to mercury contained in amalgam restorations. Compared with patients with lesions in other locations, patients with lesions near the amalgam restoration have a higher rate of positive patch test results to mercury. When the amalgam restorations are removed, patients with a positive result have a higher remission rates (47-100% depending on the study) than that of patients without this positive result.

Although the assessment of hepatic function in the treatment of otherwise healthy southern European and Japanese patients with oral lichen planus may be warranted, similar screening in British and American patients appears to be of limited benefit. Formal studies are still ongoing. Consider hepatic biochemical testing only when patients have proven oral lichen planus and suspected liver disease.

Oral Lichen Planus Medication

Topical corticosteroids are the mainstay of medical treatment of oral lichen planus, although rarely, corticosteroids may be administered intralesionally or systemically. Some topical corticosteroid therapies may predispose the patient to oral pseudomembranous candidosis. However, this condition is rarely if ever symptomatic, and it generally does not complicate healing of the erosions related to oral lichen planus. Topical antimycotics (eg, nystatin, amphotericin) may be prescribed when an infection is present.

Erosive oral lichen planus that is recalcitrant to topical corticosteroids may respond to topical tacrolimus. Other potential therapies for recalcitrant oral lichen planus include hydroxychloroquine, azathioprine, mycophenolate, dapsone, systemic corticosteroids, and topical and systemic retinoids.

Corticosteroids

    Fluocinolone (Synalar, Synalar-HP, Fluonid)

     Clobetasol (Cormax, Olux, Temovate)

    Beclomethasone (Beclovent, Vanceril)

     Triamcinolone (Amcort, Aristocort, Aristospan)

     Prednisolone (Delta-Cortef, Prednisol TBA injection)

 

Immunosuppressants

Azathioprine (Imuran)

 

Further Outpatient Care

Re-examine patients with oral lichen planus (OLP) during active treatment, and monitor lesions for reduction in mucosal erythema and ulceration and alleviation of symptoms. Continue active treatment and try alternative therapies until erythema, ulceration, and symptoms are controlled. Follow up with patients with oral lichen planus at least every 6 months.

Advise patients with oral lichen planus to pay attention to when symptoms are exacerbated or when lesions change. Such changes generally indicate a phase of increased erythematous or erosive disease.

In view of the potential association of oral lichen planus with oral SCC, an appropriate specialist should follow up with the patients every 6-12 months. In addition, advise patients to regularly examine their mouths and seek the help of a specialist if persistent red or ulcerative oral mucosal lesions develop.

Candidal cultures or smears may be obtained periodically. Infections can be controlled with topical antimycotic preparations. These tests may be of limited clinical value because oral C albicans is present in at least 70% of all healthy persons.

Deterrence/Prevention

Patients with oral lichen planus may have a slightly increased risk of oral cancer, although the precise risk is unknown.

The risk of oral cancer in patients with oral lichen planus may be reduced by means of the following:

• Elimination of smoking and alcohol consumption
• Effective treatment of atrophic, erosive, and plaque oral lichen planus lesions
• Consumption of a nutritious diet including fresh fruit and vegetables
• Elimination of C albicans superinfection
• Clinical examination with any exacerbation of symptoms or change in lesion presentation
• Regular clinical examination and repeat biopsy as required. Oral brush biopsy can be used to limit the number of scalpel biopsies. The frequency of brush biopsy for oral lichen planus patient follow-up has not been established. However, if the clinical features of the lesions change, scalpel biopsy should be repeated.

Complications

Oral lichen planus and its treatment may predispose people to oral C albicans superinfection.

Patients with oral lichen planus may have a slightly increased risk of oral cancer, which they may be able to reduce (see Deterrence/Prevention).

Oral SCC in patients with oral lichen planus is a feared complication and a controversial issue. In retrospective studies, fewer than 5% of patients with oral lichen planus who were not using tobacco products developed oral SCC. Atrophic, erosive, and plaque lesions may be at greater risk of malignant change, although SCC may arise in the unaffected oral mucosa as well. The most important risk factors of oral SCC remain the concomitant use of alcohol and tobacco products. Any additive effect of oral lichen planus is difficult to detect in patients who use both.

Proposed reasons for the increased risk of oral SCC in patients with oral lichen planus include the following:

• Compared with healthy mucosa, the oral mucosa affected by oral lichen planus may be more sensitive to C albicans and to the exogenous mutagens found in tobacco, alcohol, and betel quid.
• In patients with oral lichen planus, the chronic inflammatory response and the simultaneous healing response of epithelial wounds may increase the likelihood of cancer-forming gene mutations.

References:

1. Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: report of an international consensus meeting. Part 1. Viral infections and etiopathogenesis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Jul 2005;100(1):40-51. [Medline].

2. Thongprasom K, Dhanuthai K, Sarideechaigul W, Chaiyarit P, Chaimusig M. Expression of TNF-alpha in oral lichen planus treated with fluocinolone acetonide 0.1%. J Oral Pathol Med. Mar 2006;35(3):161-6. [Medline].

3. Lopez-Jornet P, Camacho-Alonso F. Quality of life in patients with oral lichen planus. J Eval Clin Pract. Feb 2010;16(1):111-3. [Medline].

4. Shan J, Ma JM, Wang R, Liu QL, Fan Y. Proliferation and Apoptosis of Peripheral Blood Mononuclear Cells in Patients with Oral Lichen Planus. Inflammation. Nov 8 2012;[Medline].

5. Pendyala G, Joshi S, Kalburge J, Joshi M, Tejnani A. Oral Lichen Planus: A Report and Review of an Autoimmune-Mediated Condition in Gingiva. Compend Contin Educ Dent. Sep 2012;33(8):e102-e108. [Medline].

 

PITYRIASIS ROSEA

http://emedicine.medscape.com/article/1107532-overview

http://www.youtube.com/watch?v=MysEyK9Pgx0

http://www.dailymotion.com/video/xm7gmi_natural-ways-to-treat-pityriasis-rosea_animals#.UQ07JfLE2H4

Background

Pityriasis rosea (PR) is a common benign papulosquamous disease that was originally described by Camille Melchior Gibert in 1860. Pityriasis denotes fine scales, and rosea translates as rose colored or pink. Pityriasis rosea can have a number of clinical variations. Its diagnosis is important because it may resemble secondary syphilis.

Pityriasis Rosea Clinical Presentation

History

The history should include questions about close contacts with similar eruptions. This finding is uncommon because most cases of pityriasis rosea are sporadic, as pityriasis rosea is thought to reflect a weakly contagious disease. A history of medication intake should be obtained because several medications have been shown to cause a similar exanthem.

• The disease typically begins with a solitary macule that heralds the eruption (called the herald spot/patch), which is usually a salmon-colored macule. This initial lesion enlarges over a few days to become a patch with a collarette of fine scale just inside the well-demarcated border.
• Within the next 1-2 weeks, a generalized exanthem usually appears, although it may occur from hours to months after the herald patch. This secondary phase consists of bilateral and symmetric macules with a collarette scale oriented with their long axes along cleavage lines. This phase tends to resolve over the next 6 weeks, but variability is common.
• Pruritus is common, usually of mild-to-moderate severity, and it occurs in 75% of patients.

Physical

• The herald patch is usually a single pink patch, 2-10 cm in diameter, on the neck or the trunk with a fine collarette scale (see following image). It is observed in more than 50% of patients, and it may occur as multiple lesions or in atypical locations.

• Herald patch. Courtesy of the Drexel Department of Dermatology slide collection.
• About 1-2 weeks after the herald patch is seen, the generalized eruption appears, although it has been known to occur from hours to 3 months later. It consists of salmon-colored macules or patches, 0.5-1.5 cm in diameter, with a collarette scale, often described as having a cigarette paper–like appearance. The long axes of the lesions are oriented in a parallel fashion along cleavage lines, giving the classic Christmas tree pattern (see following image). These secondary lesions most commonly occur on the trunk, the abdomen, the back, and the proximal upper extremities.

 

• Christmas tree distribution of lesions on the trunk. Courtesy of the Drexel Department of Dermatology slide collection.
• Pruritus occurs in 75% of patients and is severe in 25%.
• Lymphadenopathy is uncommon, but, when present, it is usually observed in African Americans.
• Atypical pityriasis rosea occurs in 20% of patients.
• These variations can be separated into changes in the lesions and/or their distribution. Variable distribution can be difficult to evaluate.
• Photosensitivity may occur. Photoexacerbated and photoprotected forms have been documented, although photosensitivity is not a classic manifestation of the disease.
• Lesions may be localized to single areas, such as the abdomen, the groin, the axilla, the distal extremities, the palms, and the soles.
• An inverse pityriasis rosea may be seen. This form manifests as lesions on the face and the distal extremities, and it is more common in children than in adults. The herald patch may be the only manifestation of the disease.
• A unilateral variant in which the lesions do not cross the midline has been described.
• Drug-induced cases are frequently observed without the herald patch.
• Variations in lesion morphology are noteworthy.
• Atypical, large patches tend to be fewer iumber. They may coalesce to form a variant known as pityriasis circinata et marginata of Vidal. The primary lesions may be papules, vesicles, pustules, or urticarial or purpuric plaques. Pityriasis rosea may first be evident with widespread, intensely pruritic papulovesicles in an unusual distribution, such as on the neck and the scalp.
• Papular pityriasis rosea tends to have scaling papules in the normal distribution; this form is more common in children than in adults.
• Erythema multiforme–like plaques may be evident.
• Oral involvement may occur as punctate hemorrhages, ulcers, papulovesicles, bullae, or erythematous plaques. Most studies find the incidence to be less than 10%; however, one study reported them in as many as 16% of patients.
• Purpuric pityriasis rosea is seen in both adults and children, and it follows the usual presentation of the disease.
• African American children may have more frequent papular lesions and facial and scalp involvement than is usually described. Also of interest is that many patients have resolution of lesions within 2 weeks.

Causes

Pityriasis rosea may represent a viral exanthem (and at times enanthem).

• Pityriasis rosea–like drug eruptions may be difficult to distinguish from non–drug-induced cases. Medication-induced eruptions have been reported with captopril, metronidazole, isotretinoin, penicillamine, levamisole, bismuth, gold, barbiturates, ketotifen, clonidine, aspirin, and omeprazole. A single case has been reported with terbinafine. Imatinib mesylate and etanercept have also been implicated.
• Certain vaccinations, such as the BCG vaccine or the diphtheria vaccine, have been reported to cause similar eruptions.
• Lesions are also thought to be increased in individuals with high stress levels.

Differential Diagnoses

• Erythema Dyschromicum Perstans
• Lichen Planus
• Nummular Dermatitis
• Pityriasis Lichenoides
• Psoriasis, Guttate
• Seborrheic Dermatitis
• Syphilis
• Tinea Corporis

Laboratory Studies

• One must be careful to rule out syphilis.
• A screening rapid plasma reagin (RPR) test or a VDRL test should be ordered for appropriate individuals.
• One should be aware of the prozone phenomenon seen in secondary syphilis and request titration of the RPR test.
• An HIV test should also be considered in these patients.
• Other laboratory tests are usually normal and, therefore, unhelpful. Changes in the white blood cell count and differential, as well as increases in erythrocyte sedimentation rate, total serum protein level, globulin level, and albumin level, are rarely reported.

Pityriasis Rosea Treatment & Management

http://emedicine.medscape.com/article/1107532-treatment

http://www.dailymotion.com/video/xm7gmi_natural-ways-to-treat-pityriasis-rosea_animals#.UQ07JfLE2H4

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

    Hydrocortisone topical (Westcort)

     Betamethasone topical (Diprolene, Betatrex)

     Clobetasol (Temovate)

 

Antihistamines

Diphenhydramine (Benadryl, Belix)

 

References:

1. Amer A, Fischer H, Li X. The natural history of pityriasis rosea in black American children: how correct is the “classic” description?. Arch Pediatr Adolesc Med. May 2007;161(5):503-6. [Medline].

2. Rasi A, Tajziehchi L, Savabi-Nasab S. Oral erythromycin is ineffective in the treatment of pityriasis rosea. J Drugs Dermatol. Jan 2008;7(1):35-8. [Medline].

3. Drago F, Broccolo F, Rebora A. Pityriasis rosea: an update with a critical appraisal of its possible herpesviral etiology. J Am Acad Dermatol. Aug 2009;61(2):303-18. [Medline].

 

WHAT IS DANDRUFF (SEBORRHEA)?

 

http://www.medicinenet.com/seborrhea/article.htm#what_is_dandruff_seborrhea

 

 

 

It is a common form of skin eczema that occurs in parts of the body with high oil (sebum) production. Body areas that are commonly affected include the scalp, ears, face, chest, and folds of skin, such as the underarms or the skin below breasts or overhanging abdominal folds. The cause of seborrhea is unknown, although a yeast that often lives on the skin, Malassezia furfur, may play a role.

One common manifestation of seborrhea that affects the scalp is dandruff. Scalp seborrhea can also present as thick, flaky, localized patches of scale. On the face, seborrhea produces reddish-brown, dry-looking, or thick, greasy scales on the eyebrows, sides of the nose, and behind the ears. Reddish, scaly patches may also appear in the folds of skin mentioned above. Although skin affected by seborrhea may feel “dry,” moisturizing only makes them redder.

Scalp seborrhea and dandruff do not cause permanent hair loss. Often, scalp seborrhea doesn’t even itch significantly. Seborrhea can appear during infancy, starting shortly after birth and lasting several months. It may affect the scalp (“cradle cap“) or produce scaly patches on the body. Adults of all ages may develop seborrhea, too, especially on the scalp and face.

 

 

Some people who have weakened immune systems, such as those on chemotherapy or those with HIV disease or certaieurological disorders, may have very severe seborrhea. It is important to emphasize, however, that seborrhea is a very common condition, affecting perhaps 5% of the population (with men predominating). The vast majority of those who have it are completely healthy and have no internal or immune problems.

What treatments are available for dandruff?

Treatment of seborrhea (dandruff) is directed at fighting the skin inflammation. This is done either directly, by using cortisone-based creams and lotions (which reduce inflammation), or by reducing the yeast that builds up on scaly areas and adds to the problem. Note, though, that seborrhea is not a yeast infection.

WHAT IS SEBORRHEIC DERMATITIS?

 

http://www.medicinenet.com/seborrheic_dermatitis/article.htm#what_is_seborrheic_dermatitis

 

 

Seborrheic dermatitis is a chronic skin inflammation that becomes worse and better spontaneously. Seborrheic dermatitis causes an eczema-type eruption commonly affecting portions of the head and upper torso. Seborrheic dermatitis is also known as seborrhea.

What are risk factors for seborrheic dermatitis?

Although almost all patients with seborrheic dermatitis are generally entirely healthy there does seem to be an association with diseases of the central nervous system and AIDS.

What causes seborrheic dermatitis?

The causes of seborrheic dermatitis are poorly understood. Since this condition tends to occur in areas of heavy sebum production, it is felt that oily skin may be a factor leading to seborrheic dermatitis. In addition, it seems that many patients with seborrheic dermatitis have excessive growth of a normal skin yeast (Pityrosporum or Malassezia) in the affected areas. Whether this common microorganism really leads to seborrheic dermatitis or is just a secondary phenomenon remains to be determined.

The fact that topical antifungal medications are effective in controlling this disease has led some to conclude that this is a fungal condition. However, this theory is not yet accepted.

What are seborrheic dermatitis symptoms and signs?

The rash itself is characteristically red and scaling but occasionally can become weepy and oozy. The scaling can be extensive enough to be called dandruff and can be the patient’s major complaint.

The distribution of this rash is often of great help in making the diagnosis. In adults areas commonly involved include the scalp, the outer ear and external auditory canal, the forehead, the brows, the eyelids, the cheeks adjacent to the nose, including the folds that extends from the nose to the sides of the mouth, and less commonly the armpits, the mid-chest, and mid-back regions. In babies, the rash causes a scalp eruption commonly called “cradle cap.” It can also be more extensive and involve the diaper area as well. Although in both adults and children the rash may have no symptoms, it commonly causes itching, especially in the scalp.

How is seborrheic dermatitis diagnosed?

The diagnosis of seborrheic dermatitis is almost always made clinically, meaning that the doctor knows it when he/she sees it. Occasionally, a scraping of skin under a drop of potassium hydroxide is examined under a microscope to exclude a fungal infection. It would be rare that a skin biopsy would be required for diagnosis.

What is the treatment for seborrheic dermatitis?

Treatment of hair-bearing areas, like the scalp, often includes the use of a shampoo that may contain one or more of the following ingredients:

• tar
• antifungal antibiotic
• zinc pyrithione
• selenium sulfide

In addition, the application of a topical steroid lotion or solution of weak to moderate potency is popular.

For non-hair-bearing areas, the application of a weak to moderately potent topical steroid or topical antifungal cream is frequently effective. The use of tacrolimus (Protopic) or pimecrolimus (Elidel) ointments can be effective but is quite an expensive alternative.

It needs to be stressed that since this condition is incurable but easily controllable, if the disease is active and the treatment is stopped, one should expect the seborrheic dermatitis to recur. One should also use effective medications just enough to control the symptoms. Excessive treatment of apparently normal skin is economically wasteful as well as potentially dangerous.

 

ALOPECIA AREATA

 

http://emedicine.medscape.com/article/1069931-clinical

http://www.youtube.com/watch?v=G6GvrOUlBA4

 

Background

Alopecia areata is a recurrent nonscarring type of hair loss that can affect any hair-bearing area. Clinically, alopecia areata can manifest many different patterns. Although medically benign, alopecia areata can cause tremendous emotional and psychosocial distress in affected patients and their families.

Pathophysiology

The exact pathophysiology of alopecia areata remains unknown. The most widely accepted hypothesis is that alopecia areata is a T-cell–mediated autoimmune condition that is most likely to occur in genetically predisposed individuals.

    Autoimmunity

    Cytokines

    Innervation and vasculature

    Viral etiology

Clinical Presentation

History

The natural history of alopecia areata is unpredictable. Extreme variations in duration and extent of the disease occur from patient to patient. Alopecia areata most often is asymptomatic, but some patients (14%) experience a burning sensation or pruritus in the affected area. The condition usually is localized when it first appears. Of patients with alopecia areata, 80% have only a single patch, 12.5% have 2 patches, and 7.7% have multiple patches. No correlation exists between the number of patches at onset and subsequent severity. Alopecia areata most often affects the scalp (66.8-95%); however, it can affect any hair-bearing area. The beard is affected in 28% (males; see first image below), eyebrows in 3.8%, and extremities in 1.3% of patients (see second image below). More than one area can be affected at once.

Alopecia areata affecting the beard.

 

 

 

Alopecia areata affecting the arms.

• Localized alopecia areata: Episodes of localized (< 50% involvement) patchy alopecia areata usually are self-limited; spontaneous regrowth occurs in most patients within a few months, with or without treatment.
• Extensive alopecia areata: Extensive (>50% involvement) forms of alopecia areata are less common. Alopecia totalis or alopecia universalis are reported to occur at some point in 7% of patients; alopecia areata involving more than 40% hair loss is seen in 11%. The proportion of patients with alopecia totalis appears to decrease with every decade of life.
• In 30% of patients with alopecia totalis, complete hair loss occurred within 6 months after onset of disease. Sharma et al  reported a mean progression period to alopecia totalis of 4 months after onset. The natural evolution of alopecia totalis is unpredictable, but recurrences of alopecia areata (not necessarily alopecia totalis) are expected.
• In a study involving 736 patients, the relapse rate was 90% over 5 years. One percent of children and 10% of adults can experience long-lasting regrowth. Forty-four percent of children and 34% of adults experience a significant period of normal or near-normal hair growth. Twenty-two percent of children and 34% of adults do not experience regrowth.
• Associated conditions: Because some of the entities associated with alopecia areata occur uncommonly in the general population, a large number of patients with alopecia areata need to be examined to confirm whether an increased prevalence of these conditions exists among patients with alopecia areata. Unfortunately, most studies are performed on small groups; therefore, the data should be interpreted carefully.
• Atopic dermatitis is seen in 9-26% of patients with alopecia areata. In the general population, the prevalence of atopic dermatitis in children in temperate developed countries varies from 5-20%. In adults, the prevalence decreases to 2-10%. Some authors have found atopy to be a poor prognostic factor for alopecia areata.
• Vitiligo is seen with an incidence varying from 1.8-3% compared with 0.3% in control subjects. Also see Vitiligo.
• Clinically evident thyroid disease was found in 0.85% of 1700 patients with alopecia areata.The prevalence of thyroid disease determined on a clinical or laboratory basis varies among studies from 0.85-14.7%. The incidence of thyroid disease in control subjects is estimated to be 0.17-2%. The presence of microsomal antibodies is found in 3.3-16% of patients. Antibodies can be found with or without signs or symptoms of thyroid disease, but patients with positive autoantibodies have a higher incidence of functional abnormalities found on thyroid-releasing hormone tests (26% vs 2.8%). The incidence of thyroid microsomal and thyroglobulin antibodies in control subjects is 7%. Other studies have not supported these results. A study in 100 patients with alopecia areata failed to find an increased incidence of circulating autoantibodies, including mitochondrial and thyroglobulin antibodies.
• Collagen-vascular diseases have been found in 0.6-2% of patients with alopecia areata, while the incidence in control subjects is 0.17%. The incidence of alopecia areata in 39 patients with lupus erythematous was 10% in a study by Werth et al,  in contrast to 0.42% of general dermatologic patients.
• Diabetes mellitus was found to be more common in control subjects (1.4%) than in patients with alopecia areata (0.4%). The occurrence of alopecia areata may protect against the appearance of type I diabetes mellitus. However, the incidence of type I diabetes mellitus was significantly higher in relatives of patients with alopecia areata compared with the general population.
• Alopecia areata is seen in 6-8.8% of patients with Down syndrome, but only 0.1% of patients with alopecia areata have Down syndrome. The high frequency of alopecia areata in patients with Down syndrome suggests that a genetic linkage for alopecia areata may exist on chromosome 21.
• Anxiety, personality disorders, depression, and paranoid disorders are seen with increased prevalence varying from 17-22% of patients, and the lifetime prevalence of psychiatric disorders is estimated to be 74% in patients with alopecia areata. Psychiatric problems are seen in both children and adults. No association has been made between the severity of the psychiatric disorder and that of alopecia areata.
• Stressful life events within the 6-month period preceding episodes of alopecia areata were significantly higher in patients with alopecia areata compared with patients with androgenetic alopecia or tinea capitis. Major stress factors (eg, death in family) were reported in 12% of patients.
• Others associations in some studies include pernicious anemia, myasthenia gravis, ulcerative colitis, lichen planus, and Candida endocrinopathy syndrome.
• Precipitating factors: A precipitating factor can be found in 15.1% of patients with alopecia areata. Major life events, febrile illnesses, drugs, pregnancy, trauma, and many other events have been reported, but no clear conclusions can be drawn. Despite these findings, most patients with alopecia areata do not report a triggering factor preceding episodes of hair loss.

Physical

The presence of smooth, slightly erythematous (peach color) or normal-colored alopecic patches is characteristic. The presence of exclamation point hairs (ie, hairs tapered near proximal end) is pathognomonic but is not always found. A positive result from the pull test at the periphery of a plaque usually indicates that the disease is active, and further hair loss can be expected. Additionally, hair loss on other hair-bearing areas also favors the diagnosis. The most common presentation is the appearance of one or many round-to-oval denuded patches. No epidermal changes are associated with the hair loss.

Alopecia areata can be classified according to its pattern. Hair loss most often is localized and patchy (see image below).

Patchy alopecia areata.

A reticular pattern occurs when hair loss is more extensive and the patches coalesce. An ophiasis pattern occurs when the hair loss is localized to the sides and lower back of the scalp (see image below).

Ophiasis pattern of alopecia areata.

Conversely, sisaipho (ophiasis spelled backwards) pattern occurs when hair loss spares the sides and back of the head (see image below).

Sisaipho pattern of alopecia areata.

Alopecia totalis occurs with 100% hair loss on the scalp (see image below).

 

Alopecia totalis.

Alopecia universalis occurs with complete loss of hair on all hair-bearing areas. Alopecia areata usually is focal; however, it can be diffuse, thereby mimicking telogen effluvium (TE) or the type of androgenetic alopecia seen in women (see image below).

 

Diffuse alopecia areata.

Dermoscopy

The application of dermoscopy to the evaluation of hair loss is only recently being pioneered. Dermoscopy is safe and simple, and may have great potential in the care of alopecia. However, it’s diagnostic accuracy will need to be validated by well-designed studies.

The presence of yellow dots seems to be a specific feature of alopecia areata and has been reported to be present in 95% of patients, regardless of their disease stages. Following histopathological correlation, these yellow dots represent degenerated follicular keratinocytes and sebum contained within the ostium of hair follicles. Although occasionally seen in advanced male-pattern hair loss, yellow dots are not seen in cases of female-pattern hair loss, scaring alopecia, or telogen effluvium.

Other dermoscopic signs reported include black dots, tapering hairs, broken hairs, and clustered short vellus hairs.

Nail involvement

Nail involvement is found in 6.8-49.4% of patients and most commonly is seen in patients with severe forms of alopecia areata. Pitting is the most common finding. Several other abnormalities have been reported (eg, trachyonychia, Beau lines, onychorrhexis, onychomadesis, koilonychia, leukonychia, red lunulae). Fingernails predominantly are affected.

Differential Diagnoses

       Androgenetic Alopecia

       Pseudopelade, Brocq

       Syphilis

       Telogen Effluvium

       Tinea Capitis

       Trichotillomania

Medical Care

Treatment is not mandatory because the condition is benign, and spontaneous remissions and recurrences are common. Treatments used are believed to stimulate hair growth, but no evidence indicates they can influence the ultimate natural course of alopecia areata. Treatment modalities usually are considered first according to the extent of hair loss and the patient’s age.

Assessment of the efficacy of a treatment must be considered with care because the condition is highly unpredictable in presentation, evolution, and response to treatment. Little data exist regarding the natural evolution of the condition. For example, in patients with less than 40% scalp involvement, a study showed no benefit with treatment (minoxidil 1% and topical immunotherapy) over placebo.The high spontaneous remission rate makes clearly assessing the true efficacy of a therapy difficult unless appropriate controls with placebo treatment are studied.

For patients with extensive alopecia areata (>40% hair loss), little data exist on the natural evolution. The rate of spontaneous remission appears to be less than in patients with less than 40% involvement. Vestey and Savin reviewed 50 patients with extensive alopecia areata. Of the 50 patients, 24% experienced spontaneous complete or nearly complete regrowth at some stage during the observation period of 3-3.5 years. The relapse rate is high in patients with severe forms of alopecia areata.

Patients with alopecia totalis or alopecia universalis usually have a poorer prognosis, and treatment failure is seen in most patients with any therapy.

Because alopecia areata is believed to be an autoimmune condition, different immunomodulators have been used to treat this condition. Additional treatment options for alopecia areata include minoxidil and other treatment modalities.

Topical treatments

Corticosteroids

Corticosteroid therapies can include intralesional injections or topical application.

• For intralesional steroids, few studies are available regarding efficacy; however, they are used widely in the treatment of alopecia areata.
• Intralesional steroids are the first-line treatment in localized conditions.
• In a study including 84 patients, regrowth on treated areas was present in 92% of patients with patchy alopecia areata and 61% of patients with alopecia totalis. Regrowth persisted 3 months after treatment in 71% of patients with patchy alopecia areata and 28% of patients with alopecia totalis. Regrowth usually is seen within 4-6 weeks in responsive patients. Patients with rapidly progressive, extensive, or long-standing alopecia areata tend to respond poorly.
• Another study showed regrowth in most patients (480) treated with intralesional steroids, except in 2 patients with alopecia universalis.
• Hair growth may persist for 6-9 months after a single injection.
• Injections are administered intradermally using a 3-mL syringe and a 30-gauge needle.
• Triamcinolone acetonide (Kenalog) is used most commonly; concentrations vary from 2.5-10 mg/mL. The lowest concentration is used on the face. A concentration of 5 mg/mL is usually sufficient on the scalp.
• Less than 0.1 mL is injected per site, and injections are spread out to cover the affected areas (approximately 1 cm between injection sites; see image below).

Corticosteroid injection.

• Adverse effects mostly include pain during injection and minimal transient atrophy (10%). The presence of atrophy should prompt a reduction in the triamcinolone acetonide concentration and avoidance of the atrophic site.
• Injections are administered every 4-6 weeks.
• Although intralesional injections of triamcinolone acetonide are usually recommended for alopecia areata with less than 50% involvement, a report showed that 6 of 10 patients had regrowth. Although injections may work in extensive alopecia areata, results are unlikely if no response is observed at 6 months (personal observation).
• For topical steroids, again, few studies have been performed regarding efficacy in the treatment of alopecia areata; they can however be useful, especially in children who cannot tolerate injections.
• Fluocinolone acetonide cream 0.2% (Synalar HP) twice per day induced a satisfactory-to-excellent response in 61% of patients, which was maintained in 71% of patients. Children younger than 10 years responded better, as did patients with a duration of hair loss of less than 1 year.
• Betamethasone dipropionate cream 0.05% (Diprosone) showed similar efficacy.
• A 2005 study by Tosti et al in patients with alopecia totalis or alopecia universalis showed that the use of 2.5 g of clobetasol propionate under occlusion with a plastic film 6 d/wk for 6 months induced regrowth in 8 (28.5%) of 28 patients. Regrowth was seen 6-14 weeks after the onset of therapy. Regrowth was maintained for at least 6 months after cessation of therapy in 5 (62.5%) of 8 patients. Even though only 17.8% of patients showed long-term benefits from that treatment, it should be kept in mind that the study was performed in a subgroup of patients that is usually refractory to treatment.
• Treatment must be continued for a minimum of 3 months before regrowth can be expected, and maintenance therapy often is necessary.
• Despite these data, the authors do not believe that monotherapy with a topical steroid has been of great benefit in the authors’ practice.
• The most common adverse effect is local folliculitis, which appears after a few weeks of treatment. Telangiectases and local atrophy also have been reported. No systemic adverse effects have been reported.

Immunotherapy

Topical immunotherapy is defined as the induction and periodic elicitation of an allergic contact dermatitis by topical application of potent contact allergens.

• Commonly used agents for immunotherapy include squaric acid dibutylester (SADBE) and diphencyprone (DPCP).These 2 sensitizers are not present in the natural or industrial environment. Dinitrochlorobenzene (DNCB) has become less popular as a result of reports that it is mutagenic in the Ames assay (a bacterial assay).
• No rigorous toxicologic and pharmacologic studies have been performed on the use of these agents in humans.
• Although DPCP and SADBE have not been found mutagenic in the Ames assay, neither is approved by the US Food and Drug Administration, and unknowns still exist concerning their safety profiles.
• No contaminants have been found in SADBE. Acetone solutions and alcohol solutions of SADBE are equally stable for 2 months under storage conditions.
• DPCP occasionally can contain mutagenic contaminants; therefore, it should be screened periodically to ensure purity. No formal data are available on DPCP regarding its longevity in solution.
• Cosmetically acceptable regrowth with topical immunotherapy rates in patients with severe alopecia areata (>50% involvement) varies from 22-68%. Most studies have a success rate of 30-50%. Wiseman et al  retrospectively reported the results of a large cohort of 148 consecutive patients treated with DPCP.
• Their analysis showed that the cumulative patient response at 32 months was 77.9%.
• The response rate varied with the extent of the alopecia. Cosmetically acceptable regrowth was seen in 17.4% of patients with alopecia totalis or alopecia universalis, 60.3% in patients with 75-99% hair loss, 88.1% in patients with 50-74% hair loss, and 100% regrowth in those with 25-49% hair loss.
• Age at onset was also a significant variable, with older age at onset leading to a better prognosis. A lag period of 3 months was usually present between the onset of therapy and the presence of regrowth.
• The median time to achieve significant regrowth was 12.2 months. Some patients showed regrowth on the treated side after 18 months of therapy.
• No benefit is achieved with continuing therapy after 24 months in the absence of regrowth.
• The relapse rate after reaching significant regrowth was 62.6%.
• In a report of a 5-year experience with the use of DPCP, 97 subjects received continued therapy with DPCP. A response rate of greater than 75% was seen in 15% at 6 months, 49% at 12 months, 53% at 18 months, and 56% at 24 months. The only variable that seemed to affect response to treatment was the baseline extent of the alopecia areata. A greater than 75% response rate was seen in 100% of patients with 25-49% hair loss at baseline, 77% of those with 50-74% loss at baseline, 54% of those with 75-99% loss at baseline, 50% of alopecia totalis patients, and 41% of alopecia universalis patients demonstrated a response. Maintenance treatment (once every 1-4 wk) appeared to reduce the risk of relapse (>25% hair loss). Only 18% of patients experienced relapse on maintenance therapy, compared with 57% in those who discontinued treatment
• The type of alopecia areata before treatment, duration of the disease, and the presence of nail changes were found to predict a lower response to treatment. Age at onset and sex of the patient do not appear to influence the prognosis. Controversy exists concerning whether atopy is an adverse prognosis factor.
• Topical immunotherapy has been used for almost 20 years; no serious adverse effects have been reported.
• The most common side effect, which is desired, is a mild contact dermatitis (redness, scaling, itching).
• Adverse effects include cervical lymphadenopathy and pigment changes. Vitiligo developed on the application site in 6.7-7.5% of patients. Transient leukoderma on a distant untreated area has been reported. Of patients who develop vitiligo, 31% (4 of 13) had a history of vitiligo. Only 0.75% of patients developed hyperpigmentation. Confetti-type dyschromia (ie, hyperpigmentation, hypopigmentation) has been described as an adverse effect of DPCP treatment and occurred in 1.6% of 243 patients treated. Less common adverse effects include erythema multiforme–like eruptions and urticaria, which were reported in 3 patients treated with DPCP.
• The mechanism of action of topical immunotherapy is unknown. Antigenic competition has been hypothesized. That is, the introduction of a second antigen can initiate a new infiltrate containing T-suppressor cells and suppressor macrophages that may modify the preexisting infiltrate and allow regrowth.
• Because topical immunotherapy involves the production of contact sensitivity in a previously naive patient, it is best to seek approval for the treatment by the ethics review board and to have the patient sign an informed consent.
• Both SADBE and DPCP appear to be equally effective. Acetone-based solutions usually are preferred because they evaporate quickly, allowing patients to wear a hat or wig immediately after treatment. Quick drying also decreases the chances of dissemination to other body parts by contact.
• Treatment is provided weekly.
• The patient first is sensitized directly on the scalp with a 2% concentration on a small area (2 cm).
• The following week, a low concentration (0.0001%) is applied.
• The concentration is increased slowly every week as needed until a mild tolerable allergic contact dermatitis is elicited. Many concentrations are available that achieve this goal.
• Treating only half of the head allows the physician to use the untreated half as a control. Once regrowth occurs on the treated half, treatment can be applied to the entire scalp. If regrowth initially occurs on both sides, spontaneous remission is likely, although treatment cannot be excluded as the cause.
• Avoid severe contact dermatitis. Patients are advised to avoid light exposure on the scalp for 48 hours because light degrades the chemical. Patients also are advised not to wash the scalp for 48 hours.
• Initial regrowth may be seen at weeks 12-24. Once cosmetically acceptable regrowth is achieved, the treatment can be tapered gradually. Almost all patients relapse if the treatment is discontinued, and maintenance treatment is needed.

Anthralin

The efficacy of anthralin was assessed in 3 studies, which unfortunately were uncontrolled.

• Both short-contact and overnight treatments have been used. Anthralin concentrations varied from 0.2-1%.
• A 2004 study by Tang et al showed no benefit in using anthralin. Other studies showed a response rate of 20-75%, respectively, for patchy alopecia areata and a 25% response rate for alopecia totalis. The mean time to response was 11 weeks, and the mean time to cosmetic response was 23 weeks. Anthralin was used by Tang et al in balding C3H/HeJ mice, which is one animal model for alopecia areata. Half the body was treated with anthralin 0.2%, while the other side was treated with the vehicle ointment. Regrowth was seen on the treated side in 64% of mice after 10 weeks. Four mice had almost complete regrowth. The untreated side showed either no regrowth or continued hair loss. Cytokine studies performed with an RNase protection assay showed that tumor necrosis factor-alpha and -beta were inhibited in mice that responded to treatment.
• Most patients experienced irritant contact dermatitis. Whether the dermatitis is necessary for efficacy remains under debate.
• Cosmetically acceptable regrowth was maintained during therapy in 71% of responders. No correlation exists between duration of the current episode and response to treatment.
• Adverse effects include pruritus, erythema, scaling folliculitis, local pyoderma, and regional lymphadenopathy. Withholding treatment for a few days results in rapid disappearance of adverse effects. Treatment then can be reinstituted, but anthralin should be left on for shorter periods. Staining of clothes and skin can be a concern.
• The mechanism of action of anthralin is unknown. Most likely, it creates inflammation by generating free radicals, which have antiproliferative and immunosuppressive actions.

Minoxidil

Minoxidil appears to be effective in the treatment of alopecia areata in patients with extensive disease (50-99% hair loss). Response rates in that group vary from 8-45%. Minoxidil was of little benefit in patients with alopecia totalis or alopecia universalis.

• The 5% solution appears to be more effective.
• No more than 25 drops are applied twice per day regardless of the extent of the affected area.
• Initial regrowth can be seen within 12 weeks, but continued application is needed to achieve cosmetically acceptable regrowth.
• Minoxidil usually is well tolerated. Adverse effects include distant hypertrichosis (5%) and irritation (7%).
• The exact mechanism of action of minoxidil remains unclear. Minoxidil does not appear to have either a hormonal or an immunosuppressant effect. Minoxidil most likely has a direct mitogenic effect on epidermal cells, both in vitro and in vivo. Anagen-phase hair bulbs plucked from men applying minoxidil showed a significant increase in proliferation index as measured by DNA flow cytometry. Minoxidil also has been shown to prolong the survival time of keratinocytes in vitro. Finally, minoxidil may oppose intracellular calcium entry. Calcium influx normally enhances epidermal growth factors to inhibit hair growth. Minoxidil is converted to minoxidil sulfate, which is a potassium channel agonist and enhances potassium ion permeability, thus opposing the entry of calcium into cells. Local vasodilatation does not appear to play a primary role in hair growth associated with minoxidil.

Systemic treatments

Psoralen plus UV-A

Many studies have been performed regarding the efficacy of psoralen plus UV-A (PUVA) in the treatment of alopecia areata, and the initial response rate varies from 20-73%. The relapse rate, unfortunately, is high (50-88%). Most patients relapse within a few months (mean 4-8 mo) after treatment is stopped.

• Both systemic and topical PUVA therapies have been used.
• The number of treatments required for regrowth varies, but 20-40 treatments usually are sufficient in most cases.
• A younger age at onset, a longer duration of disease, and the presence of alopecia totalis or alopecia universalis appear to indicate a poorer outcome.
• Taylor and Hawk published 10 years of experience with PUVA. The initial response rate (>90% regrowth) was comparable to other studies and was 43.8% for partial alopecia areata and 50% for alopecia totalis and alopecia universalis. However, after excluding patients with vellus hair regrowth and patients who relapsed rapidly in the follow-up period (approximately 4 mo), they found the success rate to be, at best, 6.3% for partial alopecia areata and 12.5% for alopecia totalis and alopecia universalis. They concluded that PUVA generally is not an effective long-term treatment for alopecia areata.
• PUVA is a relatively safe treatment modality; adverse effects include burning and, possibly, an increased risk of skin cancer.

Prednisone

The use of systemic steroids for the treatment of alopecia areata is sometimes justifiable, but hair loss frequently follows discontinuation of the medication and benefits must be carefully weighed against long-term risks. Some authors support a beneficial role of systemic steroids in halting the progression of alopecia areata, but many others have had poor results with this form of therapy.

• The rate of regrowth varies greatly (27-89%), and many dose regimens have been used in these studies.
• Although the initial regrowth appears promising, the prednisone dose necessary to maintain cosmetic growth usually must be high enough that adverse effects are inevitable, and most patients relapse after therapy is discontinued.
• Some benefit was shown using minoxidil 2% solution applied twice per day following a 6-week taper of prednisone, but the relapse rate remained at a minimum of 50% at 4 months in the treated group.
• Adverse effects from systemic therapy were common in these reports and included diabetes, weight gain, hypertension, psychological changes, osteoporosis, suppression of the adrenocorticotropic axes, striae, acne, hypertrichosis, and purpura.
• Systemic steroids most likely are effective via their immunosuppressive effects.
• An initial benefit may occur by using systemic prednisone in some patients, but the relapse rate is high, and it does not appear to alter the course of the condition.
• Systemic prednisone is not an agent of choice for alopecia areata because of the adverse effects associated with both short- and long-term treatment.

Cyclosporine

Cyclosporine has been used both topically and systemically in the treatment of alopecia areata.

• Topical cyclosporine has not proven to be effective in severe alopecia areata because no patient (0 of 10) showed benefit with application of a 10% cyclosporin A (CsA) solution twice per day for 12 months.
• Another study of 14 patients using a 5% solution of cyclosporine twice per day for 4-6 months reported vellus growth in 3 of 14 patients and normal hair growth in 3 patients with patchy alopecia areata. No regrowth was seen in 8 of the patients.
• Neither study showed systemic absorption of CsA, and routine blood examination showed only a transient increase of hepatic enzymes in 1 patient.
• Oral cyclosporine was effective in the DEBR model for alopecia areata. All rats had a full pelage by 5 weeks of treatment with 10 mg/kg/d, 5 d/wk for 7 weeks. Studies in humans also have proven efficacy with doses of 6 mg/kg/d for 3 months in 6 patients. All patients experienced regrowth, and cosmetically acceptable regrowth was seen in 3 of 6 patients. Unfortunately, all patients relapsed within 3 months of discontinuation of cyclosporine. No evidence indicates that CsA can prevent hair loss during an active episode because reports have described patients taking CsA who developed alopecia areata while they were under treatment for unrelated conditions.
• The mechanism of action of cyclosporine remains unclear. It may act through its immunosuppressive effect, because, in patients who regrew hair, clearance of immune cells from the hair follicles and alteration in the balance of regulatory lymphocytes occurred (ie, decrease of the CD4/CD8 ratio). Cyclosporine causes hypertrichosis in patients treated for conditions unrelated to hair loss. The mechanism by which cyclosporine stimulates hair growth remains unknown.
• In conclusion, topical cyclosporine has shown limited efficacy. Although systemic CsA appears to be effective in alopecia areata, the adverse effect profile, the recurrence rate after treatment discontinuation, and thus, the inability to produce long-term remissions, make CsA unattractive for the treatment of alopecia areata.

Tacrolimus

Regrowth was shown on the application site of topical tacrolimus in 2 studies using the DEBR model. Oral tacrolimus was ineffective. No benefit was shown in the use of topical tacrolimus for alopecia areata in a small 2005 study by Price et al that included 11 patients.

Interferon

A study of 11 patients with alopecia areata ranging from patchy alopecia areata to alopecia universalis showed no benefit using intralesional interferon alfa-2 (1.5 million IU, 3 times per wk for 3 wk).

Dapsone

Dapsone at 50 mg twice per day was used in a 6-month, double-blind, placebo-controlled study. Of patients in the study, 54% (7 of 13) withdrew from the dapsone group because of adverse effects such as malaise. Of the remaining 6 patients, 3 experienced generalized growth of terminal hair, compared with 4 (4 of 13) patients in the placebo group, who experienced only sparse patchy regrowth of vellus hair. The authors concluded that although dapsone showed some efficacy, the high incidence of adverse effects rendered it unacceptable. Another study showed a rate of success comparable to the occurrence of spontaneous regrowth reported in the literature.

Methotrexate

Joly reported 22 patients with long-standing, severe alopecia areata who responded well to methotrexate, with or without systemic corticosteroids. Although the results from that study are surprisingly good, a more standardized study involving more patients is needed because other dermatologists have not had such good efficacy with methotrexate.

Immunomodulators

Class Summary

Because alopecia areata is believed to be an autoimmune condition, different immunomodulators have been used to treat the condition. Exact mechanism of action of topical immunotherapy is unknown. Antigenic competition was hypothesized (ie, introduction of a second antigen can initiate a new infiltrate containing T-suppressor cells and suppressor macrophages that may modify preexisting infiltrate and allow regrowth).

    Cyclosporine (Sandimmune, Neoral)

    Methoxsalen (8-MOP, Oxsoralen)

    Anthralin (Dritho-Scalp 0.5% cream, Anthra-Derm 1% cream, Drithocreme 1%, Micanol 1% cream)

 

Glucocorticoids

    Clobetasol propionate (Temovate)

    Prednisone (Deltasone, Meticorten, Sterapred)

    Triamcinolone (Kenalog 10 mg/mL or 40 mg/mL)

    Betamethasone dipropionate cream 0.05% (Diprosone)

 

Vasodilators

Minoxidil topical (Rogaine Extra Strength).

 

References:

 

 1. Chang KH, Rojhirunsakool S, Goldberg LJ. Treatment of severe alopecia areata with intralesional steroid injections. J Drugs Dermatol. Oct 2009;8(10):909-12. [Medline].

2. El-Zawahry BM, Bassiouny DA, Khella A, Zaki NS. Five-year experience in the treatment of alopecia areata with DPC. J Eur Acad Dermatol Venereol. Mar 2010;24(3):264-9. [Medline].

3. van den Biggelaar FJ, Smolders J, Jansen JF. Complementary and alternative medicine in alopecia areata. Am J Clin Dermatol. 2010;11(1):11-20. [Medline].

4. Willemsen R, Haentjens P, Roseeuw D, Vanderlinden J. Hypnosis in refractory alopecia areata significantly improves depression, anxiety, and life quality but not hair regrowth. J Am Acad Dermatol. Mar 2010;62(3):517-8. [Medline].

5. Karadag Köse O, Güleç AT. Clinical evaluation of alopecias using a handheld dermatoscope. J Am Acad Dermatol. Aug 2012;67(2):206-14. [Medline].

ACNE VULGARIS

 

http://emedicine.medscape.com/article/1069804-overview

http://www.youtube.com/watch?v=JULJhv6uBgM

 

Background

Acne vulgaris is a common skin disease that affects an estimated 80% of Americans at some time during their lives. Twenty percent will have severe acne, which results in permanent physical and mental scarring. Acne vulgaris is American’s most common skin disease and is characterized by noninflammatory, open or closed comedones and by inflammatory papules, pustules, and nodules. Acne vulgaris typically affects the areas of skin with the densest population of sebaceous follicles; these areas include the face, the upper part of the chest, and the back.

Acne Vulgaris Clinical Presentation

History

Local symptoms of acne vulgaris may include pain or tenderness.

Systemic symptoms are most often absent in acne vulgaris. Severe acne with associated systemic signs and symptoms such as fever is referred to as acne fulminans. Severe acne, characterized by multiple comedones, without the presence of systemic symptoms, is known as acne conglobata. This severe form of acne frequently heals with disfiguring scars. Additionally, acne vulgaris may have a psychological impact on any patient, regardless of the severity or the grade of the disease.

Physical Examination

Acne vulgaris is characterized by comedones, papules, pustules, and nodules in a sebaceous distribution (eg, face, upper chest, back). A comedone is a whitehead (closed comedone) or a blackhead (open comedone) without any clinical signs of inflammation. Papules and pustules are raised bumps with obvious inflammation. The face may be the only involved skin surface, but the chest, back, and upper arms are often involved.

In comedonal acne, patients develop open and closed comedones but may not develop inflammatory papules or nodules.

Acne, grade I; multiple open comedones.

Mild acne is characterized by comedones and a few papulopustules. Note the image below.

Acne, grade II; closed comedones.

Moderate acne has comedones, inflammatory papules, and pustules. Greater numbers of lesions are present than in milder inflammatory acne. Note the image below.

Acne, grade III; papulopustules.

Nodulocystic acne is characterized by comedones, inflammatory lesions, and large nodules greater than 5 mm in diameter. Scarring is often evident. Note the image below.

Acne, grade IV; multiple open comedones, closed comedones, and papulopustules, plus cysts.

Causes

The main underlying cause of acne is a genetic predisposition. In addition the following aggravating factors are recognized:

• Cosmetic agents and hair pomades may worsen acne.
• Medications that can promote acne development include steroids, lithium, some antiepileptics, and iodides.
• Congenital adrenal hyperplasia, polycystic ovary syndrome, and other endocrine disorders associated with excess androgens may trigger the development of acne vulgaris. Even pregnancy may cause a flare-up.
• Mechanical occlusion with headbands, shoulder pads, back packs, or under-wire bras can be aggravating factors
• Excessive sunlight may either improve or flare acne. In any case, the ultraviolet exposure ages the skin.

Differential Diagnoses

       Acne Conglobata

       Acne Fulminans

       Acne Keloidalis Nuchae

       Acneiform Eruptions

       Folliculitis

       Perioral Dermatitis

       Rosacea

       Sebaceous Hyperplasia

       Syringoma

       Tuberous Sclerosis

Acne Vulgaris Treatment & Management

Medical Care

Treatment should be directed toward the known pathogenic factors involved in acne. These include follicular hyperproliferation, excess sebum, P acnes, and inflammation. The grade and severity of the acne help in determining which of the following treatments, alone or in combination, is most appropriate. When a topical or systemic antibiotic is used, it should be used in conjunction with benzoyl peroxide to reduce the emergence of resistance.

Topical treatments

Topical retinoids are comedolytic and anti-inflammatory. They normalize follicular hyperproliferation and hyperkeratinization. Topical retinoids reduce the numbers of microcomedones, comedones, and inflammatory lesions. They may be used alone or in combination with other acne medications. The most commonly prescribed topical retinoids for acne vulgaris include adapalene, tazarotene, and tretinoin. These retinoids should be applied once daily to clean, dry skin, but they may need to be applied less frequently if irritation occurs. Skin irritation with peeling and redness may be associated with the early use of topical retinoids and typically resolves within the first few weeks of use. The use of mild, nonirritating cleansers and noncomedogenic moisturizers may help reduce this irritation. Alternate-day dosing may be used if irritation persists. Topical retinoids thin the stratum corneum, and they have been associated with sun sensitivity. Instruct patients about sun protection. Also see Sunscreens and Photoprotection.

Topical antibiotics are mainly used for their role against Propionibacterium acnes. They may also have anti-inflammatory properties. Topical antibiotics are not comedolytic, and bacterial resistance may develop to any of these agents. The development of resistance is lessened if topical antibiotics are used in combination with benzoyl peroxide.Commonly prescribed topical antibiotics for acne vulgaris include clindamycin (or less commonly erythromycin) alone or in combination with benzoyl peroxide. Clindamycin is available in a variety of topical agents. They may be applied once or twice a day. Gels and solutions may be more irritating than creams or lotions. Clindamycin has maintained better efficacy than erythromycin, which is infrequently used.

Benzoyl peroxide products are also effective against P acnes, and bacterial resistance to benzoyl peroxide has not been reported.Benzoyl peroxide products are available over the counter and by prescription in a variety of topical forms, including soaps, washes, lotions, creams, and gels. Benzoyl peroxide products may be used once or twice a day. These agents may occasionally cause a true allergic contact dermatitis. More often, an irritant contact dermatitis develops, especially if used with tretinoin or when accompanied by aggressive washing methods. If intensive erythema and pruritus develop, a patch test with benzoyl peroxide is indicated to rule out allergic contact dermatitis.

Systemic treatments

Systemic antibiotics are a mainstay in the treatment of acne vulgaris. These agents have anti-inflammatory properties, and they are effective against P acnes. The tetracycline group of antibiotics is commonly prescribed for acne. The more lipophilic antibiotics, such as doxycycline and minocycline, are generally more effective than tetracycline. Greater efficacy may also be due to less P acnes resistance to minocycline. However, P acnes resistance is becoming more common with all classes of antibiotics currently used to treat acne vulgaris. P acnes resistance to erythromycin has greatly reduced its usefulness in the treatment of acne. Subantimicrobial therapy or concurrent treatment with topical benzoyl peroxide may reduce the emergence of resistant strains.

Although continued use of systemic tetracycline group antibiotics was believed to result in colonization with tetracycline-resistant Staphylococcus aureus, this does not appear to be true. A study by Fanelli et al found that S aureus remained sensitive to tetracycline even after prolonged use of that antibiotic for acne. This has significant ramifications when considering efforts to control the spread of methicillin-resistant S aureus (MRSA) because tetracycline group antibiotics are currently one of the primary options for outpatient treatment of MRSA.

Other antibiotics, including trimethoprim alone or in combination with sulfamethoxazole, and azithromycin, reportedly are helpful.

Some hormonal therapies may be effective in the treatment of acne vulgaris. Oral contraceptives increase sex hormone–binding globulin, resulting in an overall decrease in circulating free testosterone. Combination birth control pills have shown efficacy in the treatment of acne vulgaris.

Spironolactone may also be used in the treatment of acne vulgaris.Spironolactone binds the androgen receptor and reduces androgen production. Adverse effects include dizziness, breast tenderness, and dysmenorrhea. Dysmenorrhea may be lessened by coadministration with an oral contraceptive. Periodic evaluation of blood pressure and potassium levels is appropriate. Pregnancy must be avoided while taking spironolactone because of the risk of feminization of the male fetus.

Isotretinoin is a systemic retinoid that is highly effective in the treatment of severe, recalcitrant acne vulgaris. Isotretinoin causes normalization of epidermal differentiation, depresses sebum excretion by 70%, is anti-inflammatory, and even reduces the presence of P acnes. Isotretinoin therapy should be initiated at a dose of 0.5 mg/kg/d for 4 weeks and increased as tolerated until a cumulative dose of 120-150 mg/kg is achieved. Coadministration with steroids at the onset of therapy may be useful in severe cases to prevent initial worsening. Some patients may respond to doses lower than the standard recommendation dosages. A lower dose (0.25-0.4 mg/kg/d) may be as effective as the higher dose given for the same time period and with greater patient satisfaction. Lower intermittent dosing schedules (1 week out of each month) are not as effective.

Isotretinoin is a teratogen, and pregnancy must be avoided. Contraception counseling is mandatory, and 2 negative pregnancy test results are required prior to the initiation of therapy in women of childbearing potential. The baseline laboratory examination should also include cholesterol and triglyceride assessment, hepatic transaminase levels, and a CBC count. Pregnancy tests and laboratory examinations should be repeated monthly during treatment.

Acne can be a very depressing situation. It freezes personality development in the adolescent stage and may create hostility, anger, and antisocial behavior. Associated mood changes and depression have also been reported during treatment. Isotretinoin may heighten feelings of depression and suicidal thoughts.Do not administer isotretinoin to a depressed or suicidal teenager. Although a cause-and-effect relationship has not been established, patients should be informed of this potential effect and must sign a consent form acknowledging they are aware of this potential risk.

A US Food and Drug Administration–mandated registry is now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information on this registry, see iPLEDGE. This registry aims to further decrease the risk of pregnancy and other unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.

While using isotretinoin, the patient is considered at high risk for abnormal healing and the development of excessive granulation tissue following procedures. Many dermatologists delay elective procedures, such as dermabrasion or laser resurfacing (eg, with carbon dioxide laser or erbium:YAG laser), for up to 1 year after completion of therapy. Other procedures to be avoided during therapy include tattoos, piercings, leg waxing, and other epilation procedures. Note the images below.

Acne with reactive hyperpigmentation; before treatment.

 

 

Acne with reactive hyperpigmentation; after treatment.

Procedural treatments include manual extraction of comedones and intralesional steroid injections. Additionally, some patients may benefit from superficial peels that use glycolic or salicylic acid. Phototherapy using red light or blue light and photodynamic therapy are being assessed as potential treatments for acne. The usefulness of some fractional laser treatments in the management of acne is also being evaluated.

Diet

Diet therapy has been suggested. Kligman, Fulton, and Plewig performed a study on chocolate, having teenage patients with acne consume 1 bar of chocolate each day. Some of the patients improved and some worsened, but the vast majority were unchanged. This study helped decrease the emphasis on diet as a causal factor in acne vulgaris. However, investigators always returned to the diet question. Data suggest that the westernization of certain Native American populations and the related consumption of unhealthy “junk” foods (eg, potato chips, soft drinks) has had a negative impact on general and skin health, resulting acne flares.

Investigators have also focused on a low-glycemic diet to avoid stress from high-carbohydrate diets and to reduce insulin levels. Studies have been encouraging, so the author recommends the “South Beach Diet” and provides patients with the glycemic index of foods. The author recommends that acne patients eat nothing higher than 70 on the glycemic index.

Medication Summary

The following information primarily pertains to the treatment of Propionibacterium acne vulgaris.

Antibiotics used to treat anaerobic infections usually suffice for other types of Propionibacterium infections. These include the penicillins, carbapenems, and clindamycin. In addition, vancomycin and teicoplanin (investigational) have been used. Some of these antibiotics are discussed after the treatment of acne vulgaris. Daptomycin has been used for the treatment of Propionibacterium osteomyelitis.

Retinoid-like Agents

    Topical tretinoin (Retin-A Micro, Atralin, Avita, Tretin-X)

     Adapalene (Differin)

     Tazarotene (Tazorac)

     Isotretinoin (Claravis, Amnesteem, Sotret)

 

Antibiotics, Other

    Tetracycline

     Minocycline (Solodyn, Minocin)

     Doxycycline (Doryx, Adoxa, Doxy 100, Vibramycin)

     Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

     Clindamycin (Cleocin)

     Clindamycin topical (ClindaGel, Cleocin-T)

     Erythromycin topical (Akne-mycin)

     Daptomycin (Cubicin)

 

Aldosterone Antagonists, Selective

Spironolactone (Aldactone)

 

Estrogens/Progestins

    Ethinyl estradiol, drospirenone, and levomefolate (Beyaz)

     Ethinyl estradiol and norethindrone (Estrostep Fe)

     Ethinyl estradiol and drospirenone (Yaz)

 

Acne Products

    Erythromycin and benzoyl peroxide (Benzamycin)

     Clindamycin and tretinoin (Ziana, Veltin)

     Clindamycin and benzoyl peroxide (Acanya, Duac CS, BenzaClin)

     Azelaic acid (Azelex, Finacea, Finacea Plus)

     Benzoyl peroxide (BenzEFoam, PanOxyl, Neutrogena On The Spot, Invisible Acne Treatment).

 

 

References:

 

1. [Guideline] Strauss JS, Krowchuk DP, Leyden JJ, et al. Guidelines of care for acne vulgaris management. J Am Acad Dermatol. Apr 2007;56(4):651-63. [Medline].

2. Lee JW, Yoo KH, Park KY, Han TY, Li K, Seo SJ, et al. Effectiveness of Conventional, Low-dose and Intermittent Oral Isotretinoin in the Treatment of Acne: A Randomized, Controlled Comparative study. Br J Dermatol. Nov 29 2010;[Medline].

3. Halvorsen JA, Stern RS, Dalgard F, Thoresen M, Bjertness E, Lien L. Suicidal ideation, mental health problems, and social impairment are increased in adolescents with acne: a population-based study. J Invest Dermatol. Feb 2011;131(2):363-70. [Medline].

4. Fanelli M, Kupperman E, Lautenbach E, Edelstein PH, Margolis DJ. Antibiotics, Acne, and Staphylococcus aureus Colonization. Arch Dermatol. Aug 2011;147(8):917-21. [Medline].

 

ROSACEA

 

http://emedicine.medscape.com/article/1071429-overview

http://www.youtube.com/watch?v=EhCc9aOtKsk

http://www.dailymotion.com/video/xsqm10_acne-rosacea-tretment_lifestyle#.UQ0zwPLE2H4

 

Background

Rosacea is a common condition characterized by symptoms of facial flushing and a spectrum of clinical signs, including erythema, telangiectasia, coarseness of skin, and an inflammatory papulopustular eruption resembling acne.

An expert committee assembled by the National Rosacea Society explicitly defined and classified rosacea in April 2002 into 4 different subtypes (erythematotelangiectatic type, papulopustular, phymatous, and ocular) based on specific clinical signs and symptoms. This categorization was an important step in the treatment of rosacea. Currently, the therapeutics of rosacea empirically target the signs and symptoms of the disease because investigators do not understand the details of its pathophysiology. Therefore, this classification system aides clinicians in treatment by highlighting the preponderance of one or more of the clustering signs of presentation and, thus, helps to specify which therapeutic approach to initiate.

The diagnosis of rosacea is a clinical diagnosis. Skin biopsy may be necessary to exclude other disease states that mimic the clinical presentation of rosacea. For example, the clinician must exclude polycythemia vera, connective-tissue diseases (eg, lupus erythematous, dermatomyositis, mixed connective-tissue disease), photosensitivity, carcinoid syndrome, mastocytosis, long-term application of topical steroids, contact dermatitis, and photosensitivity before making the diagnosis of rosacea.

Rosacea is defined by persistent erythema of the central portion of the face lasting for at least 3 months. Supporting criteria include flushing, papules, pustules, and telangiectasias on the convex surfaces. Secondary characteristics are burning and stinging, edema, plaques, a dry appearance, ocular manifestations, and phymatous changes. The prevalence of these findings designates the subclassification of the presentation and, additionally, the therapeutic options.

Erythematotelangiectatic type

Central facial flushing, often accompanied by burning or stinging, is the predominant sign in erythematotelangiectatic rosacea (ETR). The redness usually spares the periocular skin. These patients typically have skin with a fine texture that lacks a sebaceous quality characteristic of other subtypes. The erythematous areas of the face at times appear rough with scale likely due to chronic, low-grade dermatitis. Frequent triggers to flushing include acutely felt emotional stress, hot drinks, alcohol, spicy foods, exercise, cold or hot weather, and hot baths and showers. These patients also report that the burning or stinging is exacerbated when topical agents are applied.

Papulopustular rosacea

Papulopustular rosacea (PPR) is the classic presentation of rosacea. Patients are typically women of middle age who predominately present with a red central portion of their face that contains small erythematous papules surmounted by pinpoint pustules. One may elicit a history of flushing. Telangiectasias are likely present but may be difficult to distinguish from the erythematous background in which they exist. See the images below.

 

Acne rosacea. Courtesy of Dirk Elston, MD.

 

Pustular rosacea. Courtesy of Dirk Elston, MD.

Phymatous rosacea

Phymatous rosacea is defined as marked skin thickenings and irregular surface nodularities of the nose, chin, forehead, one or both ears, and/or the eyelids. Four distinct histologic variants can occur with rhinophyma (associated changes of the nose) that include glandular, fibrous, fibroangiomatous, and actinic. The mainstays of treatment are isotretinoin topical application and surgical correction. This varies from other rosacea subtypes.

Ocular rosacea

Ocular manifestations may precede the cutaneous signs by years. Yet, frequently they develop concurrently with dermatologic manifestations. The ocular manifestations include blepharitis, conjunctivitis, inflammation of the lids and meibomian glands, interpalpebral conjunctival hyperemia, and conjunctival telangiectasias. Patients may describe eye stinging or burning, dryness, irritation with light, or foreign body sensation. Ocular rosacea, similar to phymatous rosacea, has a distinct therapeutic management. Therefore, dermatologists must ask their patients specifically about ocular symptoms and perform a thorough physical examination to rule out this type of rosacea.

Pathophysiology

The etiology of rosacea is unknown. However, several factors, such as vasculature, climatic exposures, dermal matrix degeneration, chemicals and ingested agents, pilosebaceous unit abnormalities, microbial organisms, ferritin expression, reactive oxygen species (ROS), increased neoangiogenesis, and dysfunction of antimicrobial peptides (AMPs), likely play a role in its development.Furthermore, the distinct subtype of rosacea is likely determined by a patient’s unique sensitivity to these triggers.

Vasculature

Increased blood flow to the blood vessels of the face and increased numbers of blood vessels that are closer to the surface of the face are thought to be responsible for the redness and flushing associated with rosacea. Furthermore, vasodilatation, the normal response to hyperthermia, is thought to be more pronounced or exaggerated in those individuals with rosacea.

Climatic exposures

Some evidence suggests that harsh climatic exposures damage cutaneous blood vessels and dermal connective tissue. This also includes exposure to solar irradiation, which may explain why rosacea predominately affects the facial convexities and has a tendency to flare in the spring. However, other studies suggest the contrary, in that most patients’ symptoms do not worsen in the sunlight and do not flare with an acute exposure to ultraviolet (UV) light.

Dermal matrix degeneration

Rosacea involves associated damage to the endothelium and degeneration of the dermal matrix. However, it is not known whether the initial damage is in the dermal matrix and this leads to poor tissue support of cutaneous vessels, causing pooling of serum, inflammatory mediators, and metabolic waste, or whether the initial abnormality exists in the cutaneous vasculature and this leads to leaky vessels and delayed clearance of serum proteins, inflammatory mediators, and metabolic waste, thus resulting in matrix degeneration.

Chemicals and ingested agents

Spicy foods, alcohol, and hot beverages were traditionally thought to trigger flushing in patients with rosacea. However, most evidence does not support dietary factors playing a central role in the pathogenesis. Moreover, certain medications, such as amiodarone, topical steroids, nasal steroids, and high doses of vitamins B-6 and B-12, may cause flares for patients with rosacea.

Perivascular versus perifollicular inflammation

An inflammatory infiltrate may exist in a perivascular and/or a perifollicular location; however, evidence is conflicting regarding which location predominates. To answer this question, more studies need to be designed to categorize subtypes of rosacea because the answer varies depending on the subclassification.

Microbial organisms

Demodex species (mites that normally inhabit human hair follicles) may play a role in the pathogenesis of rosacea. Some studies suggest that Demodex prefers the skin regions that are affected in rosacea, such as the nose and cheeks.Research also supports that an immune response of helper-inducer T-cell infiltrates occurs, surrounding the Demodex antigens in patients with rosacea. Yet, conflicting evidence indicates that Demodex does not induce an inflammatory response in patients with rosacea. Moreover, Demodex is found in large numbers of healthy individuals without rosacea. More studies need to be performed to determine whether Demodex truly is pathogenic.

Additionally, inconclusive evidence suggests that Helicobacter pylori is associated with the etiology of rosacea. However, many of the studies have not controlled for confounding variables that influence H pylori prevalence, such as sex, age, socioeconomic status, and medications. Furthermore, these studies were not statistically powered to account for the ubiquitous nature of H pylori infection.

Ferritin expression

Iron catalyzes the conversion of hydrogen peroxide to free radicals, which leads to tissue injury by damaging cellular membranes, proteins, and DNA. At the cellular level, iron that is not metabolized is stored as ferritin. In a 2009 study, skin biopsy specimens from patients with rosacea were immunohistochemically analyzed, and the number of ferritin-positive cells was significantly higher in affected individuals compared with control subjects. Additionally, higher ferritin positivity correlated with more advanced subtypes of rosacea. Thus, increased release of free iron from proteolysis of ferritin can result in oxidative damage to the skin, which may contribute to the pathogenesis of rosacea.

Reactive oxygen species

Early in the inflammatory process, reactive oxygen species (ROS) are released by neutrophils, which are postulated to have a central role in the inflammation associated with rosacea. Free radicals, such as superoxide anions and hydroxyl radials, in addition to other reactive molecules, such as molecular oxygen, singlet oxygen, and hydrogen peroxide, comprise many of the ROS that lead to oxidative tissue damage. Several mechanisms explain how ROS result in skin inflammation, most notably the deactivation of natural defenses caused by excessive oxidant stress from ROS; chemical and oxidative modification of proteins and lipids by ROS; alteration of the lipid balance in rosacea patients, which, iormal proportions would suppress the creation of ROS; production of cytokines and other inflammatory mediators by keratinocytes, fibroblasts, and endothelial cells damaged by ROS; and the generation of ROS by cathelicidins, which are found in greater amounts in the facial skin of affected individuals.

Neoangiogenesis and vascular endothelial growth factor (VEGF) overexpression

Studies performed using video capillaroscopy on erythematotelangiectatic rosacea lesions showed increased neoangiogenesis and blood vessel enlargement. Multiple immunohistochemistry studies showed increased VEGF expression in vascular endothelium in lesional versus nonlesional skin of rosacea patients. Cuevas et al used topical dobesilate, an inhibitor of angiogenic growth factor, for the treatment of erythematotelagiectatic rosacea and reported an improvement in erythema and telangiectasia after 2 weeks.

Antimicrobial peptides

AMPs are small molecular weight proteins that are a part of the innate immune response and have demonstrated broad-spectrum antimicrobial activity against bacteria, viruses, and fungi. They are rapidly released upon injury and/or infection of the skin, and they have been implicated in the pathogenesis of many inflammatory skin diseases. Cathelicidins and β-defensins are 2 well-known types of AMPs, of which the former has been shown to be expressed in abnormally high levels in patients with rosacea.

Specifically, the LL-37 peptide form of cathelicidin, in addition to proteolytically processed forms of LL-37, have been found in significantly different amounts in rosacea patients compared with healthy individuals. LL-37 is expressed by polymorphonuclear leukocytes and lymphocytes. LL-37 interacts with endothelial cells and stimulates angiogenesis both in vitro and in vivo. It also modulates the expression of VEGF.Injection of LL-37 and these novel peptides derived from LL-37 into mice induced inflammation, erythema, and telangiectasia; therefore, researchers hypothesized that an excess of cathelicidins coupled with abnormal processing caused disease.

Physical

The disease consists of a spectrum of symptoms and signs, with most patients failing to develop every stage of disease. Variable erythema and telangiectasia are seen over the cheeks and the forehead. Inflammatory papules and pustules may be predominantly observed over the nose, the forehead, and the cheeks. Extrafacial involvement uncommonly occurs over the neck and the upper part of the chest. Prominence of sebaceous glands may be noted, with the development of thickened and disfigured noses (rhinophyma) in extreme cases. Unlike acne, patients generally do not report greasiness of the skin; instead, they may experience drying and peeling. The absence of comedones is another helpful distinguishing feature. Ocular lymphedema may be prominent but is uncommon. The condition generally does not produce scarring.

Rhinophyma may occur as an isolated entity, without other symptoms or signs of rosacea. Rhinophyma can be disfiguring and therefore distressing for patients. Some authorities consider rhinophyma to represent a different disease process, although phymatous rosacea is considered one of the four subtypes of rosacea.

Lymphedema may be marked periorbitally, and, on occasion, it is the presenting symptom.

Symptoms of ocular rosacea may be accompanied by conjunctival injection, and, rarely, chalazion and episcleritis may occur.

Rosacea fulminans (pyoderma faciale) is fortunately a rare complication and is characterized by the development of nodules and abscesses with sinus tract formation accompanied by systemic signs. Patients often have low-grade fever, elevated ESR, and possibly elevated white blood cell count.

Both seborrhea and seborrheic dermatitis/blepharitis are not uncommonly observed in patients with rosacea. The reasons for these associations are not well understood.

A rare granulomatous variant of rosacea (acne agminata/lupus miliaris disseminatus faciei) can manifest with inflammatory erythematous or flesh-colored papules distributed symmetrically across the upper part of the face, particularly around the eyes and the nose. The lesions tend to be discrete, and surrounding erythema is not a marked feature but may be present. These patients often do not have a history of flushing. This pattern of rosacea is sometimes associated with scarring and may be resistant to conventional treatment. See the image below.

Lupus miliaris disseminatus faciei. Courtesy of Dirk Elston, MD.

 

Diagnostic Considerations

The differential diagnosis largely depends on the pattern of rosacea. Erythematotelangiectatic rosacea (ETR) can resemble seborrheic dermatitis, lupus erythematosus, and other photodermatoses. Carcinoid syndrome and mitral valve incompetence are overlooked causes of erythema and telangiectasia. Acneiform rosacea may be simulated by acne, bromoderma and iododerma, perioral dermatitis, and pustular folliculitis. Acne agminata can be indistinguishable from lupus vulgaris and cutaneous sarcoidosis.

Differential Diagnoses

       Lupus Erythematosus, Acute

       Perioral Dermatitis

       Sarcoidosis

       Seborrheic Dermatitis

Medical Care

Before the initiation of therapy, the triggering factors that exacerbate the patient’s rosacea should be identified and avoided if possible. These factors may be unique to each individual patient. Common triggering factors include hot or cold temperatures, wind, hot drinks, caffeine, exercise, spicy food, alcohol, emotions, topical products that irritate the skin and decrease the barrier, or medications that cause flushing. Some patients find that regular facial massage reduces lymphedema. Rosacea fulminans is treated with moderately high doses of prednisolone (30-60 mg/d) followed by oral isotretinoin.

Sunscreen

The use of daily broad-spectrum sunscreen is recommended for all patients with rosacea. A sunscreen that protects against both UV-A and UV-B light should be selected. Physical blockers such as titanium dioxide and zinc oxide are well tolerated. Additionally, the sunscreen should contain protective silicones such as dimethicone or cyclomethicone. Green-tinted sunscreens can provide coverage of the erythema.

The patient is encouraged to avoid astringents, toners, menthols, camphor, waterproof cosmetics requiring solvents for removal, or products containing sodium lauryl sulfate.

Laser

Nonablative laser is effective against rosacea by remodeling of the dermal connective tissue and improving the epidermal barrier.The major disadvantage of this therapy is its cost because it is not covered by insurance. It requires 1-3 treatments 4-8 weeks apart to achieve the best results.

Vascular lasers are the mainstay of rosacea therapy. These include pulsed dye laser (585 or 595 nm), the potassium-titanyl-phosphate laser (532 nm), and the diode-pumped frequency-doubled laser (532 nm). These wavelengths allow selective absorption by oxyhemoglobin, leading to vessel reduction with minimal damage to surrounding tissue or scarring. To be effective against deeper facial vessels, longer wavelengths of lasers are required, including the diode laser (810 nm), the long-pulsed Alexandrite laser (755 nm), and the long-pulsed Nd:YAG laser (1064 nm).

Intense pulsed-light therapy is a multichromatic laser with different targets, including melanin and hemoglobin. Therefore, it is also useful for facial rejuvenation, affecting vascular lesions, pigmented lesions, and hair.

Surgical Care

Permanent telangiectasia may be treated by electrosurgery or the 585-nm pulsed dye laser. However, facial erythema is not improved, and new telangiectasias develop with the passage of time. Cosmetic improvement of rhinophyma may be produced by mechanical dermabrasion, carbon dioxide laser peel, and surgical shave techniques.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Topical metronidazole is commonly used as a first-line agent. Topical azelaic acid, sulfacetamide products, and topical acne medications are also commonly used. Topical and oral antibiotics are also very effective, and for oral rosacea, they are usually considered as a first-line therapy. Retinoids are advocated by some authorities.

In addition to the agents listed below, anecdotal evidence indicates effective treatment of rosacea with medications that reduce flushing, including beta-blockers, clonidine, naloxone, ondansetron, and selective serotonin reuptake inhibitors.

Oral contraceptive therapy has been helpful in patients who provide historical information of worsening rosacea with their hormonal cycle.

Dapsone has been used in severe, refractory rosacea, and dapsone has been particularly beneficial for patients who cannot take isotretinoin.

Immunosuppressants

Tacrolimus ointment (Protopic)

 

Antibiotics, Other

    Metronidazole gel 0.75% or 1% (MetroGel, Noritate, MetroLotion)

     Erythromycin (E.E.S., Erythrocin, Ery-Tab) tab or 2% topical solution

      Clindamycin topical (Cleocin T, Clindagel, Evoclin)

     Tetracycline

     Minocycline (Dynacin, Minocin, Solodyn)

     Doxycycline (Oracea, Doryx, Periostat, Vibramycin)

     Clarithromycin (Biaxin, Biaxin XL)

 

Retinoid-Like Agents

    Tretinoin topical (Avita, Retin-A, Retin-A Micro)

     Isotretinoin (Amnesteem, Claravis, Sotret)

 

Corticosteroids

Prednisolone (Millipred, Orapred, Veripred, Flo-Pred)

 

Antihypertensive Agents

    Amiloride

    Spironolactone (Aldactone)

     Triamterene (Dyrenium)

 

Acne Agents, Topical

    Benzoyl peroxide (Benzig, PanOxyl, Zapzyt, Acne Clear Maximum Strength)

     Azelaic acid (Azelex, Finacea)

     Sodium sulfacetamide and sulfur (Klaron, Ovace)

 

References:

1. Schauber J, Gallo RL. Antimicrobial peptides and the skin immune defense system. J Allergy Clin Immunol. Aug 2008;122(2):261-6. [Medline].

2.Laquer V, Hoang V, Nguyen A, Kelly KM. Angiogenesis in cutaneous disease: part II. J Am Acad Dermatol. Dec 2009;61(6):945-58; quiz 959-60. [Medline].

3.Tisma VS, Basta-Juzbasic A, Jaganjac M, et al. Oxidative stress and ferritin expression in the skin of patients with rosacea. J Am Acad Dermatol. Feb 2009;60(2):270-6. [Medline].

4.Jones DA. Rosacea, reactive oxygen species, and azelaic acid. J Clin Aesthetic Derm. Jan 2009;2(1):26-30.

5. Van Zuuren EJ, Kramer S, Carter B, Graber MA, Fedorowicz Z. Interventions for rosacea. Cochrane Database Syst Rev. Mar 16 2011;3:CD003262. [Medline].

FOLLICULITIS

 

1. https://www.clinicalkey.com/topics/dermatology/folliculitis.html

2. http://www.youtube.com/watch?v=W9JMNjzu8mE

 

What is folliculitis?

Folliculitis is an infection in the hair follicles. Each hair on your body grows out of a tiny pouch called a follicle. You can have folliculitis on any part of your body that has hair. But it is most common on the face and scalp and areas rubbed by clothing, such as the thighs and groin.

 

What causes folliculitis?

It usually is caused by bacteria. It also can be caused by yeast or another type of fungus.

You may get folliculitis if you have damaged hair follicles. Shaving or wearing clothes that rub the skin can irritate the follicles, which can lead to folliculitis. They also can become blocked or irritated by sweat, machine oils, or makeup. When the follicles are injured, they are more likely to become infected.

You are more likely to get folliculitis if you:

• Use a hot tub, whirlpool, or swimming pool that is not properly treated with chlorine.
• Wear tight clothes.
• Use antibiotics or steroid creams for long periods.
• Use or work with substances that can irritate or block the follicles. Examples include makeup, cocoa butter, motor oil, tar, and creosote.
• Have an infected cut, scrape, or surgical wound. The bacteria or fungi can spread to nearby hair follicles.
• Have a disease such as diabetes or HIV that lowers your ability to fight infection.

What are the symptoms?

Folliculitis usually looks like red pimples with a hair in the center of each one. The pimples may have pus in them, and they may itch or burn. When the pimples break open, they may drain pus, blood, or both.

“Hot tub folliculitis” most often appears about 72 hours after you’ve been in a hot tub or spa. Many small pimples appear on your stomach and sometimes on your arms and legs. You might have a mild fever and have an upset stomach. Most of the time, this kind of folliculitis goes away on its own in 7 to 10 days.

How is folliculitis diagnosed?

Your doctor will check your skin and ask about your health and activities. He or she may do tests to find out what is causing your folliculitis and to make sure you don’t have a different problem, such as impetigo or heat rash. Testing a sample of the fluid in the pimples or a sample of tissue can help your doctor learn what is causing the infection.

How is it treated?

Mild folliculitis usually heals on its own in about 2 weeks. You can take care of yourself at home with:

• Warm compresses made with white vinegar or Burow’s solution. These may ease itching and help healing.
• Medicated shampoo. It can be used to treat folliculitis on the scalp or beard.

 

          

 

 

 

 

 

References:

1. Habif TM. Principles of diagnosis and anatomy. In: Habif TP, ed. Clinical Dermatology. 5th ed. Philadelphia, Pa: Mosby Elsevier; 2009:chap 1.

2. Habif TM. Bacterial infections. In: Habif TP, ed. Clinical Dermatology. 5th ed. Philadelphia, Pa: Mosby Elsevier; 2009:chap 9.

3. Pasternack MS, Swartz MN. Cellulitis, necrotizing faciitis, and subcutaneous tissue infections. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 7th ed. Philadelphia, Pa: Elsevier Churchill Livingstone; 2009:chap 90.