Allergic diseases. Anaphylactic shock. Quincke’s edema. Oral manifestation of allergic lesions (erythema multiforme, reccurent aphtous stomatitis).

 

 

Hypersensitivity

Hypersensitivity refers to excessive, undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system. Hypersensitivity reactions require a pre-sensitized (immune) state of the host. Hypersensitivity reactions can be divided into four types: type I, type II, type III and type IV, based on the mechanisms involved and time taken for the reaction. Frequently, a particular clinical condition (disease) may involve more than one type of reaction.

 

TYPE I HYPERSENSITIVITY

Type I hypersensitivity is also known as immediate or anaphylactic hypersensitivity. The reaction may involve skin (urticariaand eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) and gastrointestinal tract (gastroenteritis). The reaction may cause a range of symptoms from minor inconvenience to death. The reaction usually takes 15 – 30 minutes from the time of exposure to the antigen, although sometimes it may have a delayed onset (10 – 12 hours).

Immediate hypersensitivity is mediated by IgE. The primary cellular component in this hypersensitivity is the mast cell or basophil. The reaction is amplified and/or modified by platelets, neutrophils and eosinophils. A biopsy of the reaction site demonstrates mainly mast cells and eosinophils.

The mechanism of reaction involves preferential production of IgE, in response to certain antigens (often called allergens). The precise mechanism as to why some individuals are more prone to type-I hypersensitivity is not clear. However, it has been shown that such individuals preferentially produce more of TH2 cells that secrete IL-4, IL-5 and IL-13 which in turn favor IgE class switch. IgE has very high affinity for its receptor (Fcε; CD23) on mast cells and basophils.

A subsequent exposure to the same allergen cross links the cell-bound IgE and triggers the release of various pharmacologically active substances (figure 1). Cross-linking of IgE Fc-receptor is important in mast cell triggering. Mast cell degranulation is preceded by increased Ca++ influx, which is a crucial process; ionophores which increase cytoplasmic Ca⁺⁺also promote degranulation, whereas, agents which deplete cytoplasmic Ca⁺⁺ suppress degranulation.

The agents released from mast cells and their effects are listed in Table 1. Mast cells may be triggered by other stimuli such as exercise, emotional stress, chemicals (e.g., photographic developing medium, calcium ionophores, codeine, etc.),anaphylotoxins (e.g., C4a, C3a, C5a, etc.). These reactions, mediated by agents without IgE-allergen interaction, are not hypersensitivity reactions, although they produce the same symptoms.

 

 

 

 

The reaction is amplified by PAF (platelet activation factor) which causes platelet aggregation and release of histamine, heparin and vasoactive amines. Eosinophil chemotactic factor of anaphylaxis (ECF-A) and neutrophil chemotactic factors attract eosinophils and neutrophils, respectively, which release various hydrolytic enzymes that cause necrosis. Eosinophils may also control the local reaction by releasing arylsulphatase, histaminase, phospholipase-D and prostaglandin-E, although this role of eosinophils is now in question.

 Cyclic nucleotides appear to play a significant role in the modulation of immediate hypersensitivity reaction, although their exact function is ill understood. Substances which alter cAMP and cGMP levels significantly alter the allergic symptoms. Thus, substances that increase intracellular cAMP seem to relieve allergic symptoms, particularly broncho-pulmonary ones, and are used therapeutically (Table 2). Conversely, agents which decrease cAMP or stimulate cGMP aggravate these allergic conditions.

 

 

 

Table 2 – Relationship between allergic symptoms and cyclic-nucleotides
Lowering of cyclic-AMP	elevation of cyclic-AMP
stimulation of α-adrenergic receptor (nor-epinephrin, phenyl-epinephrin) or blocking of β-adrenergic receptor (propanolol)	stimulation of β-adrenergic receptor (epinephrine, isoproterenol) blocking of α-adrenergic receptor (phenoxybenzamine) inhibition of phosphodiesterase (theophylline) binding of histamine-2 or PGE to their receptors
elevation of cyclic-GMP
stimulation of γ-cholinergic receptor (acetyl choline, carbacol)
WORSENING OF SYMPTOMS	IMPROVEMENT OF SYMPTOMS

 

Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests (fig. 1A), measurement of total IgE and specific IgE antibodies against the suspected allergens. Total IgE and specific IgE antibodies are measured by a modification of enzyme immunoassay (ELISA). Increased IgE levels are indicative of an atopic condition, although IgE may be elevated in some non-atopic diseases (e.g., myelomas, helminthic infection, etc.).

There appears to be a genetic predisposition for atopic diseases and there is evidence for HLA (A2) association.

Figure 1A close-up view of intradermal skin test with multiple positive allergen responses 

Symptomatic treatment is achieved with anti-histamines which block histamine receptors. Chromolyn sodium inhibits mast cell degranulation, probably, by inhibiting Ca⁺⁺ influx. Late onset allergic symptoms, particularly bronchoconstriction which is mediated by leukotrienes, are treated with leukotriene receptor blockers (Singulair, Accolate) or inhibitors of thecyclooxygenase pathway (Zileutoin). Symptomatic, although short term, relief from bronchoconstriction is provided by bronchodilators (inhalants) such as isoproterenol derivatives (Terbutaline, Albuterol). Thophylline elevates cAMP by inhibiting cAMP-phosphodiesterase and inhibits intracellular Ca⁺⁺ release is also used to relieve bronchopulmonary symptoms.

The use of IgG antibodies against the Fc portions of IgE that binds to mast cells has been approved for treatment of certain allergies, as it can block mast cell sensitization.

Hyposensitization (immunotherapy or desensitization) is another treatment modality which is successful in a number of allergies, particularly to insect venoms and, to some extent, pollens. The mechanism is not clear, but there is a correlation between appearance of IgG (blocking) antibodies and relief from symptoms. Suppressor T cells that specifically inhibit IgE antibodies may play a role.

TYPE II HYPERSENSITIVITY

Type II hypersensitivity is also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues. The antigens are normally endogenous, although exogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. Drug-induced hemolytic anemia, granulocytopenia and thrombocytopenia are such examples. The reaction time is minutes to hours. Type II hypersensitivity is primarily mediated by antibodies of the IgM or IgG classes and complement (Figure 2). Phagocytes and K cells may also play a role.

Figure 2. Type II cytotoxicity mechanism

The lesion contains antibody, complement and neutrophils. Diagnostic tests include detection of circulating antibody against the tissues involved and the presence of antibody and complement in the lesion (biopsy) by immunofluorescence. The staining pattern is normally smooth and linear, such as that seen in Goodpasture’s nephritis (renal and lung basement membrane) (figure 3A) and pemphigus (skin intercellular protein, desmosome) (figure 3B).

Figure 3A   Immunofluorescent stain of immunoglobulin G (IgG) showing linear pattern in Goodpasture’s syndrome

Figure 3B Pemphigus vulgaris – immunofluorescence 

Treatment involves anti-inflammatory and immunosuppressive agents.

TYPE III HYPERSENSITIVITY

Type III hypersensitivity is also known as immune complex hypersensitivity. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis), lungs (e.g., aspergillosis), blood vessels (e.g., polyarteritis), joints (e.g., rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms.

The reaction may take 3 – 10 hours after exposure to the antigen (as in Arthus reaction). It is mediated by soluble immune complexes. They are mostly of the IgG class, although IgM may also be involved. The antigen may be exogenous (chronic bacterial, viral or parasitic infections), or endogenous (non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE). The antigen is soluble and not attached to the organ involved. Primary components are soluble immune complexes and complement (C3a, 4a and 5a). The damage is caused by platelets and neutrophils (Figure 4). The lesion contains primarily neutrophils and deposits of immune complexes and complement. Macrophages infiltrating in later stages may be involved in the healing process.

Figure 4. Mechanism of damage in immune complex hypersensitivity

The affinity of antibody and size of immune complexes are important in production of disease and determining the tissue involved. Diagnosis involves examination of tissue biopsies for deposits of immunoglobulin and complement by immunofluorescence microscopy. The immunofluorescent staining in type III hypersensitivity is granular (as opposed to linear in type II such as seen in  Goodpasture’s syndrome). The presence of immune complexes in serum and depletion in the level of complement are also diagnostic. Polyethylene glycol-mediated turbidity (nephelometry) binding of C1q and Raji cell test are utilized to detect immune complexes. Treatment includes anti-inflammatory agents.

TYPE IV HYPERSENSITIVITY

Type IV hypersensitivity is also known as cell mediated or delayed type hypersensitivity. The classical example of this hypersensitivity is tuberculin (Montoux) reaction (figure 5)

Figure 5 
Mantoux intradermal tuberculin skin test for tuberculosis

which peaks 48 hours after the injection of antigen (PPD or old tuberculin). The lesion is characterized by induration and erythema.

Table 3  –   Delayed hypersensitivity reactions
Type	Reaction time	Clinical appearance	Histology	Antigen and site
contact	48-72 hr	eczema	lymphocytes, followed by macrophages; edema of epidermis	epidermal (organic chemicals, poison ivy, heavy metals, etc.)
tuberculin	48-72 hr	local induration	lymphocytes, monocytes, macrophages	intradermal (tuberculin, lepromin, etc.)
granuloma	21-28 days	hardening	macrophages, epitheloid and giant cells, fibrosis	persistent antigen or foreign body presence (tuberculosis, leprosy, etc.)

Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases (tuberculosis, leprosy, blastomycosis, histoplasmosis, toxoplasmosis, leishmaniasis, etc.) and granulomas due to infections and foreign antigens. Another form of delayed hypersensitivity is contact dermatitis (poison ivy (figure 6), chemicals, heavy metals, etc.) in which the lesions are more papular. Type IV hypersensitivity can be classified into three categories depending on the time of onset and clinical and histological presentation (Table 3).
 

Figure 6 Poison Ivy

Mechanisms of damage in delayed hypersensitivity include T lymphocytes and monocytes and/or macrophages. Cytotoxic T cells (Tc) cause direct damage whereas helper T (TH1) cells secrete cytokines which activate cytotoxic T cells and recruit and activate monocytes and macrophages, which cause the bulk of the damage (figure 4). The delayed hypersensitivity lesions mainly contain monocytes and a few T cells.

Major lymphokines involved in delayed hypersensitivity reaction include monocyte chemotactic factor, interleukin-2, interferon-gamma, TNF alpha/beta, etc.

Diagnostic tests in vivo include delayed cutaneous reaction (e.g. Montoux test (figure 5)) and patch test (for contact dermatitis). In vitro tests for delayed hypersensitivity include mitogenic response, lympho-cytotoxicity and IL-2 production.

Corticosteroids and other immunosuppressive agents are used in treatment.

Table 5 – Comparison of Different Types of hypersensitivity
characteristics	type-I (anaphylactic)	type-II (cytotoxic)	type-III (immune complex)	type-IV (delayed type)
antibody	IgE	IgG, IgM	IgG, IgM	None
antigen	exogenous	cell surface	soluble	tissues & organs
response time	15-30 minutes	minutes-hours	3-8 hours	48-72 hours
appearance	weal & flare	lysis and necrosis	erythema and edema, necrosis	erythema and induration
histology	basophils and eosinophil	antibody and complement	complement and neutrophils	monocytes and lymphocytes
transferred with	antibody	antibody	antibody	T-cells
examples	allergic asthma, hay fever	erythroblastosis fetalis, Goodpasture’s nephritis	SLE, farmer’s lung disease	tuberculin test, poison ivy, granuloma

 

Anaphylaxis.

 

Introduction

Anaphylaxis is a sudden onset (or rapidly progressive) severe systemic allergic reaction, affecting multiple organs. Its onset may be heralded by skin and/or mucosal changes (flushing, urticaria, angio-oedema) and progress to include life-threatening airway, lung and/or circulation problems.

However, it is important in outlining guidelines to emphasise the importance of prompt administration of adrenaline (epinephrine) and resuscitation measures. Antihistamine use is included in the guidelines but there is a lack of evidence either to support or refute their value in the treatment of anaphylaxis. They are certainly very much secondary in importance and useful to treat cutaneous manifestations of anaphylaxis but without relieving airway symptoms or hypotension. Administration of antihistamines should certainly never delay administration of adrenaline (epinephrine). There is a similar lack of evidence for use of steroids, although they may have value in preventing a biphasic reaction.

 

Incidence

The number of people who suffer severe systemic allergic reactions is increasing. The incidence is about 1-3 reactions per 10,000 population per annum, although anaphylaxis is not always recognised, so certain UK studies may underestimate the incidence.

 

Aetiology

An anaphylactic reaction occurs when an allergen reacts with specific IgE antibodies on mast cells and basophils (type 1 hypersensitivity reaction), triggering the rapid release of stored histamine and the rapid synthesis of newly formed mediators. These cause capillary leakage, mucosal oedema and ultimately shock and asphyxia. Anaphylactic reactions can vary in severity and rate of progression – they may progress rapidly (over a few minutes) or occasionally in a biphasic manner. Rarely, manifestations may be delayed by a few hours (adding to diagnostic difficulty), or persist for more than 24 hours. Anaphylactoid reactions are not IgE-mediated but cause similar mast cell activation.

A significant number of cases of anaphylaxis are idiopathic.

The most common triggers of anaphylaxis:

·           Foods:

o     Peanuts.

o     Pulses .

o     Tree nuts (e.g. brazil nut, almond, hazelnut).

o     Fish and shellfish.

o     Eggs.

o     Milk.

o     Sesame.

·           Venom, for example:

o     Bee stings.

o     Wasp stings.

·           Drugs, including:

o     Antibiotics.

o     Opioids.

o     Non-steroidal anti-inflammatory drugs (NSAIDs).

o     Intravenous (IV) contrast media.

o     Muscle relaxants.

o     Other anaesthetic drugs.

 

 

Presentation

There is often (but not always) a history of previous sensitivity to an allergen, or recent history of exposure to a new drug (e.g. vaccination). Initially, patients usually develop skin symptoms, including generalised itching, urticaria and erythema, rhinitis, conjunctivitis and angio-oedema.

Signs that the airway is becoming involved include itching of the palate or external auditory meatus, dyspnoea, laryngeal oedema (stridor) and wheezing (bronchospasm). General symptoms include palpitations and tachycardia (as opposed to bradycardia in simple vasovagal episode at immunisation time), nausea, vomiting and abdominal pain, feeling faint – with a sense of impending doom; and, ultimately, collapse and loss of consciousness.

Airway swelling, stridor, breathing difficulty, wheeze, cyanosis, hypotension, tachycardia and reduced capillary filling suggest impending severe reaction.

If no history is available in a collapsed patient, use an ABCDE advanced life-support approach (see box, below) to recognise and treat an anaphylactic reaction. Treat life-threatening problems as you find them. The basic principles of treatment are the same for all age groups.

Differential diagnosis

Life-threatening conditions:

·           Sometimes an anaphylactic reaction can present with symptoms and signs that are very similar to life-threatening asthma – this is most common in children.

·           A low blood pressure (BP) – or normal in children – with a petechial or purpuric rash can be a sign of septic shock.

·           Seek help early if there are any doubts about the diagnosis and treatment.

Non-life-threatening conditions – these usually respond to simple measures:

·           Faint (vasovagal episode).

·           Panic attack.

·           Breath-holding episode in a child.

·           Idiopathic (non-allergic) urticaria or angio-oedema.

Emergency treatment

Treatment in an emergency means following without delay a systematic assessment and treatment plan.

Quick reference anaphylaxis algorithm ·   Rapid assessment: o  Airway: look for and relieve airway obstruction; call for help early if there are signs of obstruction. Remove any traces of allergen remaining (e.g. nut fragments caught in teeth, with a mouthwash; bee stings without compressing any attached venom sacs). o  Breathing: look for and treat bronchospasm and signs of respiratory distress. o  Circulation: colour, pulse and BP. o  Disability: assess whether responding or unconscious. o  Exposure: assess skin with adequate exposure, but avoid excess heat loss. ·   Consider anaphylaxis when there is compatible history of rapid-onset severe allergic-type reaction with respiratory difficulty and/or hypotension, especially if there are skin changes present. ·   Give high-flow oxygen – using a mask with an oxygen reservoir (greater than 10 litres min-1 to prevent reservoir collapse). ·   Lie the patient flat: o  Raise the legs (care, as this may worsen any breathing problems). o  In pregnant patients, use a left lateral tilt of at least 15° (to avoid caval compression). ·   Adrenaline (epinephrine) intramuscularly (IM) in the anterolateral aspect of the middle third of the thigh (safe, easy, effective): o  Adult IM dose 0.5 mg IM (= 500 micrograms = 0.5 mL of 1:1000) adrenaline (epinephrine). o  Child IM dose (the equivalent volume of 1:1000 adrenaline (epinephrine) is shown in brackets): §  >12 years: 500 micrograms IM (0.5 mL), i.e. the same as the adult dose. 300 micrograms (0.3 mL) if the child is small or prepubertal. §  >6-12 years: 300 micrograms IM (0.3 mL). §  <6 years: 150 micrograms IM (0.15 mL). o  Note: half doses of adrenaline (epinephrine) may be safer for patients on amitriptyline, imipramine, monoamine oxidase inhibitor (MAOI) or beta-blocker. ·   When skills and equipment are available: o  Establish airway (in anaphylaxis, airway obstruction from tissue swelling is difficult to overcome and early expert intubation is ofteeeded). o  IV fluid challenge: §  Insert one or more large-bore IV cannulae (enable the highest flow). §  Use intraosseous access (if trained to do so) in children when IV access is difficult. §  Give a rapid fluid challenge: §  Adults – 500 mL of warmed crystalloid solution (e.g., Hartmann’s or 0.9% saline) in 5-10 minutes if the patient is normotensive or one litre if the patient is hypotensive. §  Use smaller volumes (e.g. 250 mL) for adult patients with known cardiac failure and use closer monitoring (listen to the chest for crepitations after each bolus). §  The use of invasive monitoring, e.g., central venous pressure (CVP), can help to assess fluid resuscitation. §  For children – give 20 mL/kg of warmed crystalloid. o  Chlorphenamine (after initial resuscitation). Dose depends on age: §  >12 years and adults: 10 mg IM or IV slowly. §  >6-12 years: 5 mg IM or IV slowly. §  >6 months-6 years: 2.5 mg IM or IV slowly. §  <6 months: 250 micrograms/kg IM or IV slowly. o  Hydrocortisone (after initial resuscitation). Dose depends on age: §  >12 years and adults: 200 mg IM or IV slowly. §  >6-12 years: 100 mg IM or IV slowly. §  >6 months-6 years: 50 mg IM or IV slowly. §  <6 months: 25 mg IM or IV slowly. o  Monitor: §  Pulse oximetry §  ECG §  BP

Monitoring

·   All critically ill patients should be given oxygen.

·   Maintain the PaO₂ as close to normal as possible (approximately 13 kPa or 100 mm Hg).

·   When/if a pulse oximeter is available:

o  Titrate the oxygen to maintain an oxygen saturation of 94-98%.

o  In the sickest patients this is not always possible so you may have to accept a lower value, i.e., above 8 kPa (60 mm Hg), or 90-92% oxygen saturation on a pulse oximeter.

·   A normal SpO₂ on oxygen does not necessarily mean ventilation is adequate (because the pulse oximeter detects oxygenation and not hypercapnia). The patient may be breathing inadequately (with a high PaCO₂).

·   Use bag-mask ventilation while calling urgently for expert help. In an anaphylactic reaction, upper airway obstruction or bronchospasm can make bag mask ventilation difficult or impossible.

·   Consider early tracheal intubation (if equipment and expertise are available). If the patient is intubated, give high-concentration oxygen with a self-inflating bag.

Blood pressure – reassess the pulse rate and BP regularly (every 5 minutes).

Aim for:

·   In adults, normal BP (or a systolic BP greater than 100 mm Hg).

·   In children:

o  0 to1 month: minimum 50-60 mm Hg.

o  >1 to12 months: minimum 70 mm Hg.

o  >1 to 10 years 70+ (age in years x 2) mm Hg.

o  >10 years: minimum 90 mm Hg.

·   If the patient does not improve, repeat the fluid challenge.

·   If there are symptoms and signs of cardiac failure (shortness of breath, increased heart rate, raised JVP, a third heart sound, and inspiratory crackles in the lungs on auscultation):

o  Decrease or stop the fluid infusion.

o  Seek expert help (inotropes or vasopressors may be needed).

Follow-up

When time allows:

·           Immediate:

o     Take a full history from the patient (relatives, friends, and other staff).

o     Review the patient’s notes and charts. Study both absolute and trends of values relating to vital signs.

o     Check that important routine medications are prescribed and being given.

o     Review the results of laboratory or radiological investigations.

o     Consider what level of care is required by the patient, e.g., transport to hospital if in the community.

o     In the patient’s notes, make complete entries of your findings, assessment and treatment. Record the patient’s response to therapy.

o     Consider definitive treatment of the patient’s underlying condition.

·           In the long term:

o     Refer to an allergist or allergy clinic to try to identify the allergen, so that it can be avoided in future.

o     Organise self-use of pre-loaded pen injections for future attacks (e.g. EpiPen®; containing 0.3 mL of 1 in 1000 strength (that is, 300 micrograms) for adults; and for children 0.3 mL of 1 in 2000 (150 micrograms)). This again may be best done in allergy clinics.

o     Give a written self-management plan and arrange to teach the patient and relatives how to use syringes

 

Angioedema

Angioedema or Quincke’s edema is the rapid swelling (edema) of the dermis, subcutaneous tissue,mucosa and submucosal tissues.

Symptoms:

•         The skin of the face, normally around the mouth, and the mucosa of the mouth and/or throat, as well as the tongue, swell up over the period of minutes to several hours.

•         The swelling can also occur elsewhere, typically in the hands. The swelling can be itchy or painful.

•         There may also be slightly decreased sensation in the affected areas due to compression of the nerves. 

•         Urticaria(hives) may develop simultaneously.

•         In severe cases, stridor of the airway occurs, with gasping or wheezy inspiratory breath sounds and decreasing oxygen levels. 

 

Causative factors:

•         Food related products for Quincke’s edema associated with urticaria.

•         Drugs like penicillin, aspirin, phenytoin and others,

•         Infection- bacterial and viral

•         Venoms, medication and food can induce anaphylaxis in sensitized individuals.

•          

•         Hereditary angio-oedema is an autosomal-dominant disorder associated with recurrent episodes of edema of the subcutaneous tissue without.

•          

•         Onset is usually in early childhoodbut may be delayed even into late adult life.

 

Treatment

•         Angioneurotic odema is a medical emergency, it always better to seek the medical help immediately

 

•         To give airway support in case of medical support

•         Antihistamines

•         Corticosteroids

•         Adrenaline in acute condition

•         C1 esterase inhibitors in case of hereditary angioneurotic edema

 

Erythema multiforme

Erythema multiforme (EM) is an acute, self-limited, and sometimes recurring skin condition that is considered to be a type IV hypersensitivity reaction associated with certain infections, medications, and other various triggers.

Symptoms:

•         Fever

•         General ill feeling

•         Itching of the skin

•         Joint aches

•         Multiple skin lesions:

–       Start quickly and may return

–       May spread

–       May appear as a nodule, papule, or macule and may look like hives

–       Central sore surrounded by pale red rings, also called a “target”, “iris”, or “bulls-eye”

–       May have vesicles and blisters of various sizes (bullae)

–       Located on the upper body, legs, arms, palms, hands, or feet

–       May involve the face or lips

–       Usually even on both sides (symmetrical)

 

 

History:

•         In EM, there may be no prodrome or a mild upper respiratory tract infection.

•         The rash starts abruptly, usually within 3 days. It starts on the extremities, being symmetrical and spreading centrally.

•         Half of children with the rash have recent herpes labialis.

•         It usually precedes the erythema multiforme by 3 to 14 days but it can sometimes be present at the onset.

Examination:

•         The iris or target lesion is the classical feature of the disease.

•         Initially there is a dull red flat spot or wheal that enlarges slightly up to 2 cm over 24 to 48 hours.

•         In the middle, a small bump, vesicle, or bulla develops, flattens, and then may clear. The intermediate ring forms and becomes raised, pale, and swollen. The periphery slowly becomes purple and forms a concentric lesion, resembling a target. Some lesions are atypical targets with only 2 concentric rings.

•         The Koebner phenomenon may occur. This is where a lesion occurs along the line of trauma and it is typical of psoriasis and lichen planus.

•         Lesions appear first on the extensor surfaces of the periphery and extend centrally. The palms, neck and face are often involved but the soles and flexures of the extremities less often.

•         There may be mucosal involvement in 70% of patients but it tends to be mild and limited to just one mucosal surface (for example mouth or vulva).

•         Oral lesions are most common with lips, palate and gingiva affected. There may be red conjunctivae and tearing, but eye involvement tends to be mild.

•         Genital involvement can produce painful hemorrhagic bullae and erosions.

Investigations:
No specific investigations are indicated.

•         Nikolsky’s sign is positive

•         A punch biopsy may be required to confirm diagnosis.

Management:
In recurrent disease due to HSV, antiviral therapy is helpful.

•         Symptomatic treatment may include analgesics, mouth wash and local skin care.

•         Steroid creams may be used. If the mouth is very sore, attention may have to be given to hydration and nutrition.

•         Lubricating drops for eyes may be required.

 

Skin Tests

Scratch test (also known as a puncture or prick test). This test is done by placing a drop of a solution containing a possible allergen on the skin, and a series of scratches or needle pricks allows the solution to enter the skin. If the skin develops a red, raised itchy area (called a wheal), it usually means that the person is allergic to that allergen. This is called a positive reaction.

 

Intradermal test. 

Intradermal test. After examining and cleaning the skin, a small amount of the allergen is injected just under the skin, similar to a tuberculosis test.

•          During this test, a small amount of the allergen solution is injected into the skin.

•         An intradermal allergy test may be done when a substance does not cause a reaction in the skin prick test but is still suspected as an allergen for that person.

•          The intradermal test is more sensitive than the skin prick test but is more often positive in people who do not have symptoms to that allergen (false-positive test results).

 

 

Patch test.

 For a skin patch test, the allergen solution is placed on a pad that is taped to the skin for 24 to 72 hours. This test is used to detect a skin allergy called contact dermatitis.

 

 

Allergy blood tests

•         Allergy blood tests look for substances in the blood called antibodies. Blood tests are not as sensitive as skin tests but are often used for people who are not able to have skin tests.

•         The most common type of blood test used is the enzyme-linked immunosorbent assay (ELISA, EIA). It measures the blood level of a type of antibody (called immunoglobulin E, or IgE) that the body may make in response to certain allergens. IgE levels are often higher in people who have allergies or asthma.

•         Other lab testing methods, such as radioallergosorbent testing (RAST) or an immunoassay capture test (ImmunoCAP, UniCAP, or Pharmacia CAP), may be used to provide more information.

 

 

References:

1.        Danilevskiy M.F. et al. “ Diseases of the mucous membrane of the mouth.” – K.: “Medytsyna”, 2010.

2.        Bruch J.M. Clinical oral medicine and pathology/ J.M. Bruch, N.S. Treister// London.:Humana Press, 2010

3.        Cawson R. E. Cawson’s essentials of oral pathology and oral medicine. Seventh edition/ Cawson R. E. et. al. //Elsevier science limited, 2002.

4.        Slootweg P. Dental pathology – a practical introduction/ P.J. Slootweg// Berlin.: Springer, 2007.

5.        Da Silva J.D. Oxford American Handbook of Clinical Dentistry (Oxford American Handbooks in Medicine) / J.D. Da Silva et al.// Oxford University Press, 2007.

6. http://en.wikipedia.org/wiki/Anaphylaxis
7. http://pathmicro.med.sc.edu/mobile/m.immuno-17.htm
8. http://www.patient.co.uk/doctor/anaphylaxis-and-its-treatment
9. http://en.wikipedia.org/wiki/Angioedema
10. http://en.wikipedia.org/wiki/Erythema_multiforme

 

 

Information was prepared by Sukhovolets I.O.