Main symptoms and syndromes of diseases of stomach and intestine

Main symptoms and syndromes of diseases of stomach and intestine. Methods of clinical, laboratory and instrumental examination in acute and chronic gastritis, peptic stomacfh and duodenal ulcer, enteritis and colitis

Gastritis

         Gastritis is a common рrоblem and its incidence is increasing. It is best defined as «an inflammatory response to gastric mucosal injury». Various previous classifications have been superseded by the Sydney system, which takes account of the aetiological role of Helicobacter pylori and integrates the clinical presentation, endoscopic findings, histological appearance and anatomical involvement of different regions of the stomach.

         There is a little association between symptoms, endoscopic abnormality, histological abnormality, anatomical distribution of any abnormalities found, and the presence or absence of  H.pylori infection or other causative factors. Endoscopy alone is not diagnostic of any particular form of gastritis, though various abnormalities may be seen including erythema, erosions and haemorrhage. Gastritis is now best classified as follows.

                  Criteria for diagnosis of the gastritis.

The term gastritis should be reserved for histologically documented inflammation of the gastric mucosa. Gastritis is not the mucosal erythema seen during endoscopy and is not interchangeable with “dyspepsia.” The etiologic factors leading to gastritis are broad and heterogeneous. Gastritis has been classified based on time course (acute vs. chronic), histologic features, and anatomic distribution or proposed pathogenic mechanism .

         The correlation between the histologic findings of gastritis, the clinical picture of abdominal pain or dyspepsia, and endoscopic findings noted on gross inspection of the gastric mucosa is poor. Therefore, there is no typical clinical manifestation of gastritis.

Acute Gastritis.

         The most common causes of acute gastritis are infectious. Acute infection with H. pylori induces gastritis. However, H. pylori acute gastritis has not been extensively studied. Reported as presenting with sudden onset of epigastric pain, nausea, and vomiting, limited mucosal histologic studies demonstrate a marked infiltrate of neutrophils with edema and hyperemia. If not treated, this picture will evolve into one of chronic gastritis. Hypochlorhydria lasting for up to 1 year may follow acute H. pylori infection.

         The highly acidic gastric environment may be one reason why infectious processes of the stomach are rare. Bacterial infection of the stomach or phlegmonous gastritis is a rare potentially life-threatening disorder, characterized by marked and diffuse acute inflammatory infiltrates of the entire gastric wall, at times accompanied by necrosis. Elderly individuals, alcoholics, and AIDS patients may be affected. Potential iatrogenic causes include polypectomy and mucosal injection with India ink. Organisms associated with this entity include streptococci, staphylococci, Escherichia coli, Proteus, and Haemophilus. Failure of supportive measures and antibiotics may result in gastrectomy.

Chronic Gastritis.

         Chronic gastritis is identified histologically by an inflammatory cell infiltrate consisting primarily of lymphocytes and plasma cells, with very scant neutrophil involvement. Distribution of the inflammation may be patchy, initially involving superficial and glandular portions of the gastric mucosa. This picture may progress to more severe glandular destruction, with atrophy and metaplasia. Chronic gastritis has been classified according to histologic characteristics. These include superficial atrophic changes and gastric atrophy.

         The next stage is atrophic gastritis. The inflammatory infiltrate extends deeper into the mucosa, with progressive distortion and destruction of the glands. The final stage of chronic gastritis is gastric atrophy. Glandular structures are lost; there is a paucity of inflammatory infiltrates. Endoscopically the mucosa may be substantially thin, permitting clear visualization of the underlying blood vessels.   

 Gastric glands may undergo morphologic transformation in chronic gastritis. Intestinal metaplasia denotes the conversion of gastric glands to a small intestinal phenotype with small-bowel mucosal glands containing goblet cells. The metaplastic changes may vary in distribution from patchy to fairly extensive gastric involvement. Intestinal metaplasia is an important predisposing factor for gastric cancer.

         Chronic gastritis is also classified according to the predominant site of involvement. Type A refers to the body-predominant form (autoimmune) and type B is the central-predominant form (H. pylori-related). This classification is artificial in view of the difficulty in distinguishing these two entities. The term AB gastritis has been used to refer to a mixed antral/body picture.

         Type A Gastritis. The less common of the two forms involves primarily the fundus and body, with antral sparing. Traditionally, this form of gastritis has been associated with pernicious anemia in the presence of circulating antibodies against parietal cells and intrinsic factor; thus it is also called autoimmune gastritis. H. pylori infection can lead to a similar distribution of gastritis. The characteristics of an autoimmune picture are not always present.

         Parietal cell antibodies and atrophic gastritis are observed in family members of patients with pernicious anemia. These antibodies are observed in up to 20% of individuals over age 60 and in ~20% of patients with vitiligo and Addison’s disease. About half of patients with pernicious anemia have antibodies to thyroid antigens, and about 30% of patients with thyroid disease have circulating anti-parietal cell antibodies. Anti-intrinsic factor antibodies are more specific than parietal cell antibodies for type A gastritis, being present in ~40% of patients with pernicious anemia. Another parameter consistent with this form of gastritis being autoimmune in origin is the higher incidence of specific familial histocompatibility haplotypes such as HLA-B8 and -DR3.

         The parietal cell-containing gastric gland is preferentially targeted in this form of gastritis, and achlorhydria results. Parietal cells are the source of intrinsic factor, lack of which will lead to vitamin B12 deficiency and its sequelae (megaloblastic anemia, neurologic dysfunction).

         Gastric acid plays an important role in feedback inhibition of gastrin release from G cells. Achlorhydria, coupled with relative sparing of the antral mucosa (site of G cells), leads to hypergastrinemia. Gastrin levels can be markedly elevated (>500 pg/mL) in patients with pernicious anemia. ECL cell hyperplasia with frank development of gastric carcinoid tumors may result from gastrin trophic effects. The role of gastrin in carcinoid development is confirmed by the observation that antrectomy leads to regression of these lesions. Hypergastrinemia and achlorhydria may also be seen ion-pernicious anemia-associated type A gastritis.

         Type B gastritis. Type B, or antral-predominant, gastritis is the more common form of chronic gastritis. H. pylori infection is the cause of this entity. Although described as “antral-predominant,” this is likely a misnomer in view of studies documenting the progression of the inflammatory process towards the body and fundus of infected individuals. The conversion to a pan-gastritis is time-dependent-estimated to require 15 to 20 years. This form of gastritis increases with age, being present in up to 100% of people over age 70. Histology improves after H. pylori eradication. The number of H. pylori organisms decreases dramatically with progression to gastric atrophy, and the degree of inflammation correlates with the level of these organisms. Early on, with antral-predominant findings, the quantity of H. pylori is highest and a dense chronic inflammatory infiltrate of the lamina propria is noted accompanied by epithelial cell infiltration with polymorphonuclear leukocytes.

         Multifocal atrophic gastritis, gastric atrophy with subsequent metaplasia, has been observed in chronic H. pylori-induced gastritis. This may ultimately lead to development of gastric adenocarcinoma. H. pylori infection is now considered an independent risk factor for gastric cancer. Worldwide epidemiologic studies have documented a higher incidence of H. pylori infection in patients with adenocarcinoma of the stomach as compared to control subjects. Seropositivity for H. pylori is associated with a three- to sixfold increased risk of gastric cancer. This risk may be as high as ninefold after adjusting for the inaccuracy of serologic testing in the elderly. The mechanism by which H. pylori infection leads to cancer is unknown. However, eradication of H. pylori as a general preventative measure for gastric cancer is not recommended.

DIAGNOSIS OF H.PYLORI

Histology

 H. pylori can be detected histologically on biopsy of gastric mucosa obtained at endoscopy and stained with haematoxylin and eosin or Giemsa stains.

Rapid urease activity test

 H. pylori produces urease that is required for gastric colonization by H. pylori and that may protect it from the effects of gastric acid. This urease producing activity of the organism is utilized for diagnosis by placing the biopsy specimen in urea and assessing ammonia release that changes the color of the solution.

Culture  

      Biopsies obtained can be cultured on special medium and sensitivities to antibiotics can be ascertained.

Urea breath test with BC or 14C

     This is a quick and easy way of detecting the presence of H. pylori by urease production with release of labelled C02 detected on a mass spectrometer. This test indicates active infection but is expensive.
     Serological test

      An ELISA test for the detection of serum IgG antibodies to helicobacter proteins is used. This test has good sensitivity and specificity but it caot differentiate recent or previous infection. IgG titers fall by 50% after eradication.

          Miscellaneous Forms of Gastritis.

         Lymphocytic gastritis is characterized histologically by intense infiltration of the surface epithelium with lymphocytes. The infiltrative process is primarily in the body of the stomach and consists of mature T cells and plasmacytes. The etiology of this form of chronic gastritis is unknown. It has been described in patients with celiac sprue, but whether there is a common factor associating these two entities is unknown. No specific symptoms suggest lymphocytic gastritis. A subgroup of patients has thickened folds noted on endoscopy. These folds are often capped by small nodules that contain a central depression or erosion; this form of the disease is called varioliform gastritis. H. pylori probably plays no significant role in lymphocytic gastritis. Therapy with glucocorticoids or sodium cromoglycate has obtained unclear results.

         Marked eosinophilic infiltration involving any layer of the stomach (mucosa, muscularis propria, and serosa) is characteristic of eosinophilic gastritis. Affected individuals will often have circulating eosinophilia with clinical manifestation of systemic allergy. Involvement may range from isolated gastric disease to diffuse eosinophilic gastroenteritis. Antral involvement predominates, with prominent edematous folds being observed on endoscopy. These prominent antral folds can lead to outlet obstruction. Patients can present with epigastric discomfort, nausea, and vomiting. Treatment with glucocorticoids has been successful.

         Occasionally, a surgically obtained full-thickness biopsy of the stomach may be required to exclude malignancy.

Treatment

The treatment of gastritis depends on the cause of the problem. Some causes may resolve by themselves over time, or may be relieved by stopping the ingestion of irritating substances such as alcohol, tobacco, and aspirin. Some dietary changes will no doubt be recommended, although the bland diet often prescribed in the past is no longer thought to be necessary. Medications are often necessary to relieve symptoms, eradicate an infection such as H. pylori, and prevent or treat complications from gastritis such as an ulcer.

Lifestyle

The cure for gastritis caused by ingesting irritating substances is to stop the long-term use of these substances, which may include:

– Alcohol

– Tobacco

– Acidic beverages such as coffee, carbonated beverages, and fruit juices with citric acid

– NSAIDS, such as aspirin and ibuprofen – switch to other pain relievers (like acetominophen)

– Eat a fiber-rich diet

– Avoid high fat .

Medications

Helicobactor pylori infestation, a common bacterial cause of gastritis and ulcers, is typically treated with a combination of drugs. The typical combination includes antibiotics, a bismuth compound, and a proton pump inhibitor. (Proton pump inhibitors reduce stomach acid secretion.) These drugs are usually taken for at least 14 days.

In addition to the medications used for Helicobacter pylori infection, other medications that may be used to relieve symptoms of gastritis include those that reduce stomach acid secretion:

– Antacids such as calcium carbonate and magnesium hydroxide with aluminum salts

– H2 blockers such as ranitidine, cimetidine, nizatidine, and famotidine

– Proton pump inhibitors such as omeprazole and lansoprazole

– Drugs that reduce stomach acid secretion help protect against or treat ulcers. Other drugs used for ulcers include:

– Misoprostol – protects against the major intestinal toxicity of NSAIDS, and can reduce the formation of ulcers

– Sucralfate – helps to heal ulcers in the stomach

Treatment in chronic gastritis is aimed at the sequelae and not the underlying inflammation. Patients with pernicious anemia will require parenteral vitamin B12 supplementation on a long-term basis. Eradication of H. pylori is not routinely recommended unless PUD or a low-grade MALT lymphoma is present.

 

Peptic Ulcer

Peptic ulcer is a general chronic and relapsing disease characterized by seasonal exacerbations with ulceration of the stomach wall or the duodenum.

History. Abdominal pain is common to many gastrointestinal disorders, including DU and GU, but has a poor predictive value for the presence of either DU or GU. Up to 10% of patients with NSAID-induced mucosal disease with a complication (bleeding, perforation, and obstruction) without antecedent symptoms. Despite this poor correlation, a careful history and physical examination are essential components of the approach to a patient suspected  of  having peptic ulcers.

            Variation in the intensity or distribution of the abdominal pain, as well as the onset of associated symptoms such as nausea and/or vomiting, may be indicative of an ulcer complication. Dyspepsia that becomes constant, is no longer relieved by food or antacids, or radiates to the back may indicate a penetrating ulcer (pancreas). Sudden onset of severe, generalized abdominal pain may indicate perforation. Pain worsening with meals, nausea, and vomiting of undigested food suggest gastric outlet obstruction. Tarry stools or coffee ground emesis indicate bleeding.

Pathphysiology. Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer.

Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs, H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, mucosal blood flow, cellular restitution, and epithelial renewal.

Most patients with duodenal ulcers have impaired duodenal bicarbonate secretion, which has also proven to be caused by H pylori because its eradication reverses the defect. The combination of increased gastric acid secretion and reduced duodenal bicarbonate secretion lowers the pH in the duodenum, which promotes the development of gastric metaplasia (ie, the presence of gastric epithelium in the first portion of the duodenum). H pylori infection in areas of gastric metaplasia induces duodenitis and enhances the susceptibility to acid injury, thereby predisposing to duodenal ulcers. Duodenal colonization by H pylori was found to be a highly significant predictor of subsequent development of duodenal ulcers in one study that followed 181 patients with endoscopy-negative, nonulcer dyspepsia^.

Etiology

Peptic ulcer disease (PUD) may be due to any of the following:

^–          H pylori infection

^–          Drugs

^–          Lifestyle factors

^–          Severe physiologic stress

^–          Hypersecretory states (uncommon)

^–          Genetic factors

H pylori infection

H pylori infection and NSAID use account for most cases of PUD. The rate of H pylori infection for duodenal ulcers in the United States is less than 75% for patients who do not use NSAIDs. Excluding patients who used NSAIDs, 61% of duodenal ulcers and 63% of gastric ulcers were positive for H pylori in one study. These rates were lower in whites than ionwhites. Prevalence of H pylori infection in complicated ulcers (ie, bleeding, perforation) is significantly lower than that found in uncomplicated ulcer disease.

Drugs

NSAID use is a common cause of PUD. These drugs disrupt the mucosal permeability barrier, rendering the mucosa vulnerable to injury. As many as 30% of adults taking NSAIDs have GI adverse effects. Factors associated with an increased risk of duodenal ulcers in the setting of NSAID use include history of previous peptic ulcer disease, advanced age, female sex, high doses or combinations of NSAIDs, long-term NSAID use, concomitant use of anticoagulants, and severe comorbid illnesses.

Although the prevalence of NSAID gastropathy in children is unknown, it seems to be increasing, especially in children with chronic arthritis treated with NSAIDs. Case reports have demonstrated gastric ulceration from low-dose ibuprofen in children, even after just 1 or 2 doses

Corticosteroids alone do not increase the risk for PUD; however, they can potentiate ulcer risk in patients who use NSAIDs concurrently.

The risk of upper GI tract bleeding may be increased in users of the diuretic spironolactoneor serotonin reuptake inhibitors with moderate to high affinity for serotonin transporter^.

Lifestyle factors

Evidence that tobacco use is a risk factor for duodenal ulcers is not conclusive. Support for a pathogenic role for smoking comes from the finding that smoking may accelerate gastric emptying and decrease pancreatic bicarbonate production. However, studies have produced contradictory findings. In one prospective study of more than 47,000 men with duodenal ulcers, smoking did not emerge as a risk factor.However, smoking in the setting of H pylori infection may increase the risk of relapse of PUD.Smoking is harmful to the gastroduodenal mucosa, and H pylori infiltration is denser in the gastric antrum of smokers.

Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis. Evidence that consumption of alcohol is a risk factor for duodenal ulcer is inconclusive. A prospective study of more than 47,000 men with duodenal ulcer did not find an association between alcohol intake and duodenal ulcer.

Little evidence suggests that caffeine intake is associated with an increased risk of duodenal ulcers.

Severe physiologic stress

Stressful conditions that may cause PUD include burns, CNS trauma, surgery, and severe medical illness. Serious systemic illness, sepsis, hypotension, respiratory failure, and multiple traumatic injuries increase the risk for secondary (stress) ulceration.

Stress ulceration and upper-GI hemorrhage are complications that are increasingly encountered in critically ill children in the intensive care setting. Severe illness and a decreased gastric pH are related to an increased risk of gastric ulceration and hemorrhage.

Hypersecretory states (uncommon)

The following are among hypersecretory states that may, uncommonly, cause PUD:

• Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia type I (MEN-I)
• Antral G cell hyperplasia
• Systemic mastocytosis
• Basophilic leukemias
• Cystic fibrosis
• Short bowel syndrome
• Hyperparathyroidism

Physiologic factors

In up to one third of patients with duodenal ulcers, basal acid output (BAO) and maximal acid output (MAO) are increased. In one study, increased BAO was associated with an odds ratio [OR] of up to 3.5, and increased MAO was associated with an OR of up to 7 for the development of duodenal ulcers. Individuals at especially high risk are those with a BAO greater than 15 mEq/h.

Genetics

More than 20% of patients have a family history of duodenal ulcers, compared with only 5-10% in the control groups. In addition, weak associations have been observed between duodenal ulcers and blood type O. Furthermore, patients who do not secrete ABO antigens in their saliva and gastric juices are known to be at higher risk. The reason for these apparent genetic associations is unclear. A rare genetic association exists between familial hyperpepsinogenemia type I (a genetic phenotype leading to enhanced secretion of pepsin) and duodenal ulcers. However, H pylori can increase pepsin secretion, and a retrospective analysis of the sera of one family studied before the discovery of H pylori revealed that their high pepsin levels were more likely related to H pylori infection.

Additional etiologic factors

Any of the following may be associated with PUD:

• Hepatic cirrhosis
• Chronic obstructive pulmonary disease
• Allergic gastritis and eosinophilic gastritis
• infection
• Uremic gastropathy
• Henoch-Schönlein gastritis
• Corrosive gastropathy
• Bile gastropathy
• Autoimmune disease
• Crohn disease
• Other granulomatous gastritides
• Phlegmonous gastritis and emphysematous gastritis
• Other infections, including Epstein-Barr virus, HIV, Helicobacter heilmannii, herpes simplex,
• Chemotherapeutic agents, such as 5-fluorouracil (5-FU), methotrexate (MTX), and cyclophosphamide
• Local radiation resulting in mucosal damage, which may lead to the development of duodenal ulcers
• Use of crack cocaine, which causes localized vasoconstriction, resulting in reduced blood flow and possibly leading to mucosal damage

CLINICAL FEATURES

         Abdominal pain is common to many gastrointestinal disorders, including DU and GU, but has a poor predictive value for the presence of either DU or GU. Up to 10% of patients with NSAID-induced mucosal disease can present with a complication (bleeding, perforation, and obstruction) without antecedent symptoms. Despite this poor correlation, a careful history and physical examination are essential components of the approach to a patient suspected of having peptic ulcers.

         Variation in the intensity or distribution of the abdominal pain, as well as the onset of associated symptoms such as nausea and/or vomiting, may be indicative of an ulcer complication. Dyspepsia that becomes constant, is no longer relieved by food or antacids, or radiates to the back may indicate a penetrating ulcer (pancreas). Sudden onset of severe, generalized abdominal pain may indicate perforation. Pain worsening with meals, nausea, and vomiting of undigested food suggest gastric outlet obstruction. Tarry stools or coffee ground emesis indicate bleeding.

Physical Examination

         Epigastric tenderness is the most frequent finding in patients with GU or DU. Pain may be found to the right of the midline in 20% of patients. Unfortunately, the predictive value of this finding is rather low. Physical examination is critically important for discovering evidence of ulcer complication. Tachycardia and orthostasis suggest dehydration secondary to vomiting or active gastrointestinal blood loss. A severely tender, boardlike abdomen suggests a perforation. Presence of a succussion splash indicates retained fluid in the stomach, suggesting gastric outlet obstruction.

         Duodenal ulceration is very common in the developed world, affecting about 1 per 1000 population, bu: the cause of duodenal ulcer diathesis remains unknown. Recent attention has focused on the potential role of Helicobacter pylori, which is found in at least 95 % of cases. NSAIDs may also play a role in some patient. Multiple and resistant ulcers should prompt investigation for a gastrinoma.

         Features suggestive of peptic ulceration include:

–  intermittent epigastric pain related to eating

– epigastric pain causing nocturnal wakening

–  relief of pain by certain bland food and alkalis

–  a close relationship of pain to cigarette smoking

–  response to H2- and proton pump inhibitors

Diagnostic Evaluation.

         In view of the poor predictive value of abdominal pain for the presence of a gastroduodenal ulcer and the multiple disease processes that can mimic this disease, the clinician is often confronted with having to establish the presence of an ulcer. Documentation of an ulcer requires either a radiographic (barium study) or an endoscopic procedure.

         Barium examination of the stomach and duodenum reveals an ulcer, 1 cm in diameter (arrow), in the duodenal bulb with radiating folds.

Barium studies of the proximal gastrointestinal tract are still commonly used as a first test for documenting an ulcer. The sensitivity of older single-contrast barium meals for detecting a DU is as high as 80%, with a double-contrast study providing detection rates as high as 90%. Sensitivity for detection is decreased in small ulcers (<0.5 cm), presence of previous scarring, or in postoperative patients. A DU appears as a well-demarcated crater, most often seen in the bulb. A GU may represent benign or malignant disease. Typically, a benign GU also appears as a discrete crater with radiating mucosal folds originating from the ulcer margin. Ulcers >3 cm in size or those associated with a mass are more often malignant. Unfortunately, up to 8% of GUs that appear to be benign by radiographic appearance are malignant by endoscopy or surgery. Radiographic studies that show a GU must be followed by endoscopy and biopsy.

Many patients, however, do not have symptoms, and become aware of their ulcers only when complications occur. Suspected ulcers are best investigated by endoscopy although high-quality barium meal examination can still provide useful information. Antral biopsy during endoscopy is helpful to confirm the presence or absence of Helicobacter infection.

         Complications of duodenal ulceration include haemorrhage, pyloric stenosis caused by scarring, and perforation, leading to acute peritonitis and pneumoperytoneum.

         Duodenal ulcers usually respond to treatment with H2-receptor antagonists (e.g. cimetidine, ranitidine) or proton-pump inhibitors (e.g. omeprazole). Other drugs including bismuth preparations, may be used and “triple therapy” may be useful when Helicobacter is found. Maintenance therapy with a proton-pump inhibitor or an H2-receptor antagonist may be required event relapse.

Treatment of the ulcer diseases.

The main goals for treating a peptic ulcer include eliminating the underlying cause (particularly H. pylori infection or use of NSAIDs), preventing further damage and complications, and reducing the risk of recurrence. Medication is almost always needed to alleviate symptoms and must be used to eradicate H. pylori. Surgery is required for certain serious or life-threatening complications of peptic ulcers and may be considered if medications are not working. Even with medications, many lifestyle factors, including making changes in diet, are important.

Lifestyle

Doctors used to recommend eating bland foods with milk and only small amounts of food with each meal. We now know that these eating habits are not necessary for the treatment of ulcers. Dietary and other lifestyle measures that should help, however, include: eat a diet rich in fiber, especially from fruits and vegetables; this may reduce your risk of developing an ulcer in the first place and may speed your recovery if you already have one. The vitamin A may be an added benefit from these foods.

Foods containing flavonoids, like apples, celery, cranberries (including cranberry juice), onions, and tea may inhibit the growth of H. pylori. Quit smoking. Receive treatment for alcohol abuse.

Medications

If you have H. pylori, you will probably be prescribed three different medications. “Triple therapy” (including a proton pump inhibitor [for example, omeprazole] to reduce acid production and two antibiotics to get rid of the organism) is commonly used to treat H. pylori-related ulcers. Instead of one of the antibiotics, bismuth salicylate may be the third medication recommended. This drug, available over the counter, coats and soothes the stomach, protecting it from the damaging effects of acid. Two, rather than three, drug regimens are currently being developed.

Some of the same drugs are used for non-H. pylori ulcers as well as for symptoms (like indigestion) due to ulcers of any cause:

– Antacids, available over the counter, may relieve heartburn or indigestion but will not treat an ulcer

– H2 blockers, such as cimetidine, ranitidine, nizatidine, and famotidine, reduce gastric acid secretion.

– Misoprostol – can be used preventively if patient take a lot of NSAIDs because it helps to protect the stomach from the damaging effects of these pain killers. Does not cure existing ulcers.

– Proton-pump inhibitors, including esomeprazole, lansoprazole, omeprazole, pantoprazole, and rabeprazole, decrease gastric acid production. This is the number one choice of medications for treating ulcers.

– Sucralfate makes a coating over the ulcer crater, protecting it from further damage.

 

Small intestine

Malabsorption

         Malabsorption is the most common presenting feature of small intestinal disease and is characterized by failure to digest or absorb, or both, nutrients from the intestinal tract.

         Gluten enteropathy (coeliac disease)

                  A gluten-free diet relieves symptoms and reverses the biopsy appearances in most patients. Small intestinal lymphoma and carcinoma are more common in patients with coeliac disease than in general population; extra-gastrointestinal cancers are also more common. The effect of a gluten-free diet on the risk of these complications is unclear.

         In dermatitis herpetifomis a gluten-sensitive enteropathy is accompanied by a bullous skin eruption, Bacterial overgrowth.

         Small intestinal bacterial overgrowth commonly accompanies the reduction of gastric acidity by drugs or surgery, blind loops and motility disorders. It is an important consideration in the elderly. Diagnosis is supported with a glycocholate or hydrogen breath test.

Inflammatory bowel disease

Inflammatory bowel disease is a term that encompasses two main conditions: ulcerative colitis and Crohn’s disease.

Crohn’s disease

         Crohn’s disease is a chronic granulomatous inflammatory disease of unknown cause, which is becoming more common. The prevalence in the UK is about 3 per 100.000. The terminal ileum and colon are principally involved, but the disease may affect any part of intestinal tract, often with discontinuous patches of inflammation of all the bowel wall structures («skip» lesions). Initially, aphthoid ulcers may be seen at endoscopic examination with macroscopically normal intervening mucosa. Subsequently, more severe inflammation leads to more extensive ulceration and oedema of the mucosa and ultimately fibrosis can cause bowel strictures.

      Crohn’s disease can be controlled in most patients with short-term courses of corticosteroids, and aza-thioprine is useful in resistant patients. Other drugs which may be helpful include 5-aminosalicylic acid, cyclosporin and interferon. Surgery is required for the relief of obstruction and the correction of fistulae. Nu¬tritional support, either enteral or parenteral, corrects malnutrition thus making a major contribution to the patient’s well-being.

Ulcerative colitis

         Ulcerative colitis has a stable incidence and prevalence of 6 and 100 per 100.000. It is primarily a mucosal disease that extends for a variable distance and in a continuous fashion, around the colon from the rectum, which is always

         Endoscopy reveals the severity of the disease and allows biopsy, which may show goblet cell depletion, crypt abscesses, distortion of the architecture with little submucosal inflammation and no granulomas (in contrast to Crohn’s disease). Barium enema may show characteristic findings. Other important investigations include TBC, erythrocyte sedimentation rate (ESR) or C-reactive protein, serum albumin and stool microscopy and culture to exclude an infective or parasitic cause for symptoms.

         Medical treatment involves the control of disease activity with short courses of corticosteroids or azathi-oprine, or both, the maintenance of remission with sul-phosalazine or one of the preparations designed to deliver 5-aminosalicylic acid to the colon (mesalazine or olsalazine) and the correction of anaemia. Surgery is required if medical management fails, and to prevent acute and chronic complications such as perforation or carcinoma. Pan-proctocolectomy with a permanent ieostomy is usually necessary, although pouch procedures involving ileoanal anastomoses are currently fashonable. Maintenance of good nutrition is essential.