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МІНІСТЕРСТВО ОХОРОНИ ЗДОРОВ'Я УКРАЇНИ Харківський національний медичний університет

Modul 3. Internal medicine. Contents module №3. Theme 4. Management of patients with chronic abdominal pain

Guidelines for students and interns

Модуль 3. Внутрішня медицина. Змістовний модуль № 3. Тема 4. Ведення хворих з хронічним абдомінальним болем

Методичні вказівки для студентів та лікарів-інтернів

Рекомендовано вченою радою ХНМУ. Протокол № 11 від 21.12.2011.




Module 3. Internal medicine. Contents module№ 3. Theme 4. Manage­ment of patients with chronic abdominal pain / comp. Oleg Babak, Galyna Fadeyenko, Olga Gaponova. - Kharkiv: KNMU, 2012. - 36 p.

Compilers     Oleg Babak

Galyna Fadeyenko Olga Gaponova

Модуль 3. Внутрішня медицина. Змістовний модуль № 3. Тема 4. Ведення хворих з хронічним абдомінальним болем: Метод. вказ. для студентів та лікарів-інтернів/ Упор. О.Я. Бабак, Г.Д. Фадєєнко, О.Г. Га-понова. - Харків: ХНМУ, 2012. - 36 с.

Упорядники    Бабак О.Я.

Фадєєнко Г.Д. Гапонова О.Г.


General Outcome

The students should be able to list and describe different conditions which can cause chronic abdominal pain, manage the main investigations dif­ferentiating it's causes, know modern strategies of diagnostics and treatment of chronic abdominal pain, manage psychosocial presentations of chronic ab­dominal pain.

Student must know:

Modern standarts of diagnostics and treatment of patients with chronic abdominal pain.

Differential diagnosis of different causes of abdominal pain.

Drawing the plan of appropriate investigations.

Role of instrumental and laboratory methods of investigations.

Strategy of management of patients with chronic abdominal pain de­pending on etiological factors.

Conservative and surgical treatment.

Following management of patients.

Prognosis and working capacity.

The evaluation of any patient with a complaint of abdominal pain is challenging. Abdominal pain can be benign and self-limited or a harbinger of a serious life-threatening disease. Chronic abdominal pain poses a particularly challenging clinical problem. Not only is the management of chronic abdominal pain a frequently daunting task, but also the possibility of overlooking a struc­tural or organic disorder is always a concern. Many disorders discussed else­where in this text can produce chronic abdominal pain (table 1). Many of these diagnoses require careful consideration and clinical interrogation, in addition to appropriate diagnostic testing, to discern whether the entity is indeed the cause of the patient's pain. Diagnosis of a functional gastrointestinal disorder is gen­erally considered once potential causes of organic chronic abdominal pain have been confidently excluded. Although the causes of chronic abdominal pain are varied, the pathophysiologic pathways that produce chronic pain are common to many of them. Functional abdominal pain syndrome (FAPS) serves as a model to illustrate many of the complex issues involved in caring for patients with chronic abdominal pain.

Table 1.

Differential Diagnosis of Chronic or Recurrent Abdominal Pain

_Structural (or Organic) Disorders_

Inflammatory: appendicitis, celiac disease, eosinophilic gastroenteri­tis, fibrosing mesenteritis (mesenteric panniculitis), inflammatory bowel dis­eases, pelvic inflammatory diseases, primary sclerosing cholangitis_

Vascular: celiac artery syndrome, mesenteric ischemia, superior mes-enteric artery syndrome_

Metabolic: diabetic neuropathy, familial Mediterranean fever, heredi­tary angioedema, porphyria,_

Neuromuscular: anterior cutaneous nerve entrapment syndrome, myo-fascial pain syndrome, slipping rib syndrome, thoracic nerve radiculopathy_

Other: abdominal adhesions, abdominal neoplasms, anaphylaxis, chronic pancreatitis, endometriosis, gallstones, hernias, intestinal malrota-tion, intestinal obstruction, lactose intolerance, peptic ulcer disease, small intestinal and pelvic lipomatosis_

Functional Gastrointestinal Disorders: biliary pain (gallbladder or sphincter of Oddi dysfunction, functional abdominal pain syndrome, functional (nonulcer) dyspepsia, gastroparesis, irritable bowel syndrome, levator ani syndrome_


Abdominal pain is considered chronic when it has been occurring con­stantly or intermittently over at least six months. Abdominal pain is considered acute when it has been occurring for several days and subacute when it has been occurring more than several days but less than 6 months. These arbitrary definitions are often helpful when formulating a differential diagnosis. The clinician initially must adopt a broad-based approach, which necessarily be­comes more focused as the evaluation ensues. Importantly, although typical patterns of presentation are useful to remember, some patients, especially im-munosuppressed and older persons, may present with atypical features.


Assessment includes 4 major components:

1. History.

2. Physical examination.

3. Psychosocial assessment.

4. Investigations.

1. The sensitivity of history and physical examination are low. Epigas­tric pain and gastroduodenal pathology, RUQ pain and hepatobiliary pathology, and suprapubic pain and gynaecological pathology are the only findings with specificity >50%. The physical examination should be integrated with findings from the history and other collateral information to focus the diagnostic work-up on possible diagnoses.

Pain may arise from any system, including the genitourinary, gastroin­testinal, and gynecologic tracts. The aetiology of chronic abdominal pain is so wide that only the more common causes can be covered here.

Anyhow, the initial step in evaluating a patient with chronic abdominal pain is to elicit a detailed history from the patient. The chronology of the pain, including its abruptness of onset and duration, and its location and possible radiation should be determined. Visceral pain emanating from the digestive tract is perceived in the midline, because of the relatively symmetrical bilateral innervation of the organs, but is diffuse and poorly localized. Referred pain is ordinarily located in the cutaneous dermatomes that share the same spinal cord level as the affected visceral inputs. The patient should be questioned about the intensity and character of the pain, with the understanding that these parameters are subjective. The patient's perception of precipitating, exacerbating, or miti­gating factors may be useful when diagnostic possibilities are considered.

Symptoms assessment: The localisation of pain from abdominal vis­cera, especially the small bowel, is imprecise. Most of the digestive tract is perceived in the midline due to its symmetric innervation. Exceptions include pathologies of the ascending/descending colon and gallbladder, which may present with one-sided pain due to unilateral innervation. The location of pain and the patient's perception of the anatomical distribution can sometimes help to narrow the differential diagnosis and guide diagnostic evaluation:

Epigastric and upper abdominal pain can indicate oesophageal (e.g., gas­troesophageal reflux), stomach (e.g., gastritis), duodenal (e.g., ulcer), gall­bladder (e.g., cholecystitis), or pancreatic (e.g., pancreatitis) origin.

Lower abdominal pain can indicate large bowel involvement, and later-alisation may help to distinguish between descending/sigmoid colon (e.g., left-sided diverticulitis) and ascending/caecum (e.g., Crohn's ileocolitis), or appen­dix (e.g., appendicitis).

Pelvic pain can suggest gynaecological origin (e.g., ovarian cysts, PID) or chronic pelvic pain syndrome (e.g., interstitial cystitis, endometriosis, ure-thral syndrome, or changes and dysfunction of the pelvic muscles).

Localised point of maximal pain in the anterior abdomen can indicate chronic abdominal wall pain or abdominal cutaneous nerve entrapment syn­drome. Localised pain can also arise at specific sites such as the kidneys, uret­ers, and ovaries, or from a source of focal peritoneal irritation.

Information about exacerbating and relieving factors may provide fur­ther clues: Pain made worse by eating (postprandial pain) may indicate gastric ulcer, chronic pancreatitis, gallstones, abdominal ischaemia (also called ab­dominal angina), or functional disorders such as irritable bowel syndrome, functional dyspepsia, or postprandial distress syndrome (postprandial fullness). Pain relieved by eating suggests duodenal peptic ulcer disease. Pain relieved by

defecation may indicate irritable bowel syndrome. Pain associated with men­strual cycle suggests gynaecological origin. Additional symptoms of dyspare-unia, dysmenorrhoea, pain with defecation, and infertility suggest endometrio-sis. Pain associated with urinary urgency and frequent urination suggests inter­stitial cystitis. Pain in the anterior abdomen that is accentuated by physical activity can indicate chronic abdominal wall pain or abdominal cutaneous nerve entrapment syndrome.

Pain due to organic conditions (e. g., ulcers, cholelithiasis, pancreatitis) is generally circumscribed, unlike pain due to functional disorders. Radiation of the pain to the shoulder indicates cholelithiasis, to the inguinal and genital re­gion nephrolithiasis, to the back, pancreatic diseases, aortic aneurysm, or ulcer penetration).

Increased pain while lying down occurs with reflux disease and pancreas diseases. More intense pain while standing occurs with hernias. Increased pain with movement indicates abdominal wall processes (such as trauma), vertebro-genic pain (such as discopathy), or reflux disease.

When initially attempting to determine whether the patient's pain is caused by an organic or functional process, the clinician should search for clues in the patient's history and physical examination that support or refute the diag­nosis of a progressive, serious, chronic underlying illness. Such features in the history include fever, night sweats, appetite change, weight loss, and nocturnal awakening.

2. Physical examination. The physical examination should first fo­cus on the vital signs. Fever, tachycardia, tachypnoea, and hypotension suggest an acute illness requiring urgent evaluation. A head and neck examination is useful for non-specific signs of intra-abdominal pathology, including: temporal wasting, sunken eyes, and prominent clavicles, suggesting significant weight loss; dry mucosal membranes, indicating volume depletion; icteric sclera, indi­cating hepatobiliary disease; pale conjunctiva, suggesting anemia. Peripheral vascular disease is suggested by diminished pulses and may co-exist with intes­tinal angina or mesenteric ischaemia. Pain on deep inspiration suggests referred pain from the lungs or RUQ/LUQ pain.

The abdominal examination should use a combination of inspection, auscultation, percussion, and palpation. The most critical step for a patient with an acute exacerbation of chronic abdominal pain is to ascertain promptly whether a surgical abdomen is present. Although most causes of chronic ab­dominal pain do not require immediate surgical treatment, a complication re­lated to a disease process ordinarily associated with chronic abdominal pain may present acutely (e.g., intestinal perforation in a patient with inflammatory bowel disease). Furthermore, a patient who has experienced chronic abdominal pain may present with acute pain related to another disease process (e.g., acute

mesenteric ischemia in a patient with underlying irritable bowel syndrome [IBS]). The abdomen should be auscultated to detect an abdominal bruit, be­cause the presence of a bruit may suggest chronic mesenteric ischemia (intesti­nal angina). Abdominal palpation for the presence of organomegaly, masses, and ascites and examination for hernias are particularly pertinent.

In some cases examination is unremarkable, but rebound tenderness, guard­ing, or tenderness on palpation require urgent consideration. Precise localisation of the pain in the anterior abdomen with positive Carnett's sign (i.e., increase of pain/tenderness on re-palpation during contraction of abdominal muscles, suggest­ing abdominal wall origin) can help to differentiate between abdominal wall pain and intra-abdominal pathology. Careful rectal examination and pelvic examination are part of a thorough evaluation. Bleeding, diarrhoea, discharge/mucus, tenderness, rectal masses, or obstruction can provide important additional clues for underlying disease processes. In females with pelvic/lower abdominal pain, gynaecological examination should be considered.

Other physical findings that suggest an underlying organic illness in­clude signs of malnutrition (e.g., muscle wasting or edema), vitamin deficien­cies, or extraintestinal processes (e.g., arthropathy or skin changes). Although not entirely specific, the closed eyes sign is often seen in patients with FAPS. Physical examination should include skin and mouth for non-specific findings such as ulcers, vesicles, angiomata, bleeding or bruising, or specific lesions (e.g., erythema nodosum).

The pelvic girdle, lower back, and thorax (ribs and spine) should be ex­amined, since this may yield clues about symptoms wrongly attributed to ab­dominal organs.

3. Psychosocial assessment. The association between chronic ab­dominal pain and a history of PTSD, abuse, somatisation, anxiety, and depres­sion is well recognised. Evaluation of psychosocial factors can help to deter­mine an appropriate management plan and minimise unnecessary investiga­tions. Affective disturbance can both result from and contribute to the experi­ence of chronic pain. Clinical presentation, symptom severity, and response to treatment can all vary according to mental state abnormalities. Symptom fluc­tuations and mental state should be monitored closely.

4. Investigations.Specific algorithms for the diagnostic work-up of chronic abdominal pain do not exist. Appropriate investigations should be tai­lored to history and examination findings and be made on a case-by-case basis. In the absence of alarm features, laboratory and imaging tests should be ordered in a conservative and cost-effective manner.

1. Laboratory

The laboratory evaluation can be helpful, but the clinician must first dis­till pertinent facets of the history and physical examination to focus the labora­

tory assessment. Injudicious use of laboratory testing is costly and can confuse the clinical picture and even lead to complications. It is worth emphasizing that an abnormal laboratory test result does not necessarily prove causality in rela­tion to a patient's chronic pain syndrome. The clinician must exercise the ut­most discretion when ordering and interpreting the results of laboratory tests. The patient should be asked about previous investigations as, owing to the chronicity of their symptoms, many patients will already have been investigated and existing information may be available for review. Standard laboratory tests include:

FBC with differential, to screen for infection or anaemia. The platelet count and ESR may signify an inflammatory process.

• Serum electrolytes, glucose, creatinine, and urea for metabolic causes.

• Liver function tests, lipase, and amylase, particularly in patients with upper abdominal pain.

Urine analysis and urine culture to help exclude UTI and interstitial cystitis.

Additional laboratory tests based on the individual case include:

Stool tests for culture, ova and parasites, and Giardia antigen should be done if bacterial, parasitic, or protozoal cause of abdominal pain is suspected.

• Urine or serum pregnancy test: this should also be done prior to radio-graphic or endoscopic investigations.

Serology testing for Helicobacter pylori in patients with upper GI symptoms, including early satiety and epigastric discomfort (i.e., dyspeptic symptoms).

• Vaginal swabs, pap smears, beta-human chorionic gonadotropin, pros­tate-specific antigen, and urine cytology can be helpful in certain cases with pelvic and lower abdominal pain.

2. Endoscopy

Endoscopic and imaging studies have important roles in diagnosing and excluding many causes of chronic abdominal pain. Upper endoscopy and colonoscopy, as well as capsule endoscopy, may be indicated in selected cases. Available imaging investigations include barium and radionuclide studies, ultrasonography, computed tomography, magnetic resonance imaging, positron emission tomography (PET), and conventional angiography. The indications for each of these radiologic investigations differ, as do their potential to clarify an individual clinical situation.

All patients >50 years old with abdominal pain should have a GI tract endoscopy.

Colonoscopy is indicated if the pain is in the lower abdomen and/or it is associated with changes in bowel habit.

Upper endoscopy is indicated if the pain is localised in the upper abdo­men, particularly if other upper GI symptoms (early satiety, nausea, vomiting) are present. There are no guidelines suggesting when these tests in younger (<50 years old) patients should be ordered.

3. Imaging

Further investigations depend on the clinical findings.

Upper abdominal ultrasound may be indicated to evaluate RUQ or epi­gastric pain, particularly if elevated liver or pancreatic enzymes are found.

Pelvic abdominal ultrasound and trasvaginal and/or transrectal ultra­sound is indicated for evaluating lower abdominal pain.

CT scanning can help to evaluate dilated intestinal loops; exclude partial intestinal obstruction; detect abnormalities in other abdominal organs (e.g., pancreas, liver, kidneys); identify inflammatory processes (e.g., inflammatory bowel disease, diverticulitis, abscesses); and investigate retroperitoneal or pel­vic masses.

If all investigations are negative, the likely diagnosis is a functional GI disorder. The diagnosis of specific functional disorders depends on the pres­ence and characteristics of additional associated symptoms. Irritable bowel syndrome and functional dyspepsia are the most common causes of chronic abdominal pain in adults.

If the pain is located in the abdomen rather than the pelvic region, and is not related to food intake or defecation, a diagnosis of functional abdominal pain syndrome (FAPS) may be appropriate. FAPS, also called chronic idio-pathic abdominal pain or chronic functional abdominal pain, describes recur­rent, continuous or near-continuous abdominal pain not related to gut function, associated with loss of daily activities, and present for >6 months. Like other functional GI disorders, FAPS cannot be explained by structural or metabolic disorders, and it is believed to be related to altered pain perception and pain modulation circuits.


Pain Originating from the Stomach and Small Intestine

Distribution. Pain originating from the stomach and small intestine can be generally classified as follows: L chronic gastritis

L functional gastric disorders (gastric irritation) L ulcerous disease (duodenal ulcer, gastric ulcer) L gastric carcinoma L rare disorders

L complaints secondary to general diseases.

Diagnosis. The differential diagnosis is based on the medical history, clinical findings, imaging (endoscopy, radiologic examination), and biopsy with a histologic analysis.

A detailed medical history is particularly important in gastric diseases. Functional stomach disorders (irritable stomach) are characterized by their relatively indefinite character. They generally occur irregularly and have no periodicity. The pain is frequently accentuated immediately after eating.

Endoscopy is most important for diagnosis of obscure epigastric pain, dys-phagia, heartburn, and gastrointestinal bleeding. Another indication is an unclear iron deficiency anemia. Radiologic examinations are helpful, particularly in cases of paraesophageal hiatus hernia, motility disorders, Zenker diverticulitis, external compression, or stenoses that cannot be detected endoscopically.

Endosonography can be used to detect intramural processes, espe­cially the extent and depth of infiltration of neoplasms, as well as lymph node metastases.

Chronic Gastritis

Type A, B and C gastritis must be distinguished.

Type A Gastritis. Type A gastritis (autoimmune gastritis) primarily af­fects the gastric body and fundus. It is caused by autoimmune processes. It is typically associated with pernicious anemia. Autoantibodies against parietal cells and intrinsic factor are typical. Gastrin is increased. The risk of develop­ment of a gastric carcinoma is significantly increased in chronic-atrophic type A gastritis. Endoscopic surveillance is therefore indicated.

Type B Gastritis. Type B gastritis (bacterial gastritis) is primarily local­ized in the gastric antrum and is typically caused by Helicobacter pylori (Hp). It is more common than type A gastritis and is associated with gastric ulcers, duodenal ulcer, and mucosa-associated lymphoid tissue (MALT) lymphoma.

Type C Gastritis. Type C gastritis (chemical gastritis) is caused by chemical irritation, i. e., reflux of bile (bile gastritis) or duodenal contents (re­flux gastritis) and most importantly drugs, in particular use of NSAIDs (NSAID gastropathy).

Rare Cases of Gastritis. Rare, chronic forms of gastritis are lympho-cytic, eosinophilic, and granulomatous gastritis.

Diagnosis. Chronic gastritis can only be confirmed by histology. There is no clear relationship to typical clinical symptoms. The majority of patients with histologically demonstrated chronic gastritis are asymptomatic.

Functional Dyspepsia

Continuous epigastric pain, loss of appetite, nausea, and frequent vomit­ing are the main symptoms. Eating tends to exacerbate the symptoms and there is generally no periodicity or diurnal rhythm. This information from the medi­cal history generally distinguishes this complaint from an ulcer. The lack of the

typical endoscopic changes with irritable stomach is decisive for differential diagnosis.


The central feature of ulcers is infection with Helicobacter pylori (Hp). There has been a radical change in the understanding of ulcers. The eradication of the Hp infection in patients with ulcers not only heals the acute lesion but generally prevents recurrence and complications of ulcers. Only about 10% of patients infected with Hp in industrialized countries develop an ulcer, but 95% of patients with a duodenal ulcer are infected with Hp.

This indicates that Hp infection alone is not sufficient to cause an ulcer. Hp generates conditions that, together with additional risk factors, cause an ulcer: stress, smoking, and a genetic predisposition.

Helicobacter pylori Detection. The presence of Hp can be confirmed

L histologically by Giemsa or Warthin-Starry staining of gastric antrum biopsies

L by urease activity either with a fast urease test in the biopsy specimen or an exhalation test with 13C or 14Clabeled urea L by culture from gastric antrum biopsies

L by serology: serology is, however, not generally useful, because Hp colonizes approximately 10% of persons under 30 and approximately 60% of persons of 60 years, while only 10% of infected persons develop an ulcer.

Clinical Features and Differential Diagnosis. Strongly localized pain is characteristic for ulcers, as compared to irritable stomach and acute gas­tritis. In acute gastritis a diffuse pain upon palpation is generally present in the epigastric region. Many patients with ulcers can point to the exact loca­tion of the spontaneous pain and the pain upon palpation. The maximum pain is to the left of the abdominal mid-line with gastric ulcers and to the right with duodenal ulcers.

The character of the pain is important in differential diagnosis versus biliary colic (period and diurnal rhythm of the pain). The pain characteristics and the diurnal rhythm typical for ulcers are particularly important. A biliary colic lasts for one to three days, ulcer pain for three to five weeks. Ulcer pain generally disappears after eating within a few minutes while biliary pain does not. Ulcer pain is virtually never accompanied by nausea while nausea is very frequent with biliary diseases. Appetite is not affected, unlike with gastritis and carcinoma. If the character of the pain is not typical in spite of other signs of an ulcer, the possibility of complications must be considered:

L with continuous and back pain: penetration

L with nausea and vomiting: stenosis.

An ulcer episode, like acute gastritis, can be triggered by stress situa­tions (surgery, serious trauma), alcohol abuse, or drugs (including NSAIDs).

Ulcers occur at all ages, particularly after puberty. Carcinoma incidence in­creases with age but can also be observed in 20- to 30-year-olds.

Diagnosis. The mainstay of ulcer diagnosis is endoscopy. Multiple biop­sies from and around the ulcer are key for differentiating benign from malig­nant stomach ulcers.

Radiologic diagnosis is no longer common, but when performed, an ulcer niche, may be visible under tangential setting as a contrast agent bulge in the region of the gastric curvature. The ulcer niche is visible as a persistent contrast spot in the direct frontal view. About 85% of ulcer niches are on the minor curvature of the stomach. The remaining 15% occur at the major curvature, the dorsal wall (back pain), and in the pyloric re­gion. Gastric carcinomas can also form niches. Indirect ulcer signs are spastic retractions on the wall opposite the ulcer, referred to as ulcer fin­gers. They are not specific for ulcers, because they are also observed with various tumors. After healing an hourglass stomach may develop, which results from shrinkage of the minor curvature by scar tissue and spastic retraction of the major curvature.

Duodenal Ulcer. More than 95% of duodenal ulcers occur in the duo­denal bulb. Untreated they are characterized by spontaneous healing and recur­rence. 60% of untreated cases recur within one year and 80-90% within two years. 95-100% are associated with Hp infection.

The main symptom is pain, that typically occurs 90 minutes to three hours postprandial and is relieved by eating (food relief). Asymptomatic ulcers are common.

Complications are penetration, particularly into the pancreas (constant pain in the back), stomach outlet obstruction (pain increased postprandially, vomiting), perforation, and hemorrhage.

Postbulbar ulcers are rare. The clinical symptoms correspond to the clas­sical duodenal ulcer, but postbulbar ulcers bleed more frequently.

Gastric Ulcer. The peak incidence of gastric ulcers is in the sixth dec­ade of life and thus about 10 years later than with duodenal ulcers. Men are affected more frequently than women. Benign gastric ulcers are most com­monly localized adjacent to the corpus-antrum border. Gastric erosions and ulcers are often caused by NSAIDs. Gastric ulcers not associated with NSAIDs are generally caused by Hp infection. The pain is less typical than in duodenal ulcers and increases after eating. Nausea and vomiting occur even without gastric outlet obstruction, in contrast to the duodenal ulcer. Asymptomatic courses are common.

It is important to note that gastric ulcers, much more commonly than duodenal ulcers, can be caused by carcinoma. Histologic diagnosis is therefore mandatory and the healing must be monitored endoscopically.

Ulcer Associated with Other Diseases. Duodenal ulcer, is frequently observed in patients with: cirrhosis of the liver, chronic obstructive jaundice, chronic pancreatitis, chronic lung disease, especially emphysema, chronic renal insufficiency, general arteriosclerosis, polycythemia vera, hyperparathyroidism, systemic mastocytosis.

Gastric ulcers, are frequently observed: with NSAID use, in smokers, after chemotherapy.

Use of aspirin and other NSAIDs causes gastric ulcers much more fre­quently than duodenal ulcers. Ulcers and strictures of the small and large intes­tine also occur.

Stress-induced Erosions. Stress-induced erosions and ulcers are often multiple and frequently occur in areas of the stomach with high activity, after shock, massive burns (Curling ulcer), sepsis, and after serious trauma.

Hemorrhage is frequent, particularly in patients on respirators and with coagulation disorders.

Cushing Ulcer. Gastric ulcers frequently occur after brain trauma, brain surgery, or in patients with elevated brain pressure (Cushing ulcer).

Zollinger-Ellison Syndrome. Ulcers are a complication of Zollin-ger-Ellison syndrome. Gastrinomas (most frequently originating from non-p-pancreatic islet cells or duodenal G cells), through overproduction of gastrin, increase secretion of gastric acid and are thus responsible for the formation of ulcers. Zollinger-Ellison syndrome should be considered in the following situa­tions:

L peptic ulcers with atypical localization (esophagus, postbulbus, je-junal), multiple occurrence (approximately 10%), and resistance to treatment.

L aqueous diarrhea, with or without steatorrhea, with or without hypo-kalemia and its consequences.

L gastric hypersecretion and increased serum gastrin levels.

L prominent gastric mucosa folds, as with Menetrier disease

L 25% of cases are associated with multiple endocrine adenomatosis type I (Wermer syndrome). Zollinger-Ellison syndrome must be considered in patients with signs of hyperparathyroidism or hypophyseal tumor. The family medical history is particularly important in view of the inheritance.

L Fasting serum gastrin levels are elevated. Massive hyperchlorhydria and hypergastrinemia (> 1000 pg/mL) are diagnostic. Increased serum gastrin levels are also found in achlorhydria (e. g., pernicious anemia, after vagotomy, stomach resection). In Zollinger-Ellison syndrome serum gastrin levels in­crease significantly in response to calcium infusion or after secretin administra­tion. These provocation tests are useful for identification of Zollinger-Ellison syndrome in patients with borderline serum gastrin levels (200-1000 pg/mL).

Late Complications of Ulcer Disease. Pyloric Stenosis. Pyloric steno­sis is a late complication of chronic recurring ulcers. The character of ulcer pain is changed and loss of appetite occurs. Feelings of fullness and discomfort after meals, which are not present in uncomplicated ulcers indicate stenosis. A steno­sis is very likely with vomiting that relieves or cures late pain and with vomit­ing of food from the previous day. If endoscopic examination identifies empty stomach secretion and food 12 hours after eating, this supports the diagnosis.

Food and liquid retention can often be detected by sonography. The di­agnosis is confirmed radiologically by slow pyloric passage, dilatation of the stomach, and marked dilution of the contrast agent by stomach secretion and food residues. The nature of the pyloric stenosis (benign or malignant) can generally be defined by endoscopy and histology.

Gastric Carcinoma. Epidemiology and Risk Factors. 85% of malignant tumors in the stomach are adenocarcinomas. They can grow as space-filling processes or diffusely infiltrate the stomach wall (linitis plastica). Non-Hodgkin lymphoma and leiomyosarcoma are malignant gastric tumors. Nitrates in food, which are converted to carcinogenic nitrites by bacteria, play an important role in the development of the gastric carcinoma. Hp infection also seems to play a significant role. Patients with chronic atro-phic type A gastritis are at particular risk for carcinoma. Gastric carcinomas are more frequent in patients with blood group A.

Clinical Features. In contrast to ulcers, the symptoms of gastric carci­noma are less typical. They start slowly, are uncharacteristic, and are not peri­odic. There is generally no history of stomach complaints. Typical features are the persistence or progression of the complaints and the appearance of general symptoms, particularly weakness (anemia) and weight loss. Iron-deficiency anemia frequently precedes the local symptoms by weeks or months. In con­trast to ulcer symptoms, carcinoma pain is not relieved by antacids and is not periodic. In about one-quarter of cases there is no pain, but rather unspecific complaints (feeling of fullness, discomfort, belching, nausea). In other cases the complaints are more diffuse, e. g., loss of appetite andweight loss. Vomiting is typical for tumors in the antrum or cardia. Cardiac carcinoma extending to the esophagus typically causes dysphagia.

Diagnosis. The carcinoma is generally palpable only in advanced cases. The early cases are either not sensitive to palpation or present with diffuse pain. A Vir-chow gland above the left clavicle is typical for advanced gastric carcinoma.

Endoscopy and histology are usually diagnostic. If endoscopy suggests gastric carcinoma, a negative biopsy does not rule out a carcinoma. Close endo-scopic-histologic monitoring is necessary for early detection of gastric carci­noma. Failure of an ulcer to heal after four to eight weeks of medical therapy or early recurrence are indications for a malignant or complicated ulcer.

Detection of early cancer by endoscopy improves prognosis. Early can­cer, defined as carcinoma restricted to mucosa and submucosa, is generally cured bysurgery.

Rare Gastric Diseases. Malignant Lymphoma. Malignant lymphoma is similar to gastric carcinoma. Primary gastric lymphoma is rare.

However, the stomach is the most common extranodal localization of a non-Hodgkin lymphoma. The prognosis of malignant lymphoma is signifi­cantly better than that of gastric carcinoma. Infection with Hp is associatedwith the development of gastric lymphoma, particularly the MALT lymphoma. The eradication of the Hp infection causes a regression of the MALT lymphoma in about 50% of patients.

Lymphoma of the small intestine can also be a complication of sprue.

Leiomyoma. This tumor is rare (approximately 1% of all tumors). The most important clinical symptom is hemorrhage. Endoscopy and radiography show a semispherical, well-circumscribed tumor with central ulceration.

Gastrointestinal Stroma Tumors (GIST). GIST are mesenchymal tumors of the gastrointestinal tract, 60-70% of which are localized in the stomach. They were until recently frequently classified as leiomyomas or leiomyosarco-mas, but have a specific cellular origin and a specific pathogenesis. GIST are identified by mutations of the cKIT protooncogene and activation of the KIT receptor tyrosine kinase, and like chronic lymphatic leukemia, respond to treatment with the specific tyrosine kinase inhibitor imatinib mesylate.

Intestinal Polyposis. In contrast to Menetrier disease, gastric mucosa with intestinal polyposis shows a predominantly normal, smooth aspect with diffusely distributed individual polyps at endoscopy. Gastric polyps are more frequent in patients with chronic atrophic gastritis, particularly in pernicious anemia. The complaints are uncharacteristic. Depending on the extent and loca­tion of the tumors, the polyps may be asymptomatic, may present as gastritis, or result in sudden stenosis. The tumors often bleed, resulting in anemia that may dominate the clinical picture. The diagnosis must be histologically confirmed.

Hamartomatous polyps occur in the colon and the small intestine in Peutz-Jeghers syndrome and juvenile polyposis. Malignancy is rare compared to familiar adenomatous polyposis, Gardner and Turcot syndromes, and heredi­tary nonpolyposis colorectal carcinoma.

Very Rare Gastric Diseases. Syphilis, tuberculosis, sarcoidosis, Crohn disease, eosinophilic gastritis, or phlegmonous gastritis are extremely rare causes of gastric complaints. Endoscopy and biopsy are generally diagnostic. With many diseases the diagnosis can only be confirmed if organs other than the stomach are affected (e. g., sarcoidosis, Crohn disease, tuberculosis).

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