Ulcer-like syndrome (acidism syndrome)
The classic clinical picture is vividly demonstrated in adolescents. The leading manifestation is a specific pain pattern.
- Nature of pain: paroxysmal, prolonged.
- Relation to food intake: typical "hunger pains" occurring on an empty stomach, as well as nocturnal attacks. Complete or partial relief of pain after eating is characteristic.
- Localization: epigastric region (projection of the stomach) and pyloroduodenal zone (umbilical region), where palpation reveals local tenderness.
- Dyspeptic component: patients are troubled by heartburn and vomiting, though appetite is generally fully preserved.
- Trophological status: objective examination may reveal thinning of the subcutaneous adipose tissue.
- Anamnesis: genetic predisposition to acid-related diseases plays a crucial role (e.g., the presence of peptic ulcer disease or erosive gastritis in close relatives).
Gastric hypersecretion syndrome and its consequences
Excessive hydrochloric acid production triggers a cascade of pathological changes in the upper gastrointestinal tract.
- Mucosal damage: formation of peptic ulcers of the stomach and duodenum. Due to hypersecretion, they are often multiple and recurrent.
- Concomitant pathologies: development of reflux esophagitis and ulcerative enteritis.
- Complications: prolonged course leads to life-threatening conditions—perforation of the organ wall, profuse gastrointestinal bleeding, and cicatricial strictures.
Clinically, the syndrome manifests as progressive deterioration of the patient's general condition, increasing pain intensity, and persistent dyspepsia.
Differential diagnosis: functional dyspepsia
The main "competitor" to peptic ulcer disease in diagnosis is functional dyspepsia (FD). It occurs in 3.5–27% of children and adolescents.
- Essence of the pathology: this is a diagnosis of exclusion. It is established only when diagnostic minimums (mandatory upper GI endoscopy) reveal no organic changes explaining the symptoms.
- Diagnostic criteria (Rome IV criteria): presence of pain, burning in the epigastrium, feeling of postprandial fullness, or early satiety. Symptoms must occur at least 4 days per month for the last 2 months (or persist for many weeks throughout the year).
- Etiology of FD: multifactorial. Includes gastric motility disorders, visceral hypersensitivity, genetic predisposition, and low-grade mucosal inflammation (following infections or food allergy).
- Important distinction: in FD, symptoms do not decrease after defecation and are not associated with changes in stool frequency or consistency. This is a key difference from irritable bowel syndrome (IBS).
Clinical variants of FD are divided into ulcer-like (pain dominates), dyskinetic (nausea, fullness), and unspecified. Modern classification also distinguishes postprandial distress syndrome and epigastric pain syndrome.
Differential search in exacerbations and complications
Exacerbation of peptic ulcer disease requires the exclusion of a wide range of pathologies: erosive gastroduodenitis, pancreatitis, cholelithiasis, gastroesophageal reflux disease (GERD), and acute appendicitis.
- Stenosing ulcer of the antrum in adolescents can simulate early toxicosis (hyperemesis gravidarum). However, in toxicosis, abdominal pain is absent, nausea is agonizing and aggravated by odors, and vomiting occurs more frequently in the morning and is independent of food.
- Gastrointestinal bleeding of ulcer etiology is differentiated from erosive gastritis, Mallory-Weiss syndrome, gastric cancer, and swallowed blood from the respiratory tract.
- Abdominal pain syndrome in general requires the exclusion of inflammatory bowel diseases (Crohn's disease, ulcerative colitis, which may present with an epigastric component), celiac disease, giardiasis, gastrointestinal food allergy, and carbohydrate intolerance (e.g., lactase deficiency).
Laboratory and instrumental confirmation
- Laboratory data: in uncomplicated courses, complete blood count, urinalysis, biochemistry, coagulogram, and coprogram remain within normal limits. This reliably excludes acute inflammatory processes, renal pathology, and pronounced metabolic shifts.
- X-ray examination: barium swallow imaging reveals a direct radiological sign—the "niche" sign in the antrum or duodenal bulb, representing an accumulation of contrast medium directly within the ulcer crater.
For differential diagnosis of peptic ulcer disease and IBS, remember the defecation rule: if abdominal pain subsides after going to the toilet, look for the problem in the intestine (IBS); if pain depends solely on food, the problem is in the upper levels (ulcer or dyspepsia).
Class and exam questions
Can Helicobacter pylori gastritis without an ulcer cause severe pain?
No, the mere detection of H. pylori in the absence of an ulcer defect does not provoke dyspeptic symptoms and does not replace the diagnosis of peptic ulcer disease.
How to distinguish a stenosing ulcer from hyperemesis gravidarum in adolescents?
In ulcers, abdominal pain remains the leading symptom. In toxicosis, pain is absent, nausea is almost constant, aggravated by odors, and vomiting usually occurs in the morning and does not depend on food.
What diseases are excluded in gastrointestinal bleeding?
The differential series includes erosive gastritis, Mallory-Weiss syndrome, gastric cancer, and blood swallowed during respiratory bleeding.
What else to study on this topic
- Rome IV criteria for functional dyspepsia
- Postprandial distress syndrome and epigastric pain syndrome
- Differential diagnosis with inflammatory bowel diseases (Crohn's disease, ulcerative colitis)
- Extraintestinal causes of abdominal pain (celiac disease, parasitoses, food allergy)
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