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Patient A., 64 years old, a working pensioner (lead engineer of the mine), complains of recurrent epigastric pain, more on the right in 1.5-2 hours after eating, sometimes at night, heartburn, sour belching. The pain is local in nature, does not radiate, decreases after dairy food. Medical history: for 2 years, pain and heartburn periodically occurred, which were relieved by taking milk, sometimes Maalox and Almagel. Six months ago, he was examined, gastroduodenitis was detected, he took Omez 20 mg 2 times and Maalox. Within 3 months, clinical manifestations were absent, recently pains reoccurred and increased in intensity, especially at night, heartburn and belching occurred daily. The patient is a smoker, for the last 3 years, he has been smoking 2 packs of cigarettes a day. His work involves daily shifts. The father was operated on for gastric bleeding (he does not know the cause). On examination: the skin is of normal color, turgor is preserved. Peripheral lymph nodes are not palpable. Lungs are without pathological changes. The borders of the heart are normal. Pulse - 70 beats per minute, high, blood pressure - 130/70 mm Hg. The tongue is covered with a white coating. The abdomen is involved in breathing. On superficial palpation, he reports significant tenderness in the right subcostal area and in the epigastrium. On deep palpation, the intestinal parts are not changed. Liver is along the edge of the costal arch, gallbladder symptoms (Kehr’s, Murphy’s, Ortner’s) are negative. The spleen is not palpable. EGD: the esophagus is patent, the cardiac sphincter is tightly closed, the folds of the esophageal mucosa are normal. In the antrum of the stomach, foci of edema and intense hyperemia are determined, as well as single submucosal hemorrhages. The duodenal bulb is deformed, on the posterior wall of the bulb there is a stellate post-ulcer scar, on the front wall there is a deep ulcerative defect (up to the muscle layer) measuring 10 × 12 mm, significantly enlarged hyperemic folds of the mucous membrane, forming an inflammatory torus, hang over the defect. Along the rest length duodenal mucosa is with foci of hyperemia. Questions: 1. Suggest the most likely diagnosis. 2. Justify your diagnosis. 3. Plan and justify additional laboratory and instrumental investigations of the patient. 4. What will be your treatment strategy during the acute attack and in the inter-attack period? 5. After 2 months of maintenance therapy, the symptoms disappeared completely, there is a white scar at the site of the ulcer in EGD, a specimen was taken for cytological examination from the foci of edema and hyperemia in the stomach, Helicobacter pylori was found in great numbers. What is your further strategy? Justify your choice.

Reading Document

1) Most likely diagnosis

Chronic Helicobacter pylori-associated duodenal ulcer disease (peptic ulcer disease), currently in exacerbation: active ulcer of the anterior wall of the duodenal bulb (10×12 mm, deep), with cicatricial deformation of the bulb from a previous ulcer; concomitant antral gastritis (hyperemic-edematous, likely erosive/hemorrhagic).

2) Justification

This is most consistent with duodenal ulcer because of:
  • Typical pain rhythm: epigastric/right epigastric pain 1.5-2 h after meals and night pain (“hungry/night pain” pattern)
  • Relief with food/antacids/milk, classic for duodenal ulcer
  • Relapsing course over years with temporary response to acid suppression
  • Risk factors:
    • heavy smoking (2 packs/day)
    • likely persistent H. pylori infection (later confirmed in high load)
  • Endoscopic proof:
    • active deep ulcer defect in duodenal bulb (anterior wall), 10×12 mm
    • inflammatory rim/torus and hyperemic enlarged folds around ulcer
    • stellate scar on posterior wall and bulb deformation = prior ulcer and chronic recurrent disease
    • antral inflammatory changes (edema, hyperemia, submucosal hemorrhages) supporting associated gastroduodenitis
No evidence here for biliary colic/cholecystitis (negative Murphy/Kehr/Ortner), cardiac pain, or pancreatitis pattern.

3) Additional investigations (with rationale)

A. Laboratory

  1. CBC
    • assess occult/chronic blood loss (Hb), inflammatory response.
  2. Iron studies (if anemia): ferritin, transferrin saturation.
  3. Fecal occult blood test
    • detect chronic microbleeding from ulcer/erosions.
  4. Basic biochemistry: ALT/AST, bilirubin, ALP, creatinine, urea, electrolytes, glucose
    • baseline safety before prolonged therapy; differential with hepatobiliary disease.
  5. Amylase/lipase (if atypical pain appears)
    • exclude pancreatic pathology.

B. H. pylori diagnostics

(Needed for etiologic treatment and cure confirmation)
  1. During EGD: rapid urease test + histology (antrum and corpus biopsies).
  2. Noninvasive alternatives: 13C urea breath test or stool antigen test.
  3. Test-of-cure (mandatory): breath test or stool antigen
    • ≥4 weeks after antibiotics and ≥2 weeks off PPI.

C. Instrumental

  1. Repeat EGD with biopsy as indicated
    • confirm healing, complications, and monitor severe antral lesions.
  2. Abdominal ultrasound
    • exclude concomitant hepatobiliary pathology in right upper abdominal tenderness.
  3. If alarm signs develop (weight loss, recurrent bleeding, persistent vomiting): urgent reassessment/endoscopy.

4) Treatment strategy

During acute exacerbation

  1. PPI-based anti-ulcer treatment
    • e.g., omeprazole 20 mg BID (or equivalent potent PPI).
  2. Immediate H. pylori eradication regimen (if not yet treated definitively):
    • Preferred in many regions: bismuth quadruple therapy 10-14 days
      (PPI BID + bismuth + tetracycline + metronidazole),
      or guideline-appropriate concomitant/non-bismuth regimen based on local resistance.
  3. Mucosal protection / symptom relief
    • sucralfate and/or alginate/antacid as needed.
  4. Risk-factor control
    • strict smoking cessation (critical for healing and recurrence prevention),
    • avoid NSAIDs/alcohol if present.
  5. Diet/lifestyle
    • regular meals, avoid late-night irritant foods that worsen symptoms.
  6. Monitor for complications
    • bleeding, perforation, penetration, gastric outlet obstruction signs.

Inter-attack (maintenance/remission period)

  1. Confirm eradication of H. pylori (test-of-cure as above).
  2. Continue PPI step-down strategy for a limited period based on healing and symptoms.
  3. If high-risk recurrence persists (continued smoking, prior complicated ulcer, mandatory NSAIDs), consider longer gastroprotection plan.
  4. Secondary prevention:
    • no smoking, avoid ulcerogenic drugs, treat comorbid reflux/dyspepsia, follow-up if symptoms recur.

5) Situation after 2 months: symptoms resolved, white scar on EGD, but high-load H. pylori detected. Further strategy

This means ulcer healed morphologically but infection persists.
So the next step is definitive eradication therapy now (if not already effective), because persistent H. pylori strongly predicts relapse and complications (bleeding, recurrent ulcer, possible malignant risk in chronic gastritis pathway).

Recommended approach

  1. Start evidence-based eradication regimen for 14 days (prefer regimen different from any prior failed exposure and adapted to local resistance):
    • commonly bismuth quadruple therapy if not previously used.
  2. Adherence counseling (very important): exact dosing, no missed doses, side-effect management.
  3. Continue PPI during eradication and for short post-eradication healing support if needed.
  4. Mandatory test-of-cure:
    • 13C breath test or stool antigen,
    • timing: ≥4 weeks post-antibiotics and ≥2 weeks after stopping PPI.
  5. If still positive: second-line rescue regimen with different antibiotics (guided by prior regimens, and susceptibility testing where available).

Why this is the correct choice

  • Clinical remission and scar do not equal etiologic cure.
  • Eradication of H. pylori is the key intervention that reduces recurrence and ulcer complications long-term.
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