Introduction: Helicobacter pylori (H. pylori) has a well-known association with peptic ulcer disease (PUD) and gastritis. However, other helicobacter species cause similar diseases. We present a case of a patient with H. heilmanni infection causing PUD and significant gastrointestinal (GI) bleeding. Case Description/Methods: A 63-year-old man with CAD s/p stent on aspirin and recent root canal procedure who was taking ibuprofen for several weeks presented with a one day history of mixed melena and hematochezia. He had no prior history of PUD or GI bleeding. EGD revealed two Forrest class III gastric ulcers and three duodenal ulcers including a 7 mm Forrest class IIc ulcer. Gastric biopsies were taken. He required 3 units of packed red blood cells (PRBCs), and was discharged on pantoprazole BID with a Hgb of 8 g/dl and biopsy results pending. The following day, he presented with similar symptoms, requiring ICU admission for Hgb 5.4 g/dl and blood pressure 77/52 mm Hg. He required 5 units PRBCs without pressor support. Repeat EGD revealed a 12 mm Forest class IIb duodenal ulcer (image 1) which was injected with epinephrine, and a single hemoclip was placed with hemostatic control. Prior EGD biopsy results showed chronic gastritis and helicobacter-like species found to be Helicobacter heilmanni by genotyping, and negative for concurrent H. pylori. The patient was treated with triple therapy with pantoprazole, amoxicillin and clarithromycin. Repeat EGD 2 months after treatment confirmed eradication of H. heilmanni and healing of all ulcers. Discussion: H. heilmanni was first described as an organism causing gastritis in humans in 1987 under its former name Gastrospirillum hominis. H. heilmanni is found in less than 1% of patients undergoing EGD for upper GI symptoms compared to H. pylori which is found in as many as 60% of patients with similar symptoms. Complications of H. heilmanni infection in patients include: 82% developing gastritis, 16% PUD, 2% gastric cancer, and, in our patient’s case, severe GI bleeding. Concurrent infection with H. pylori and H. heilmanni infection is uncommon and identification of H. heilmanni via H. pylori via stool antigen or rapid urease testing has unclear efficacy. Our case highlights the need for H. heilmanni to be recognized as a potential cause of PUD and further testing might need to be considered when H. pylori testing is negative. Ultimately, definitive diagnosis is done via genetic PCR amplification, and treatment is possible using the same antibiotic regimen as H. pylori.Figure 1.: Duodenal ulcer with adherent clot (Forest class IIb).
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