S5462 Large Gastric Ulcer Caused by Sarcina ventriculi Colonization in a Patient With Cirrhosis

Introduction: Peptic ulcer disease (PUD) is the discontinuation in the inner lining of the gastrointestinal tract due to increased gastric acid secretion. The most common risk factor in developing PUD is Helicobacter pylori infection. However, PUD caused by other organisms in vulnerable patients, such as cirrhotics is seldomly documented. By describing the clinical course and treatment of PUD due to Sarcinaventriculi (SV) infection in a cirrhotic, clinicians can be better equipped to treat PUD in special patient populations, such as those with cirrhosis. Case Description/Methods: A 61-year-old woman with history of compensated hepatitis C cirrhosis status post treatment and end stage renal disease on intermittent dialysis presented to our emergency department with large coffee-ground emesis. Associated symptoms include epigastric pain and anorexia. On admission, labs were notable for a hemoglobin drop 11.7 to 7.8. Patient had no known varices. Hepatology was consulted and recommended starting intravenous pantoprazole, octreotide, ceftriaxone, and endoscopy (EGD). EGD was notable for a 10 cm gastric ulcer extending from the antrum to the distal body with heaped up edges, concerning for malignancy. Biopsies were taken. Computed tomography (CT) abdominal/pelvis was ordered for possible staging and notable for circumferential gastric thickening with perigastric fat stranding as well as multiple peripancreatic/retrocaval lymph nodes. A repeat EGD was performed with additional biopsies as CT findings could be more reactive as opposed to malignant. All biopsies were notable for gastric antral type mucosa with reactive changes, colonized by SV. Infectious disease was consulted for treatment of ulcer with SV colonization. Patient was started on metronidazole and ciprofloxacin for a 10-day course, with repeat endoscopy in 8 weeks to confirm resolution. Discussion: SV is an anaerobic gram-positive coccus. In rare cases, SV causes gastric ulcers and gastric perforation. Our patient was treated with antibiotics and was eventually discharged without complications. Although, SV colonization can mimic malignancy as in our patient, all her biopsies were negative for cancer. This case is significant for clinicians caring for cirrhotics. Cirrhotic patients are at higher risk of developing large, potentially fatal ulcers caused by rare organisms such as SV. Multiple biopsies should be taken to rule out malignancy, and these patients should be treated with antibiotics to prevent recurrence.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001149308.76419.9a
Primary Topic
Helicobacter pylori-related gastroenterology studies
Type
article
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article

S5462 Large Gastric Ulcer Caused by Sarcina ventriculi Colonization in a Patient With Cirrhosis

Lauren Thompson, Adaobi Ahanotu
The American Journal of Gastroenterology
Helicobacter pylori-related gastroenterology studies
article

S5462 Large Gastric Ulcer Caused by Sarcina ventriculi Colonization in a Patient With Cirrhosis

Lauren Thompson, Adaobi Ahanotu
article en

Abstract

Introduction: Peptic ulcer disease (PUD) is the discontinuation in the inner lining of the gastrointestinal tract due to increased gastric acid secretion. The most common risk factor in developing PUD is Helicobacter pylori infection. However, PUD caused by other organisms in vulnerable patients, such as cirrhotics is seldomly documented. By describing the clinical course and treatment of PUD due to Sarcinaventriculi (SV) infection in a cirrhotic, clinicians can be better equipped to treat PUD in special patient populations, such as those with cirrhosis. Case Description/Methods: A 61-year-old woman with history of compensated hepatitis C cirrhosis status post treatment and end stage renal disease on intermittent dialysis presented to our emergency department with large coffee-ground emesis. Associated symptoms include epigastric pain and anorexia. On admission, labs were notable for a hemoglobin drop 11.7 to 7.8. Patient had no known varices. Hepatology was consulted and recommended starting intravenous pantoprazole, octreotide, ceftriaxone, and endoscopy (EGD). EGD was notable for a 10 cm gastric ulcer extending from the antrum to the distal body with heaped up edges, concerning for malignancy. Biopsies were taken. Computed tomography (CT) abdominal/pelvis was ordered for possible staging and notable for circumferential gastric thickening with perigastric fat stranding as well as multiple peripancreatic/retrocaval lymph nodes. A repeat EGD was performed with additional biopsies as CT findings could be more reactive as opposed to malignant. All biopsies were notable for gastric antral type mucosa with reactive changes, colonized by SV. Infectious disease was consulted for treatment of ulcer with SV colonization. Patient was started on metronidazole and ciprofloxacin for a 10-day course, with repeat endoscopy in 8 weeks to confirm resolution. Discussion: SV is an anaerobic gram-positive coccus. In rare cases, SV causes gastric ulcers and gastric perforation. Our patient was treated with antibiotics and was eventually discharged without complications. Although, SV colonization can mimic malignancy as in our patient, all her biopsies were negative for cancer. This case is significant for clinicians caring for cirrhotics. Cirrhotic patients are at higher risk of developing large, potentially fatal ulcers caused by rare organisms such as SV. Multiple biopsies should be taken to rule out malignancy, and these patients should be treated with antibiotics to prevent recurrence.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 41%
Helicobacter pylori-related gastroenterology studies
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