Abdominal Pain, Gastrointestinal Bleeding, and Weight Loss in a 17-Year-Old Male

Abstract

A 17-year-old male presented to his primary care physician with a 2-week history of epigastric pain. The pain was localized, burning, temporarily relieved by meals, and occasionally awakened him from sleep. He denied fever, chills, cough, vomiting, or changes in bowel habits. He also denied use of nonsteroidal anti-inflammatory drugs, illicit drugs, or alcohol. There was no history of travel or trauma. His physical examination was remarkable only for epigastric tenderness. Laboratory values including complete blood count (CBC), chemistry, liver panel, erythrocyte sedimentation rate (ESR) and serum Helicobacter pylori immunoglobulin G (IgG) were negative. He was empirically treated with omeprazole. However, his pain progressed in severity and he avoided oral intake. An abdominal ultrasound was normal. Upper endoscopy showed irregular, ulcerated folds extending from the gastroesophageal junction to the antrum ( Fig. 1). Biopsies showed chronic active gastritis with poorly formed granulomas with central necrosis (Fig. 2). Hematoxylin and eosin (H&E) and Giemsa stains were negative for H. pylori. Acid fast bacilli (AFB), periodic acid-Schiff (PAS), and Gomori methenamine silver (GMS) stains were negative for mycobacteria and fungi.After having lost 10 pounds in 10 days, he was referred to our center for further evaluation. He developed hematemesis, which lowered his hematocrit level to 30.4%. ESR had elevated to 33 and C-reactive protein (CRP) was 7.6 mg/l. An urgent upper endoscopy revealed friable tissue, multiple nodules, ulcers throughout the stomach, and active bleeding. The esophagus and duodenum were normal. Biopsies showed poorly formed granulomas with central necrosis. Viral cultures, cytomegalovirus (CMV) polymerase chain reaction, AFB stain, and H. pylori were negative. Extensive workup, including tuberculin skin test, blood culture, rapid plasma reagin for syphilis, human immunodeficiency virus test, histoplasma antibody, screen Brucella antibody, antinuclear antibody, angiotensin-converting enzyme, chronic granulomatous disease test, and celiac panel were negative. Stool studies, including ova and parasites, culture, H. pylori antigen, and Clostridium difficile were negative. Chest X-ray was normal and abdominal computed tomography scan showed thickening and inflammation of the stomach and proximal duodenum. Upper gastrointestinal series with small bowel followthrough barium study showed mucosal disease in the distal esophagus, stomach, distal ileum, and proximal colon. Colonoscopy was normal except for lymphoid nodular hyperplasia. Biopsies were normal. He improved clinically with a protein pump inhibitor (PPI) and iron as his only medications.Three months later, he was seen in clinic for a follow-up visit. He remained asymptomatic, had regained his weight, and his hematocrit and ESR had normalized. He continued to take once daily PPI. A surveillance upper endoscopy showed normal mucosa throughout but biopsies showed

Rare Gastric Lesions Associated with Helicobacter pylori Infection: A Histopathological Review

“…They are also often in contact with a damaged pit (where H. pylori are commonly found) and are frequently accompanied by prominent neutrophilic infiltration, which distinguishes them from the granulomas that are observed in Crohn disease or sarcoidosis [6,7]. However, this characteristic morphology and localization has not been consistently reported in subsequent studies [18,23,24,40-42]. Therefore, there are no distinct histologic features that could be used to confirm H. pylori –associated GG.…”

Magnifying Endoscopic Features of Granulomatous Gastritis

“…We read with interest the case presentation published in a recent issue of Digestive Diseases and Sciences, focusing on granulomatous gastritis and its association with Helicobacter pylori (H. pylori) infection [1]. To date, wide variety of endoscopic features have been reported in granulomatous gastritis cases.…”

Clinicopathological characteristics and aetiological factors of granulomatous gastritis

“…33,[42][43][44][45][46] However, gastric granulomas can also precede H. pylori infection, persist after eradication or even spontaneously resolve. 6,33,43,[47][48][49][50] Furthermore, GG is not very common, considering the prevalence of H. pylori in most populations.…”

“…Moreover, eradication can lead to granuloma resolution, albeit sometimes only several months later 33,42–46 . However, gastric granulomas can also precede H. pylori infection, persist after eradication or even spontaneously resolve 6,33,43,47–50 . Furthermore, GG is not very common, considering the prevalence of H. pylori in most populations.…”