Duodenal diverticula (DD) are commonly encountered in the periampullary region but rarely on the lateral wall of the duodenum. They can develop complications such as diverticulitis, bleeding, and perforation. A 69-year-old healthy woman presented with melena due to a bleeding lesion in a lateral DD that was treated with hemoclipping. Two days later, she developed fever, hypotension, and an elevated CRP with mild abdominal pain and had no signs of peritonitis. A CT scan with oral contrast showed a large diverticulum at the junction of the descending and horizontal part of the duodenum and a perforation with minimal clinical symptoms that was successfully treated conservatively. Although causality could not be established, a retroperitoneal perforation following endoscopic hemostasis was a suspected complication of hemostatic clipping. Physicians should have a low threshold for a CT scan in the case of raised fever or inflammatory markers following endoscopic management of DD.
Background Gastrointestinal involvement in sarcoidosis is rare, and clinically apparent disease occurs in fewer than 1% of patients. The stomach is the most frequently affected site, although presentations are usually indolent. Perforation is exceedingly rare, and to our knowledge, this is the first case of gastric perforation attributable to sarcoidosis. Case Presentation A 30‐year‐old woman presented with 4 months of bilateral lower extremity paresthesia, pleuritic chest pain, progressive dyspnea, abdominal discomfort, and 50 lb unintentional weight loss. Angiotensin‐converting enzyme and soluble interleukin‐2 receptor were markedly elevated, and autoimmune serologies and extensive infectious workup were negative. Imaging revealed abdominal and pelvic lymphadenopathy, hepatosplenomegaly, and bilateral cavitary pulmonary opacities with mediastinal and hilar lymphadenopathy. During admission, she developed acute abdominal pain with pneumoperitoneum. Emergent laparotomy revealed a 6‐mm gastric perforation repaired with a Graham patch, with biopsies revealing lymphohistiocytic aggregates and multinucleated giant cells containing asteroid bodies. Subsequent endobronchial ultrasound–guided mediastinal node biopsy demonstrated granulomatous lymphadenitis, and a bronchoalveolar lavage showed a cD4/CD8 ratio of 15:1, suggesting sarcoidosis. Glucocorticoids were deferred due to surgical repair initially, and hydroxychloroquine was started. Subsequent lung wedge resection confirmed non‐necrotizing granulomas. Mycophenolate mofetil was then added and replaced by methotrexate with clinical improvement and resolution of symptoms. Conclusion Gastric perforation can be a severe complication in sarcoidosis, particularly in patients with multisystemic symptoms that are not otherwise explained. Multidisciplinary involvement is needed to appropriately treat these patients.
Background In clinical hepatology practice, pretreatment liver enzyme screening plays a key role in making management decisions, such as initiation of antituberculosis therapy or surveillance of chronic hepatitis B. Unrecognized extrahepatic sources of aminotransferase elevations can lead to misdiagnosis, inappropriate treatment alteration, and unnecessary invasive or costly investigations. Case Presentation We present two cases of active young males who were undergoing liver biochemical testing for therapeutic decision‐making for other underlying illnesses. Patient one was undergoing baseline liver enzyme testing prior to first‐line antituberculosis treatment initiation while patient two was undergoing surveillance for e‐antigen‐negative hepatitis B infection. Both patients had asymptomatic aminotransferase elevations mimicking acute hepatocellular injury. There was a marked and disproportionate elevation of aspartate aminotransferase (AST) relative to alanine aminotransferase (ALT), in the setting of otherwise normal cholestatic and synthetic parameters. Targeted history revealed heavy resistance weight training prior to testing. Measurement of serum creatine kinase (CK) confirmed exercise‐induced muscle injury, demonstrating elevated CK concentrations that paralleled the AST trajectory. Cessation of strenuous training led to rapid normalization of aminotransferases and a decline in CK levels, without interruption of tuberculosis management or unwarranted antiviral initiation. Conclusion Clinically silent exertional muscle injury is an underappreciated mimicker of acute liver injury. In patients presenting with isolated or disproportionate AST elevation, confirming a myogenic enzyme source via CK quantification can prevent misdiagnosis, eliminate unnecessary liver‐directed workup, and avoid inappropriate modification or initiation of essential pharmacotherapy.
Background Gastritis cystica profunda (GCP) is an uncommon gastric lesion characterized by displacement of cystically dilated glands into the submucosa. It may present as a submucosal mass mimicking gastrointestinal stromal tumor (GIST). The coexistence of GCP with high‐grade dysplasia is extremely uncommon and may pose a significant diagnostic challenge by simulating invasive carcinoma. Case Presentation We report a case of a 54‐year‐old patient whose endoscopic and radiographic features suggested a GIST in the gastric cardia. Surgical resection was performed. Histopathological examination revealed cystically dilated glands extending into the submucosa, lined by high‐grade dysplastic epithelium. Importantly, the muscularis mucosae was focally disrupted, and the submucosal component comprised both dysplastic and nondysplastic glands displaced together within smooth muscle bundles derived from the muscularis mucosae and accompanied by lamina propria‐type stroma, supporting mucosal prolapse rather than true invasion. A final diagnosis of high‐grade dysplasia arising in GCP was established. Conclusion This case highlights an important diagnostic pitfall in distinguishing pseudoinvasion from true invasive carcinoma in submucosal gastric lesions. Recognition of this entity and careful assessment of the muscularis mucosae together with the character of the displaced glands are essential to avoid overstaging and unnecessary aggressive management.
A 78-year-old woman presented with sudden-onset lower extremity edema, abdominal pain, and loss of appetite that developed the day after she fell off her bicycle. Computed tomography showed a simple hepatic cyst, 17 cm in diameter, compressing the inferior vena cava (IVC). Her symptoms resolved following laparoscopic deroofing. Notably, the cyst had remained stable at 12 cm 2 and 4 years prior, without any evidence of IVC compression. Although many guidelines for asymptomatic simple hepatic cysts published to date do not recommend treatment or follow-up regardless of size, our experience suggests the importance of monitoring simple hepatic cysts larger than 12 cm.
