Introduction: Pancreatic serous cystadenomas (PSCA) which represent one-third of pancreatic cystic neoplasms are typically benign asymptomatic lesions usually found incidentally on imaging studies at the body or tail of the pancreas. When symptomatic, presents typically with abdominal pain and a palpable mass. We report a case with PSCA presented as chronic diarrhea due to pancreatic duct (PD) obstruction with further enlargement over the years leading to biliary and partial duodenal obstruction. Case Description/Methods: A 65-year-old man with chronic diarrhea and a remote history of Hodgkin's Lymphoma treated with Mantle and pelvic radiation. Initially diagnosed as radiation enteritis, presented to our clinic with worsening diarrhea, flatulence, bloating, and weight loss. Endoscopic evaluation was negative for celiac disease or microscopic colitis. Diarrhea responded to empiric trial of pancreatic enzymes and he regained weight. CT scan of abdomen done to determine the etiology of exocrine pancreatic insufficiency (EPI) revealed a 3.7 cm complex cystic mass in the in the head of the pancreas with PD dilation and atrophy of the body and tail (Figure). Endoscopic ultrasound showed pancreatic mass with involvement of SMA and portal vein. Fine needle aspiration was not diagnostic. CT-guided biopsy was consistent with PSCA. 4 years later he complained of pale stools and dark urine; labs revealed ALT 495, alkaline phosphatase 463, bilirubin 4.5. MRI showed cyst enlargement to 5.7 cm with biliary dilation. Surgical consultation deemed him not to be a surgical candidate because of radiation induced vascular disease. ERCP with fully covered stent placement led to resolution of symptoms and normalization of liver tests. A year later ERCP with stent exchange showed compression of the duodenum distal to the stent leading to partial obstruction. Discussion: PSCA is usually an incidental finding on imaging studies. EPI is most commonly a result of chronic pancreatitis. Our patient presented with chronic diarrhea due to EPI as a result of PD obstruction by a PSCA. This case underscores the importance of imaging the pancreas in all patients with EPI to evaluate for potential underlying neoplasm causing obstruction of the PD. Our case also highlights that PSCA although benign if in the head of the pancreas can grow in size leading to gastric outlet obstruction and obstructive jaundice which can be associated with significant morbidity if the patient is not a surgical candidate.[1694] Figure 1. There is an approximately 4.0 cm x 3.7 cm ill-defined complex mass in the head of the pancreas.
cholecystocutaneous fistulae with either laparoscopic or open cholecystectomies and fistulae resections have been described with good success. Cholecystocutaneous fistulae in the setting of gallbladder malignancy have poor outcomes due to the spread to adjacent structures. Improved imaging diagnosis of gallstone and gallbladder disease, antibiotic therapies, early surgical intervention for gallbladder disease, and endoscopic alleviation of biliary outflow obstructions have made such a presentation of cholecystocutaneous fistula a rarely seen phenomenon.[2811] Figure 1. A patient found to have cholecystocutaneous fistula with (A) gallbladder extruding from the abdominal wall, (B) occlusion cholangiogram post-removal of multiple common bile duct stones showing dilated CBD and cholelithiasis in an irregular, contracted gallbladder, and (C) CT scan showing a mass (star) with extrusion of gallbladder through the liver and skin (arrow).
Introduction: Esophageal parakeratosis (EP) is an uncommon finding with largely unknown clinical implications and malignant potential. Here, we report a case of severe esophageal parakeratosis. Case Description/Methods: Patient is a 69-year-old African American male with history significant alcohol and cocaine abuse, prior tobacco abuse, keloids, gastroesophageal reflux, food impaction, and progressive dysphagia for 20 years with 40-pound weight loss. Patient's first esophagogastroduodenoscopy (EGD) in 2000 revealed moderate esophagitis and a distal esophageal stricture with 9 mm lumen bougie dilated to 12 mm, but dysphagia persisted. Repeat EGDs between 2006 and 2016 showed whitish plaques with no evidence of fungal organisms. Given classic appearance of EOE, he was trialed on empiric fluticasone and budesonide with no improvement in dysphagia. In September 2021, he was hospitalized with severe dysphagia. EGD (Figure) at this time showed gray, yellow frondlike lesion replacing esophageal lumen from mid to distal esophagus with mucosal friability. His dysphagia transiently responded to repeat dilations, but continued to recur and worsen. Unfortunately, patient continued to have weight loss and dysphagia unresponsive to dilations. The patient was then started on gastric tube feedings. He was offered surgery due to the severity of his symptoms, but he declined. Most recently, the patient underwent endoscopic mucosal resection with deeper tissue samples revealing superficial fragments of laterally spreading squamous cell carcinoma of the esophagus. Discussion: In this case, there was a high clinical suspicion for malignancy, leading the endoscopist to obtain deeper tissue samples via endoscopic mucosal resection as superficial fragments of the esophagus only revealed parakeratosis. It is important to trust clinical judgment, especially if there is a high suspicion for malignancy. Tylosis also has a known association with EP and often presents with areas of thickened skin plaques on palms and feet. Tylosis has a strong association with head, neck, and esophageal squamous cell carcinoma. The patient had no family history of tylosis and no cutaneous features. Despite this, a careful inspection of the entire EP area with targeted biopsies should be obtained to evaluate for dysplasia. This case represents EP with years of no evidence of squamous cell cancer despite aggressively searching for it, which at least anecdotally suggests a precancerous potential for EP.
Figure 1. 1a Kaposi sarcoma lesions, 1b CT imaging of abdomen and pelvis showing ascites.
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