Development of a non-functional pancreatic neuroendocrine tumor and a duodenal ulceration after cholecystoduodenostomy in a cat

A six-year-old Ragdoll with previous extrahepatic biliary tract obstruction due to cholangiohepatitis, treated with cholecystoduodenostomy, was presented for acute vomiting, hyporexia, and weight loss. Abdominal ultrasound examination revealed randomly distributed hepatic nodules and dilated biliary ducts. Gastroduodenoscopy showed a patent cholecystoduodenostoma but disclosed a perforated duodenal ulceration. Conversion to celiotomy revealed extensive liver pathology, a discrete pancreatic nodule, and a duodenal ulcer opposite to the cholecystoduodenostoma. The cat was euthanized intra-operatively and necropsy was performed. The intrahepatic biliary tract of the right liver lobes was obstructed and severely dilated, whereas bile from the left lobes drained through the cholecystoduodenostoma. Histopathologic diagnoses were a primary pancreatic tumor, positive for glucagon on immunohistochemistry, with liver metastases, chronic purulent cholecystitis, and duodenal ulceration. To the authors’ knowledge, this is the first report in which the development of pancreatic neoplasia is described in a cat with a history of biliary tract disease.

The Pathogenesis of Duodenal Ulcer and the Role of Helicobacter pylori in This Disease: A Systematic Review

Background: The pathogenesis of duodenal ulcer has never been explained although the first description of this disease in medical literature appeared in 1817. Marshall et al. concluded that Helicobacter pylori was the most important etiological factor for duodenal ulcer in 1988, but the etiology based on this bacterium is controversial and how the bacterial infection leads to ulceration is presently unknown. Objectives: This study aims to identify the cause of duodenal ulcer, address the controversial issues surrounding Helicobacter pylori, elucidate the roles of gastric acid, and describe the pathological process of duodenal ulceration. Methods: First, a comprehensive systematic review on peptic ulcers (including gastric ulcer and duodenal ulcer) was conducted and the results were summarized. Second, a recently published causal relationship was employed to identify the etiology of peptic ulcers. Third, novel concepts and methods were applied to analyze the existing data on duodenal ulcer. Results: The etiology of duodenal ulcer and the roles of Helicobacter pylori and gastric acid in this disease were identified. The controversies surrounding Helicobacter pylori were addressed, and many characteristics and phenomena/observations of duodenal ulcer were elucidated. The pathological process of duodenal ulceration was described. Conclusion: Existing data accumulated over the past 300 years was sufficient, when analyzed using novel concepts, to understand the pathogenesis of duodenal ulcer. Duodenal ulcer is not an infectious disease caused by the infection of Helicobacter pylori, but a psychosomatic disease triggered by psychological stress. Helicobacter pylori plays a secondary role in only the late phase of duodenal ulceration.

Duodenal Ulceration following Holmium Laser Lithotripsy

The epidemiology of peptic ulcer disease (PUD) has changed considerably in the last several decades. Previously a chronic disease characterized by frequent recurrences with a high rate of surgical interventions, it is now largely a self-limited disease that is medically managed. The role of acid suppression was widely recognized as being important in the pathogenesis of PUD in the 19th century, while it was not until the 1980s and 1990s that the importance of Helicobacter pylori infection was identified. Today, PUD is largely caused by either H. pylori infection or nonsteroidal anti-inflammatory drug use. However, other less common etiologies of this disease are becoming more relevant as the prevalence of H. pylori decreases and proton pump inhibitor therapy is increasingly common. Here, we report a case of duodenal ulceration following bilateral rigid ureteroscopy with holmium laser lithotripsy.

Ischemic Duodenal Ulceration after Transarterial Chemoembolization for Hepatocellular Carcinoma: A Case Report

Drug-eluting bead transarterial chemoembolization (DEB-TACE) is a well-established, minimally invasive interventional treatment for nonresectable hepatocellular carcinoma (HCC). Generally, TACE is regarded as safe and effective with a low complication rate. However, remote gastrointestinal ischemia due to the carryover of embolic material into visceral arteries is a rare but serious complication of TACE. In this report, we present a case of duodenal ulceration with contained perforation and severe necrotizing pancreatitis after TACE in a patient with nonresectable HCC and underlying hepatitis C virus associated with Child-Pugh stage B liver cirrhosis. This patient showed, for the first time, complete endoscopic and clinical recovery within 2 months of conservative treatment. Considering the high mortality rate from surgical intervention in all previously reported patients, the significant recovery potential demonstrated by our case suggests conservative treatment with antibiotics and parenteral nutrition combined with close clinical, radiological, and endoscopic monitoring should be considered in all clinically stable patients without signs of peritonism or septic sequelae.