Helicobacter pylori is an established cause of many gastrointestinal pathologies including peptic ulcer disease, gastritis, and gastric cancer. It is an entity that affects the global population, and its true nature has only been known since the 1980s. Although there is much known about H. pylori including its pathophysiology, detection, and eradication, resistance to current therapy models is common. This is problematic because untreated or inadequately treated H. pylori increases morbidity and mortality related to gastric cancer and peptic ulcer disease among others. In order to improve the treatment and reduce resistance, there is significant ongoing research identifying new detection and eradication methods for H. pylori. This review aims to highlight what has already been established regarding H. pylori’s epidemiology, pathophysiology, detection, and treatment as well as the most current and novel research involving detection and treatment of H. pylori.

No abstract

No abstract

Among the many potential causes and risk factors for acute portal venous thrombosis, viral hepatitis has been regarded as a rare associated condition. We present the first case in the literature of a 30-year-old previously healthy male who presented with acute portal venous thrombosis associated with acute hepatitis A virus (HAV) infection, describing the probable pathophysiology mechanism, work-up and treatment pursued. We encourage that hepatitis A serological markers should be routinely included in the investigation for acute portal venous thrombosis of unknown aetiology, in unvaccinated patients with risk factors of a recent HAV exposure.

No abstract

No abstract

No abstract

markedly distended, non-tender abdomen, with a positive fluid wave and shifting dullness. Laboratory findings revealed body fluid studies with a SAAG ratio less than 1.1 indicating malignancy, but a high hepatic venous pressure gradient pointing to portal hypertension, with multiple cytology findings negative for malignant cells, however with good synthetic liver function. CT abdomen pelvis upon presentation was unremarkable, and consistent with previous imaging findings of known hepatectomy. After repeated paracentesis and multiple courses of antibiotic therapies for SBP, with recurrent ascites, complicated by hyponatremia with no mental status changes, further management of the case involved interventional radiology placing a Denver shunt to control the ascites. After a couple of months, the patient was followed up and found to have progression of disease with cancer seeding into the peritoneum with omental caking. Discussion: We strongly believe the patient's recurrent ascites of unknown origin was most likely a case of recurrent malignancy in ascitic fluid, masquerading as intrahepatic portal hypertension. We hope that this case report highlights that although in the setting of poorly differentiated gallbladder adenocarcinoma with local metastasis and negative margin resections, malignant ascites can occur and must not be mistaken for portal hypertension given the conflicting SAAG ratio and HPVG.