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Gastric hyperplastic polyps are usually associated with chronic gastritis including Helicobacter pylori gastritis and postantrectomy stomachs. Here, we report on a series of 12 patients with portal hypertension secondary to liver cirrhosis, who were found to have a unique histological type of gastric polyp on endoscopy.Retrospective chart review of 12 patients with portal hypertension, who presented with histologically diagnosed gastric hyperplastic polyps. These polyps were reviewed and compared with hyperplastic polyps from 21 patients who did not have portal hypertension.The endoscopic appearances of portal hypertension-associated polyps varied considerably, with sizes ranging up to 18 mm. They were sessile or pedunculated, singular or multiple, found in the antrum or body of the stomach, and endoscopically appeared to be typical hyperplastic polyps. Histopathological examination, however, showed mucosal hyperplasia and extensive vascular proliferation and granulation tissue formation.The unique histological appearance of gastric hyperplastic polyps in patients with portal hypertension polyps is described. The exact pathogenetic mechanism of polyp formation is unclear although it seems possible that the underlying cause is mucosal injury that is vascular in nature rather than being secondary to surface inflammation. Although there is an emerging evidence of the neoplastic potential of usual hyperplastic polyps, the natural history of portal hypertension-associated polyps is unknown. Identification and management of portal hypertension-associated gastric polyps present a particular dilemma, as these patients often have coagulopathies and vascular ectasias. Therefore, the natural history and endoscopic features of gastric polyps arising in portal hypertensive patients warrants further exploration.

Sessile serrated adenomas (SSAs) are associated with colorectal carcinomas (CRCs) that demonstrate high microsatellite instability (MSI-H). Currently, SSAs are managed clinically in a similar fashion to adenomatous polyps (APs). We studied the natural history of SSA by analyzing the outcome of previously undiagnosed SSAs and comparing it with that of hyperplastic polyps (HPs) and APs. All colorectal polyps diagnosed between 1980 and 2001 as HP were selected for study. Polyps identified as possible SSAs were reviewed by 3 pathologists, and the diagnosis was confirmed. Clinical follow-up was obtained for each SSA patient and matched with control HP and AP patients. In total, 1402 colorectal polyps diagnosed as HP were examined and 81 polyps in 55 patients (5.8%) were rediagnosed as SSA. Of these, 40 SSA patients had no previous history of either CRC or AP with high-grade dysplasia (HGD). Of these 40 patients, 5 developed subsequent CRCs and 1 developed AP with HGD. The incidence of subsequent CRCs was significantly higher in SSA patients than in control patients with HP (12.5% vs. 1.8%) and AP (12.5% vs. 1.8%). All of the subsequent CRCs or APs with HGD developed in the proximal colon. Four of the 5 CRCs demonstrated a high microsatellite instability phenotype. We conclude that SSAs are high-risk lesions, with 15% of the SSA patients developing subsequent CRCs or APs with HGD. This incidence is higher than that of the control HP and AP patients, and would support close endoscopic follow-up in patients harboring SSAs.

Giant cell hepatitis (GCH) is a rare form of hepatitis that has a generally poor prognosis.1 The disease often takes a progressive course, with the development of cirrhosis within months requiring transplantation or leading to death in a high percentage of cases.2 Diagnosis of GCH is made when hepatocellular multinucleate giant cells are found on liver biopsy.2 The etiology is unclear but is thought to include viruses including typical viral hepatitis, cytomegalovirus, rubella, parvovirus, paramyxovirus, human herpes virus, and human papilloma virus. Other postulated etiologies include autoimmune disorders, drug toxicities, alpha 1antitrypsin deficiency, and haemosiderosis. Therapy for GCH is controversial although successful treatment with ribavirin and/or interferon has been described in both non-transplant and transplant patients.

There are occasional pediatric reports of parvovirus B19-associated transient acute hepatitis and hepatic failure. A case of a 34-year-old immunocompetent woman who developed severe and prolonged but self-limited acute hepatitis and myelosuppression following acute parvovirus B19 infection is reported. Parvovirus B19 may be the causative agent in some adult cases of acute non-A-E viral hepatitis and acute liver failure.

Collecting duct carcinoma of the kidney is unique and rarely reported. The histological and ultrastructural characteristics of this tumor are well described in the pathological literature. However, there are few reports documenting the clinical presentation and long-term prognosis in patients with this unusual malignancy. Collecting duct carcinoma arises from the epithelium of the collecting tubules within the medulla and secondarily invades the renal cortex. The tumor occurs in a younger age group than is typical for renal cell carcinoma and most patients appear to have metastatic disease at presentation. We describe a case of this uncommon tumor and review the literature.