Serum thrombopoietin levels are elevated in patients with an early stage of chronic viral hepatitis. As the disease progresses from mild fibrosis to cirrhosis, decreased production of thrombopoietin may contribute to the further development of thrombocytopenia in cirrhosis.

Patients with CH-C have evidence of enhanced hepatic iron accumulation and lipid peroxidation compared to those with CH-B. In CH-C, hepatic siderosis and lipid peroxidation are improved with successful IFN treatment. These results suggest that hepatic lipid peroxidation and iron may potentially play contributory roles in the pathogenesis of CH-C.

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Background : Endoscopic retrograde cholangiopancreatography (ERCP) and associated procedures have been reported to be difficult to perform in patients with Billroth II gastrectomy. We evaluated the feasibility of using an oblique-viewing endoscope equipped with a cannula deflector for these procedures in such patients. Patients and Methods : Twenty-four patients with Billroth II gastrectomy were enrolled in the present study and underwent ERCP, endoscopic sphincterotomy, endoscopic nasobiliary drainage, expandable metal stent placement or tube stent placement. All procedures were performed with an oblique-viewing endoscope equipped with a cannula deflector. Results : In all patients, afferent loops were entered. Reaching the papilla of Vater was achieved in 22 (91.7%) patients, in whom all planned procedures were accomplished. One patient experienced acute pancreatitis, hemorrhage from the papilla of Vater after sphincterotomy, and intestinal perforation. Conclusions : We believe an oblique-viewing endoscope equipped with a cannula deflector to be useful in performing ERCP and associated procedures in many patients with Billroth II gastrectomy. However, one should be aware of major complications, such as perforation, that may occur.

Serum thrombopoietin levels are elevated in patients with an early stage of chronic viral hepatitis. As the disease progresses from mild fibrosis to cirrhosis, decreased production of thrombopoietin may contribute to the further development of thrombocytopenia in cirrhosis.

Recent reports suggest the hepatic iron concentration (HIC) may influence the activity of hepatitis and the response to interferon (IFN) therapy in patients with chronic hepatitis C (CH-C). We have evaluated iron status in 28 patients with CH-C and determined if pretreatment iron status can predict the response to IFN-alpha therapy in these patients. Increased serum iron, transferrin saturation, and ferritin levels were observed in 3 (11%), 11 (39%), and 5 (18%) patients, respectively. Hepatic iron deposits were histologically detected in 17 (61%) patients, and 14 of them had stainable hepatocytic iron. However, all HIC values were within the normal range (203-1279 microg/g). Seven of 17 patients treated with IFN-alpha for 6 mo had normalization of serum transaminases and disappearance of serum HCV-RNA (responders). Nonresponders had a significantly higher median HIC compared with responders (710 vs 343 microg/g, respectively; p < 0.05). There was no significant difference in other pretreatment iron parameters, serum HCV-RNA level, or HCV-genotype between responders and nonresponders. In conclusion, mild hepatic iron accumulation occurs in patients with CH-C. Increased hepatic iron stores are associated with poor response to IFN therapy. Pretreatment HIC may be an additional host-specific parameter with a predictive value for responsiveness to IFN therapy, in addition to well-known predictive viral factors.

Wereport here a case of an unusual extrahepatic portosystemic venous shunt in a 37-year-old woman without liver cirrhosis or portal hypertension, whodeveloped portal systemic encephalopathy. Angiography demonstrated an inferior mesenteric-caval shunt characterized by the presence of direct communicationof the inferior mesenteric vein with the left internal iliac vein. After the treatment with percutaneous transcatheter embolization of the shunt via a femoral vein approach using coils, she had no episode of portal systemic encephalopathy. (Internal Medicine 40: 887-890, 2001)

Hepatic lipid peroxidation can occur in PBC and may be an early event in bile duct destruction. At advanced stages of PBC, hepatocellular lipid peroxidation may play a role in hepatocyte injury during cholestasis.