Time‐dependent Cox regression model is superior in prediction of prognosis in primary sclerosing cholangitis

Kirsten Muri Boberg, Giuseppe Rocca, Thore Egeland, Annika Bergquist, Ulrika Broomé, Llorenc Caballeria, Roger Chapman, Rolf Hultcrantz, Stephen Mitchell, Albert Pares, Floriano Rosina, Erik Schrumpf – 30 December 2003 – More precise prognostic models are needed for prediction of survival in patients with primary sclerosing cholangitis (PSC), particularly for the selection of candidates for liver transplantation. The aim of this study was to develop a time‐dependent prognostic model for the calculation of updated short‐term survival probability in PSC.

α‐Fetoprotein mRNA in the circulation as a predictor of postsurgical recurrence of hepatocellular carcinoma: A prospective study

Masayoshi Ijichi, Tadatoshi Takayama, Masayuki Matsumura, Yasushi Shiratori, Masao Omata, Masatoshi Makuuchi – 30 December 2003 – α‐fetoprotein (AFP) messenger RNA (mRNA) has been proposed as a marker of hepatocellular carcinoma (HCC) cells disseminated into the circulation, but its clinical significance remains controversial. We prospectively assessed the prognostic value of AFP mRNA in patients undergoing curative hepatic resection for HCC.

Contribution to antimitochondrial antibody production: Cleavage of pyruvate dehydrogenase complex‐E2 by apoptosis‐related proteases

Shuji Matsumura, Judy Van De Water, Hiroto Kita, Ross L. Coppel, Takao Tsuji, Kazuhide Yamamoto, Aftab A. Ansari, M. Eric Gershwin – 30 December 2003 – Patients with PBC produce a directed, specific response to a single immunodominant autoepitope of PDC‐E2 within the inner lipoyl domain. In contrast, immunized animals react to multiple epitopes and rarely recognize the inner lipoyl domain. In other autoimmune diseases, apoptosis plays a critical role in antigen presentation; the caspases and granzyme B are the key proteases in the generation of autoepitopes.

Effect of liver transplantation on inflammatory bowel disease in patients with primary sclerosing cholangitis

Igor Dvorchik, Michael Subotin, A. Jake Demetris, John J. Fung, Thomas E. Starzl, Samuel Wieand, Kareem M. Abu‐Elmagd – 30 December 2003 – This report investigates the influence of liver transplantation and concomitant immunosuppression on the course of progression of inflammatory bowel disease (IBD) and discusses statistical methodology appropriate for such settings.

Relationship of health‐related quality of life to treatment adherence and sustained response in chronic hepatitis C patients

David Bernstein, Leah Kleinman, Chris M. Barker, Dennis A. Revicki, Jesse Green – 30 December 2003 – Interferon therapy may exacerbate health‐related quality of life (HRQL) deficits associated with hepatitis C virus (HCV) early in the course of therapy. Treatment with polyethylene glycol–modified interferon (peginterferon) alfa‐2a (40 kd) provides improved sustained response over interferon alfa‐2a, but its effect on HRQL is unknown.

Hepatic arterial buffer response in patients with advanced cirrhosis

Veit Gülberg, Klaus Haag, Martin Rössle, Alexander L. Gerbes – 30 December 2003 – Hepatic arterial buffer response (HABR) is considered an important compensatory mechanism to maintain perfusion of the liver by hepatic arterial vasodilation on reduction of portal venous perfusion. HABR has been suggested to be impaired in patients with advanced cirrhosis. In patients with hepatopetal portal flow, placement of a transjugular intrahepatic portosystemic shunt (TIPS) reduces portal venous liver perfusion.

Polymorphism of the N‐acetyltransferase 2 gene as a susceptibility risk factor for antituberculosis drug–induced hepatitis

Yi‐Shin Huang, Herng‐Der Chern, Wei‐Juin Su, Jaw‐Ching Wu, Shinn‐Liang Lai, Shi‐Yi Yang, Full‐Young Chang, Shou‐Dong Lee – 30 December 2003 – Antituberculosis drug–induced hepatitis is one of the most prevalent drug‐induced liver injuries. Isoniazid is the major drug incriminated in this hepatotoxicity. Isoniazid is mainly metabolized to hepatotoxic intermediates by N‐acetyltransferase (NAT). However, the association of polymorphic NAT acetylator status and antituberculosis drug–induced hepatitis is debatable.

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