Macroscopic Portal Vein Thrombosis in HCC Patients.

Macroscopic portal vein invasion (PVT) by hepatocellular carcinoma (HCC) in the liver is one of the most important negative prognostic factors for HCC patients. The characteristics of a large cohort of such patients were examined. We found that the percent of patients with PVT significantly increased with increasing maximum tumor diameter (MTD), from 13.7% with tumors of MTD <5cm to 56.4% with tumors of MTD >10cm. There were similar numbers of HCC patients with very large tumors with and without PVT. Thus, MTD alone was insufficient to explain the presence of PVT, as were high AFP levels, since less than 50% of high AFP patients had PVT. However, the percent of patients with PVT was also found to significantly increase with increasing blood alpha-fetoprotein (AFP) levels and tumor multifocality. A logistic regression model that included these 3 factors together showed an odds ratio of 17.9 for the combination of MTD>5.0cm plus tumor multifocality plus elevated AFP, compared to low levels of these 3 parameters. The presence or absence of macroscopic PVT may therefore represent different HCC aggressiveness phenotypes, as judged by a significant increase in tumor multifocality and AFP levels in the PVT positive patients. Factors in addition to MTD and AFP must also contribute to PVT development.

Hepatitis B Virus Reactivation under Treatment with Nilotinib.

Hepatitis B virus (HBV) reactivation with imatinib, a tyrosine kinase inhibitor, has been reported in chronic myeloid leukemia. Nilotinib is a more potent second generation tyrosine kinase inhibitor and it inhibits the Src-family kinase LCK and hamper proliferation and function of CD8 (+) T lymphocytes. CD8 (+) T lymphocytes are the main cellular subset responsible for viral clearance in patients with HBV infection. We report a case of HBV reactivation under treatment with nilotinib. Fatal HBV reactivation is not usually related to death in chronic myeloid leukemia patients who have an expectation of longevity with well-tolerated oral drugs. Thus, screening for latent chronic HBV infections including assessment of hepatitis B surface antigen (HBsAg), antibody to hepatitis B core antigen (anti-HBc antibody) and antibody to hepatitis B surface antigen (anti-HBs), especially at countries with intermediate and high prevalence of HBsAg is warranted. Treatment with nucleoside analogs and close monitoring may be life-saving in this context. HOW TO CITE THIS ARTICLE: Temel T, Gunduz E, Sadigova E, Teke HU, Ozgenel SM, Ozakyol AH. Hepatitis B Virus Reactivation under Treatment with Nilotinib. Euroasian J Hepato-Gastroenterol 2015;5(2):112-114.

A Case Report of Ulcerative Colitis Induced by Therapy of Colorectal Carcinoma.

Although patients with ulcerative colitis have an increased risk for colon cancer which is associated with disease activity, location of involvement or the accompanying primary sclerosing cholangitis, ulcerative colitis induced by resections for colorectal carcinoma or chemotherapy drugs are very rare as case presentations in the literature. Fifty-nine year-old female patient with the diagnosis of sigmoid colon carcinoma have been developed ulcerative colitis 2 months after low anterior resection and oral capecitabine treatment. Development of colitis after colon cancer may be associated with some causes as mutual genetic factors that take part at the pathophysiological mechanisms liable from occurrence of ulcerative colitis and colorectal carcinoma, chemotherapy agents, perioperative stress and underlying silent ulcerative colitis. It is unclear which role is certain. Increasing reports like this case will be useful in resolving this issue. HOW TO CITE THIS ARTICLE: Temel T, Ozgenel SM, Canaz F, Arik D, Tokmak S, Ozakyol AH. A Case Report of Ulcerative Colitis Induced by Therapy of Colorectal Carcinoma. Euroasian J Hepato-Gastroenterol 2015;5(2):115-117.