Association of heart failure in homozygous beta-thalassemia with the major histocompatibility complex.

Background: In beta-thalassemia major, heart failure primarily affecting left ventricular systolic function is the most common complication and cause of death. Apart from iron deposition, it has been recently reported that myocarditis might be another contributing factor in the pathogenesis of acute or chronic heart failure, acting possibly through an autoimmune mechanism. In an attempt to assess the role of immunogenetic factors in the development of heart failure associated with beta-thalassemia major, we studied the frequency of major histocompatibility antigens/alleles A, B, DR, and DQ in homozygous beta-thalassemic patients with and without heart failure primarily affecting the left ventricle.

Apolipoprotein E epsilon4 allele as a genetic risk factor for left ventricular failure in homozygous beta-thalassemia.

In homozygous beta-thalassemia, the organ damage is mainly attributed to excessive iron deposition through the formation of oxygen free radicals. Despite appropriate transfusion and chelation therapy and low ferritin levels, patients still develop organ failure, heart failure being the main cause of death. This study was designed to determine whether the decreased antioxidant activity of the apolipoprotein E (APOE) 4 allele could represent a genetic risk factor for the development of left ventricular failure (LVF) in beta-thalassemia homozygotes.

Interferon-alpha 2b treatment of chronic hepatitis C in haemodialysis patients.

Nineteen haemodialysis (HD) patients with chronic hepatitis C were treated with interferon-alpha 2b (IFN-alpha) at a dose of 3 or 1 MU thrice weekly for 6 months and were followed-up for another 14 months without treatment. Six patients discontinued treatment because they either presented severe side-effects to IFN-alpha or had complications of their primary disease. Levels of AST and ALT were within normal limits on the 2nd month of treatment and remained so throughout the treatment and the follow-up period in all patients except one who showed an elevation of transaminase levels 2 months after the end of treatment.

Interferon treatment of chronic active hepatitis B: effect of a six month treatment regimen.

In this study of 17 patients with chronic active hepatitis B, the loss of hepatitis B virus DNA, the return to normal of alanine aminotransferase activities, and histological improvement after six months' treatment with 3 million units three times weekly with interferon alfa-2b, was achieved in 40% of hepatitis B e antigen (HBeAg) positive/anti HBe negative patients, and 41.66% of HBeAg negative/anti HBe positive patients. The reappearance of hepatitis B virus DNA was seen in most patients when treatment was stopped, although a higher percentage of HBeAg positive/anti HBe negative patients (20%) had a sustained loss of hepatitis B virus DNA, return to normal alanine aminotransferase activities, and histological improvement compared with HBeAg negative/anti HBe positive patients (8.