[Early hepatic complication in frst year after bone marrow transplantation in major beta thalassemic patients]

Bone marrow transplantation is a good therapeutic modality for beta thalassemia. Liver complications is one of the major causes of morbidity and mortality following BMT. Determination of the factors of liver injury leads to earlier diagnosis after BMT and improves prognosis. We studied 113 major Beta thalassemic patients who have been transplanted from 1990- 2000 in bone marrow transplantation center of Shariati Hospital. 62 were male and 51 were female. 27 patients were class one, 56 were class two and 30 were class three. The median age of each classes were 6.5, 6.3 and 8.7 year. Conditioning regime consisted of busulfan [3.5-4mg/Kg] and cyclophophamide [40-50 mg/kg]. For GVHD prophylaxis we gave cyclosporine +/- metothrexate. Grade of liver fibrosis defined by biopsy in all patients before BMT. All patients and their donors tested for HBsAg, HBsAb, HCVAb, CMVAb with RIA method. We assessed causes of liver dysfunction before and after transplantation and effect of high ferritin level on liver function. Hepatic dysfunction in first year after transplantation were seen in 86 [76%] patients. Causes of liver dysfunction were consisted of 53.1% GVHD, 15.93% cyclosporine hepatotoxicity, 5.3% conditioning regime hepatotoxicity and 1.77% VOD. In all three classes hepatic GVHD, cyclosporine toxicity, death and normal liver function post BMT had significant relation with hepatic dysfunction before BMT [p=0.001]. In patients with ferritin level more than 1000, there were significant hepatotoxicity with conditioning regime [p=0.001]. 17 [15.04%] of patients have been died. In this study we determined incidence and causes of hepatic dysfunction before and after BMT in major beta thalassemic patients. According to our study the incidence of hepatic dysfunction was 76.1% and hepatic GVHD and drug hepotoxicity were the most common causes of hepatic dysfunction in all three classes. Serum ferritin level had not significant relation to GVHD, cyclosporine hepatotoxicity and VOD

[Early hepatic complication in first year after bone marrow transplantation in major beta thalassemic patients]

Bone marrow transplantation is a good therapeutic modality for beta thalassemia. Liver complications is one of the major causes of morbidity and mortality following BMT. Determination of the factors of liver injury leads to earlier diagnosis after BMT and improves prognosis. We studied 113 major Beta thalassemic patients who have been transplanted from 1990- 2000 in bone marrow transplantation center of Shariati Hospital. 62 were male and 51 were female. 27 patients were class one, 56 were class two and 30 were class three. The median age of each classes were 6.5, 6.3 and 8.7 year. Conditioning regime consisted of busulfan [3.5-4mg/Kg] and cyclophophamide [40-50 mg/kg]. For GVHD prophylaxis we gave cyclosporine +/- metothrexate. Grade of liver fibrosis defined by biopsy in all patients before BMT. All patients and their donors tested for HBsAg, HBsAb, HCVAb, CMVAb with RIA method. We assessed causes of liver dysfunction before and after transplantation and effect of high ferritin level on liver function. Hepatic dysfunction in first year after transplantation were seen in 86 [76%] patients. Causes of liver dysfunction were consisted of 53.1% GVHD, 15.93% cyclosporine hepatotoxicity, 5.3% conditioning regime hepatotoxicity and 1.77% VOD. In all three classes hepatic GVHD, cyclosporine toxicity, death and normal liver function post BMT had significant relation with hepatic dysfunction before BMT [p=0.001]. In patients with ferritin level more than 1000, there were significant hepatotoxicity with conditioning regime [p=0.001]. 17 [15.04%] of patients have been died. In this study we determined incidence and causes of hepatic dysfunction before and after BMT in major beta thalassemic patients. According to our study the incidence of hepatic dysfunction was 76.1% and hepatic GVHD and drug hepotoxicity were the most common causes of hepatic dysfunction in all three classes. Serum ferritin level had not significant relation to GVHD, cyclosporine hepatotoxicity and VOD