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44, P=0.11). However, the Spearman correlation test showed no linear correlation between iron changes and the time of biopsy (Spearman correlation coefficient=0.005, P=0.99). The Mann-Whitney test showed no significant difference in iron changes between males and females (P=0.15 and 0.08, respectively). Additionally, according to the Mann-Whitney test, there was no significant difference between patients Docetaxel in vitro changes (P=0.28 and 0.78, respectively). The Mann-Whitney test showed no significant difference between transplantation using bone marrow and transplantation using the peripheral blood in terms of iron and fibrosis changes (P=0.36 and 0.7, respectively). Discussion Iron depletion by phlebotomy Vatalanib (PTK787) 2HCl after HSCT can cause cirrhosis regression in patients with iron overload.5 The use of iron chelators such as Deferoxamine after HSCT has the same effect.15 Deferoxamine should not be administered immediately after transplantation because it can interfere with engraftment. In one study in Pesaro, 48 patients who had been regularly followed-up after transplantation for homozygous beta thalassemia were enrolled in a program of regular phlebotomy. Patients were eligible for this study if they were in prognostic classes 2 or 3 before transplantation; the 2-year follow-up examinations showed serum ferritin levels greater than 2,000 ��g/L and the 2-year post-transplant liver biopsies showed moderate or severe iron overload without phlebotomy. In this study thirty-five (85%) patients were hepatitis C seropositive. The results of the study showed that EX 527 nmr serum ferritin and HIC were reduced after repeated phlebotomy (P Value= 0.0001), but the degree of hepatic fibrosis was not significantly changed (P Value 0.18).8 In this study, fibrosis and iron overload before HSCT were not compared with the values after HSCT (prior to phlebotomy). In our center, most patients with beta thalassemia major were treated with phlebotomy after successful transplantation, but some of them had not received this treatment, because did not consent to phlebotomy or they had not regular follow-up. The main selection criterion in our study was liver fibrosis before transplantation (prognostic classes 2 or 3) regardless of the severity of iron accumulation in the liver or serum ferritin level. In this study we have shown that liver fibrosis alone before HSCT (with any degree of hepatic iron overload) can cause liver fibrosis progression after HSCT. In patients with mild to moderate iron overload, a gradual spontaneous decrease of iron overload after HSCT was almost sufficient to normalize iron levels16, but this did not occur in patients with severe iron overload at the time of transplant; in these patients, there may be progression of liver damage after HSCT.