Iron overload is associated with low anti‐müllerian hormone in women with transfusion‐dependent β‐thalassaemia

Please cite this paper as: Chang H, Chen M, Lu M, Chern J, Lu C, Yang Y, Jou S, Lin D, Yang Y, Lin K. Iron overload is associated with low anti‐müllerian hormone in women with transfusion‐dependent β‐thalassaemia. BJOG 2011;118:825–831. Objective To investigate anti‐müllerian hormone (AMH) as a best test of ovarian reserve in women with transfusion‐dependent β‐thalassaemia, and the relationship between AMH and iron overload. Design and setting A case–control study in a tertiary medical centre. Population Twenty‐nine women with transfusion‐dependent β‐thalassaemia and 29 healthy controls of a similar age were recruited. Methods Blood sampling, questionnaires and medical record reviews were used. Main outcome measures The history of iron overload‐related morbidities, haematological phenotypes, serum levels of AMH and ferritin, and hormonal profiles were analysed. Results The serum levels of AMH, luteinising hormone, and estradiol were lower in women with transfusion‐dependent β‐thalassaemia than in age‐matched normal controls. In women with transfusion‐dependent β‐thalassaemia, the serum AMH level was significantly inversely related to the ferritin level, but not related to the presence of hypogonadotrophic hypogonadism, diabetes and haematological phenotypes. The serum ferritin level was positively associated with advanced age and the presence of hypogonadotrophic hypogonadism in the study participants. However, the inverse relationship between AMH and ferritin still exists after further adjustment for advanced age in women with transfusion‐dependent β‐thalassaemia. Conclusions The present study indicates that the serum AMH levels in women with transfusion‐dependent β‐thalassaemia are lower when compared with normal healthy women of a similar age, and are significantly negatively correlated with their serum ferritin levels. This implies that ovarian function might be impaired by the chronic iron overload status in women with transfusion‐dependent β‐thalassaemia.