Bone histomorphometry in @entity1 and adolescents with @entity8674 : @entity68 -associated focal XXXX .

@entity1 @entity851 @entity4772 @entity417 @entity101 @entity68 @entity170 @entity442 @entity10545 @entity79 @entity2331 @entity74 @entity8453 @entity8674 @entity2395
@entity2395 / @entity8453 is a @entity74 that causes chronic @entity417 and increased erythropoiesis. Consequently, an expansion of bone marrow spaces may contribute to @entity2331 / @entity170 . However, the pathogenesis of bone changes is not yet known. We, therefore, carried out the study on bone histomorphometry and biochemical and hormonal profiles in @entity1 and adolescents with suboptimally treated @entity8674 with the hope of gaining some new insight into the cellular and structural alterations of thalassemic bone. Seventeen @entity1 underwent iliac crest bone biopsy for histomorphometric analyses. @entity79 ( @entity79 ) measurements were performed by dual energy x-ray absorptiometry. Most @entity1 had @entity851 and delayed bone age. @entity79 was low especially at the lumbar spine. Serum @entity442 levels were almost always low. Bone histomorphometry revealed @entity101 , osteoid maturation time, and mineralization lag time, which indicate impaired bone matrix maturation and defective mineralization. In addition, @entity68 deposits appeared along mineralization fronts and osteoid surfaces. Moreover, focal @entity10545 were found together with focal @entity68 deposits. Dynamic bone formation study revealed reduced bone formation rate. These findings indicate that delayed bone maturation and focal @entity4772 are the pathogenesis of @entity79 in suboptimally blood-transfused thalassemics with @entity68 overload. @entity68 deposits in bone and low circulating @entity442 levels may partly contribute to the above findings.
