Chronic erythroid hyperplasia and accelerated bone turnover.
Bone atrophy is generally thought to be the etiology of the decreased skeletal mass and fractures found in patients with ineffective hematopoiesis and associated erythroid hyperplasia. A bone biopsy from a patient with chronic erythroid hyperplasia and diffuse cortical osteopenia revealed a normal trabecular bone volume, excess osteoid, numerous osteoblasts, and increased osteoclastic resorptive surface. The increased fractional labeled surfaces and widely spaced double tetracycline labels indicated accelerated bone turnover, despite demonstrable iron deposits at the calcification front and cement lines and a low serum level of 25-hydroxyvitamin D. The relationship between the expanded marrow space and trabecular bone suggests that local marrow factors may be responsible for the rapid bone remodeling.
D000328:Adult; D001706:Biopsy; D001847:Bone Diseases / Q000209:etiology* / Q000473:pathology; D001855:Bone Marrow Diseases / Q000150:complications* / Q000503:physiopathology; D001842:Bone and Bones / Q000378:metabolism / Q000473:pathology; D005260:Female; D006410:Hematopoiesis; D006455:Hemoglobins, Abnormal / Q000378:metabolism; D006801:Humans; D007085:Ilium / Q000473:pathology; D008903:Minerals / Q000378:metabolism
D006455:Hemoglobins, Abnormal; D008903:Minerals; C041119:hemoglobin Bibba