Prevention of thrombocytic defects in the br/br rabbit with folic acid and vitamin B12: analogy with the T.A.R. syndrome in humans.
Brachydactylia in the rabbit results from in utero haemorrhages leading to necrosis and post-natal amputations. Foetal liver study on day 14 to 16 of gestation, the critical period for thrombosis, reveals abnormalities of haematopoietic tissue. We observe a rarefaction of erythropoietic tissue and a defect of the megakaryocytic series resulting in erythrocyte macrocytosis and thrombopenia. Vitamin treatment (Folic acid + vitamin B12) administered to pregnant females prevents the above disorders and lead to production of mature forms in all the haematopoietic series. The T.A.R. syndrome (thrombocytopenia with absent radii) in humans, presents similarities with the physiological and clinical description of the br/br rabbit. Consequently, our research concerning the br/br foetuses seems to be a model for the study of several types of brachydactylia in humans either due to a vitamin deficiency or not.
D000818:Animals; D002452:Cell Count; D005260:Female; D005492:Folic Acid / Q000627:therapeutic use*; D005865:Gestational Age; D006410:Hematopoiesis; D006801:Humans; D017880:Limb Deformities, Congenital; D008099:Liver / Q000166:cytology / Q000196:embryology; D008533:Megakaryocytes / Q000166:cytology; D011247:Pregnancy; D011817:Rabbits; D013577:Syndrome; D013921:Thrombocytopenia / Q000209:etiology / Q000517:prevention & control*; D014805:Vitamin B 12 / Q000627:therapeutic use*
D005492:Folic Acid; D014805:Vitamin B 12