Boucher-Ehrensperger M, Petter C
Int J Vitam Nutr Res. 1984;54(2-3):199-203.
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.
兔子的短指畸形是由子宫内出血导致坏死和出生后截肢引起的。在妊娠第14至16天（血栓形成的关键时期）对胎儿肝脏进行研究，发现造血组织存在异常。我们观察到红细胞生成组织稀少以及巨核细胞系列存在缺陷，导致红细胞大细胞症和血小板减少。给怀孕母兔进行维生素治疗（叶酸 + 维生素B12）可预防上述病症，并使所有造血系列产生成熟形式。人类的T.A.R.综合征（血小板减少伴桡骨缺失）与br/br兔子的生理和临床描述相似。因此，我们对br/br胎儿的研究似乎是研究人类几种类型短指畸形的模型，无论其是否由维生素缺乏引起。
