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一只猫因肾脏过度排磷和明显的维生素 D 代谢异常而导致佝偻病。

Rickets caused by excessive renal phosphate loss and apparent abnormal vitamin D metabolism in a cat.

作者信息

Henik R A, Forrest L J, Friedman A L

机构信息

Department of Medical Sciences, University of Wisconsin, Madison, WI 53706, USA.

出版信息

J Am Vet Med Assoc. 1999 Dec 1;215(11):1644-9, 1620-1.

Abstract

Rickets was diagnosed in a 1-year-old cat with a history of weakness, osteopenia, and recurrent fractures. Processes causing rickets include vitamin D deficiency caused by inadequate, nutrition, lack of exposure to sunlight, defective metabolism of parent vitamin D to active metabolites, inherited vitamin D receptor defects, hypoparathyroidism, chronic renal failure, renal loss of phosphate, or malabsorptive states resulting from gastrointestinal or hepatic diseases. On the basis of analysis of serum 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D2 and D3 concentrations, serum biochemical analysis, and urinary fractional clearance of electrolytes, the causes of rickets in our cat, were most compatible with a combination of excessive loss of phosphorus via the kidneys and deficient or abnormal hepatic 25-hydroxylation of vitamin D. Calcifediol treatment and twice daily administration of phosphate salts resulted in clinical improvement and increases in mineralization of the skeleton, as evidenced on radiographic evaluation.

摘要

一只1岁的猫被诊断为佝偻病,该猫有虚弱、骨质减少和反复骨折的病史。导致佝偻病的病因包括营养不足引起的维生素D缺乏、缺乏阳光照射、母体维生素D向活性代谢产物的代谢缺陷、遗传性维生素D受体缺陷、甲状旁腺功能减退、慢性肾衰竭、肾脏磷酸盐流失,或由胃肠道或肝脏疾病导致的吸收不良状态。根据血清25-羟基维生素D3以及1,25-二羟基维生素D2和D3浓度分析、血清生化分析和电解质的尿部分清除率,我们这只猫的佝偻病病因最符合经肾脏过度流失磷以及肝脏维生素D 25-羟化不足或异常的综合情况。骨化二醇治疗以及每日两次给予磷酸盐导致了临床症状改善和骨骼矿化增加,这在影像学评估中得到了证实。

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