锂诱导的肾性尿崩症引发的高渗性非酮症昏迷。
Hyperosmolar nonketotic coma precipitated by lithium-induced nephrogenic diabetes insipidus.
作者信息
Azam H, Newton R W, Morris A D, Thompson C J
机构信息
Department of Diabetes, Ninewells Hospital and Medical School, Dundee, Scotland, UK.
出版信息
Postgrad Med J. 1998 Jan;74(867):39-41. doi: 10.1136/pgmj.74.867.39.
A 45-year-old man, with a 10-year history of manic depression treated with lithium, was admitted with hyperosmolar, nonketotic coma. He gave a five-year history of polyuria and polydipsia, during which time urinalysis had been negative for glucose. After recovery from hyperglycaemia, he remained polyuric despite normal blood glucose concentrations; water deprivation testing indicated nephrogenic diabetes insipidus, likely to be lithium-induced. We hypothesize that when this man developed type 2 diabetes, chronic polyuria due to nephrogenic diabetes insipidus was sufficient to precipitate hyperosmolar dehydration.
一名45岁男性，有10年躁郁症病史，一直用锂盐治疗，因高渗性非酮症昏迷入院。他有5年多尿和烦渴病史，在此期间尿液分析葡萄糖呈阴性。高血糖恢复后，尽管血糖浓度正常，他仍多尿；禁水试验表明为肾性尿崩症，可能由锂盐所致。我们推测，当该男子患2型糖尿病时，肾性尿崩症所致的慢性多尿足以引发高渗性脱水。
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