Dorfman S G, Ruark G W, Agus Z S, Jacobs R L, Young R L
Arch Intern Med. 1977 Oct;137(10):1479-81.
A 38-year-old physician developed polyuria and hypodipsia four days after the onset of an upper respiratory tract infection. Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI). Skull roentgenograms, EEG, and lumbar puncture were normal. The polyuria and hypodipsia slowly resolved without treatment. Normal urinary concentration ability was achieved by the 48th day, but a residual elevation in serum osmolarity persisted for one year. Review of the literature failed to show previous documentation of transient DI with elevated serum osmolarity from an acute, febrile illness. The mechanism is speculative, but may be related to a subclinical encephalitis. The true frequency of this syndrome and its relationship to the frequent observation of transient polydipsia and polyuria in "benign" febrile illness remains to be determined.
一名38岁的内科医生在上呼吸道感染发病四天后出现多尿和烦渴减退。随后的检查显示存在伴有脱水的浓缩功能缺陷,给予血管加压素注射(垂体后叶素)后部分得到纠正,符合部分性中枢性尿崩症(DI)。头颅X线片、脑电图和腰椎穿刺均正常。多尿和烦渴减退未经治疗缓慢缓解。到第48天时恢复了正常的尿浓缩能力,但血清渗透压仍持续升高一年。文献回顾未发现先前有关于急性发热性疾病导致血清渗透压升高的短暂性尿崩症的记录。其机制尚属推测,但可能与亚临床脑炎有关。该综合征的实际发生率及其与“良性”发热性疾病中常见的短暂性烦渴多饮和多尿的关系仍有待确定。