Hill A R, Uribarri J, Mann J, Berl T
Department of Medicine, State University of New York Health Science Center, Brooklyn 11203.
Am J Med. 1990 Apr;88(4):357-64. doi: 10.1016/0002-9343(90)90489-z.
Patients with hyponatremia due to tuberculosis have shown variable responses to water loading in previous small studies, ranging from persistent antidiuresis to a normal diuresis. Although tuberculosis is considered a cause of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), circulating vasopressin has been documented in only a few cases. We studied a larger group of patients to determine whether it can be suppressed by a short-term reduction in osmolality.
Twenty-eight hyponatremic patients (mean age +/- SD: 40 +/- 10 years) with pulmonary or miliary tuberculosis underwent a clinical evaluation, measurement of blood and urine chemistry values, and (in 22) a water load of 20 mL/kg. Volume status was evaluated by urine sodium concentration, blood and urine urea nitrogen, and plasma renin activity. Endocrine, renal, and other recognized causes of SIADH were excluded.
All 22 patients exhibited a decline in urine osmolality and an increase in free water clearance after water loading. Water excretion was fully normal in seven of 22, with the remainder showing variable impairment of diluting ability and/or volume excreted. Plasma vasopressin, measured in 11 of 22 patients as well as in six others not subjected to water loading, was detectable despite hypo-osmolality in 16 of 17. Vasopressin levels declined after water loading, from 1.85 +/- 1.32 to 0.77 +/- 0.25 pg/mL (p less than 0.05). The majority of patients had the euthyroid sick syndrome but normal adrenal responses to cosyntropin. Although several patients had mild volume depletion when studied, this factor did not appear to explain the defect in water excretion. Hyponatremia resolved predictably within days to weeks of antituberculous therapy.
Circulating vasopressin remains detectable in hyponatremic patients with tuberculosis and is responsive to changes in osmolality. A downsetting of osmoregulation induced by active tuberculosis ("reset osmostat") could explain this abnormality, but we cannot exclude an unidentified non-osmotic stimulus that can be counteracted by water loading.
在先前的小型研究中，因结核病导致低钠血症的患者对水负荷的反应各不相同，从持续性抗利尿到正常利尿。尽管结核病被认为是抗利尿激素分泌不当综合征（SIADH）的一个病因，但仅有少数病例记录到循环血管加压素的存在。我们研究了一组更大规模的患者，以确定其是否能通过短期降低渗透压来抑制。
28例患有肺结核或粟粒性结核的低钠血症患者（平均年龄±标准差：40±10岁）接受了临床评估、血液和尿液化学值测量，以及22例患者进行了20 mL/kg的水负荷试验。通过尿钠浓度、血液和尿液尿素氮以及血浆肾素活性评估容量状态。排除了SIADH的内分泌、肾脏及其他已知病因。
所有22例患者在水负荷后尿渗透压均下降，自由水清除率增加。22例中有7例水排泄完全正常，其余患者显示稀释能力和/或排泄量存在不同程度的损害。在22例患者中的11例以及另外6例未进行水负荷试验的患者中测量血浆血管加压素，尽管17例中有16例存在低渗，但仍可检测到。水负荷后血管加压素水平下降，从1.85±1.32降至0.77±0.25 pg/mL（p<0.05）。大多数患者患有甲状腺功能正常的病态综合征，但肾上腺对促肾上腺皮质激素的反应正常。尽管在研究时有几名患者存在轻度容量不足，但该因素似乎无法解释水排泄缺陷。抗结核治疗数天至数周内，低钠血症可得到预期缓解。
患有结核病的低钠血症患者中仍可检测到循环血管加压素，且其对渗透压变化有反应。活动性结核病引起的渗透调节下调（“渗透压调定点重置”）可以解释这种异常，但我们不能排除一种未明确的非渗透性刺激因素，而水负荷可以抵消这种刺激。
