Yamamoto T, Fukuyama J, Kabayama Y, Harada H
Kishiwada Tokushukai Hospital, Osaka, Japan.
Clin Endocrinol (Oxf). 1998 Dec;49(6):785-92. doi: 10.1046/j.1365-2265.1998.00621.x.
Hyponatraemia is often observed in patients with ACTH deficiency who are thought not to suffer from volume depletion. Their high plasma AVP levels relative to plasma osmolality are presumed to be maintained by non-osmotic mechanisms. We attempted to assess volume status from changes in selected clinical measurements related to body fluid balance in the course of i.v. fluid supplementation and following glucocorticoid (GC) replacement in ACTH-deficient patients, and to interpret plasma AVP levels in the context of the estimated volume status.
This report consists of three parts. First, an ACTH-deficient patient with hyponatraemia and volume depletion who was followed through volume replacement to recovery after GC replacement is described (case report). Secondly, medical records of five ACTH-deficient patients with hypovolaemia and hyponatraemia were surveyed retrospectively to observe changes in serum levels of sodium, uric acid (UA) and haematocrit (Hct) following i.v. fluid supplementation of low sodium content (retrospective study). Thirdly, five ACTH-deficient patients with or without overt dehydration were studied with regard to body weight, blood pressure, serum sodium, total proteins, Hct and blood urea nitrogen before and after GC replacement (prospective study). Plasma AVP levels were measured after i.v. fluid supplementation without GC replacement in the patients of the retrospective study, and before and after GC replacement in the patients of the prospective study.
The first patient became more hyponatraemic after i.v. fluid supplementation and recovered ultimately from hyponatraemia after GC replacement. In five patients studied retrospectively, the serum sodium levels fell progressively following i.v. fluid supplementation, concurrent with reduction in UA levels and Hct, which indicated the dilutional nature of the hyponatraemia. In the patients observed prospectively, the accumulation of fluid and sodium was indicated by a rise in body weight, blood pressure and serum sodium levels and a decline in Hct and total proteins after GC replacement. Plasma AVP levels rose similarly in patients with dilutional hyponatraemia and in patients with borderline hyponatraemia before GC replacement.
Patients with untreated ACTH deficiency may have either of two kinds of hyponatraemia--i.e. borderline hyponatraemia associated with subclinical hypovolaemia, or dilutional hyponatraemia. Similarity of plasma AVP levels in two hyponatraemic states suggests their AVP secretion is regulated by non-osmotic, non-volume mechanisms, possibly released from GC suppression at low plasma osmolality.
低钠血症常见于促肾上腺皮质激素(ACTH)缺乏且无容量耗竭的患者。相对于血浆渗透压,其较高的血浆血管加压素(AVP)水平被认为是由非渗透机制维持的。我们试图通过与体液平衡相关的特定临床指标在静脉补液过程中以及ACTH缺乏患者糖皮质激素(GC)替代治疗后的变化来评估容量状态,并结合估计的容量状态来解释血浆AVP水平。
本报告由三部分组成。首先,描述了一名ACTH缺乏、低钠血症且有容量耗竭的患者,在接受容量补充直至GC替代治疗后恢复(病例报告)。其次,回顾性调查了5例ACTH缺乏、低血容量和低钠血症患者的病历,以观察低钠含量静脉补液后血清钠、尿酸(UA)和血细胞比容(Hct)水平的变化(回顾性研究)。第三,对5例有或无明显脱水的ACTH缺乏患者在GC替代治疗前后的体重、血压、血清钠、总蛋白、Hct和血尿素氮进行了研究(前瞻性研究)。回顾性研究的患者在未进行GC替代治疗的静脉补液后测定血浆AVP水平,前瞻性研究的患者在GC替代治疗前后测定血浆AVP水平。
首例患者在静脉补液后低钠血症加重,最终在GC替代治疗后从低钠血症中恢复。在回顾性研究的5例患者中,静脉补液后血清钠水平逐渐下降,同时UA水平和Hct降低,这表明低钠血症具有稀释性。在前瞻性观察的患者中,GC替代治疗后体重增加、血压升高、血清钠水平升高以及Hct和总蛋白降低表明有液体和钠的潴留。在稀释性低钠血症患者和GC替代治疗前临界低钠血症患者中,血浆AVP水平同样升高。
未经治疗的ACTH缺乏患者可能有两种低钠血症,即与亚临床低血容量相关的临界低钠血症或稀释性低钠血症。两种低钠血症状态下血浆AVP水平的相似性表明其AVP分泌受非渗透、非容量机制调节,可能是在低血浆渗透压时由GC抑制释放。