MECHANISMS OF HYPOPHOSPHATEMIA IN HUMANS WITH HEATSTROKE

被引:20
作者
BOUCHAMA, A
CAFEGE, A
ROBERTSON, W
ALDOSSARY, S
ELYAZIGI, A
机构
[1] KING FAISAL SPECIALIST HOSP & RES CTR, DEPT MED, RIYADH 11211, SAUDI ARABIA
[2] KING FAISAL SPECIALIST HOSP & RES CTR, DEPT BIOL & MED RES, RIYADH 11211, SAUDI ARABIA
[3] KING FAISAL SPECIALIST HOSP & RES CTR, DEPT PHARM, RIYADH 11211, SAUDI ARABIA
关键词
HYPERTHERMIA; RENAL THRESHOLD FOR PHOSPHATE; COOLING;
D O I
10.1152/jappl.1991.71.1.328
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Hypophosphatemia is common in heatstroke, but little is known about its mechanism. We investigated 10 consecutive patients with heatstroke (mean age 58 +/- 2 yr) whose mean rectal temperature at admission was 42.3 +/- 0.2-degrees-C. Eight patients presented with hypophosphatemia [0.48 +/- 0.08 mmol/l, normal range (NR) 0.8-1.4 mmol/l], associated with increased fractional excretion of phosphate (19.8 +/- 6.4%, NR 6-20%) relative to plasma phosphate levels and reduced renal threshold for phosphate (0.55 +/- 0.08 mmol/l glomerular filtrate, NR 0.8-1.4 mmol/l). Plasma parathyroid hormone (75.0 +/- 5 pmol/l) and calcium (2.24 +/- 0.02 mmol/l) levels and fractional excretion of calcium were normal (1.66 +/- 0.27%). There was no evidence of uricosuria or aminoaciduria, and only one patient had glucosuria. Arterial carbon dioxide was decreased in eight patients (28 +/- 1.1 Torr); however, none had elevated blood pH (7.35 +/- 0.02). The results suggest that heat-stroke-related hypophosphatemia is associated with abnormal phosphaturia independent of the parathyroid hormone level, and there is no evidence of tubular dysfunction.
引用
收藏
页码:328 / 332
页数:5
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