Urinary loss of thiamine is increased by low doses of furosemide in healthy volunteers
Urinary loss of thiamine is increased by low doses of furosemide in healthy volunteers
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DOI：
10.1016/s0022-2143(99)90203-2
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发表时间：
1999-09-01
期刊：
影响因子：
--
通讯作者：
Ezra, D
中科院分区：
文献类型：
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作者：
Rieck, J;Halkin, H;Ezra, D
在一些充血性心力衰竭和饮食中硫胺素摄入量低的患者中，延长速尿治疗与尿中硫胺素丢失和硫胺素缺乏有关。在大鼠中，利尿剂引起的硫胺素尿丢失仅依赖于利尿增加，与使用的利尿剂类型无关。我们研究了单次静脉注射速尿（1、3和10 mg）和生理盐水（750 mL）对6名志愿者尿硫胺素排泄的影响。在长达6个时期,呋喃苯胺酸诱导剂量依赖性增加尿流和钠排泄率(意思是+ / - SD),从51 + / - 17毫升/小时在基线89 + / - 29 mL / h, 110 + / - 38毫升/小时,183 + / - 58毫升/小时(F = 10.4, P < .002)和从5.1 + / - 2.3更易与h到9.4 + / - 6.8更易/ h, 12.1 + / - 2.6更易/ h,和20.9 + / - 10.6更易与h (F = 6.3, P < .005)三个剂量分别为(104 + / - 35毫升/小时和13.0 + / - 6.2更易与盐水/ h)。在此期间，硫胺素排泄率从基线水平（利尿剂干预前四个24小时的平均值）的6.4 +/- 5.1 nmol/h翻了一番，达到11.6 +/- 8.2 nmol/h （F = 5.03, P < 0.01，所有四种干预措施之间没有差异），然后在接下来的18小时内返回到6.1 +/- 3.9 nmol/h。硫胺素排泄率与尿流率相关（r = 0.54, P < 0.001），干预方式和钠排泄率无进一步影响。这些发现补充了我们之前的动物实验结果，表明持续的利尿量为100 mL/h，可诱导人类受试者尿中硫胺素损失的非特异性但显著增加。在持续利尿的患者中，当可能存在饮食不足时，应考虑补充硫胺素。
Prolonged furosemide treatment is associated with urinary loss of thiamine and thiamine deficiency in some patients with congestive heart failure and low dietary thiamine intake. In the rat, diuretic-induced thiamine urinary loss is solely dependent on increased diuresis and is unrelated to the type of diuretic used. We studied the effects of single intravenous doses of furosemide (1, 3, and 10 mg) and of normal saline infusion (750 mL) on urinary thiamine excretion in 6 volunteers. Over a 6-hour period, furosemide induced dose-dependent increases in urine flow and sodium excretion rates (mean +/- SD), from 51 +/- 17 mL/h at baseline to 89 +/- 29 mL/h, 110 +/- 38 mL/h, and 183 +/- 58 mL/h (F = 10.4, P < .002) and from 5.1 +/- 2.3 mmol/h to 9.4 +/- 6.8 mmol/h, 12.1 +/- 2.6 mmol/h, and 20.9 +/- 10.6 mmol/h (F = 6.3, P < .005) for the three doses, respectively (104 +/- 35 mL/h and 13.0 +/- 6.2 mmol/h for the saline infusion). During this period the thiamine excretion rate doubled from baseline levels (mean of four 24-hour periods before the diuretic interventions) of 6.4 +/- 5.1 nmol/h to 11.6 +/- 8.2 nmol/h (F = 5.03, P < .01, for all four interventions, no difference being found between them), then returning over the following 18 hours to 6.1 +/- 3.9 nmol/h. The thiamine excretion rate was correlated with the urine flow rate (r = 0.54, P < .001), with no further effect of the type of intervention or sodium excretion rate. These findings complement our previous results in animals and indicate that sustained diuresis of >100 mL/h induces a nonspecific but significant increase in urinary loss of thiamine in human subjects. Thiamine supplements should be considered in patients undergoing sustained diuresis, when dietary deficiency may be present.