Trimethoprim-sulfamethoxazole therapy in outpatients: Is hyperkalemia a significant problem?
Trimethoprim-sulfamethoxazole therapy in outpatients: Is hyperkalemia a significant problem?
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DOI：
10.1159/000013483
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发表时间：
1999-05-01
影响因子：
4.2
通讯作者：
Perazella, MA
中科院分区：
文献类型：
--
作者：
Alappan, R;Buller, GK;Perazella, MA
进行了一项前瞻性随机临床研究，以确定标准剂量甲氧苄啶-磺胺甲恶唑联合治疗对门诊患者血清钾浓度的影响。97名患者接受口服抗生素治疗各种感染。51例接受甲氧苄啶-磺胺甲恶唑（甲氧苄啶，320 mg/天;磺胺甲恶唑，1,600 mg/天）治疗的患者构成治疗组，而46例接受其他抗生素治疗的患者作为对照组。测定血清钾、钠、氯浓度、血清二氧化碳含量、血尿素氮水平、血清肌酐水平和血清葡萄糖浓度。治疗组的基线血清钾浓度为4.30 +/-（SD）0.36 mmol/l，治疗第5天显著升高（p < 0.001）至4.66 +/- 0.45 mmol/l。治疗第5天平均血清钾浓度的亚组分析未能检测到临床相关的高钾血症。在血清肌酐水平等于或大于1.1 mg/dl（K+，4.83 +/- 0.48 mmol/l）的患者中，与血清肌酐水平< 1.1 mg/dl（K+，4.63 +/- 0.44 mmol/l）的患者相比，第5天的钾浓度无显著差异（p = 0.3）。虽然糖尿病患者的血清钾浓度（K+，4.91 +/- 0.44 mmol/l）高于非糖尿病患者（K+，4.61 +/- 0.44 mmol/l），但差异无统计学意义（p = 0.055）。年龄大于或等于50岁的患者（K+，4.82 +/- 0.59 mmol/l）在第5天的血清钾浓度与年龄< 50岁的患者（K+，4.55 +/- 0.28 mmol/l）有显著差异（p = 0.046）。相比之下，对照组的基线血清钾浓度为4.37 +/- 0.45 mmol/l，药物治疗5天后降低（p = 0.1）至4.22 +/- 0.4 mmol/l。甲氧苄啶-磺胺甲恶唑疗法，当用于治疗各种感染时，导致大多数患者血清钾浓度升高。用这种药物治疗5天后，与对照组相比，治疗组的血清钾浓度出现统计学显著性升高。而甲氧苄啶-磺胺甲恶唑组仅3例（6%）发生严重高钾血症（K+ ≥ 5.5mmol/l）。此外，接受治疗的患者亚组均未发生具有临床意义的高钾血症。这表明，与获得性免疫缺陷综合征患者和轻度肾功能不全的住院患者相比，门诊患者在接受这种抗菌方案治疗时发生重度或危及生命的高钾血症的几率较低。然而，门诊病人的危险因素，可能会导致高钾血症的发展时，应仔细监测与甲氧苄啶磺胺甲恶唑治疗。
A prospective, randomized clinical study was undertaken to determine the effect of standard-dose trimethoprim-sulfamethoxazole combination treatment on serum potassium concentrations in outpatients treated in an ambulatory clinic. Ninety-seven patients were treated with oral antibiotics for a variety of infections. Fifty-one patients treated with trimethoprim-sulfamethoxazole (trimethoprim, 320 mg/day; sulfamethoxazole, 1,600 mg/ day) constituted the treatment group, while 46 patients treated with other antibiotics served as controls. Serum potassium, sodium, and chloride concentrations, serum carbon dioxide content, blood urea nitrogen level, serum creatinine level, and serum glucose concentration were measured. The baseline serum potassium concentration in the treatment group was 4.30 +/- (SD) 0.36 mmol/l, and it increased significantly (p < 0.001) to 4.66 +/- 0.45 mmol/l on day 5 of therapy. Subgroup analysis of mean serum potassium concentration on day 5 of therapy failed to detect clinically relevant hyperkalemia. In patients with a serum creatinine level equal to or greater than 1.1 mg/dl (K+, 4.83 +/- 0.48 mmol/l), a nonsignificant difference (p = 0.3) in the potassium concentration was noted on day 5 as comapred with patients with a serum creatinine level < 1.1 mg/dl (K+, 4.63 +/- 0.44 mmol/l). Although diabetics had a higher serum potassium concentration (K+, 4.91 +/- 0.44 mmol/l) than nondiabetics (K+, 4.61 +/- 0.44 mmol/l), the difference was not statistically significant (p = 0.055). Patients aged greater than or equal to 50 years (K+, 4.82 +/- 0.59 mmol/l) had a significantly different (p = 0.046) serum potassium concentration on day 5 than patients aged < 50 years (K+, 4.55 +/- 0.28 mmol/l). In contrast, the baseline serum potassium concentration in the control group was 4.37 +/- 0.45 mmol/l, and it decreased (p = 0.1) to 4.22 +/- 0.4 mmol/l on 5 days of drug therapy. Trimethoprim-sulfamethoxazole therapy, when used to treat a variety of infections, leads to an increase in serum potassium concentration in most patients. After 5 days of therapy with this drug, the treatment group developed a statistically significant rise in the serum potassium concentration as compared with the control group. However, severe hyperkalemia (K+ greater than or equal to 5.5 mmol/l) occurred in only 3 patiens (6%) treated with trimethoprim-sulfamethoxazole. In addition, none of the subgroups of treated patients developed clinically important hyperkalemia. This suggests that outpatients, in contrast to acquired immunodeficiency syndrome patients and hospitalized patients with mild renal insufficiency, develop severe or life-threatening hyperkalemia less commonly when treated with this antimicrobial regimen. However, outpatients having risk factors which may predispose to the development of hyperkalemia should be carefully monitored when treated with trimethoprim-sulfamethoxazole.