Wilson H K, Keuer S P, Lea A S, Boyd A E, Eknoyan G
Arch Intern Med. 1982 Mar;142(3):517-20.
To determine the efficacy of phosphate replacement in the therapy for diabetic ketoacidosis (DKA), 44 patients were randomly assigned to three treatment groups: those who received no phosphate replacement, those who received 15 mmole of sodium phosphate at the fourth hour, or those who received 15 mmole of sodium phosphate at 2, 6, and 10 hours. All patients were treated with intravenous insulin injection (0.1 units/kg/hr), fluids, and potassium. Four hours after a 15-mmole sodium phosphate infusion, the serum phosphate level was 2.8 +/- 0.8 mg/dL vs 2.1 +/- 0.8 mg/dL in the control patients; however, this dose was insufficient to maintain the serum phosphate level at 16 and 24 hours. Forty-five millimoles of phosphate prevented severe hypophosphatemia in all but one patient and produced substantially higher phosphate levels at 8, 16, and 24 hours. Phosphate therapy did not affect the duration of DKA, dose of insulin required to correct the acidosis, abnormal muscle enzyme levels, glucose disappearance, or morbidity and mortality. Although theoretically appealing, phosphate therapy is not an essential part of the therapy for DKA in most patients.
为确定补充磷酸盐在糖尿病酮症酸中毒(DKA)治疗中的疗效,44例患者被随机分为三组治疗组:未接受磷酸盐补充的患者、在第4小时接受15毫摩尔磷酸钠的患者,或在第2、6和10小时接受15毫摩尔磷酸钠的患者。所有患者均接受静脉注射胰岛素(0.1单位/千克/小时)、补液和补钾治疗。输注15毫摩尔磷酸钠4小时后,血清磷酸盐水平为2.8±0.8毫克/分升,而对照组患者为2.1±0.8毫克/分升;然而,该剂量不足以在16小时和24小时维持血清磷酸盐水平。45毫摩尔的磷酸盐除1例患者外可预防所有患者发生严重低磷血症,并在8、16和24小时产生显著更高的磷酸盐水平。磷酸盐治疗不影响DKA的持续时间、纠正酸中毒所需的胰岛素剂量、异常肌肉酶水平、血糖清除率或发病率和死亡率。尽管从理论上讲很有吸引力,但在大多数患者中,磷酸盐治疗并非DKA治疗的必要组成部分。