Sporer K A, Ernst A A, Conte R, Nick T G
Section of Emergency Medicine, Louisiana State University School of Medicine, New Orleans 70112.
Am J Emerg Med. 1992 Sep;10(5):403-5. doi: 10.1016/0735-6757(92)90063-4.
The purpose of the study was to determine the incidence of ethanol-induced hypoglycemia. All nondiabetic patients who had blood alcohol levels above 0.10% and a random serum chemistry drawn (including glucose) were included. Over a 6-month study period, 378 patients were included in the study. Fifteen patients (4%) presented with hypoglycemia (glucose less than 67 mg%). Of these, four (1%) were profoundly hypoglycemic (glucose less than 50 mg%). Two hundred and fifty three patients (67%) patients were normoglycemic (glucose 67-106 mg%) and 110 patients (29%) were hyperglycemic (glucose greater than 106 mg%). Nonfasting glucose measurements from a control group of 96 nondiabetic, nonintoxicated patients were compared with those of the study group. Two patients (2%) presented with hypoglycemia and none (0%) presented with profound hypoglycemia. Forty-five patients (47%) presented with normoglycemia, and 49 (51%) with hyperglycemia. There were no statistically significant differences found in the hypoglycemia rate between the intoxicated patients and nonintoxicated control population (odds ratio of 0.75; P greater than .05). Four of 378 intoxicated patients (1%) had profound hypoglycemia (less than 50 mg/dL) compared with none (0%) of the 96 nonintoxicated patients. Intoxicated patients had a statistically significant lower rate of hyperglycemia in comparison with the nonintoxicated control group (29% versus 51%; P less than .0001). Age, sex, race, ethanol level, and serum electrolyte measurement had no predictive value for hypoglycemia in intoxicated patients. The anion gap was consistently elevated in hypoglycemic patients in comparison with normoglycemic patients (P less than .05). Hypoglycemia appears to occur as frequently in an ethanol-intoxicated population as in a population without elevated ethanol levels.(ABSTRACT TRUNCATED AT 250 WORDS)
该研究的目的是确定乙醇诱导的低血糖症的发生率。纳入所有血液酒精浓度高于0.10%且进行了随机血清化学检测(包括血糖)的非糖尿病患者。在为期6个月的研究期间,共有378名患者纳入研究。15名患者(4%)出现低血糖(血糖低于67mg%)。其中,4名患者(1%)为严重低血糖(血糖低于50mg%)。253名患者(67%)血糖正常(血糖67 - 106mg%),110名患者(29%)血糖过高(血糖高于106mg%)。将96名非糖尿病、未中毒患者的对照组非空腹血糖测量结果与研究组进行比较。2名患者(2%)出现低血糖,无人出现严重低血糖。45名患者(47%)血糖正常,49名患者(51%)血糖过高。中毒患者与未中毒对照人群的低血糖发生率无统计学显著差异(优势比为0.75;P大于0.05)。378名中毒患者中有4名(1%)出现严重低血糖(低于50mg/dL),而96名未中毒患者中无人出现严重低血糖。与未中毒对照组相比,中毒患者的血糖过高发生率具有统计学显著降低(29%对51%;P小于0.0001)。年龄、性别、种族、乙醇水平和血清电解质测量对中毒患者的低血糖无预测价值。与血糖正常的患者相比,低血糖患者的阴离子间隙持续升高(P小于0.05)。乙醇中毒人群中低血糖的发生率似乎与乙醇水平未升高的人群一样频繁。(摘要截断于250字)