ACTA ENDOCRINOLOGICA (BUC)

Background. Alcohol ingestion can induce either a hypoglycemia or a hyperglycemia,\r\nin patients with acute and chronic ethanol poisoning, unknown with diabetes mellitus.\r\nAim. The aim of this study was to evaluate whether 5 hours prolonged oral glucose\r\ntolerance test (5h-OGTT) is useful in evaluating the abnormalities of glucose metabolism in\r\nacute and chronic ethanol poisoning, in comparison with standard methods (fasting blood\r\nglucose - FBG, and/or 2h-OGTT).\r\nMethods. 497 consecutive patients were enrolled in a 34 months cross sectional study.\r\nIn all cases, glucose tolerance was assessed by a 75-g oral glucose tolerance, OGTT 2 hours,\r\nprolonged to 5 hours. The relationship between clinical and biochemical variables of ethanol\r\npoisoning (liver status, lipid profile, metabolic syndrome) and glucose tolerance was\r\ninvestigated. Risk factors for hypoglycemia in ethanol poisoning were identified.\r\nResults. 349 subjects presented acute ethanol poisoning, and 148 subjects had chronic\r\nethanol poisoning. 254 patients (51.10%) had documented alcoholic liver disease (ALD -\r\nclinical, biochemical and imagistic criteria). Glucose metabolism abnormalities were\r\nrecorded in 143 subjects with chronic ethanol poisoning and ALD (96.63%), and in 207\r\ncases with acute alcohol poisoning (59.31%). 371 patients (74.65%) showed normal FBG,\r\ndiabetes mellitus (DM) was diagnosed in 54 subjects (10.86%), impaired glucose tolerance\r\n(IGT) in 43 subjects (8.65%), delayed hypoglycemia in 172 subjects (34.60%) and normal\r\nglucose tolerance (NGT) in 147 subjects (29.57%) using OGTT and ADA diagnosis criteria.\r\nHypoglycemia was recorded in more than two thirds of acutely poisoned patients, when alcohol\r\nlevel was 0.5-1.5 g/L. Impaired glucose tolerance (IGT) were recorded in half of patients with\r\nblood ethanol levels > 2.5 g/L.\r\nConclusions. OGTT 2 hours and OGTT 5 hours revealed the same number of patients\r\nwith diabetes mellitus. Frequent co morbidities in patients with ethanol poisoning influence\r\nthe prolonged OGTT and revealed .especially delayed hypoglycemia, and IGT, as an indicator\r\nof alcoholic liver disease (ALD).

Introduction. In the community, hypoglycemic coma is commonly caused by therapies for diabetes mellitus, or excessive alcohol consumption. Little information is available on the causes and outcome of hypoglycemic coma in non-diabetic patients. Patients and Methods. We retrospectively surveyed adult patients admitted to a regional emergency hospital with hypoglycemic coma in a 18-years period, identifying 80 admissions of 79 patients. 72 cases (91.14%) presented hypoglycemic coma induced by anti-diabetic medications in attempted suicide. The others had hypoglycemic coma induced by deliberate selfpoisoning with other drugs influencing glucose metabolism, sometimes associated with excessive consumption of alcohol. Results. A history of psychiatric illness was present in 15 patients (19%), and 2 cases (2.53%) had chronic alcoholism. Neurological manifestations of hypoglycemia were the principal reason for admission, observed in all patients, and 15 patients (19%) had precipitated convulsions. Although some patients received treatment for hypoglycemia before admission, hypoglycemia recurred in 12 cases (15.19%) in hospital. Morbidity included ventricular arrhythmias (8.86%), non-cardiogenic acute pulmonary edema (1.26%), and transient neurological disturbances, in 2 elderly patients. Two cases died following admission, but death was not the direct result of hypoglycemia. Therapeutic measures consisted in antidote therapy, toxin removal, and supportive therapy. Conclusion. Though drug-induced hypoglycemic coma is rarely encountered in medical practice (2.44% in our study), management of these patients represents a challenging task in every practitioner.