[Value of biguanide in therapy of diabetes mellitus].

BACKGROUND AND OBJECTIVES: Biguanides have been used in treatment of diabetes mellitus for over 30 years now. Due to frequent occurrence of lactic acidosis, particularly in patients with serious contraindications to biguanide therapy and in cases of non-compliance with dosage instructions, buformin and phenformin were taken off the market in most European countries at the end of the seventies. Metformin continued to be allowed, since the risk of lactic acidosis is 20 times less than with phenformin or buformin due to the different pharmacokinetic properties of the substance. Plenty of clinical experience has been gained with metformin, documented in a large number of reliable long-term studies.
FINDINGS: Metformin lowers fasting blood glucose levels by an average of 25% (17 to 37%), postprandial blood glucose by up to 44.5% and HbA1c bei 1.5% (0.8 to 3.1%) Metformin reduces raised plasma insulin levels in cases of metabolic syndrome by as much as 30% and reduces the "insulin requirement" of type 2 insulin-treated diabetics by 15 to 32%. It has well documented effects on various rheological parameters. In overweight type 2 diabetics, metformin shows the same level of hypoglycaemic effect as all of the important sulfonylurea derivatives used in Europe. The active mechanism of these derivatives is, however, concentrated solely on reduction of blood glucose. This mechanism does not take into account the remaining risk constellation involved in insulin resistance. Biguanides, similarly to weight reduction, lead to a reduction of hyperinsulinaemia, which is by contrast exacerbated by sulfonylureas and, in particular, exogenous insulin.
CONCLUSION: The risk of lactic acidosis can probably be eliminated entirely if dosage instructions and contraindications are observed carefully. The cause of such neglect in 83% of all cases was limited on renal function (serum creatinine > 1.5 mg%). Regarding morbidity and mortality from lactic acidosis, metformin therapy is no riskier than treatment with the sulfonylurea derivative glibenclamide, taking into account the incidence of fatal hypoglycaemias with the latter.