Contraindications to the use of metformin.

نویسندگان

  • G C Jones
  • J P Macklin
  • W D Alexander
چکیده

van der Meu-len JH, et al. Empirical evidence of design-related bias in studies of diagnostic tests.SORT statement and quality of reports of randomised trials. A comparative before-and-after evaluation. of methodological factors in randomised controlled trials and the association with a journal policy to promote adherence to the Consolidated Standards of Reporting Trials (CONSORT) checklist. Contraindications to the use of metformin Evidence suggests that it is time to amend the list A ccording to the United Kingdom prospective diabetes study, patients with type 2 diabetes randomised to intensive treatment with metformin, sulphonylurea, or insulin had similar degrees of glycaemic control and significantly reduced microvascular end points. 1 The study showed that the use of metformin in obese patients reduced cardiovas-cular events. The group treated with metformin had no hypoglycaemia and less weight gain. Treatment with metformin rather than diet alone produced a significant reduction in relative risk in all cause mortality (36%, P=0.011), diabetes related deaths (42%, P=0.017), any diabetes related end point (32%, P=0.0023), and myocardial infarction (39%, P=0.01). Metformin is the only oral hypoglycaemic agent proved to reduce cardiovascular risk and is now recog-nised as the treatment of choice in overweight patients with type 2 diabetes. Lactic acidosis associated with metformin is a rare condition with an estimated prevalence of one to five cases per 100 000. 2 Although classically lactic acidosis associated with metformin has been thought of as lac-tic acidosis secondary to accumulation of metformin, the evidence for this is poor. Metformin does not affect lactate concentrations in patients with type 2 diabetes, 3 is excreted solely through the kidney, and has a short half life— accumulation of metformin therefore rarely occurs in the absence of advanced renal failure. 4 Accumulation of metformin alone is rarely reported as a cause of lac-tic acidosis, and tissue hypoxia acting as a " trigger " is found in most instances. Accumulation of metformin does not correlate with lactate concentrations or mortality. Mortality is predicted by the severity of underlying hypoxia. 5 Metformin should therefore be discontinued when tissue hypoxia is suspected. A recent review of cases of lactic acidosis associated with metformin, which was published between May 1995 and January 2000, concluded that no mortality was associated with metformin alone. 6 Another study noted that the rates of lactic acidosis in the United States before the approval of metformin were no different from the rates observed in users of metformin. …

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عنوان ژورنال:
  • BMJ

دوره 326 7379  شماره 

صفحات  -

تاریخ انتشار 2003