Can phenformin-induced lactic acidosis be prevented?

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Phenformin and lactic acidosis.

Thirty-eight patients who presented with diabetes and a changed state of consciousness satisfied the criteria for lactic acidosis. Sixteen patients were non-ketotic, and 15 of these were receiving phenformin on admission. In all but one of these 15 patients, however, additional renal or cardiovascular abnormalities, or both, could be identified, which supported a multifactorial aetiology for la...

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Phenformin-induced lactic acidosis in an older diabetic patient: a recurrent drama (phenformin and lactic acidosis).

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Lactic acidosis occurring during phenformin therapy.

Case history The patient was a 47-year-old woman who developed diabetes mellitus in 1965. She was initially controlled on chlorpropamide and phenformin. However, her diabetic control became less satisfactory and insulin therapy was substituted in October 1967. Subsequently her diabetes became unstable and phenformin 100-150 mg daily was added in November 1968. Since then her blood glucose level...

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Can albuterol be blamed for lactic acidosis?

Albuterol is an uncommonly recognized culprit in causing lactic acidosis. While treating asthmatics, lactic acidosis creates a paradoxical situation in which, despite improvement in bronchospasm, patients look more dyspneic as a compensatory mechanism for metabolic acidosis. This might lead to misinterpretation of the situation with increased albuterol dosing, creating a sort of vicious cycle u...

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Lactic acidosis and hyperamylasaemia associated with phenformin therapy.

Introduction Lactic acidosis, first described by Clausen (1925), is most frequently seen accompanying hypotension and impaired tissue perfusion, but has been reported in association with many other conditions such as phenformin therapy, non-ketotic diabetic acidosis, ethanol ingestion and glycogen storage disease (Oliva, 1970; Lancet, 1973). Recently, an association was suggested between non-ke...

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ژورنال

عنوان ژورنال: BMJ

سال: 1976

ISSN: 0959-8138,1468-5833

DOI: 10.1136/bmj.2.6042.972