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Metformin associated lactic acidosis.

P J Phillips·R Scicchitano·A R Clarkson·H R Gilmore
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Abstract

A case of lactic acidosis occurring in association with inappropriate and excessive metformin therapy and a high serum metformin concentration is described. In the other 23 cases of metformin associated lactic acidosis reported to December 1977, renal, cardiovascular and liver disease were common. Although metformin is less likely to cause lactic acidosis than phenformin, neither drug should be prescribed in the presence of renal, hepatic or cardiovascular disease.

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AcidosisFemaleHumansLactatesMetforminMiddle AgedCase ReportsJournal Article

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BibTeXRIS

P J Phillips, R Scicchitano, A R Clarkson, H R Gilmore. 1978. Metformin associated lactic acidosis.. https://doi.org/10.1111/j.1445-5994.1978.tb04524.x

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PubMed1979

Studies of acidosis in the ischaemic heart by phosphorus nuclear magnetic resonance.

1. Phosphorus-nuclear-magnetic-resonance measurements were made on perfused rat hearts at 37 degrees C. 2. With the improved sensitivity obtained by using a wide-bore 4.3 T superconducting magnet, spectra could be recorded in 1 min. 3. The concentrations of ATP, phosphocreatine and Pi and, from the position of the Pi resonance, the intracellular pH (pHi) were measured under a variety of conditions. 4. In a normal perfused heart pHi = 7.05 +/- 0.02 (mean +/- S.E.M. for seven hearts). 5. During global ischaemia pHi drops to 6.2 +/- 0.06 (mean +/- S.E.M.) in 13 min in a pseudoexponential decay with a rate constant of 0.25 min-1. 6. The relation between glycogen content and acidosis in ischaemia is studied in glycogen-depleted hearts. 7. Perfusion of hearts with a buffer containing 100 mM-Hepes before ischaemia gives a significant protective effect on the ischaemic myocardium. Intracellular pH and ATP and phosphocreatine concentrations decline more slowly under these conditions and metabolic recovery is observed on reperfusion after 30min of ischaemia at 37 degrees C. 8. The relation between acidosis and the export of protons is discussed and the significance of glycogenolysis in ischaemic acid production is evaluated.

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