PubMed · 3322985
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M Shohat, M Nitzan. 1987-11-01. [Lactic acidosis].. https://pubmed.ncbi.nlm.nih.gov/3322985/
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Metformin is a biguanide used to treat type II diabetes mellitus. Since the recent introduction of this drug into the United States there has been considerable interest in metformin associated lactic acidosis (MALA) following intravenous contrast media. The Royal College of Radiologists published advice in November, 1996 (Advice to Members and Fellows with regard to metformin-induced lactic acidosis and X-ray contrast medium agents, RCR Publication) supporting the manufacturers' advice that metformin should not be used in the 48 h before or after intravenous (i.v.) contrast medium. We performed a systematic review of the literature and this has shown that almost all reported cases of MALA following i.v. contrast medium occurred where there was either pre-existing poor renal function or another contraindication to metformin usage. There has been only one reported case of lactic acidosis following the use of intravenous contrast medium in a patient with normal renal function. We suggest that the Royal College of Radiologists' advice should be modified and that it is safe to give i.v. contrast medium to patients on metformin with normal renal function.
In 27 of 28 children with congenital lactic acidosis, cerebrospinal fluid lactate was higher than venous blood lactate. The mean +/- SEM difference between these variables was 2.4 +/- 0.3 mmol/L (P =.0001). Girls or patients with pyruvate dehydrogenase deficiency had higher cerebrospinal fluid lactate concentrations than boys or patients with respiratory chain defects or mitochondrial DNA mutations.
Zidovudine is known to be responsible for a mitochondrial myopathy with ragged-red fibres and mitochondrial DNA depletion in muscle. Lactic acidosis alone or associated with hepatic abnormalities has also been reported. A single report mentioned the concomitant occurrence of muscular and hepatic disturbances and lactic acidosis in a patient receiving zidovudine, but muscle and liver tissues were not studied. A 57-year-old man with AIDS, who had been treated with zidovudine for 3 years, developed fatigue and weight loss. Serum creatine kinase and hepatic enzyme levels were high. Lactic acidosis was present. Liver biopsy showed diffuse macrovacuolar and microvacuolar steatosis. After withdrawal of zidovudine, creatine kinase, aspartate aminotransferase, and alanine aminotransferase levels normalised within 5 days, and lactacidaemia decreased. Acidosis persisted. The patient became confused and febrile and died 8 days after detection of high blood lactic acid. A muscle sample obtained at autopsy showed mitochondrial abnormalities with ragged-red fibres and lipid droplet accumulation. Southern blot analysis showed depletion of mitochondrial DNA, affecting skeletal muscle and liver tissue. No depletion was found in myocardium and kidney. This case emphasises that zidovudine treatment can induce mitochondrial multisystem disease, as revealed in our case by myopathy, liver steatosis and lactic acidosis.