Statin precipitated lactic acidosis?
- 1Queen’s Hospital, Belvedere Road, Burton-on-Trent, Staffordshire, DE13 0RB, UK
- 2Queen’s Hospital, Burton-on-Trent and Division of Clinical Sciences, Wolverhampton University, Wolverhampton, UK
- Correspondence to: Professor T M Reynolds Clinical Chemistry Department, Queen’s Hospital, Belvedere Road, Burton-on-Trent, Staffordshire, DE13 0RB, UK; tim.reynoldsburtonh-tr.wmids.nhs.uk
- Accepted 20 April 2004
Abstract
An 82 year old woman was admitted with worsening dyspnoea. Arterial blood gases were taken on air and revealed a pH of 7.39, with a partial pressure of CO2 (pCO2) of 1.2 kPa, pO2 of 19.3 kPa, HCO3 of 13.8 mmol/litre, and base excess of −16.3 mmol/litre: a compensated metabolic acidosis with hyperventilation induced hypocapnia, which is known to be a feature of lactic acidosis. There was also an increased anion gap ((Na140 + K4.0) – (Cl 106 + HCO3 13.8) = 24.2 mEq/litre (reference range, 7–16)), consistent with unmeasured cation. Lactate was measured and found to be raised at 3.33 mmol/litre (reference range, 0.9–1.7). After exclusion of common causes of lactic acidosis Atorvastatin was stopped and her acid–base balance returned to normal. Subsequently, thiamine was also shown to be deficient. The acidosis was thought to have been the result of a mitochondrial defect caused by a deficiency of two cofactors, namely: ubiquinone (as a result of inhibition by statin) and thiamine (as a result of dietary deficiency).
- ABGs, arterial blood gases
- bd, twice daily
- coQ10, coenzyme Q10
- HMGCoA, hydroxymethylglutaryl CoA
- od, once daily
- qds, four times daily
- P, partial pressure
- hydroxymethylglutaryl CoA reductase inhibitor
- lactic acidosis
- statin
- thiamine deficiency
- transketolase
