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Related Experiment Videos

Statin precipitated lactic acidosis?

R Neale1, T M Reynolds, W Saweirs

  • 1Queen's Hospital, Belvedere Road, Burton-on-Trent, Staffordshire, DE13 0RB, UK.

Journal of Clinical Pathology
|August 31, 2004
PubMed
Summary
This summary is machine-generated.

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An 82-year-old woman experienced lactic acidosis due to a mitochondrial defect. This was linked to statin-induced ubiquinone deficiency and thiamine deficiency, resolving after treatment.

Area of Science:

  • Biochemistry
  • Internal Medicine
  • Medical Genetics

Background:

  • Metabolic acidosis is a critical condition often associated with elevated lactate levels.
  • Identifying the underlying cause of lactic acidosis is crucial for effective treatment.

Observation:

  • An 82-year-old female presented with dyspnea and was diagnosed with compensated metabolic acidosis and hyperventilation-induced hypocapnia.
  • Laboratory results revealed an increased anion gap and elevated lactate levels, consistent with lactic acidosis.

Findings:

  • The patient's lactic acidosis resolved after the discontinuation of Atorvastatin, suggesting a link to statin therapy.
  • Subsequent thiamine deficiency was identified.
  • The acidosis was attributed to a mitochondrial defect caused by deficiencies in ubiquinone (statin-related) and thiamine (dietary).

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Implications:

  • This case highlights a potential drug-induced mitochondrial dysfunction, specifically statin-induced ubiquinone deficiency, as a cause of lactic acidosis.
  • It underscores the importance of considering cofactor deficiencies, including thiamine, in patients with unexplained metabolic acidosis.
  • This finding may prompt further investigation into the role of statins in mitochondrial health and the management of metabolic acidosis.