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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
Summary
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).
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.