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Impaired redox status and cytochrome c oxidase deficiency in patients with polymyalgia rheumatica

P Chariot1, X Chevalier, M Yerroum

  • 1Department of Pathology (Neuromuscular Disorders), Hôpital Henri-Mondor, 94000 Créteil, France. pchariot@cybercable.fr

Annals of the Rheumatic Diseases
|October 17, 2001
PubMed
Abstract

Insights

Polymyalgia rheumatica (PMR) is linked to muscular mitochondrial issues, including cytochrome c oxidase (COX) deficiency. These abnormalities suggest PMR involves mitochondrial dysfunction beyond normal aging.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Rheumatology

Background:

  • Polymyalgia rheumatica (PMR) is an inflammatory condition primarily affecting older adults.
  • The underlying pathophysiology of PMR, particularly concerning muscle involvement, remains incompletely understood.
  • Mitochondrial dysfunction is implicated in various age-related and inflammatory diseases.

Purpose of the Study:

  • To investigate redox status and muscular mitochondrial abnormalities in patients diagnosed with polymyalgia rheumatica (PMR).
  • To determine if observed mitochondrial changes in PMR are attributable solely to the aging process.

Main Methods:

  • Prospective analysis of deltoid muscle biopsies from 15 PMR patients and 15 age- and sex-matched controls.
  • Histochemical staining for cytochrome c oxidase (COX) and other markers, along with Sudan black staining.
  • Measurement of blood lactate, pyruvate, and lactate/pyruvate ratio in all participants.

Main Results:

  • Focal COX deficiency was prevalent in PMR patients (93%) and controls (60%), but significantly more common in PMR patients.
  • Ragged red fibres, indicative of mitochondrial abnormalities, were observed in 53% of PMR patients.
  • Elevated blood lactate levels or lactate/pyruvate ratios were found in 47% of PMR patients.

Conclusions:

  • Polymyalgia rheumatica (PMR) is associated with significant muscular mitochondrial abnormalities.
  • These mitochondrial alterations in PMR are not solely a consequence of the natural aging process.
  • The findings suggest a role for mitochondrial dysfunction in the pathogenesis of PMR.

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