Carnitine homeostasis in patients with rheumatoid arthritis
Myopathy is a frequent finding in patients with rheumatoid arthritis (RA). Since carnitine is important for skeletal muscle energy metabolism, carnitine metabolism was investigated in patients with RA and myopathy. Muscle strength was estimated by determination of a muscle strength index (MSI) which...
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Veröffentlicht in: | Clinica chimica acta 1999, Vol.279 (1), p.35-45 |
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Sprache: | eng |
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Zusammenfassung: | Myopathy is a frequent finding in patients with rheumatoid arthritis (RA). Since carnitine is important for skeletal muscle energy metabolism, carnitine metabolism was investigated in patients with RA and myopathy. Muscle strength was estimated by determination of a muscle strength index (MSI) which is derived from isometric measurements of muscle strength at knees and elbows. Carnitine was determined by a radioenzymatic method and 3-methylhistidine by high-performance liquid chromatography. In comparison to control subjects, patients had a reduced MSI. Both the 24-h creatinine and 3-methylhistidine excretions were reduced in patients. The plasma carnitine pool was not different between patients and control subjects, except for a higher long-chain acylcarnitine concentration in patients. Urinary excretion of carnitine was decreased in patients, also after normalization for body weight. Accordingly, renal carnitine clearance and excretion fraction were both decreased in patients. Skeletal muscle free- and total carnitine levels were increased in patients, whereas the long-chain acylcarnitine content was markedly decreased. The total skeletal muscle carnitine content showed a negative correlation with the MSI and no association with disease activity. Carnitine deficiency does not explain reduced skeletal muscle strength in patients with RA. Decreased renal carnitine excretion in patients is most likely due to reduced carnitine biosynthesis, leading to more efficient tubular carnitine reabsorption for maintaining the carnitine body stores. |
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ISSN: | 0009-8981 1873-3492 |
DOI: | 10.1016/S0009-8981(98)00161-2 |