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Abnormalities of Serum Anti-Elastin Antibodies in Patients with Polymyalgia Rheumatica.

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By Keith K. Colburn, et al • www.ProHealth.com • October 25, 2006


Journal: Journal of Musculoskeletal Pain, Vol. 14(3) 2006. pp 21-26. [Published online ahead of print. Article copies available for a fee from The Haworth Document Delivery Service: 1-800-HAWORTH. E-mail address: docdelivery@haworthpress.com Website: http://www.HaworthPress.com] Authors and affiliations: Keith K. Colburn,Marilyn C. Malto, Lawrence B. Sandberg, Euly Langga-Shariffi, Lora M. Green. Memorial Veterans Medical Center/ Loma Linda University School of Medicine/Loma Linda University Graduate School, Loma Linda, California, USA. [E-mail: Keith.Colburn@med.va.gov]. DOI: 10.1300/J094v14n03_04

Background: Antibodies [Abs] to alpha-elastin [elastin breakdown product] and tropoelastin [elastin precursor] are found in serum of all human subjects and correlate with their respective serum peptide levels. Serum elastin peptide levels vary with age and some disease states. Vascular damage is thought to be a possible mechanism in the pathogenesis of polymyalgia rheumatica [PMR] and in the closely related condition of giant cell arteritis. Damage to elastin is a characteristic of giant cell arteritis. This study was undertaken to determine if the levels of serum Abs against elastin were altered in patients with PMR by measuring the ratio of serum anti-alpha elastin to anti-tropoelastin Abs compared to age matched controls.

Methods: Sera from 37 elderly patients with PMR were compared with sera from 45 agematched, otherwise healthy osteoarthritis subjects using an enzyme-linked immunosorbent assay that measured levels of anti-alpha and anti-tropoelastin Abs.

Results: We found a decrease in anti-tropoelastin and an increase in anti-alpha-elastin immunoglobulin G Abs and in the sera of patients with PMR that were significantly different than the control levels [P < 0.008 [anti-tropoelastin] and 0.005 [anti-alpha-elastin]]. The ratio of anti-tropoelastin [synthesis] to anti-alpha-elastin [degradation] was 1.98 [PMR] versus 3.40 [control] [P < 0.001].

Conclusions: Variations in elastin metabolism were detected in PMR by the ratio of antitropoelastin to anti-alpha-elastin immunoglobulin G Abs that represents elastin synthesis and degradation, respectively. This study suggests that there was a decrease in elastin production as well as an increase in elastin destruction in patients with PMR that may be reflecting disease pathology.

Keywords. Anti-elastin antibodies, polymyalgia rheumatica




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