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Rheumatology (Oxford). 2013 Apr;52(4):599-608. doi: 10.1093/rheumatology/kes395. Epub 2013 Jan 12.

Occurrence of tendon pathologies in metabolic disorders.

Author information

1
Department of Medicine and Science of Aging, University G. d'Annunzio, Chieti-Pescara, Chieti Scalo (CH), Italy. m.abate@unich.it

Abstract

This article reviews the pathogenetic role of metabolic disorders, which are of paramount relevance to the progression of tendon damage. In diabetes, the prevalence of rheumatological diseases is high, mainly because of the deleterious effects of advanced glycation end products that deteriorate the biological and mechanical functions of tendons and ligaments. In heterozygous familial hypercholesterolaemia, most patients develop Achilles xanthomatosis, a marker of high risk for cardiovascular disease caused by cholesterol deposition in the tendons. Tendon degeneration has also been observed in non-familial hypercholesterolaemia. Monosodium urate crystal deposition in soft tissues is a hallmark of chronic gouty arthritis. In this group of diseases, the mobilization of cholesterol and uric acid crystals is presumably followed by low-grade inflammation, which is responsible for tendon degeneration. Adiposity may contribute to tendon disorders via two different mechanisms: increased weight on the load-bearing tendons and systemic dysmetabolic factors that trigger subclinical persistent inflammation. Finally, tendon abnormalities have been observed in some rare congenital metabolism disorders such as alkaptonuria.

PMID:
23315787
DOI:
10.1093/rheumatology/kes395
[Indexed for MEDLINE]

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