Abstract
BackgroundModerate joint laxity is widespread in many joints of the body, and this condition is considered to be caused by an abnormality in the collagen structure. This study was carried out to determine the serum prolidase activity in female patients with benign joint hypermobility syndrome (BJHS), and to evaluate its correlation with their clinical features.MethodsA total of 45 patients with BJHS and 40 healthy controls were included in the study. All of the patients with BJHS met the Beighton diagnostic criteria. All the patients and the control group underwent a comprehensive examination of the locomotor system and took the New York Posture Rating Test. The examination and test results were recorded. Serum prolidase activity was measured in both the groups.ResultsProlidase activity was significantly lower in patients with BJHS (479.52 ± 126.50) compared to the healthy controls (555.97 ± 128.77) (p = 0.007). We found no correlation between serum prolidase activity and Beighton scores or New York rating test scores. On the other hand, mean prolidase activity was significantly lower in patients with pes planus or hyperlordosis compared to those without (p = 0.05, p = 0.03, respectively). We did not find such a correlation with the other clinical features.ConclusionsSignificantly lower prolidase activity in patients with BJHS suggests that prolidase may affect the collagen metabolism and cause hyperlaxity.
Highlights
Moderate joint laxity is widespread in many joints of the body, and this condition is considered to be caused by an abnormality in the collagen structure
Serum prolidase activity was significantly lower in patients with benign joint hypermobility syndrome (BJHS) having pes planus compared to those without pes planus (p = 0.05)
Serum prolidase activity was significantly lower in patients with BJHS having hyperlordosis compared to those without hyperlordosis (p = 0.03) Table 4
Summary
Moderate joint laxity is widespread in many joints of the body, and this condition is considered to be caused by an abnormality in the collagen structure. Benign joint hypermobility syndrome (BJHS) is a hereditary disease characterised by musculoskeletal symptoms in patients with widespread joint laxity, independent of a systemic rheumatoid disease [1]. The incidence of BJHS is higher in females compared to males and decreases with age [3]. It may develop with some musculoskeletal symptoms which are affiliated with bones, tendons, muscles, ligaments, joints and spine. Collagen is an abundant protein of the body It is a major component of skin, tendons, ligaments, joint capsules and blood vessels [6]. Ligaments are dense bands of articular tissues that connect bones together. Reduced thickness of collagen fibrils in patients with BJHS, as suggested by the electron microscopic examination of the skin biopsy, supports this view [10]
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