Arginase, NOS activities, and clinical features in fibromyalgia patients.

OBJECTIVES

Fibromyalgia (FM) is a form of nonarticular rheumatism characterized by chronic widespread musculoskeletal aching and tender points. The aim of the present study was to investigate the effect of arginase and nitric oxide synthase (NOS) enzyme activities in FM with respect to their importance in pathogenesis, and the relationship with FM-related clinical parameters.

METHODS

After obtaining informed consent, 25 female FM patients were compared with 23 healthy female controls. NOS and arginase enzyme activities were measured spectrophometrically in sera. Tender points were examined using the protocol described by Wolfe et al. The health status of patients was assessed by Fibromyalgia Impact Questionnaire. Musculoskeletal pain was scored according to visual analog scale. Health Assessment Questionnaire, Beck depression and Beck anxiety scales, and dyspnea scores were administered to analyze functional, psychiatric, and respiratory status of the patients.

RESULTS

We found that NOS activity was significantly higher whereas arginase activity was lower in patients with FM. In the correlation analysis, NOS levels showed statistically significant positive correlation with chest pain and dyspnea parameters. NOS enzyme activities were higher in subjects with positive history of migraine, pain, and morning stiffness. On the other hand, arginase levels were lower in subjects with positive history of irritable bowel syndrome and morning stiffness.

CONCLUSION

Animal experiments have suggested that nitric oxide (NO) is an important transmitter in pain pathways. It can also stimulate cyclooxygenase activity. We observed increased NOS activity and reduced arginase activity in FM patients, which may be due to increased cyclooxygenase enzyme activity and oxidant/antioxidant imbalance. In conclusion, we think that future studies concerning clinical control of pain with selective NOS inhibitors are needed in order to determine new therapeutic approaches and the exact pathophysiologic mechanisms in FM patients.