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Plasma and platelet serotonin levels in familial Mediterranean fever

A.M. Onat, L. Özçakar, M.A. Öztürk, G. Uçar, K. Üreten, N. Dagli, S. Kiraz, İ. Ertenli, M. Çalgüneri

Gaziantep University Hospitals, Department of Rheumatology, Gaziantep, Turkey

CER3078
2007 Vol.25, N°4 ,Suppl.45 - PI 0016, PF 0020
Full Paper

Rheumatology Article

 

Abstract

OBJECTIVES:
Familial Mediterranean fever (FMF) is the most common auto-inflammatory syndrome with exaggerated acute phase and inflammatory response. After revealing the MEFV gene mutation with the finally disturbed end product pyrin, some of the mechanisms were explained. However it is still unknown what triggers or ends these periodical attacks. Moreover, the treatment of up to 30% of the patients, that are resistant to colchicine is still a problem. In this study we investigated the role of serotonin in colchicine-resistant FMF patients.
METHODS:
Twenty-four FMF patients (male/female: 15/9) and 32 age- and sex-matched healthy controls (male/female: 17/15) were included into the study. Patients were subdivided into two groups. Thirteen had FMF attacks despite regular colchicine (colchicine-resistant group), other 11 had disease under control with colchicine for at least 6-months. Sampling was done both during the attack and ten days after its cessation. Plasma and platelet serotonin levels and acute phase reactants were studied in patients and controls.
RESULTS:
Colchicine-resistant patients had plasma serotonin (5-HT) levels of 7.85 ± 1.0 nmol/l during acute attacks which significantly reduced to the levels of 6.3 ± 0.6 nmol/l (p < 0.001), after 10 days of acute attacks and these levels were significantly lower than those of attack-free patients’ and controls’ (10.7 ± 0.2 nmol/l and 10.1 ± 0.3 nmol/l, respectively). Platelet 5-HT level was 6.4 ± 0.3 nmol/109 platelets during acute attack, and this level was increased to 9.8 ± 0.5 nmol/109 platelets on the 2nd sampling, 10 days after the cessation of the acute attack (p < 0.001). They were both significantly higher than those of attack-free FMF patients (5.9 ± 0.1 nmol/109 platelets) and healthy controls (5.7 ± 0.3 nmol/109 platelets). There was a negative correlation between plasma and platelet 5-HT levels (r=-0.77, p < 0.001).
CONCLUSIONS:
Changes in plasma and platelet 5-HT levels may be related to the disturbances in 5-HT transport mechanisms or may also be attributed to the potential role of serotonin in the inflammatory cascade. Last but not least, serotonin may have a role in the pathogenesis of FMF.

PMID: 17949546 [PubMed]