Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2014 (2014), Article ID 627041, 8 pages
Research Article

Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at the University of Göteborg, P.O. Box 480, 405 30 Göteborg, Sweden

Received 12 May 2014; Revised 3 July 2014; Accepted 28 July 2014; Published 14 August 2014

Academic Editor: Giuseppe Valacchi

Copyright © 2014 Maria I. Bokarewa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Smoking deregulates neuroendocrine responses to pain supporting production of neuropeptide Y (NpY) by direct stimulation of nicotinic receptors or by inhibiting adipokine leptin. Present study addressed the effect of cigarette smoking on adipokines and pain parameters, in 62 women with fibromyalgia (FM) pain syndrome with unknown etiology. Pain was characterized by a visual analogue scale, tender point (TP) counts, pressure pain threshold, and neuroendocrine markers NpY and substance P (sP). Levels of IGF-1, leptin, resistin, visfatin, and adiponectin were measured in blood and cerebrospinal fluid. Current smokers had lower levels of leptin compared to ex-smokers (, ), while the expected NpY increase was absent in FM patients. In smokers, this was transcribed in higher VAS-pain and TP count , lower pain threshold , since NpY levels were directly related to the pain threshold () and inversely related to TP counts (). This study shows that patients with FM have no increase of NpY levels in response to smoking despite the low levels of leptin. Deregulation of the balance between leptin and neuropeptide Y may be one of the essential mechanisms of chronic pain in FM.