title: Assessment of opioid receptor μ1 gene A118G polymorphism and its association with pain intensity in patients with fibromyalgia.
abstract: Fibromyalgia may present with widespread pain and tenderness, fatigue, anxiety, and depression and is associated with a low pain threshold. The etiology of fibromyalgia is yet to be ascertained, although both genetic and environmental factors may play a role in the susceptibility of patients to fibromyalgia. Various genetic variations have been investigated to explain fibromyalgia susceptibility and differences in pain sensitivity, pain threshold, and tolerance. The A118G rs1799971 polymorphism in the opioid receptor μ1 gene (OPRM1) is one of the candidate genes. We hypothesized that the OPRM1 polymorphism may play a role in fibromyalgia susceptibility and impact the pain intensity and pain-related symptoms in fibromyalgia patients. This study comprised of 108 patients with fibromyalgia and 100 healthy controls. Overall, the 118G allele frequency was 16.3 % and was significantly lower in patients with fibromyalgia than in the control group (13.9 and 19 %, respectively). No difference was observed between fibromyalgia patients with and without the A118G allele with regard to the Beck Depression Inventory, widespread pain index, symptom severity, and Fibromyalgia Impact Questionnaire scores. All body parts of patients with fibromyalgia demonstrated lower pressure pain thresholds (PPT) compared to controls. The PPTs were higher in the 118 A/A genotype carrier fibromyalgia patients than in 118*/G carriers; however, the differences were not significant. As the A118G polymorphism frequency was lower in fibromyalgia patients, this polymorphism may exert a protective effect against fibromyalgia in Turkish women. However, the OPRM1 polymorphism does not have a significant effect on pressure pain and fibromyalgia severity.
authors.affiliation: Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Afyon Kocatepe University, Afyon, Turkey.
authors.forename: Özlem
authors.initials: Ö
authors.lastname: Solak
authors.forename: Müjgan Özdemir
authors.initials: MÖ
authors.lastname: Erdoğan
authors.forename: Handan
authors.initials: H
authors.lastname: Yıldız
authors.forename: Alper Murat
authors.initials: AM
authors.lastname: Ulaşlı
authors.forename: Fatima
authors.initials: F
authors.lastname: Yaman
authors.forename: Evrim Suna Arıkan
authors.initials: ES
authors.lastname: Terzi
authors.forename: Sena
authors.initials: S
authors.lastname: Ulu
authors.forename: Ümit
authors.initials: Ü
authors.lastname: Dündar
authors.forename: Mustafa
authors.initials: M
authors.lastname: Solak
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005260:Female; D005356:Fibromyalgia / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D010146:Pain / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology; D010147:Pain Measurement; D017288:Pain Threshold; D010641:Phenotype; D011110:Polymorphism, Genetic; D011237:Predictive Value of Tests; D065840:Protective Factors; D017450:Receptors, Opioid, mu / Q000235:genetics*; D012307:Risk Factors; D012720:Severity of Illness Index; D012737:Sex Factors; D014421:Turkey / Q000453:epidemiology
chemical_list: C485764:OPRM1 protein, human; D017450:Receptors, Opioid, mu