Catechol-O-Methyltransferase Gene Polymorphisms Are Not Associated with Multisomatoform Disorder in a Group of German Multisomatoform Disorder Patients and Healthy Controls

Abstract

The etiology of multisomatoform disorder (MSD) is largely unknown, but genetic disposition may be one of several risk factors. As pain is a major component of MSD, and polymorphisms in the catechol-O-methyltransferase (COMT) gene are associated with COMT enzymatic activity and pain sensitivity, we assumed that COMT polymorphisms could be associated with MSD. One hundred and forty-nine patients with MSD and 149 age- and sex-matched healthy controls participated in this study. The inclusion criteria for MSD were in accordance with the structured clinical interview of the diagnostic and statistical manual of mental disorders IV. DNA from MSD patients and controls was genotyped for six single-nucleotide polymorphisms (SNPs) within the COMT locus by polymerase chain reaction and restriction enzyme analysis. The distribution of COMT SNP alleles, genotypes, and haplotypes was compared between patients and controls. None of the investigated SNPs, including the functionally relevant common SNP in codon 158 (Val158Met), showed a statistically significant allelic, genotypic, or haplotypic association with MSD. We conclude that COMT polymorphisms on their own do not seem to play a relevant role as major genetic risk factors for MSD.

Catechol-O-methyltransferase gene polymorphism and chronic human pain

“…These patients show a higher prevalence of psychiatric comorbidity, worse functioning, and impaired symptom improvement compared with individuals without the disorder [88]. A recent study attempted to elucidate the possible genetic risk factors of this relatively unknown disease by exploring the association between six SNPs in the COMT gene, including rs4680 [58]. None of the SNPs investigated was found to be associated with multisomatoform disorder.…”

Neurohumoral Profiles and Childhood Adversity of Patients with Multisomatoform Disorder and Pain as the Leading Bodily Symptom

“…Subjects. The patient collective was previously investigated regarding the role of single nucleotide polymorphisms [6][7][8] as well as the difference in quantitative sensory profiles and epigenetic regulation of TRPA1 expression between patients and controls [9,11]. Altogether, 300 individuals were recruited to participate (151 patients, 149 controls).…”

“…Patients were screened for possible MSD through demonstrating a PHQ-15 score > 10 and a 36-Item Short-Form 36 (SF-36) physical component score ≤ 40 which demonstrates strong psychophysiological strain as established previously [3]. Additionally, a modified interview of the somatoform disorder section of the Structured Clinical Interview of the DSM-IV (SCID) was used [1,3,[6][7][8]. The interview (SCID) was modified to check for published diagnostic criteria of MSD [1,3] and required three currently present somatoform symptoms in addition to one pain-related symptom which are functionally disabling.…”

“…As part of the effort to understand chronic pain in somatic syndromes, single nucleotide polymorphisms (SNPs) of genes have been studied with inconsistent results. Previous studies suggest a role of SNPs in serotonergic and dopaminergic but not catecholamine-o-transferase genes in the etiology of MSD [6][7][8]. Patients with MSD and pain as the leading bodily symptom show characteristic sensory alterations as demonstrated through quantitative sensory measurements [9].…”

Interaction of the Dopaminergic and Serotonergic Systems Significantly Influences the Risk for Multisomatoform Disorder: A Controlled Pilot Study

“…However, very recently, a population-based twin study of FSS showed that those symptoms, especially chronic widespread pain, are affected by genetic influences (Kato et al, 2009). While catechol-O-methyltransferase polymorphisms seem to account for part of the variability among the pain responses of individuals (Edwards, 2006), such an association could not be demonstrated in either in FMS (Sommer et al, 2008) or in MSD ( Jacobi et al, 2010). The serotonergic and the dopaminergic systems appear to be strongly associated with the clinical picture (Sommer, 2006) and pharmacological approaches (Lawson, 2008) in FMS.…”