Which genotype of MAO gene that the patients have are likely to be most susceptible to the symptoms of fibromyalgia?

Abstract

The objective of this study was to analyze the genotype distributions and allele frequencies for the MAO-A and MAO-B polymorphism of the MAO gene among the patients with fibromyalgia syndrome (FS). One hundred and seven fibromyalgia patients and 90 unrelated healthy subjects were included into the study. Genomic DNA of 107 FS patients and 90 healthy control subjects were analyzed by polymerase chain reaction. Polymorphism of the MAO gene was: 1-1, 1-3, 3-3, 3-4. The "allele 3" had a 2.7 to 4.8-fold increased transcription activity than the "allele 1". The frequencies of the genotypes of the patients with FS and healthy controls were compared. Although no significant difference was found in genotypes of patients and controls (P = 0.0559), it is likely that "allele 3" could be a more riskful factor for FS than "allele 1" (P = 0.033). Fibromyalgia impact questionnaire was administered to FS group as well as control group. One of our findings is that, the patients whose genotype 3-3 may be mostly affected by the symptoms of FS. In conclusion, it seems plausible to say that MAOA-dependent metabolism of the biological amines may be partly related to high-activated MAO-A, allele 3, in the occurrence of FS among Turkish population.

Candidate gene studies of fibromyalgia: a systematic review and meta-analysis

“…While some gene polymorphisms including the ADRB2 [7], ADRA1A [7], COMT rs4818 [12], DRD4 [17], and MAO-A allele3 [13] showed a significant association with fibromyalgia, other gene polymorphisms such as ADRB3 [7], DRD3 [8], DAT [10], 5-HT2A receptor (rs6311) [11], COMT (rs6269, rs4633, rs4818, rs4680, rs20907, and rs16559) [12], MAO-B [13], eNOS [14], TACR1 [10], AAT [10], IL-4 [15], 5-HTTLPR (intron2 VNTR) [19], HTR3A, and 3B (some SNPs) [16] was not associated with fibromyalgia. However, there is insufficiency evidence to conclude whether the polymorphisms are associated with fibromyalgia susceptibility, because there was only one study about the association of the polymorphisms with fibromyalgia, respectively.…”

“…Four studies were excluded because they were reviews [5,36,37] or because they did not concern fibromyalgia [38]. Thus, eighteen studies met the inclusion criteria [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. Of these, three studies contained data on two different groups [7,12,20].…”

“…Thirty-three studies were identified by electronic or manual searching, and twenty-two were selected for a full-text review based on title and abstract details [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][36][37][38]. Four studies were excluded because they were reviews [5,36,37] or because they did not concern fibromyalgia [38].…”

“…All studies of three polymorphisms showed the genotype and allele frequencies of the polymorphisms except for Cohen et al's study giving only allele data [20]. There was one study for adrenergic receptor A1A (ADRA1A) [7], adrenergic receptor B2 (ADRB2) [7], adrenergic receptor B3 (ADRB3) [7], dopamine-D 3 -receptor (DRD3) [8], dopamine-D 4 -receptor (DRD4) [17], dopamine transporter (DAT) [10], 5-HT2A receptor (rs6311) [11], COMT (rs6269, rs4633, rs4818, rs4680, rs20907, and rs16559) [12], monoamine oxidase-A (MAO-A) [promoter variable number tandem repeat (VNTR), 941G/T] [13], monoamine oxidase-B (MAO-B) [13], endothelial nitric oxide synthase (eNOS) [14], tachykinin NK1 (substance P) receptor (TACR1) [10], alpha-1 antitrypsin (AAT) [10], interleukin-4 (IL-4) [15], 5-HTTLPR (intron2 VNTR) [19], 5-HT receptor 3A, and 3B (HTR3A and 3B) (some SNPs) [16], respectively (Tables 1, 2). We performed a meta-analysis on the association of the polymorphisms with fibromyalgia if there were at least two comparisons.…”

“…Significant familial aggregation, convincing demonstrations of genetic linkages and associations demonstrate an underlying genetic basis for fibromyalgia [5]. Many studies have examined the potential contribution of the candidate gene polymorphisms to fibromyalgia susceptibility, but these studies have produced diverse results [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23].…”