Erratum: An association between fibromyalgia and the dopamine D4 receptor exon III repeat polymorphism and relationship to novelty seeking personality traits

Buskila, Dan; Cohen, Hagit; Neumann, L; Ebstein, Richard P.

doi:10.1038/sj.mp.4001568

Cited by 61 publications

(28 citation statements)

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“…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.…”

Section: Studies Included In the Meta-analysismentioning

confidence: 96%

“…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].…”

Section: Studies Included In the Meta-analysismentioning

confidence: 99%

“…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].…”

Section: Studies Included In the Meta-analysismentioning

confidence: 99%

“…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].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2010

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The aim of this study was to explore whether the candidate gene polymorphisms contribute to fibromyalgia susceptibility. The authors conducted a meta-analysis on associations between serotonin transporter (5-HTT) gene-linked polymorphic region (5-HTTLPR) S/L allele, catechol-O-methltransferase (COMT) val158Met, and serotonin 2A (5-HT2A) receptor 102T/C polymorphisms and fibromyalgia susceptibility as determined using the following: (1) allele contrast, (2) recessive, (3) dominant models, and (4) contrast of homozygotes. We also performed a systematic review with available data of the candidate genes. A total of 21 separate comparisons were considered in this systematic review and meta-analysis. Seventeen candidate genes and over 35 different polymorphisms were identified in studies on fibromyalgia susceptibility. Meta-analysis of the 5-HTTLPR S/L allele and COMT val158Met failed to reveal any association with fibromyalgia. However, meta-analysis of the C allele, CC + CT genotype, and CC versus TT genotype of the 5-HT2A receptor 102T/C polymorphism showed significant association with fibromyalgia. The overall OR of the association between the C allele and fibromyalgia was 1.333 (95% CI = 1.053-1.688, P = 0.017). The ORs for the CC + CT genotype, and CC versus TT genotype showed the same pattern as that observed for the C allele (OR = 1.541, 95% CI = 1.032-2.303, P = 0.035; OR = 1.838, 95% CI = 1.151-2.936, P = 0.011). This meta-analysis demonstrates that the 5-HT2A receptor 102T/C polymorphism confers susceptibility to fibromyalgia. In contrast, no association was found between the 5-HTTLPR S/L allele, COMT val158Met, and susceptibility to fibromyalgia.

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Section: Studies Included In the Meta-analysismentioning

confidence: 96%

Section: Studies Included In the Meta-analysismentioning

confidence: 99%

Section: Studies Included In the Meta-analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2010

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“…Genetic factors influence vulnerability to fibromyalgia syndrome, but no specific genes have been definitively implicated. To date, a few studies have analyzed specific genetic polymorphisms, for instance, the serotoninergic system genotype of 5-HTT [26], catecho-Omethyltransferase gene polymorphism [27], and D4 dopamine receptor exon II repeat polymorphism [28], which were more commonly seen in FMS than in controls. However, the most associations identified thus far have been weak or inconsistent.…”

Section: Introductionmentioning

confidence: 99%

A brain-derived neurotrophic factor polymorphism Val66Met identifies fibromyalgia syndrome subgroup with higher body mass index and C-reactive protein

2011

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A common single nucleotide polymorphism (SNP) in the gene of brain-derived neurotrophic factor (BDNF) results from a substitution at position 66 from valine (Val) to methionine (Met) and may predispose to human neuropsychiatric disorders. We proposed to determine whether these BDNF gene SNPs were associated with fibromyalgia syndrome (FMS) and/or any of its typical phenotypes. Patients with FMS (N = 95) and healthy normal controls (HNC, N = 58) were studied. Serum high-sensitivity C-reactive protein (hsCRP) levels were measured using an enzyme-linked immunosorbent assay (ELISA). The BDNF SNPs were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).The BDNF SNP distribution was 65 (68%) Val/Val, 28 (30%) Val/Met, and 2 (2%) Met/Met for FMS and 40 (69%), 17(29%), and 1 (2%) for HNC, respectively. The serum high-sensitivity C-reactive protein (hsCRP)and body mass index (BMI) in FMS were higher than in HNC. The FMS with BDNF Val66Val had significantly higher mean BMI (P = 0.0001) and hsCRP (P = 0.02) than did FMS carrying the Val66Met genotype. This pattern was not found in HNC. Phenotypic measures of subjective pain, pain threshold, depression, or insomnia did not relate to either of the BDNF SNPs in FMS. The relative distribution BDNF SNPs did not differ between FMS and HNC. The BDNF Val66Met polymorphism is not selective for FMS. The BDNF Val66Val SNP identifies a subgroup of FMS with elevated hsCRP and higher BMI. This is the first study to associate a BDNF polymorphism with a FMS subgroup phenotype.

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