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GCH1-polymorphism and pain sensitivity among women with provoked vestibulodynia

Heddini, Ulrika (författare)
Karolinska Institutet
Bohm-Starke, Nina (författare)
Karolinska Institutet
Grönbladh, Alfhild (författare)
Uppsala universitet,Institutionen för farmaceutisk biovetenskap,Uppsala Univ, Div Biol Res Drug Dependence, Dept Pharmaceut Biosci, Uppsala, Sweden.
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Nyberg, Fred (författare)
Uppsala universitet,Institutionen för farmaceutisk biovetenskap,Uppsala Univ, Div Biol Res Drug Dependence, Dept Pharmaceut Biosci, Uppsala, Sweden.
Nilsson, Kent W. (författare)
Uppsala universitet,Centrum för klinisk forskning, Västerås,Uppsala Univ, Cty Council Vastmanland Cent Hosp, Clin Res Ctr, Vasteras, Sweden.
Johannesson, Ulrika (författare)
Karolinska Institutet
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 (creator_code:org_t)
2012-01-01
2012
Engelska.
Ingår i: Molecular Pain. - : SAGE Publications. - 1744-8069. ; 8, s. 68-
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Background: Provoked vestibulodynia (PVD) is a pain disorder localized in the vestibular mucosa. It is the most common cause of dyspareunia among young women and it is associated with general pain hypersensitivity and other chronic pain conditions. Polymorphism in the guanosine triphosphate cyclohydrolase (GCH1) gene has been found to influence general pain sensitivity and the risk of developing a longstanding pain condition. The aim of this study was to investigate GCH1-polymorphism in women with PVD and healthy controls, in correlation to pain sensitivity. Results: We found no correlation between the previously defined pain-protective GCH1-SNP combination and the diagnosis of PVD. Nor any correlation with pain sensitivity measured as pressure pain thresholds on the arm, leg and in the vestibule, coital pain scored on a visual analog scale and prevalence of other bodily pain conditions among women with PVD (n = 98) and healthy controls (n = 102). However, among patients with current treatment (n = 36), there was a significant interaction effect of GCH1-gene polymorphism and hormonal contraceptive (HC) therapy on coital pain (p = 0.04) as well as on pressure pain thresholds on the arm (p = 0.04). PVD patients carrying the specified SNP combination and using HCs had higher pain sensitivity compared to non-carriers. In non-HC-users, carriers had lower pain sensitivity. Conclusions: The results of this study gave no support to the hypothesis that polymorphism in the GCH1-gene contributes to the etiology of PVD. However, among patients currently receiving treatment an interaction effect of the defined SNP combination and use of hormonal contraceptives on pain sensitivity was found. This finding offers a possible explanation to the clinically known fact that some PVD patients improve after cessation of hormonal contraceptives, indicating that PVD patients carrying the defined SNP combination of GCH1 would benefit from this intervention.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine (hsv//eng)

Nyckelord

Provoked vestibulodynia
Pain
GCH1
Gene
Polymorphism
SNP
Hormonal contraceptives

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