title: GCH1-polymorphism and pain sensitivity among women with provoked vestibulodynia.
abstract: 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.
authors.affiliation: Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Division of Obstetrics and Gynecology, Stockholm, Sweden. ulrika.heddini@ds.se
authors.forename: Ulrika
authors.initials: U
authors.lastname: Heddini
authors.forename: Nina
authors.initials: N
authors.lastname: Bohm-Starke
authors.forename: Alfhild
authors.initials: A
authors.lastname: Grönbladh
authors.forename: Fred
authors.initials: F
authors.lastname: Nyberg
authors.forename: Kent W
authors.initials: KW
authors.lastname: Nilsson
authors.forename: Ulrika
authors.initials: U
authors.lastname: Johannesson
mesh_terms: D000293:Adolescent; D000328:Adult; D003278:Contraceptives, Oral, Hormonal / Q000627:therapeutic use; D005260:Female; D006136:GTP Cyclohydrolase / Q000235:genetics*; D005787:Gene Frequency / Q000235:genetics; D020022:Genetic Predisposition to Disease; D006579:Heterozygote; D006801:Humans; D016014:Linear Models; D010147:Pain Measurement; D017288:Pain Threshold; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D056650:Vulvodynia / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics* / Q000503:physiopathology; D055815:Young Adult
chemical_list: D003278:Contraceptives, Oral, Hormonal; D006136:GTP Cyclohydrolase