title: Race and Melanocortin 1 Receptor Polymorphism R163Q Are Associated with Post-Burn Hypertrophic Scarring: A Prospective Cohort Study.
abstract: The genetic determinants of post-burn hypertrophic scarring (HTS) are unknown, and melanocortin 1 receptor (MC1R) loss-of-function leads to fibrogenesis in experimental models. To examine the associations between self-identified race and MC1R single-nucleotide polymorphisms (SNPs) with severity of post-burn HTS, we conducted a prospective cohort study of burned adults admitted to our institution over 7 years. Subjects were evaluated using the Vancouver Scar Scale (VSS), asked to rate their itching, and genotyped for 8 MC1R SNPs. Testing for association with severe HTS (VSS>7) and itch severity (0-10) was based on multivariate regression with adjustment for known risk factors. Of 425 subjects analyzed, 77% identified as White. The prevalence of severe HTS (VSS>7) was 49%, and the mean itch score was 3.9. In multivariate analysis, Asian (prevalence ratio (PR) 1.54; 95% CI: 1.13-2.10), Black/African American (PR 1.86; 95% CI: 1.42-2.45), and Native American (PR 1.87; 95% CI: 1.48-2.35) race were independently associated with severe HTS. MC1R SNP R163Q was also significantly (P<0.001) associated with severe HTS. Asian race (linear regression coefficient 1.32; 95% CI: 0.23-2.40) but not MC1R SNP genotype was associated with increased itch score. We conclude that MC1R genotype may influence post-burn scarring.
authors.affiliation: Department of Surgery, UW Medicine Regional Burn Center, Harborview Medical Center, Seattle, Washington, USA. Electronic address: rfsood@uw.edu.
authors.forename: Ravi F
authors.initials: RF
authors.lastname: Sood
authors.affiliation: Department of Surgery, UW Medicine Regional Burn Center, Harborview Medical Center, Seattle, Washington, USA.
authors.forename: Anne M
authors.initials: AM
authors.lastname: Hocking
authors.affiliation: Department of Surgery, UW Medicine Regional Burn Center, Harborview Medical Center, Seattle, Washington, USA.
authors.forename: Lara A
authors.initials: LA
authors.lastname: Muffley
authors.affiliation: Department of Surgery, UW Medicine Regional Burn Center, Harborview Medical Center, Seattle, Washington, USA.
authors.forename: Maricar
authors.initials: M
authors.lastname: Ga
authors.affiliation: Department of Surgery, UW Medicine Regional Burn Center, Harborview Medical Center, Seattle, Washington, USA.
authors.forename: Shari
authors.initials: S
authors.lastname: Honari
authors.affiliation: Department of Epidemiology, University of Washington, Seattle, Washington, USA.
authors.forename: Alexander P
authors.initials: AP
authors.lastname: Reiner
authors.affiliation: Department of Epidemiology, University of Washington, Seattle, Washington, USA; Harborview Injury Prevention and Research Center, Seattle, Washington, USA.
authors.forename: Ali
authors.initials: A
authors.lastname: Rowhani-Rahbar
authors.affiliation: Department of Surgery, UW Medicine Regional Burn Center, Harborview Medical Center, Seattle, Washington, USA.
authors.forename: Nicole S
authors.initials: NS
authors.lastname: Gibran
mesh_terms: D000328:Adult; D002056:Burns / Q000097:blood* / Q000150:complications / Q000628:therapy; D017439:Cicatrix, Hypertrophic / Q000208:ethnology* / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D015331:Cohort Studies; D005260:Female; D005838:Genotype; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016012:Poisson Distribution; D020641:Polymorphism, Single Nucleotide; D015995:Prevalence; D011446:Prospective Studies; D044102:Receptor, Melanocortin, Type 1 / Q000235:genetics*; D018570:Risk Assessment; D012720:Severity of Illness Index; D014945:Wound Healing / Q000235:genetics / Q000502:physiology
chemical_list: D044102:Receptor, Melanocortin, Type 1