Patients with a high genetic risk for hidradenitis suppurativa may have an increased likelihood of developing coronary artery disease and diabetes, according to a recent study.
In the cohort study, published in JAMA Dermatology, investigators examined the genetic association between hidradenitis suppurativa (HS) and cardiometabolic diseases, specifically coronary artery disease (CAD) and diabetes. They used the UK Biobank to analyze the data from 391,481 participants of European ancestry who had a median age of 58 years (interquartile range = 51–64 years), 53% of whom were female. A polygenic risk score (PRS) for HS was used to assess the risk of developing CAD and diabetes.
The investigators found notable genetic correlations between HS and several cardiometabolic factors, including CAD (r = 0.25, P = 5.59 × 10⁻⁵), diabetes (r = 0.30, P = 4.19 × 10⁻⁶), triglycerides (r = 0.20, P = 1.81 × 10⁻⁴), and C-reactive protein (CRP) (r = 0.31, P = 1.49 × 10⁻⁴). Additionally, there was a negative genetic correlation with high-density lipoprotein (HDL) cholesterol (r = –0.21, P = 2.78 × 10⁻⁴).
The findings showed that patients with a high PRS for HS had an increased risk of both CAD and diabetes. Those in the highest quartile of genetic risk for HS had a 9% increased risk of CAD (odds ratio [OR] = 1.09, 95% confidence interval [CI] = 1.06–1.12) and a 13% increased risk of diabetes (OR = 1.13, 95% CI = 1.10–1.17) compared with those in the lowest quartile. The PRS for HS was also associated with altered expression of 58 plasma proteins, including those involved in inflammatory and metabolic pathways.
Over a median follow-up period of 13.7 years, 26,994 participants were diagnosed with CAD and 13,153 developed diabetes. A high PRS for HS was associated with a hazard ratio (HR) of 1.06 for CAD (95% CI = 1.03–1.10, P < .001) and 1.14 for diabetes (95% CI = 1.08–1.19, P < .001).
The results of the study indicated that a genetic predisposition to HS could be linked to an increased risk of cardiometabolic diseases, likely through shared inflammatory mechanisms.
Full disclosures can be found in the published study.