Read more

November 15, 2024
2 min read
Save

Genetic variants for hidradenitis suppurativa linked to cardiovascular disease, diabetes

You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

Key takeaways:

  • Patients with a high vs. low genetic risk for developing hidradenitis suppurativa were 1.09 times more likely to develop coronary artery disease.
  • They were also 1.13 times more likely to develop diabetes.

Genetic variants found in hidradenitis suppurativa may be correlated to genetic variants in coronary artery disease and diabetes, according to a study.

“Previous observational studies have described how patients with hidradenitis suppurativa (HS) are at increased risk of developing cardiovascular disease compared to the general population,” Valdemar Wendelboe Nielsen, BSc, MMed, a graduate researcher at Bispebjerg Hospital during the study and now a visiting research fellow at the University of California, San Francisco, told Healio. “While this could be due to shared risk factors such as smoking and obesity, our findings suggest that a genetic component may also explain part of this association.”

DERM1124Nielsen_Graphic_01
Data derived from Nielsen VW, et al. JAMA Dermatol. 2024;doi:10.1001/jamadermatol.2024.3779.

The cohort study included 391,481 individuals (mean age, 58 years; 53% female) and used polygenic risk scoring to identify the risks.

Valdemar Wendelboe Nielsen

Results showed that genetic variants for HS were significantly correlated with CAD and diabetes variants. In fact, patients with a high genetic risk for developing HS were 1.09 times (95% CI, 1.06-1.12) and 1.13 times (95% CI, 1.1-1.17) more likely to develop CAD and diabetes, respectively, compared with individuals with a low genetic risk for HS.

These findings remained consistent even after evaluating the rate of incidences of CAD and diabetes among these patients. After 15 years of follow-up, patients with a high genetic risk for HS saw an 8.22% (95% CI, 8.03%-8.42%) and 4.17% (95% CI, 4.02%-4.31%) incidence of CAD and diabetes, respectively, vs. 7.81% (95% CI, 7.62%-8.01%) and 3.66% (95% CI, 3.53%-3.79%) in the low-risk group.

“We found that the polygenic risk score for HS was also associated with BMI, suggesting that the increased risk of cardiometabolic disease we observed may, in part, be mediated by an indirect predisposition to obesity,” Nielsen said.

These results show a need for discussions with patients regarding smoke cessation and weight management, which could improve both HS and overall health, he added.

The study also found that high genetic risk for HS was significantly associated with the altered expression of 58 different plasma proteins.

“While it is unlikely to have a direct clinical application for risk stratification of CAD and diabetes, the polygenic risk score and its associated plasma proteomic profile should instead be regarded as instruments to explore the complex shared genetic and pathophysiologic architecture between HS and these significant comorbidities,” Nielsen told Healio. “Additional investigation into the identified proteins with altered expression and their potential roles as drug targets is warranted.”