{Reference Type}: Journal Article {Title}: New-Onset Hidradenitis Suppurativa in Psoriasis Patients: A Multi-Center, Retrospective Cohort Study. {Author}: Li CP;Lo SW;Tsai RY;Chang HC;Gau SY; {Journal}: Life (Basel) {Volume}: 14 {Issue}: 6 {Year}: 2024 Jun 6 {Factor}: 3.251 {DOI}: 10.3390/life14060730 {Abstract}: BACKGROUND: Previous research has indicated a potential correlation between hidradenitis suppurativa (HS) and psoriasis (PSO), two chronic inflammatory dermatological diseases. However, there is a lack of comprehensive evaluations that consider a variety of clinical and demographic factors, and the risk of developing HS in PSO patients remains unclear. Our study aims to examine HS risk over time among PSO patients versus matched controls while considering the influence of confounders to provide insights into the potential link between these two diseases.
METHODS: In this multi-institutional cohort study using the TriNetX database, we matched 202,318 patients with PSO with an equivalent number of individuals without PSO, using propensity score matching. The study period extended from 1 January 2005 to 31 December 2018. We computed hazard ratios and their respective 95% confidence intervals (CIs) to evaluate the probability of HS manifestation over a period of 5 years in patients with PSO in comparison to those without PSO.
RESULTS: PSO patients demonstrated a consistently higher risk of developing HS than matched controls across all analytic models with the hazard ratios (HR) ranging from 1.43 (95% CI 1.30-1.56) to 5.91 (95% CI 2.49-14.04). Stratified analyses showed the increased HS risk was observed in both genders but only significant in those aged 18-64 years. Kaplan-Meier analysis indicated PSO patients had a higher cumulative probability of developing HS over time (HR 1.77, 95% CI 1.49-1.89).
CONCLUSIONS: PSO was associated with increased HS risk, highlighting the importance of considering HS as a potential comorbidity in PSO patients and may have implications for early detection, prevention, and management strategies for both conditions. Shared inflammatory pathways, genetic components, and skin dysbiosis may contribute. Further research should elucidate underlying mechanisms.