Post-Hoc Analysis To evaluate the Association between Treatment with Interleukin-23 Antagonism and Clinical Response in Hidradenitis Suppurativa

Hidradenitis suppurativa (HS) is a long-term skin condition that causes painful lumps, boils, leaking sores, and scars. It often affects sensitive areas such as the groin, buttocks, armpits, and under the breasts. HS can be very distressing and painful. It is relatively common, affecting about 1% of the global population.

Although new biologic medicines (medicines made from living cells), which target specific parts of the immune system, have improved care for some people with HS, they do not work equally well for everyone. This research is needed because doctors currently have limited evidence to help them predict which patients are most likely to benefit from these treatments. As a result, some people may spend time on medicines that are less likely to help them. By identifying patterns linked to better or worse response, we will add to medical knowledge and help support more personalised patient care in the future.

This research will focus on one such medicine, risankizumab. Risankizumab works by blocking interleukin-23 (IL-23), an immune signal involved in inflammation. We will use the data from a clinical trial of risankizumab. We will compare people who received risankizumab with people who received placebo, which is a treatment with no active drug.

We will examine whether treatment response differs according to patient features such as sex, how severe the HS was at the start of the study, and which body areas were affected. We will measure improvement using standard HS outcome measures, including Hidradenitis Suppurativa Clinical Response (HiSCR) and International Hidradenitis Suppurativa Severity Score System (IHS4). These are scoring tools used to measure how much the disease improves. We will use statistical methods to test whether these patient features are linked to a higher or lower chance of improvement.

We will also compare our findings with results from a similar study of another IL-23-blocking medicine, guselkumab. This will help us see whether any patterns are consistent across this type of treatment, rather than being specific to one drug. We expect this study will improve understanding of why treatment responses vary in HS. In the future, this could help doctors choose treatments more effectively, improve outcomes for patients, and guide the design of better clinical trials.