Risk of hidradenitis suppurativa in patients with juvenile arthritis: A nationwide cohort study

Juvenile arthritis (JA) comprises a heterogeneous group of chronic inflammatory joint disorders of unknown aetiology, with onset before the age of 16 years.1 Studies have shown an increased odds of JA in patients with hidradenitis suppurativa (HS),2 a disease also mediated by chronic inflammation, but the potential risk of HS among patients with JA remains unexplored. All HS-free (without ICD-10 D73.2) patients < 16 years with a hospital diagnosis of inflammatory arthritis (ICD-10 M8.0 + L40.5) from the National Danish Patient Registry (1 January 1997 to 31 December 2022) were included on the day of arthritis diagnosis. Patients were age- and sex matched with controls without JA from the general population, as well as with a control group of patients previously hospitalized for elective surgical procedures (identified using predefined SKS procedure codes, including tonsil/adenoid surgery, hernia repair, urological procedures and dental/oral surgery) denoted as the ‘hospital cohort’ as a sensitivity analysis.3, 4 Patients were followed from juvenile age into adulthood until the first occurrence of HS, migration, death or end of follow-up. Comorbidities were assessed at index and during follow-up, with definitions previously described.5 Biologic treatments were identified using predefined SKS procedure codes, including TNF inhibitors (e.g. infliximab and adalimumab), interleukin inhibitors (e.g. tocilizumab and anakinra) and co-stimulation inhibitors (e.g. abatacept). Risk was assessed using Cox regression models and reported as hazard ratios (HR). A post hoc analysis compared demographics and comorbidities between population controls and patients with JA who developed HS. A total of 6352 patients with JA, 16,555 from the hospital cohort, and 31,625 population controls were included (Table 1). Mean (SD) age was 9.1 (4.5), 9.1 (4.5) and 10.0 (4.0) years, respectively. Females comprised 58.8%, 58.8% and 56.2% of each group. The incidence rate (IR) of HS was 0.33 per 1000 person-years (PY) among individuals with JA, whereas the corresponding rates were 0.23 and 0.15 in the hospital cohort and the general background population. The risk of HS in patients with JA was increased relative to both comparison groups (Figure 1). A higher HR was observed relative to the general population (HR, 2.87 [95% CI, 1.75–4.70]; p < 0.0001), whereas comparison with the hospital cohort showed a non-significant trend towards increased risk (HR, 1.67 [95% CI, 0.99–2.80]; p = 0.052). Among males with JA, the risk of HS was markedly higher than in the general population (HR, 7.34 [95% CI, 2.07–26.02]; p < 0.01) and in the hospital cohort (HR, 3.47 [95% CI, 1.06–11.40]; p = 0.04) than among females in the general population (HR, 2.41 [95% CI, 1.39–4.17]; p < 0.01) and the hospital cohort (HR, 1.41 [95% CI, 0.78–2.52]; p = 0.255); however, the latter was not statistically significant. JA patients treated with any anti-rheumatic biologic had a significantly increased risk of HS (relative to, respectively, the general population: HR, 4.86 [95% CI, 2.18–10.83]; p < 0.001 and hospital cohort: HR, 2.35 [95% CI, 1.05–5.27]; p = 0.039). In the intragroup analysis of patients with and without JA who developed HS, there was no difference in demographic factors or covariates (all p > 0.05). No clear difference in HS risk was observed between the arthritis subtypes. Our study found an increased risk of HS among patients with JA compared with both the general population and hospital-based controls; however, this should be interpreted with caution given the wide confidence intervals. Notably, the risk appeared higher among males. In conclusion, JA is associated with an elevated risk of HS, emphasizing the need for increased clinical awareness in this group of patients. None. Nadja Højgaard Pedersen and Valdemar Wendelboe Nielsen had no conflicts of interest regarding this paper. Nikolaj Holgersen has received funding for conference attending from UCB. Prof. Thyssen was previously an advisor for AbbVie, Almirall, Arena Pharmaceuticals, OM Pharma, Aslan Pharmaceuticals, Union Therapeutics, Eli Lilly & Co, LEO Pharma, Pfizer, Regeneron and Sanofi-Genzyme, a speaker for AbbVie, Almirall, Eli Lilly & Co, LEO Pharma, Pfizer, Regeneron and Sanofi-Genzyme, and received research grants from Pfizer, Regeneron and Sanofi-Genzyme. He is currently an employee of LEO Pharma. Prof. Egeberg has received research funding from Almirall, Pfizer, Eli Lilly, Novartis, Bristol-Myers Squibb, AbbVie, Janssen Pharmaceuticals, Boehringer Ingelheim, the Danish National Psoriasis Foundation, the Simon Spies Foundation and the Kgl Hofbundtmager Aage Bang Foundation and honoraria as consultant and/or speaker from Amgen, AbbVie, Almirall, Leo Pharma, Zuellig Pharma Ltd., Galápagos NV, Sun Pharmaceuticals, Samsung Bioepis Co., Ltd., Pfizer, Eli Lilly and Company, Novartis, Union Therapeutics, Galderma, Dermavant, UCB, Mylan, Bristol-Myers Squibb, McNeil Consumer Healthcare, Horizon Therapeutics, Boehringer Ingelheim and Janssen Pharmaceuticals, and is currently employed by LEO Pharma. Simon Francis Thomsen has received research support from Janssen, LEO Pharma, Novartis, Sanofi and UCB, and has been a speaker/consultant for AbbVie, Almirall, CSL, Eli Lilly, Galderma, Incyte, Janssen, LEO Pharma, Novartis, Pfizer, Sanofi, Servier, Symphogen, UCB and Union Therapeutics. No approval needed for working with the Danish Registers. All patients in the Danish registries are anonymized. The data that support the findings of this study are available from the corresponding author upon reasonable request.