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Published on: June 16, 2020
Distinct spondyloarthritis phenotypes and disease burden in patients with concomitant hidradenitis suppurativa
Montserrat Cabanillas-Paredes1, Joan Calvet1, Miriam Almirall2
1Department of Rheumatology, Parc Taulí Hospital Universitari, Institut d'Investigació i Innovació Parc Taulí (I3PT-CERCA), Universitat Autònoma de Barcelona, Sabadell, Spain; Departament de Medicina, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Objective:
To characterize the clinical phenotype and disease burden in patients with concomitant spondyloarthritis (SpA) and hidradenitis suppurativa (HS) versus patients with SpA alone.
Methods:
We conducted a multicenter, retrospective and matched case-control study. Cases were adults with SpA and dermatologist‑confirmed HS; controls had SpA without HS. Data from the preceding three years were extracted from electronic medical records.
Results:
We included 39 cases and 111 controls. Among cases, 64% had axial SpA (axSpA) and 36% peripheral SpA (pSpA). Compared with controls, patients with axSpA+HS had less HLA-B27 positivity (46%vs. 79%, p = 0.002), less radiographic sacroiliitis (60%vs. 86%, p = 0.007), and more frequent arthritis (40%vs. 23%; p = 0.081). Several comorbidities were more prevalent in axSpA+HS: active smoking (68%vs. 35%; p = 0.006), hypertension (44%vs. 17%; p = 0.011), and anxiety-depressive disorders (36%vs. 16%; p = 0.046). Among EMM, IBD was more frequent in axSpA+HS than in controls (20%vs. 3%; p = 0.020). Patients with axSpA+HS presented higher disease activity (ASDAS-CRP: 3.0 vs. 2.1, p = 0.003; CRP: 11.3 vs. 3.3 mg/L, p = 0.001), had received a greater number of different biologic agents (p = 0.028), showed more frequent csDMARD use (52%vs. 28%; p = 0.018), and had more rheumatology visits (median 9.0 vs. 7.0; p = 0.050).
Conclusions:
Concomitant SpA and HS appears to be associated with a distinct clinical phenotype and higher disease burden that translates into greater therapeutic complexity and healthcare utilization. These findings support the hypothesis that HS may form part of the broader spectrum of immune-mediated manifestations associated with SpA, although further investigation is required.
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