Therapeutic drug monitoring of adalimumab in hidradenitis suppurativa: a prospective observational study

Abstract

Background: Adalimumab (ADA) is an effective treatment for moderate to severe hidradenitis suppurativa (HS). However, nearly half of patients receiving the standard dose may lose response.

Objective: To establish therapeutic thresholds for HS-specific ADA levels, leading to more personalized treatment.

Methods: We conducted a single-center, prospective observational study of adults with HS treated with ADA (40 or 80mg/week, and 80mg/biweekly) at a specialized HS clinic (January 2023-May 2024). Serum samples were collected after ≥4 weeks of therapy to ensure steady state. Patients were stratified by physician-assessed response (low <50%, partial 50-75%, high >75% improvement). Associations of ADA concentration and clearance with response were tested using Spearman and Pearson correlations; discriminatory performance was evaluated with ROC analysis.

Results: Among 46 enrolled patients, the majority was female (60.9%) and White (54.3%), with a median age of 38 years (IQR: 30-45). ADA serum concentrations positively correlated with clinical response (r = 0.43, p = 0.002). Low responders had significantly lower concentrations than partial (p = 0.029) and high responders (p = 0.007). Clearance was inversely correlated with ADA levels (r = -0.65, p < 0.001). Receiver operating characteristic analysis identified optimal thresholds of 10.7 μg/mL for ADA concentration and 0.5 L/day for clearance.

Conclusion: Higher ADA concentrations and lower drug clearance are associated with better clinical outcomes in HS. ROC analysis identified 10.7 μg/mL (ADA concentration) and 0.5 L/day (clearance) as optimal cut-off values to differentiate low from partial/high responders. These findings suggest that therapeutic drug monitoring may help optimize ADA therapy in HS.

Keywords: adalimumab; anti-drug antibodies; biologic therapy; drug clearance; hidradenitis suppurativa; pharmacokinetics; therapeutic drug monitoring; tumor necrosis factor-alpha inhibitors.