IMPORTANCE: In a previously reported cohort of 29 patients with plaque-type psoriasis followed up for 24 weeks, clinically relevant antidrug antibody (ADA) to adalimumab was frequently found. Long-term data were lacking. We now present the extension of this study: 80 patients followed up for 1 year. OBJECTIVES: To assess the extent of ADA and its clinical consequences after 24 weeks of adalimumab treatment for psoriasis in a cohort of 80 patients. DESIGN, SETTING, AND PARTICIPANTS: A multicenter cohort study, performed in the outpatient dermatology clinic of 2 academic hospitals, included 80 sequential patients receiving adalimumab therapy for plaque-type psoriasis and had a follow-up of 1 year. Outcome assessors were not aware of the presence of antibodies to adalimumab or the adalimumab serum concentration when assessing patients' Psoriasis Area and Severity Index (PASI), and personnel analyzing serum samples were blinded to patients' PASI. INTERVENTIONS: For 80 patients treated with adalimumab for psoriasis, disease severity (PASI) was assessed, blood samples were collected, and adalimumab and ADA concentrations was determined at baseline and at weeks 12, 24, and 52. MAIN OUTCOMES AND MEASURES: Patient PASI and adalimumab and ADA concentrations. RESULTS: Antidrug antibody formed in 49% of patients, before week 24 in 90% of them. Adalimumab and ADA concentrations, clinical response and ADA concentration, and adalimumab concentration and clinical response had correlations of -0.872, -0.606, and 0.519, respectively. The adalimumab dose interval was shortened because of lack of efficacy in 15 patients, 7 with and 8 without ADA; improvement in responder status occurred in 1 of 7 and 4 of 8, respectively. CONCLUSIONS AND RELEVANCE: Patients with no ADA formation in the first 24 weeks of treatment have little chance of it in the following 24 weeks. The presence of ADA is strongly correlated with adalimumab concentration and greatly influences clinical response. If ADA is present, dose interval shortening is less useful.
IMPORTANCE: In a previously reported cohort of 29 patients with plaque-type psoriasis followed up for 24 weeks, clinically relevant antidrug antibody (ADA) to adalimumab was frequently found. Long-term data were lacking. We now present the extension of this study: 80 patients followed up for 1 year. OBJECTIVES: To assess the extent of ADA and its clinical consequences after 24 weeks of adalimumab treatment for psoriasis in a cohort of 80 patients. DESIGN, SETTING, AND PARTICIPANTS: A multicenter cohort study, performed in the outpatient dermatology clinic of 2 academic hospitals, included 80 sequential patients receiving adalimumab therapy for plaque-type psoriasis and had a follow-up of 1 year. Outcome assessors were not aware of the presence of antibodies to adalimumab or the adalimumab serum concentration when assessing patients' Psoriasis Area and Severity Index (PASI), and personnel analyzing serum samples were blinded to patients' PASI. INTERVENTIONS: For 80 patients treated with adalimumab for psoriasis, disease severity (PASI) was assessed, blood samples were collected, and adalimumab and ADA concentrations was determined at baseline and at weeks 12, 24, and 52. MAIN OUTCOMES AND MEASURES: Patient PASI and adalimumab and ADA concentrations. RESULTS: Antidrug antibody formed in 49% of patients, before week 24 in 90% of them. Adalimumab and ADA concentrations, clinical response and ADA concentration, and adalimumab concentration and clinical response had correlations of -0.872, -0.606, and 0.519, respectively. The adalimumab dose interval was shortened because of lack of efficacy in 15 patients, 7 with and 8 without ADA; improvement in responder status occurred in 1 of 7 and 4 of 8, respectively. CONCLUSIONS AND RELEVANCE: Patients with no ADA formation in the first 24 weeks of treatment have little chance of it in the following 24 weeks. The presence of ADA is strongly correlated with adalimumab concentration and greatly influences clinical response. If ADA is present, dose interval shortening is less useful.
Authors: C I Busard; S P Menting; J S van Bezooijen; J M van den Reek; B A Hutten; E P Prens; E M de Jong; M B van Doorn; P I Spuls Journal: Trials Date: 2017-02-02 Impact factor: 2.279
Authors: Robert J Moots; Ricardo M Xavier; Chi Chiu Mok; Mahboob U Rahman; Wen-Chan Tsai; Mustafa H Al-Maini; Karel Pavelka; Ehab Mahgoub; Sameer Kotak; Joan Korth-Bradley; Ron Pedersen; Linda Mele; Qi Shen; Bonnie Vlahos Journal: PLoS One Date: 2017-04-27 Impact factor: 3.240
Authors: B Gorovits; D J Baltrukonis; I Bhattacharya; M A Birchler; D Finco; D Sikkema; M S Vincent; S Lula; L Marshall; T P Hickling Journal: Clin Exp Immunol Date: 2018-03-30 Impact factor: 4.330
Authors: Y Umezawa; H Torisu-Itakura; Y Morisaki; H ElMaraghy; K Nakajo; N Akashi; H Saeki Journal: J Eur Acad Dermatol Venereol Date: 2018-11-13 Impact factor: 6.166
Authors: Jan Hillson; Tim Mant; Molly Rosano; Carolyn Huntenburg; Mehrshid Alai-Safar; Siddhesh Darne; Donna Palmer; Borislava G Pavlova; Jennifer Doralt; Russell Reeve; Niti Goel; Doris Weilert; Paul W Rhyne; Kamali Chance; John Caminis; James Roach; Tanmoy Ganguly Journal: Pharmacol Res Perspect Date: 2018-02