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N20 Experience with therapeutic drug monitoring on adalimumab in paediatric inflammatory bowel disease (pIBD)

S. Sider*1, L. Cococcioni1, A. ElZein1, S. Chadokufa1, R. Buckingham1, N. Shah1, A. Ocholi1, O. Borrelli1, F. Kiparissi1

1Great Ormond Street Hospital, London, UK


Adalimumab (Ada)/(Humira®), a TNF-α inhibitor, has been approved for the treatment of Crohn’s disease (CD), ulcerative colitis (UC) and inflammatory bowel disease Unclassified (IBDU) in Paediatric Inflammatory bowel disease (pIBD). After loading with Ada, drug levels get maintained with 2 weekly injections.


The aim of the study was to evaluate whether proactive therapeutic drug monitoring (TDM) with antibodies (AB) is enabling clinicians to improve clinical outcomes, additionally to looking at biomarkers and PCDAI/PUCAI indices. Data suggest that drug levels between 5 and 10 with negative AB should be aimed for to improve clinical outcomes and biomarkers.


Retrospective review of pIBD patients on Ada over a 4 year period. All patients were on an immunomodulator.


UC n = 9, all male, age at diagnosis 3–12 years (median 7 years) age at commencement of Ada 9-17 years (median 13 years) interval from diagnosis to Ada 1–9 years (median 6 years). Six of 9 (67%) had levels of 5.7–15.2 (median 10) with negative AB, 2/9 (22%) developed AB of 10 with levels of 0.3 and 5.9 each, no intervention in 7/8 (87%) as normal PUCAI, 1 (11%) patient did not improve and drug discontinued. 1/9 (11%) had low levels of 1–2.1 with AB of 78–192. After reloading, drug levels of 4.4 and AB of 83 with improved PUCAI. CD n = 26, 12 female, age at diagnosis 3–13 years (median 9 years) age at commencement of Ada 5.5–15 years (median 12.5 years), interval from diagnosis to Ada 0.5–11.5 years (median 3 years). 1/26 (4%) had levels of 0.8 and antibodies of 231. This patient continued with Ada treatment and improved from moderate to mild disease. 25/26 (96%) had levels of 3–17(median 9.6), 12/25 had AB of 0, 9/25 had AB of less than 20, and 2/25 had AB of 122(drug level 3.9) and 168(drug level 11.1). Seventeen/26 (65%) remained on 2 weekly Ada, 17/17 were in clinical remission with low PCDAI. 8/26 (31%) escalated treatment due to worsening of PCDAI, 6 of those (75%) by shortening intervals (to weekly) and 2 (25%) switched to vedolizumab. 1/26 discontinued Ada due to anxiety/poor compliance. IBDU: n = 4, all female, age at diagnosis 5–9 years (median 5.5 years), age at commencement of Ada 10–15 years (median 12.5 years), interval from diagnosis to Ada 5–7 years (median 5 years). All had levels of 6.1–13.8 (median 10.6), 3/4 had positive AB (median 13, range 0–168) and remained on 40 mg, 2 weekly. 1/3 had mild, 2/3 quiescent disease. 1/4 escalated treatment to vedolizumab due to worsening clinical symptoms.


Our study suggests that our approach of proactive TDM improves clinical outcomes (PUCAI/PCDAI) and increases and maintains adequate levels and reduces AB formation in some patients.