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DOP057. The influence of anti-adalimumab antibodies on adalimumab trough levels, TNF-α levels and clinical outcome

G. Bodini1, V. Savarino1,2, P. Dulbecco1,3, I. Baldissarro1,2, E. Savarino1,4,5, 1IRCCS San Martino Genova, Dipartimento di medicina interna, Genova, Italy, 2Universita di Genova, Dipartimento di medicina interna, Genova, Italy, 3Università di Genova, Dipartimento di Medicina Interna, Genova, Italy, 4University of Padua, Department of Surgery, Oncology and Gastroenterology, padova, Italy, 5Department of Surgery, Oncology and Gastroenterology, University of Padua, gastroenteroly unit, padua, Italy


There is increasing evidence on the role of low trough levels and the development of anti-TNF-α antibodies for the occurrence of lack/loss of response to Infliximab (IFX) therapy in patients with Crohn's Disease (CD). Therefore, several recent papers and guidelines suggested the need for dosing IFX concentrations and anti-IFX antibodies in order to treat better CD patients. To date, there are limited data on the role of adalimumab (ADA) through levels and anti-ADA antibodies (AAA) for the management of CD patients.

Aim: We assessed the role of AAA on ADA trough levels, TNF-α concentrations, PCR value and clinical outcome.


In this prospective observational cohort study, performed at a single tertiary referral center, 23 [14M/9F; mean age 41 (range 21–66)] infliximab-naïve patients with CD achieving disease remission and in maintenance treatment with ADA were included in a follow-up program. Blood samples were drawn at standardized time points (i.e. at 6, 12, 18, 24 months and in case of relapse) just before ADA injection. Trough serum concentration and antibodies against ADA were measured using an homogenous mobility shift assay (HMSA; Prometheus Lab, San Diego, United States). Blood samples were considered positive for they presence if AAA were >1.7 U/mL and for ADA through levels if they levels were more than >5 µg/ml. Disease activity was assessed at the same points by means of routine biochemistry and the Harvey–Bradshaw Index (HBI, remission <5, mild disease 5–7, moderate disease 8–16, severe disease >16).


We have data from 189 blood samples. AAA were observed in 42/189 (22.2%) samples, and 16/42 (38.1%) had levels of AAA >1.7 U/mL. ADA through levels were found in 183/189 (96.8%) samples, and 168/183 (91.8%) had a value of drug levels >5 µg/ml. Overall, 5/23 (21.7%) patients had AAA and 22/23 (95.6%) were positive for ADA levels. Blood samples with AAA had lower ADA trough levels [7.54 (0–26.49) vs. 9.45 (0.14–23.62); p = 0.002] and higher TNF-α concentrations [5.9 (4.1–11.5) vs. 3.6 (0–27.2); p = 0.0007] than blood samples without evidence of AAA. Moreover, patients with blood samples positive for AAA reported HBI values higher compared to patients without evidence of AAA [10 (3–17) vs. 5 (2–17); p < 0.0001]. Finally, no differences were found in terms of mean PCR values between patients with AAA and those without [8.1 (3–76.4) vs. 5.2 (2.6–56); p = 0.39].


Development and presence of AAA influence ADA trough levels and TNF-α concentrations in CD patients during maintenance treatment with ADA, thus favoring clinical relapse as demonstrated by the increased values of HBI scores.