Search in the Abstract Database

Abstracts Search 2014

* = Presenting author

P578. Adalimumab as first-line anti-TNF treatment in pediatric Crohn's disease

J. Martín-de-Carpi1, V.M. Navas-Lopez2, M. Navalón-Rubio3, E. Llerena-Santa-Cruz1, D. Gil-Ortega3, V. Varea-Calderón1, C. Sierra-Salinas2, 1Hospital Sant Joan de Deu, Pediatric Gastroenterology and Nutrition Unit, Barcelona, Spain, 2Hospital Materno Infantil, Pediatric Gastroenterology and Nutrition Unit, Malaga, Spain, 3Hospital Virgen de la Arrixaca, Pediatric Gastroenterology and Nutrition, Murcia, Spain

Background

Adalimumab (ADA), monoclonal humanized anti-TNF antibody is usually prescribed for patients who have lost response or developed intolerance to IFX. Data published thus far on the efficacy of treatment with ADA in children with CD comes from case series, retrospective studies and a clinical trial (IMAgINE 1). In the case series reported, more than 70% of patients had initially been treated with IFX. Data on short and long-term efficacy in anti-TNF naïve patients are limited.

Methods

Multicenter retrospective study that included CD anti-TNF naïve pediatric patients treated with ADA as first anti-TNF. PCDAI, fecal calprotectin (FC), CRP, ESR were measured at weeks 0, 12 and 52 of treatment.

Results

We included 40 patients (22 females) with a mean age at diagnosis of 11.3±3.7 y, a mean age at start of ADA of 12.6±2.5 y, and a median of 9 months (IQR 4.3–22.3) duration from CD diagnosis to start of treatment. The time from the onset of symptoms until diagnosis of the disease was 7 months (IQR 3–12). Mean weight was 38.7±12.2 Kg. ADA induction dose was 160/80 mg in 22 (55%) patients. Standard maintenance dose was 40 mg eow in all patients. Administration of ADA was performed in combination with thiopurines in 39 patients, of whom 37 received azathioprine, and 2 6-MP due to azathioprine-intolerance. Mean duration of combo therapy was 12 m (IQR 6–14). Baseline PCDAI was 25 (IQR 15–30). Median follow up was 24 months (IQR 12–39), 35 of 40 patients at week 12, 33 of 34 patients al week 52 and 36 of 40 patients at the end of follow-up were in clinical remission (PCDAI <10). A significant decrease was also seen in FC levels, from 747 µg/g (IQR 427–854) at start of ADA treatment to 131 µg/g (IQR 50–281) at week 12 (p = 0.001) and to 255 µg/g (IQR 38–532) at week 52; CRP 30 mg/L (IQR 14–52) at baseline to 1.5 mg/L (IQR 0.5–5) at week 12 (p < 0.0001) and 1.3 mg/L (IQR 0.4–4) at week 52 (p < 0.0001); ESR 19.5 mm (IQR 14–32) to 4.5 mm (IQR 2–12) at week 12 (p < 0.0001) and to 6 mm (IQR 3–11) at week 52 (p < 0.0001). 10 of 40 (25%) patients needed treatment intensification but only one patient continued on intensification schedule at the end of the follow-up. A total of 1901 doses were administered in all in the 40 patients [36 doses (IQR 20–70)] during 16 months (IQR 8–33) of treatment. Surgery was performed in 5 patients (12.5%) through the follow-up. No severe adverse reactions, infections or malignancies were reported.

Conclusion

ADA has shown efficacy and safety in inducing and maintaining remission in pediatric CD patients naïve to anti-TNF. Early use of ADA in our series could explain the better results compared with already published data.