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P258. Therapeutic leucocytapheresis for inflammatory bowel diseases: Demographic variables, which identify responder and non-responder patients to this non-pharmacological intervention


T. Tanaka1

1Akitsu Prefectural Hospital, Gastroenterology, Hiroshima, Japan



Background: Most patients with active inflammatory bowel disease IBD have elevated and activated myeloid leucocytes, notably CD14(+)CD16(+) monocytes, which are sources of TNF-alpha (J Immunol 2002;168:3536–42). Hence selective depletion of myeloid leucocytes by granulocyte/monocyte adsorption (GMA) with an Adacolumn is expected to alleviate inflammation. However, studies in ulcerative colitis (UC) reported contrasting efficacy, from an 85% (Suzuki, et al. Gastroenterology 2005) to a statistically insignificant level (Sands, et al. Gastroenterology 2008). Patients' demographic variables in the aforementioned studies were different. We thought that understanding these variables should save medical cost and reduce morbidity time for many patients.

Methods: In 135 UC patients including 15 paediatrics, we looked for clinical and endoscopic features which could indentify a patient as a responder or as a non-responder to GMA. Sixty-six adults were steroid dependent, the other 69 were steroid naive. Patients received up to 11 GMA sessions over 10 weeks. At entry and week 12, patients were clinically and endoscopically evaluated, allowing each patient to serve as her or his own control. Clinical activity index (CAI) 4 or less at week 12 was defined as response to GMA. Biopsies from colonoscopically detectable inflamed mucosa were processed to see the impact of GMA on leucocytes within the mucosa.

Results: Average CAI was 12.8, range 10–17. An 88 patients responded including all 15 paediatric patients with entry CAI 13–17. Five paediatric patients who did not improve after 5 sessions were given 20 mg/day prednisolone and GMA was continued, but prednisolone was tapered to 0 mg within 3 months. Over 900 biopsies were processed. Infiltrating leucocytes were overwhelmingly neutrophils and monocytes/macrophages. There was a marked reduction of infiltrating leucocytes in responders. Patients who had extensive deep UC lesions and virtually no mucosal tissue left at lesion sites were identified as non-responders. Patients with the first UC episode were identified as the best responders (100%) followed by steroid naive patients. Additionally, a short duration of UC marked a patient as a likely responder and vice versa.

Conclusions: Depleting elevated myeloid leucocytes appears to benefit patients with IBD. Accordingly, the application of GMA to treat IBD patients will continue and even expand as it is favoured by patients for its safety profile and being a non-drug intervention, good for adults as well as for children.