E Domènech ¹, J Hinojosa, M Esteve-Comas, F Gomollón, J M Herrera, G Bastida, A Obrador, R Ruiz, C Saro, M A Gassull, Spanish Group for the Study of Crohn’s Disease and Ulcerative Colitis (GETECCU)

Aliment Pharmacol Ther. 2004 Dec;20(11-12):1347-52. doi: 10.1111/j.1365-2036.2004.02288.x.

Background: Uncontrolled studies suggest that granulocyteaphaeresis might be useful in the management of active ulcerative colitis. Aim: To assess the efficacy of granulocyteaphaeresis treatment in active steroid-dependent inflammatory bowel disease. Methods: We conducted a multicentre, prospective, open, pilot study in patients with steroid-dependent inflammatory bowel disease. All patients were started on 60 mg/day of prednisone; after 1 week, a five-session programme of granulocyteaphaeresis (once per week) was started. The steroid dose was tapered weekly if there was clinical improvement. Remission was defined as an inactive clinical activity index together with complete withdrawal of steroids at week 6. The patients were followed up for at least 6 months or until disease relapse. Results: Twenty-six patients (14 ulcerative colitis, 12 Crohn’s disease) were included. More than a half had been previously treated with immunomodulators. Remission was achieved in 62 and 70% of ulcerative colitis and Crohn’s disease, respectively. During a median follow-up of 12.6 months, six of eight ulcerative colitis patients maintained their clinical remission; however, only one Crohn’s disease patient remained in remission after the first 6 months of follow-up. Conclusions: Granulocyteaphaeresis is a safe treatment option in inflammatory bowel disease. A five-session programme of granulocyteaphaeresis seems to be efficient in the treatment of steroid-dependent ulcerative colitis, but not in Crohn’s disease.

https://pubmed.ncbi.nlm.nih.gov/15606397/

https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1365-2036.2004.02288.x

Yukihiko Kawasaki ¹, Junzo Suzuki, Shigeo Suzuki, Hitoshi Suzuki

J Pediatr Gastroenterol Nutr. 2004 Oct;39(4):422-5. doi: 10.1097/00005176-200410000-00021.

Generally, UC is associated with intervals of acute exacerbation and the administration of corticosteroids is effective in bringing about a clinical remission (¹). Corticosteroids are not always effective even in doses over 1 mg/kg/day. In addition, the long-term use of corticosteroids often causes serious side effects such as growth retardation, glaucoma, hormonal disturbance, peptic ulcer, liver dysfunction and psychologic problems. Alternative treatment for active UC may be necessary to avoid the clinical problems associated with corticosteroid therapy. In recent years, leukocytapheresis (LCAP) and granulocytapheresis (GCAP) using a leukocyte removal filter has been found effective in some cases of adults with inflammatory bowel disease (^2,3). However, there have been few reports concerning the efficacy of LCAP and GCAP for UC in childhood (⁴).We report two children with severe steroid-dependent UC in whom LCAP with leukocyte removal filter was used in treatment. LCAP therapy was safe and effective in two children with refractory UC and allowed discontinuation of corticosteroid therapy with an improvement in quality of life. Prospective studies of this therapy will be needed to clarify the role of LCAP in treatment of childhood UC.

https://pubmed.ncbi.nlm.nih.gov/15448435/

https://journals.lww.com/jpgn/Fulltext/2004/10000/Leukocytapheresis_with_Leukocyte_Removal_Filter.21.aspx

Masakazu Takazoe ¹, Torao Tanaka, Kenji Kondo, Toshiki Ichimori, Toshio Shinoda Ther Apher 2002 Aug;6(4):305-11. doi: 10.1046/j.1526-0968.2002.00445.x.

The immunological and genetic pathogeneses of inflammatory bowel disease (IBD) have been well elucidated in the recent years. The pharmacologic treatment of IBDs accordingly becomes to focus upon the individual pathologic step (targeting therapy), whereas the therapeutic action is not yet a pinpoint one. It has been known recently that new drugs such as biological immunomodulating agents and anti-inflammatory cytokines have better short-term effects in some respects than the conventional drugs, and they might alter the treatment strategy of IBDs in the near future. The limitation of pharmacologic treatments mainly results from adverse effects of the drugs, i.e. infection susceptibility, oncogenesis, teratogenesis and so forth. The extracorporeal therapy such as leukocytapheresis and photopheresis is reportedly effective for IBDs probably through immunomodulation such as decrease in circulating activated T-lymphocytes and activated granulocytes that play a central role in the pathogenesis of IBD. It can be said that these extracorporeal treatment methods have advantage of rapid action and lack of serious adverse effects to drug therapy.

https://pubmed.ncbi.nlm.nih.gov/12164801/

K Yamaji ¹, H Tsuda, H Hashimoto Ther Apher  2001 Aug;5(4):287-92. doi: 10.1046/j.1526-0968.2001.00358.x.

Cytapheresis has been investigated recently for the treatment of autoimmune related diseases, such as rheumatoid arthritis (RA), inflammatory bowel disease (IBD), multiple sclerosis, and so on. A large number of physicians have indicated that patients with autoimmune diseases respond to cytapheresis treatment. The effective mechanism of cytapheresis for immune disorders is still controversial. However, the removal of the leukocyte including granulocyte, lymphocyte, and monocyte may play a crucial role in correcting imbalance of the immune system. A session of cytapheresis including leukocytapheresis (LCAP) and granulocytapheresis (GCAP) may not create a sufficient amount of cell removal for the human body. However, the cell removal can be a trigger of the immunomodulation as the treatment for immune disorder. Furthermore, not only cell removal but also reaction by blood contacting with medical device materials may play a role as an immunomodulation for immune disorders. This review introduces current cytapheresis technologies and attempts to elucidate the effective mechanism of cytapheresis for immune disorders, focused on LCAP and/or GCAP for RA or IBD.

https://pubmed.ncbi.nlm.nih.gov/11724514/