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P080. Effect of chondroitin sulphate on pro-inflammatory mediators and disease activity in patients with inflammatory bowel disease (IBD)

P.M. Linares1, M. Chaparro1, A. Algaba2, I. Guerra2, M. Román3, I. Moreno Arza3, F. Abad Santos3,4, D. Ochoa3, F. Bermejo2, J.P. Gisbert1, 1Hospital Universitario de La Princesa, IP and CIBERehd, Gastroenterology Unit, Madrid, Spain, 2Hospital Universitario de Fuenlabrada, Gastroenterology Unit, Fuenlabrada, Spain, 3Hospital Universitario de La Princesa and IP, Farmacy Unit, Madrid, Spain, 4CIBERehd, Farmacy Unit, Madrid, Spain


Chondroitin sulphate, a glycosaminoglycan that modulates NF-κB, might modulate several pro-inflammatory proteins involved in the pathogenesis of IBD. The aim of our study was to evaluate the incidence rate of relapse in patients with IBD under chondroitin sulphate treatment and its effect on the concentrations of diverse pro-inflammatory mediators in serum and urine.


Prospective observational 12-month (m) follow-up study in patients with IBD in remission for at least 6 m, starting chondroitin sulphate treatment (Condrosan®, CS Bio-ActiveTM, Bioibérica S.A., Barcelona, Spain) for osteoarthritis (OA) (dose: 800 mg o.d.). Visits were as follows: Baseline, 3rd, 6th, 9th and 12th m. CDAI and modified Truelove-Witts clinical indexes were calculated for Crohn's disease (CD) and ulcerative colitis (UC) respectively. C-reactive protein (CRP), orosomucoid, and erythrocyte sedimentation rate (ESR) were also determined. Levels of VEGFA, VEGFC, FGF2, HGF, Ang1, Ang2, TGFβ, TNFα, IL1β, -6, -12, -17, -23, ICAM1, VCAM1, MMP3 and PGE2 were quantified by ELISA. OA joint pain was evaluated by a visual analogue scale (VAS).


37 patients with IBD (19 UC, 18 CD) were included. Mean age was 59.8±19 years, and 70% were women. The mean disease duration was 12.7±17.3 years. 62% of patients were under mesalazine, 5% with sulfasalazine, 22% with thiopurines, and 3% with methotrexate. There was only one patient (with UC) that had a flare during follow-up (6th m visit). The incidence rate of relapse was 3.4% per patient-year of follow-up. That figure is lower than the relapse rate previously reported for IBD patients (16%). 12 UC and 11 CD patients completed the 12 m follow-up. In all patients with IBD, mean serum VEGFA levels were higher after 12 months of CS treatment (799 pg/mL) as compared to baseline (492 pg/mL) (P < 0.05). Further differences regarding the other studied pro-inflammatory markers were not found. At 12th m, the OA joint pain had improved in all but four patients (from 5.9 to 3.0) (P < 0.01). 43% of patients suffered adverse events, but only 5% were related to the drug.


The incidence of IBD relapse in patients under chondroitin sulphate treatment was lower than the generally reported. This treatment might modulate VEGFA serum levels, but it is not associated with modifications in the concentrations of the other studied pro-inflammatory mediators. Chondroitin sulphate decreases pain related to OA in patients with IBD.