Rivaroxaban induces mucosal healing in a rat model of trinitrobenzene sulfonic acid-induced colitis

This study was designed to identify the effect of rivaroxaban, a direct factor Xa inhibitor, on trinitrobenzene sulfonic acid [TNBS] induced colitis in rats. Twenty-four female Wistar rats were divided into 4 groups of 6 each. Group 1 received TNBS + rivaroxaban, group 2 received TNBS + methylprednisolone, group 3 received TNBS and group 4 received a saline enema. Colitis was induced in the rats by the intracolonic administration of TNBS. Rivaroxaban and methylprednisolone were given by oral gavage daily for 7 days. The rats were killed 7 days after the induction of colitis. Rivaroxaban and methylprednisolone significantly reduced gross damage and histo-pathological scores. Rivaroxaban was more effective than methylprednisolone in terms of microscopic mucosal healing. Rivaroxaban attenuated the accumulation of malonyldi-aldehyde [MDA] and transforming growth-factor [1] [TGF-Beta[1]] and the activites of myeloperoxidase [MPO], matrix metal-loproteinase-3 and tissue inhibitor of metalloproteinases-1. Methylprednisolone reduced only the activity of MPO and the accumulation of MDA and TGF-Beta[1]. Superoxide dismutase activity showed a restoration to normal levels after rivaroxaban and methylprednisolone administration. Rivaroxaban showed a therapeutic effect in the TNBS model of experimental colitis, and it seemed to be at least as effective as methylprednisolone. This effect may be brought about by the inhibition of oxidative stress and metallopro-teinase activity associated with tissue injury and remodeling

Tuberculosis and crohn's disease revisited

Crohn's Disease [CD] and Intestinal Tuberculosis [ITB] share confusingly similar clinical, endoscopic, radiological and pathological manifestations. There is no simple test for differentiating ITB from CD. Although there are a number of sensitive and specific parameters for distinguishing between CD and ITB, the differential diagnosis still remains challenging and both clinical suspicion and appropriate clinical and laboratory studies are required to establish the diagnosis. Correct diagnosis is crucial because the therapy strategies of the two diseases are dramatically different. Treatment of ITB with immunosuppressive agents would lead to worsening of the patients' condition. Likewise, unnecessary antituberculosis therapy would delay the treatment of CD. Another important consideration is the risk of reactivation TB in patients with inflammatory bowel diseases which has been significantly increased following the widespread use of anti-Tumor Necrosis Factor Alpha [TNFalpha] therapy. The majority of reactivation cases are extrapulmonary or disseminated TB. And it is widely recommended that patients with IBD who are to receive TNF inhibitor therapy should be screened for evidence of latent TB. This paper mainly reviews current literature on differential diagnosis between CD and ITB, and summarizes strategies to reduce the TB risk among candidates for TNF antagonist therapy in this specific patient population