Crohn’s disease: Infliximab is effective in the acute treatment and maintenance of fistulising or non-fistulising Crohn’s disease. The efficacy and safety of azathioprine / 6-mercaptopurine is now well established in the maintenance treatment of the disease. The autologous bone marrow transplant could be a hope of treatment in the very serious forms. Ucerous colitis: Mesalazine remains the reference treatment in the light to moderate forms. In severe forms, a prednisone treatment is indicated. In case of non-response after seven to ten days of treatment, the introduction of ciclosporin should be discussed. Azathioprine / 6-mercaptopurine should be routinely administered in the maintenance treatment of severe forms. Microscopic Colitis: Budesonide is the first-line treatment for collagen colitis. In lymphocytic colitis, treatment with 5-aminosalicylates will be started first, and in case of non-response, budesonide will be used.
The main developments in the treatment of Crohn’s disease come from the gradual arrival on the market of biological treatments. For now, these treatments consist mainly of intravenous or subcutaneous administration of proteins. The latter are either recombinant human proteins having immunoregulatory properties, or monoclonal antibodies, or finally fusion proteins.
A review article reviews inflammatory bowel disease with a focus on advances in understanding the pathogenesis of the disease.
Ulcerative colitis is a chronic relapsing disease. Self-management by the patient has been well developed in other chronic diseases, for example asthma and diabetes. This approach, partly self-managed by the patient, has been, at least, so far less well developed in inflammatory bowel diseases. Such an approach is the subject of an interesting controlled study (N = 203 patients). The patients were randomized to a group receiving detailed information on the disease and the immediate therapeutic attitude to adopt in case of recurrence; the second group was followed at fixed intervals without the possibility of initiating treatment immediately before a medical check. The frequency of recidivism was, as might be expected, identical in both groups, but the duration of recidivism and the cost of treatment were lower in the self-administered group; moreover, the patients showed their preference for the self-management of recidivism.
It must be emphasized, however, that this study was conducted in a medical setting (England) where the rapid access and availability of gastroenterologists is probably less than in Switzerland or France. However, she stresses the importance of the information given and acquired by the patient. Our patients seem indeed, at least according to the results of a study conducted in Ireland, dramatically uninformed about their disease: about 40% of patients are unaware of its chronic long-term, its exact location, its association with a development risk colorectal cancer; the majority of patients are unaware of the potential side effects of mesalazine and corticosteroids.
The treatment modalities of oral and rectal mesalazine have been regularly specified in recent years in therapeutic acquisitions. Two detailed reviews recall the important results available: the total dose administered is decisive; 2 g are superior to placebo; 3-4.8 g are more effective than lower doses; there is no sufficient data to claim that one preparation is superior to another. Balsalazide is also the subject of a detailed review.
Local mesalazine often causes compliance problems. In the form of foam, mesalazine (2 g) seems as effective as a liquid form (4 g) (controlled study, N = 250 patients).
Balsalazide is a substance only activated in the colon after release of its associated molecule (4-aminobenzoyl-B-alanine), by analogy with sulfasalazine. At high dose (6.75 g), it appears to be more effective than mesalazine (controlled study, N = 154 patients) but the dose of mesalazine used (2.4 g) is lower than current recommendations. Balsalazide (6.75 g) is identical in efficacy to sulfasalazine (3 g) with obviously better tolerance (controlled study, N = 57 patients). In the prevention of ulcerative colitis, high-dose balsalazide (3 g) is superior to “normal” dose mesalazine (1.5 g) (controlled study, N = 133 patients). It must be remembered, however, that several authors admit that the effective preventive dose of mesalazine is identical to the dose needed to achieve remission, as we have pointed out in recent years. Determination of the optimal dosage of mesalazine, and comparable substances, including balsalazide, therefore remains controversial.
The potential side effects of mesalazine have been consistently reported in recent years. It is definitively established that mesalazine should be preferred over sulfasalazine, the incidence of side effects being lower (about 20% versus 6.5%, retrospective study, N = 685 patients) .51 Renal toxicity seems negligible as already mentioned, which is confirmed by two studies. Genetic polymorphism determines fast and slow acetylators of 5-aminosalicylates; the determination of the type of acetylator, however, does not seem to predict the incidence of toxicity induced by mesalazine.
Corticosteroids represent the necessary treatment of moderate forms not responding to mesalazine and severe forms of ulcerative colitis. Budesonide, which is used predominantly in Crohn’s disease and is predominantly oral in distal and right bowel, is reviewed twice. Its efficacy by local route is admitted without confirmation of oral use. Targeting at the colon level of prednisolone is a seductive concept but its efficacy is not confirmed in a controlled study (N = 33 patients).
The need for prevention of side effects on corticoid bone is recognized and is imperative from the first treatment. We recommend a baseline mineralometry at the early stage of inflammatory bowel disease and supplementation with calcium and vitamin D. A decrease in bone mineral density may already be observed after eight weeks of prednisone treatment.