Developments in Non-pharmacological Treatment for Inflammatory Bowel Disease
Developments in Non-pharmacological Treatment for Inflammatory Bowel Disease
European Gastroenterology Review 2007 - December 2007
Published: October 2008
Published: October 2008
Ulcerative colitis (UC) and Crohn’s disease can be recognised by periods of clinical quiescence interrupted by clinical relapses that are characterised by escalating inflammation in the colon or the full length of the gastrointestinal tract, respectively. The severity of the clinical relapse is variable, but most patients require hospitalisation at some stage of their disease and many require surgery. The relapse impacts significantly on patient quality of life and employment. A key hypothesis for the relapsing–remitting nature of inflammatory bowel disease (IBD) is the suggestion that the causes of the disease and the clinical relapse are determined by distinctively different pathogenic mechanisms that are nevertheless functionally interdependent. Hence, the cause of IBD can be viewed as the collective outcome of complex multiple genetic and environmental factors leading to the phenotype of Crohn’s disease and UC. Under these circumstances the intestinal mucosa is in a state of vastly heightened immune activation, determined by the cells that underlie adaptive or acquired immunity. When the balance between luminal aggressors and mucosal defence is tilted to the advantage of the former, there is an exaggerated inflammatory response in terms of massive polymorphonuclear cell migration to the intestine.
This inflammation causes the common relapse symptoms (tiredness, diarrhoea, urgency, bleeding, abdominal pain, etc.), and may well underlie the serious complications of the disease (perforation, strictures, fistulae, megacolon, etc.). The goal of medical management of UC and Crohn’s disease is first to induce remission of active disease and then to maintain this non-symptomatic status. This is achieved by administration of drugs that interfere with the inflammatory process. Targeted treatment of active IBD involves the administration of 5-aminosalicylic acid (5-ASA) preparations, corticosteroids, tumour necrosis factor (TNF) antibodies (and other biologicals), immunosuppressants (cyclosporine, tacrolimus, etc.) and, in the case of Crohn’s disease, elemental diets and cessation of smoking. Maintenance of remission is conventionally attempted with the use of 5-ASA and azathioprine. These treatments are effective in most patients, but there is ongoing concern about the side effects of medical treatment. These range from renal problems and pancreatitis (5-ASA) to hypertension, diabetes mellitus, osteoporosis, cushingoid appearances (corticosteroids) and overwhelming infections (biologicals and immunosuppressants) that may be lethal. An alternative strategy is to remove mechanically the inflammatory mediators, the cells that produce them or the main effector cells (neutrophils) from the circulation in the hope that this interferes with the vicious cycle whereby the inflammation is self-perpetuating.1 If successful, such non-pharmacological treatment might be expected to be associated with an improved safety profile. This is increasingly becoming of major interest to the informed patient.
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