PREDICTION OF ACUTE RELAPSE OF CROHNS-DISEASE - A STUDY OF HOST NONSPECIFIC IMMUNE REACTIVITY

Authors
Citation
E. Rene, PREDICTION OF ACUTE RELAPSE OF CROHNS-DISEASE - A STUDY OF HOST NONSPECIFIC IMMUNE REACTIVITY, Canadian journal of gastroenterology, 7(2), 1993, pp. 226-231
Citations number
NO
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
08357900
Volume
7
Issue
2
Year of publication
1993
Pages
226 - 231
Database
ISI
SICI code
0835-7900(1993)7:2<226:POAROC>2.0.ZU;2-V
Abstract
In Crohn's disease, there is evidence of activation of immunological e ffector mechanisms in the mucosa. Currently, it is not clear if the ac tivated immunological processes are an appropriate response to an as y et unidentified pathogen or a pathologically increased response to a r elatively otherwise innocent challenge. The tissue damage characterist ic of Crohn's disease results from T cell-mediated granuloma formation , suggesting a delayed-type hypersensitivity reaction. However, data r egarding cellular immunity in Crohn's disease are not conclusive. Depr ession of delayed hypersensitivity was found by several authors, while others have reported normal skin-reactivity. It is still largely unkn own whether hyporesponsiveness, if present in Crohn's disease, is rela ted to clinical activity of the disease or caused by nonspecific mecha nisms such as malnutrition. A kinetic approach to the host factors was designed which analyzed the change of skin delayed hypersensitivity r eaction associated with three main evolutive events of Crohn's disease : period of stable remission; period preceding acute flare up; period preceding and following surgical resection of the diseased gut. Fluctu ations between anergic and hyperergic states were observed during Croh n's disease evolution. The influence of the host's immune response qua lity (expressed by skin delayed hypersensitivity) on the clinical cour se of Crohn's disease is discussed, and the folllowing hypothesis prop osed. The course of Crohn's disease would be dependent on the balance of phases of 'hyperergy' during which the pathogenic agents (not neces sarily specific) would easily induce acute flare-up with a high freque ncy of relapses, and alternatively phases of 'hypo-ergy' during which the pathogenic agents would hardly induce acute flare-up resulting in a low frequency of relapse. Alternatively, this hypothesis, based on d ifferences in the host response, may be the explanation of individual variation in the course of Crohn's disease. The ability to mount an im mune reaction woul be an individual characteristic and would lead to t he classic dual pattern of the course of the disease consistently foun d in different groups of patients, namely continuous course as opposed to intermittent or inactive disease.