Crohn's disease: in defense of a microvascular aetiology

Abstract

There appears little doubt that microvascular ischaemia is involved in Crohn's disease. Studies have consistently demonstrated that the number of blood vessels and the total volume of blood feeding segments of bowel with Crohn's disease are reduced. However, the aetiology of the microvascular ischaemia is yet to be determined. Potential aetiological factors that appear to be disease specific include increased mesenteric platelet aggregation and increased platelet surface expression of P-selectin and GP53. However, there are several other factors known to be raised in active and quiescent disease for which disease specificity is not yet known, including increased submucosal endothelial endothelin-1 receptor expression, increased m RNA expression for several interleukins and cytokines including TNFalpha, increased PAF and thrombomodulin and finally altered cellular adhesion molecule expression. Proving cause and effect will always be a difficult task given the self-perpetuating nature of the inflammatory and coagulation cascades and our inability at present to identify persons who subsequently develop Crohn's disease at a point prior to mucosal inflammation. Results to date however, are supportive of each of these factors, alone or in combination playing an integral part in the development of microvascular ischaemia, a pathological process which appears to precede the classic changes which characterize Crohn's disease.