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Small intestinal dysfunction has been described in patients with ulcerative colitis and in experimental animal models of colitis. This is demonstrated by a decrease in fluid, electrolyte, amino acid, fat and carbohydrate absorption as well as by deranged intestinal motility. Histopathological changes in the small intestines in colitis have not been consistently demonstrated, but there is evidence of structural and biochemical alterations as shown by increased intestinal permeability and a decrease in the expression of multiple brush border membrane enzymes such as disaccharidases and aminopetidases, in both humans and experimental animals. The pathophysiology of this dysfunction has not been elucidated, but it is thought to include alterations in neural circuitry such as increased neuronal excitability, neuronal damage and changes of neuropeptidergic innervation and receptors as well as an increase in local production of pro-inflammatory cytokines and alterations in the production of some neurohumoral mediators. In the following, we provide an update on the advancement of clinical and scientific contributions to elucidate the underlying mechanisms of the alteration of the functions of apparently intact small intestinal segments, induced by ulcerative colitis.

Impairment of Small Intestinal Function in Ulcerative Colitis: Role of Enteric Innervation