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Summary The pathogenesis of ulcerative colitis has been interpreted in terms of histamine‐release phenomena. The dominant alterations of the colon are congestion and œdema. These, together with muscular excitation, can be explained in terms of the known effects of histamine‐release agents in experimental animals. Superficial ulceration is thought to be due to simple excoriation of œdematous and congested mucosa. Deep ulceration probably arises from strains due to stretching of the mucosa where it is more firmly attached over the muscular tæniæ and in the crypts between the rugæ. In support of this interpretation is the relative absence of inflammatory cells in the submucosa until ulceration occurs. The nature of the syndrome is thought to be within the realm of the psychosomatic disorders. Augmented barrages of nervous impulses during stress may give rise to excessive production of acetylcholine in the colon, which then reacts with the tissue mast cells causing the phenomenon of “histamine‐release”. Return to normal does not take place when the stress passes if the congestion and œdema have been present for long enough to permit some fibrosis to occur in the submucosa.
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McGovern et al. (1957) studied this question.
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