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LESIONS OF THE GASTROINTESTINAL TRACT RESEMBLING REGIONAL ENTERITIS--A GRANULOMATOUS DISEASE; A REPORT OF THREE CASES.

Although regional enteritis classically involves the terminal ileum, lesions showing similar histology may involve other segments of the gastrointestinal tract, either independently or concomitantly with terminal ileum involvement. Histologically the basic reaction is non-specific chronic inflammation with a granulomatous component and a variable degree of fibrosis. Such lesions in the upper gastrointestinal tract resulted in nonspecific intestinal complaints and roentgenographically showed mucosal alterations and loss of normal motility. Those with colonic involvement were difficult to differentiate from ulcerative colitis, clinically and, in the early stages, roentgenographically. With more advanced involvement, roentgenographical diagnosis was possible.Three patients with lesions illustrating the aforementioned features were diagnosed and treated. One had lesions in the colon and terminal ileum. In the others the terminal ileum was not involved; in the second the stomach, duodenum and upper jejunum were involved, and in the third the colon was involved.

Colitis↗

Experimental regional enteritis in pigs.

Lymphatic obstruction is constantly present in regional enteritis, but its role in the pathogenesis is poorly understood. To clarify this the mesenterial lymphatics of the terminal ileum were obstructed in 21 pigs chosen for experiments because spontaneous ileitis is common in pigs. Long-lasting obstruction was produced by injecting formaline into regional lymph nodes. The growth of the pigs was retarded. Their ileum became reddish and oedematous with numerous intra-abdominal adhesions, and mucosal ulcerations. Eleven pigs developed fistulae; none had chylous ascites. Histologically the subserosa was infiltrated by round and giant cells giving an impression of granulomatous inflammation. Many lymphatics were thrombosed. The lymphoid tissue was hyperplastic. These changes became more prominent with extensive subserosal fibrosis after three weeks, when the oedema diminshed. Transmural inflammation with round cell aggregations was then the most typical feature. Purulent infection with crypt abcesses appeared near the fistulae. If the function of lymphatics is destroyed, transport of particles too big to enter blood vessels is inhibited. This produces chronic irritation and oedema with declining tissue nutrition and oxygenation, thus causing fibrosis. Moreover, the intestinal lumen is a source of infections, and the oedematous tissue is easily infected. This may lead to mucosal ulcerations and, progressively, to fistulae.

Animals↗

Effect of 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced ileitis on the motor function of non-inflamed rat gastric fundus.

During intestinal inflammation, motility disturbances are not restricted to inflamed regions, but may also occur in remote non-inflamed sites of the gastrointestinal tract. Our aim was to investigate the motor function of the gastric fundus after the induction of terminal ileitis in the rat. Ileal inflammation was induced by intraluminal installation of 2,4,6-trinitrobenzenesulphonic acid (TNBS) into the ileum. Inflammation was assessed both histologically and biochemically. Contractions and relaxations of longitudinal muscle strips from the gastric fundus were studied 36 h and 1 week later. During the acute phase of ileal inflammation (36 h), the non-inflamed stomach was distended. The contractility of longitudinal muscle strips of the gastric fundus was decreased due to a post-receptor defect. In addition, nonadrenergic noncholinergic (NANC) relaxations were inhibited due to neuronal dysfunction. Aortic contractility remained normal and the mere presence of food in the stomach did not account for the disturbed neuromuscular function in the gastric fundus. Ablation of extrinsic primary afferent neurones by capsaicin further impaired gastric fundus contractility. Transection and re-anastomosis of the jejunum reversed the effect of TNBS-induced ileitis on the neuromuscular function of the gastric fundus. One week after TNBS, cholinergic neurotransmission was increased in the gastric fundus. During acute ileitis, smooth muscle cell contractility and inhibitory NANC neurotransmission are inhibited in the non-inflamed gastric fundus. This phenomenon may be mediated by intrinsic connections within the enteric nervous system.

Animals↗