Most commonly held theory for the formation of JID is similar to that of colonic diverticulosis; increased intraluminal pressures aوٴect weak areas of the wall, leading to extrusion of the mucosa and false diverticulum formation. On histological analysis, Edwards found disruption of the muscularis mucosae by the vasculature resulting in a weakening in the wall, or as he termed it “locus minoris resistentia”. Нis weak point allows for mucosal extrusion from the lumen, resulting in the “out-pouching.” Interestingly, the jejunum is known to have a larger diameter of vessels comprising the vasa recta supplying it. Нe larger diameter of the weakened site may contribute to the observation that diverticula are more common in the proximal small bowel than the distal. Once a point of decreased resistance has been created, elevated luminal pressures create aneurismal dilation of the intestinal wall, resulting in false diverticula. Krishnamurthy et al proposed a second theory of the pathophysiology of JID. In this study, small intestine samples of seven patients were examined under light microscopy to explore the possibility of smooth muscle dysfunction. Four of these patients were found to have fibrosis and decreased quantity of smooth muscle cells. Two more demonstrated fibrosis associated with degenerative smooth muscle cells.

Нe final patient sample had neuronal and axonal degeneration. Нese findings were consistent with those of progressive sclerosis, systemic neuropathy and visceral myopathy, respectively. Concomitant existence of autoimmune or motility disorders with JID suggests an association with the formation of the diverticula. Нe majority of patients with small bowel diverticulosis are noted to have isolated duodenal disease; in a 1997 retrospective study of two hundred eight patients, 79% of patients had isolated duodenal disease. 18% of patients had jejunoileal disease and 3% had the all three segments of small bowel aوٴected While the majority of this patient population is the elderly, there are more isolated documented cases of intestinal diverticula in children and in family groups. Нese cases have been used to postulate inherited, genetic, or embryological causes for the disorder. Anderson et al described a family of eight siblings, six of whom had small intestinal diverticula. Four subjects had concomitant immunologic diseases, specificall\ rheumatoid arthritis, ulcerative colitis, thyroiditis and non-viral hepatitis.

Barton et al reported a family of patients with JID in multiple generations. Six of 10 siblings in this cohort had symptomatic JID, and one symptomatic patient had monozygotic twin children with symptomatic JID suggesting an autosomal dominant inheritance pattern. Нis study included a pathology specimen demonstrating extensive true diverticula of the jejunum (Figures 1-3), suggesting a mechanism more consistent with that of Krishnamurthy.

Symptoms

While the majority of cases of JID are asymptomatic, patients can present with a multitude of symptoms. Tsiotos et al describe a series of 112 patients with JID, 47 of whom were diagnosed incidentally [10]. Of the remaining 65 patients, 45 presented with symptoms of malnutrition or chronic pain while the remaining 20 presented with acute complications of JID.

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