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Ninety-one patients with idiopathic constipation had segmental colonic transit studied with radiopaque markers using a new simplified technique to determine frequency and type of colonic transit time (CTT) abnormalities and to determine the utility of this test in planning therapy. Colonic transit studies defined four groups: normal CTT (N = 49), right colonic stasis (N = 16), outlet obstruction (N = 12), and isolated left colonic stasis (N = 14). Right colonic stasis and outlet obstruction were associated with frequent use of digital pressure to assist defecation. Right colonic stasis was characterized by a low stool frequency (less than 3 per week) in 93% of cases and failure to respond to bran therapy. Outlet obstruction also showed a poor response to bran therapy but weekly stool frequency was higher than 3 in 46% of cases. Normal colonic transit time and isolated left colonic stasis were characterized by a normal stool frequency (5.8 +/- 0.05 and 4.2 +/- 0.1, respectively) and clinical help with the use of bran treatment (72 and 64%, respectively). Our study suggested that patients who complain of idiopathic constipation represent a heterogenous group of disorders. Segmental CTT determination is a simple, useful, and noninvasive test of patients with constipation.

Background/aims-Cryptogenetic multifocal ulcerous stenosing enteritis (CMUSE) is a rare disease whose origin is unknown. The aim of this study was to describe the clinical spectrum of CMUSE, to determine the origin and pathophysiology of the disease, and to propose a treatment strategy. Methods-A total of 220 French gastroenterology departments were contacted to review patients with unexplained small bowel strictures. Of 17 responses, 12 corresponded to a diagnosis of CMUSE. These patients were hospitalised between 1965 and 1993 and their medical records were reviewed. Results-All patients (mean age 42.1 (4.4) years) had intestinal and five had extraintestinal symptoms (peripheral neuropathy, buccal aphthae, sicca syndrome, polyarthralgia, Raynaud's phenomenon, arterial hypertension). One patient had heterozygous type I C2 deficiency (28 base pair gene deletion). Two to 25 (mean 8.3 (1.9)) small intestine strictures were found. Stenoses of the large jejunoileal arteries were observed on two and aneurysms on three of five mesenteric angiograms. Despite surgery, symptoms recurred in seven of 10 patients and strictures in four. Steroid therapy was eVective but caused dependence. One untreated patient died. Small bowel pathology showed superficial ulceration of the mucosae and submucosae, and an inflammatory infiltrate made of neutrophils and eosinophils. Conclusions-CMUSE is an independent entity characterised by steroid sensitive inflammation of the small bowel which often recurs after surgery. CMUSE may be related to a particular form of polyarteritis nodosa with mainly intestinal expression or with an as yet unclassified vasculitis. (Gut 2001;48:333-338)

1 The toxic e ects of nonsteroidal anti-in¯ammatory drugs for the lower gastrointestinal tract share certain features with in¯ammatory processes, suggesting that the release of in¯ammation cytokines such as TNF-a may damage the intestine. 2 Rats received a s.c. injection of indomethacin. Then, jejunum-ileum was taken up for the quanti®cation of ulcerations, production of TNF-a, nitrites and PGE2 ex vivo and activity of calciumindependent NO synthase and myeloperoxydase. Activation of NO metabolism and myeloperoxydase were measured as potential e ectors of TNF-a. 3 Jejunum-ileum from rats having received indomethacin (10 mg kg 71 ) produced TNF-a ex vivo. Cytokine production was associated with the onset of macroscopic ulcerations of the small intestine, and preceded nitrite production and tissue activity of myeloperoxidase. 4 Similar intestinal ulcerations and upregulation of TNF-a were obtained with¯urbiprofen (30 mg kg 71 ), chemically unrelated to indomethacin. 5 TNF-a production was proportional to the indomethacin dose (from 3 ± 20 mg kg 71 ) and correlated with the surface area of ulcerations and nitrite production, 24 h after indomethacin administration. 6 Pretreatment of rats with RO 20-1724, a type-IV phosphodiesterase inhibitor which inhibits TNF-a synthesis, substantially reduced jejunum-ileum ulcerations, TNF-a and nitrite production and tissue enzyme activities. 7 These ®ndings provide evidence that TNF-a is increased in indomethacin-induced intestinal ulcerations and support suggestions that TNF-a is involved at an early stage of nonsteroidal antiin¯ammatory drug toxicity for the small intestine.