Abstract: . . .  analysis was stratified by various aspects of the phenotypic Vienna classification, 13 age >40 years at diagnosis (SMR 1.99 (95% CI, 1.4– 2.8)), colonic involvement at diagnosis (SMR 2.1 (95% CI 1.3–3.1)), and inflammatory disease behaviour at diag- nosis (SMR 2.2 (95% CI, 1.5–3.2)) all appeared to be associated with increased mortality risk. However, in a multivariate COMMENTARIES 447 www.gutjnl.com on . . .
. . .  has been made by Sander and colleagues. 1 Now, neurogastroenter- ological research must determine whether presynaptic inhibition in the ENS has the same significance for the common symptoms of food allergy, mucosal inflammation, and brain-gut interactions in stress in humans, as is known to exist in animal models. If this proves to be the case, then additional investigation will be needed to deter- mine if it . . .
. . .  this issue of Gut, reports their results for expression of histamine receptor subtypes in the human intestinal tract from normal individuals and patients with symptoms of the irritable bowel syndrome (IBS) and/or food allergies (see page 498). Work of this nature was overdue because most of the available histologi- cal and functional data for histamine receptors in the small and large intes- tine were obtained from animal models. The . . .
. . .  cases, the average age at entry into the cohort was 42 years (higher than the average age at diagnosis of Crohn’s disease of late 20s/early 30s in most studies), and the average follow up was only three years. A recent systematic review of ‘‘hard end points’’ in popula- tion based cohorts of Crohn’s disease concluded that there was no evidence for a significant change in disease out- come over the past 40 years. 9 To sum-  . . .
. . .  centres (SMR 2.0 (95% confidence interval (CI) 1.3–3.0)) than in southern ones (SMR 1.6 (95% CI 0.8–2.7)) but this difference was not statistically significant. When the SMR analysis was stratified by various aspects of the phenotypic Vienna classification, 13 age >40 years at diagnosis (SMR 1.99 (95% CI, 1.4– 2.8)), colonic involvement at diagnosis (SMR 2.1 (95% CI 1.3–3.1)), and inflammatory disease behaviour at diag-  . . .
. . .  Sci 1989;34:1462–5. 12 Siddiqui AA, Miner PB Jr. The role of mast cells in common gastrointestinal diseases. Curr Allergy Asthma Rep 2004;4:47–54. 13 Weston AP, Biddle WL, Bhatia PS, et al. Terminal ileal mucosal mast cells in irritable bowel syndrome. Dig Dis Sci 1993;38:1590–5. 14 Libel R, Biddle WL, Miner PB Jr. Evaluation of anorectal physiology in patients with increased mast cells. Dig Dis Sci 1993;38:877–81. 15 Miner PB Jr. The role of the mast . . .
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