Giant inflammatory polyps associated with idiopathic inflammatory bowel disease

Five cases of giant inflammatory polyps associated with idiopathic inflammatory bowel disease are reported. Polyps produced intestinal obstruction in three cases; consequently, surgery was performed. In a further two cases, intestinal bleeding was improved by endoscopic polypectomy. Electron microscopy showed fibroblasts, myofibroblasts, mast cells, lymphocytes, collagen fibers, capillaries, and venules. Remnants of the original mucosal epithelial cells, smooth muscle cells, and hypertrophic autonomous nerve plexuses were noted. Nerve fibers were interwoven with the matrix of the polyps. Mast cells were closely linked with vessels, nerves, and collagen fibers. They may have an important role in the excessive granulation, angiogenesis, and fibrotic process in giant inflammatory polyps.     

Extraintestinal manifestations of idiopathic inflammatory bowel disease

Ulcerative colitis and Crohn's disease have reported associations with a spectrum of extraintestinal diseases. This association has been appropriately termed as extraintestinal manifestations because large case studies have demonstrated that between 25% to 36% of patients with either type of inflammatory bowel disease will have at least one such associated disease. The spectrum of diseases reported associated with either ulcerative colitis or Crohn's disease involves many organ systems. Some of these extraintestinal manifestations are related to active colitis--joint, skin, ocular, and oral; small bowel dysfunction--cholelithiasis and nephrolithiasis; and nonspecific manifestations such as amyloidosis and hepatobiliary diseases. The purpose of this review is to update the clinicians with the most recent literature concerning the etiology, clinical course and the therapy of the extraintestinal manifestations associated with both forms of idiopathic inflammatory bowel disease.     

Marital idiopathic inflammatory bowel disease. Crohn's disease in a husband and wife

Two cases of Crohn's disease in a husband and wife are described and compared with the seven previously reported cases of chronic idiopathic inflammatory bowel disease occurring in spouses.     

Intestinal mast cell responses in idiopathic inflammatory bowel disease

Mucosal and submucosal mast cell hyperplasia is a feature of the chronic inflammatory bowel diseases—ulcerative colitis and Crohn's disease. The mast cells are often seen to be degranulated in areas of active disease, suggesting that the inflammatory mediators released from these cells contribute to the pathophysiology of these disorders. We examined the hypothesis that epithelial cell-derived proteins, intestinal epithelial cell-associated components (ECAC), interact with the mast cells of patients with chronic inflammatory bowel disease to trigger the local release of mast cell mediators. Aliquots of human intestinal mucosal mast cell suspensions obtained from surgically resected specimens of colon or small intestine (ulcerative colitis, 12; Crohn's disease, 3; histologically normal controls, 8) were incubated with 1–100 μg/ml of colon or small bowel-derived murine ECAC or control kidney protein, or 1 μg/ml goat anti-human IgE positive control for 30 min at 37°C. Supernatants were analyzed in duplicate for histamine content by fluorometric assay. The median percent total histamine released by chronic inflammatory bowel disease mast cell suspensions to colonic epithelium-derived protein (ECAC-C) was 4% histamine (range 0–20%), such that the distribution of histamine release values in inflammatory bowel disease specimens was significantly different from the distribution of values in mast cells taken from normal mucosa (median 0%,P<0.05). The median histamine release by all chronic inflammatory bowel disease specimens was also increased in response to the ECAC preparations derived from small bowel epithelium in that a third of the inflammatory bowel disease specimens showed greater than 10% histamine release to ECAC. Normal controls did not respond to either the ECAC preparations or to the kidney protein (median 0%). Our data suggest that epithelial protein-induced release of intestinal mast cell mediators may contribute to the inflammation in these chronic gastrointestinal disorders.     

Period and generation effects on mortality from idiopathic inflammatory bowel disease

To test the hypothesis that environmental factors play a role in idiopathic inflammatory bowel disease (IBD), age, period, and generation (cohort) effects on IBD mortality in the United Kingdom and the United States were examined. The crude death rate of ulcerative colitis has declined since 1930. Plotted versus the year of birth, its age-specific death rates showed an initial rise in successive generations born between 1850 and 1900, followed by a fall in all later generations. The crude death rate of Crohn's disease increased from 1950 to 1974 and then declined. When the age-specific death rates for Crohn's disease and ulcerative colitis were superimposed, the mortality from Crohn's disease in each age group or sex began to decline at a different time, but always upon reaching the level of mortality from ulcerative colitis. It appears as if the gradual disappearance of an ulcerative colitis-associated factor in a birth-cohort fashion prevented a further rise in mortality from Crohn's disease after 1974.This study was supported by grant So 172/1-1 from the Deutsche Forschungsgemeinschaft. Part of this work was presented at the 89th meeting of the American Gastroenterological Association in New Orleans, May 16, 1988 (1).     

Thrombosis and inflammatory bowel disease.

Interaction between thrombosis and inflammation is increasingly recognized. With this, interest has arisen in the role of thrombosis in inflammatory conditions, including the inflammatory bowel diseases. Although the association between active inflammatory bowel disease and thromboembolic complications has long been known, there has been a resurgence in research into the role of thrombosis and the hemostatic system in the pathogenesis of both ulcerative colitis and Crohn's disease. Here we review the increased frequency of thromboembolic complications occurring in patients with inflammatory bowel disease; whether thrombosis might play a part in the initiation and maintenance of inflammation in inflammatory bowel disease; abnormalities of the coagulation system found in patients with inflammatory bowel disease; platelet dysfunction in inflammatory bowel disease; the mechanisms by which hemostatic processes might be proinflammatory in inflammatory bowel disease; and how these interactions might impact not only on the prevention of complications, but also on the treatment of the underlying inflammation in inflammatory bowel disease.     

Exercise and inflammatory bowel disease.

Crohn's disease and ulcerative colitis are both idiopathic inflammatory bowel diseases (IBDs) that affect 0.5% of Canadians. As yet, there is no known cure for either disease, and symptoms are treated with an array of medicines. The objective of the present review was to present the role of exercise and its impact on all facets of IBD. Exercise has been speculated to be protective against the onset of IBD, but the literature is inconsistent and weak. Preliminary studies reveal that exercise training may be beneficial to reduce stress and symptoms of IBD. Current research also recommends exercise to help counteract some IBD-specific complications by improving bone mineral density, immunological response, psychological health, weight loss and stress management ability. However, the literature advises that some patients with IBD may have limitations to the amount and intensity of exercise that they can perform. In summary, exercise may be beneficial to IBD patients, but further research is required to make a convincing conclusion regarding its role in the management of IBD and to help establish exercise regimens that can account for each IBD patient's unique presentation.     

Chlamydiae and inflammatory bowel disease.

No association was found between inflammatory bowel disease and infection with C. trachomatis or C. psittaci when patients were tested for the presence of these organisms using immunohistological, cell culture isolation, and serological techniques.     

Pathogenic factors in inflammatory bowel disease. 2. Crohn's disease.

Clues from patient and experimental animal studies suggest that events occurring early in the pathogenesis of Crohn's disease are related to an inability of the immune system to eradicate one or a number of luminal antigens resulting in persistent T cell and macrophage activation. Whether the primary abnormality rests with the nature of the luminal antigen, disturbances of antigen uptake by the mucosa, antigen handling by macrophages, or macrophage-T cell interactions remains unresolved. Given the heterogeneity of clinical presentations and experimental data, Crohn's disease may be a group of disorders associated with a number of primary defects.     

胰高血糖素样肽-2与炎症性肠病

炎症性肠病(IBD)是一组病因不明的慢性肠道炎症性疾病。胰高血糖素样肽-2(glucagon-like peptide-2,GLP-2)是胰高血糖素原(PG)基因的表达产物之一,近年来发现GLP-2具有促进肠黏膜增长、抑制炎性介质表达的作用,这可能为炎症性肠病的治疗开辟新的途径。     

Corticosteroids in inflammatory bowel disease. A review

Corticosteroids have been used for decades in the treatment of inflammatory bowel disease. Despite considerable information on the clinical response to corticosteroids in inflammatory bowel disease, much less is known concerning corticosteroids' effects on the underlying immunopathology of the disease. In this review, we discuss the known immunologic actions of corticosteroids: their effects on eicosanoid production and on modulating the humoral and cellular immune response. After reviewing the postulated immunological aberrations in inflammatory bowel disease, we speculate on the specific immunologic effects of corticosteroids in this disease.     

磷脂酶A2受体与特发性膜性肾病

特发性膜性肾病(IMN)是一种以肾小球毛细血管袢上皮侧免疫复合物沉积为特征的肾小球疾病,其致病抗体抗M型磷脂酶A2受体1(PLA2R1)抗体的发现使得IMN的诊断、预后判断和病情监测等方面取得突破性的进展。全基因组关联研究发现HLA-DQA1和PLA2R1是IMN的易感基因,进一步明确IMN的遗传学背景。最近研究发现PLA2R上引发免疫反应的主要抗原表位。本文就PLA2R与IMN的研究进展作一综述。     

High-sensitivity C-reactive protein in paediatric inflammatory bowel disease

AIM:To study whether high-sensitivity C-reactive protein(hs-CRP) measurement can aid the assessment of disease activity and glucocorticoid treatment in paediatric inflammatory bowel disease(IBD).METHODS:CRP levels were measured in 39 children with IBD undergoing colonoscopy [median age 12.8 years,Crohn's disease(CD) n=20],in 22 other children with IBD followed for acute response to glucocorticoids,and in 33 paediatric non-IBD patients.When standard CRP level was below detection limit(<5mg/L),hs-CRP was anal...     

Smoking and inflammatory bowel disease. A case control study.

A population case controlled study of smoking habits at the time of diagnosis was done in 260 patients with ulcerative colitis and 144 with Crohn's disease. Smokers had a decreased risk of acquiring ulcerative colitis in comparison with never smokers (relative risk 0.7) which appeared to be dose dependent. In former smokers a rebound effect was seen, especially in former heavy smokers, where the risk was sharply increased (relative risk 4.4). No sex difference was recorded. Smoking doubled the risk of acquiring Crohn's disease without any dose dependent pattern. In former smokers a non-significantly increased risk was observed. This might be caused by a carry over effect after stopping smoking, however, which possibly is reduced by time. No sex difference was seen.