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PubMed1985

Cytomegalovirus infection of the colon: a possible role in exacerbations of inflammatory bowel disease.

An exacerbation of idiopathic inflammatory bowel disease associated with the appearance of cytomegalovirus nuclear inclusion bodies in the colon was observed in two patients. In one, improvement in the colitis after withdrawal of corticosteroids suggested cytomegalovirus as the cause of the exacerbation. A review of the 16 reported cases of inflammatory bowel disease with cytomegalovirus superinfection of the colon indicates a high mortality rate (seven of 16), a frequent association with toxic dilatation of the colon, and a clinical course sufficiently severe to require colectomy in 10 of 16 patients. For exacerbations of inflammatory bowel disease associated with evidence of cytomegalovirus infection of the colon which are refractory to medical management withdrawal of corticosteroids and other immunosuppressive therapy should be considered. If necessary, early colectomy may be an appropriate alternative.

Adolescent↗

PubMed2002

[Immunohistologic changes of the intestinal mucosa in chronic inflammatory bowel diseases].

In the pathogenesis of inflammatory bowel disease abnormally increased immune reactions in the intestinal mucosa play a basic role. The revealing of these reactions was facilitated by the rapidly spreading immunohistological methods in last decades. This review discusses in detail the characteristic distribution of lymphocyte subsets and plasma cells in Crohn's disease and ulcerative colitis. Results indicating increased expression of adhesion molecules are also presented, as well as the different patterns of cytokine production in Crohn's disease and ulcerative colitis. The rapid epithelial turnover developing as a consequence of increased rate of proliferation and apoptosis in inflammatory bowel disease is also shown. The epithelial expression of MHC II antigen in colonic mucosa which is not observed in healthy subjects is also discussed. In addition, the pathogenetic role of lost oral tolerance in the development of inflammatory bowel is reviewed in detail.

Chronic Disease↗

PubMed1985

Metabolism of arachidonic acid in acetic acid colitis in rats. Similarity to human inflammatory bowel disease.

We recently reported that human inflammatory bowel disease mucosa contains large amounts of leukotriene B4, a potent chemotactic agent formed from arachidonic acid through the lipoxygenase pathway. To more fully evaluate the role of arachidonic acid metabolites in the mediation of intestinal inflammation, we studied arachidonate metabolism in an animal model: acetic acid colitis in the rat. Incubation of acetic acid colitis mucosa with arachidonic acid resulted in the production of leukotriene B4 and a series of monohydroxy fatty acids, all products of the lipoxygenase pathway, plus much smaller amounts of cyclooxygenase products including prostaglandin E2. All of these metabolities were made in significantly greater quantities by mucosa from acetic acid-treated rats than by controls. The pattern of arachidonate metabolism in acetic acid colitis was strikingly similar to that in human inflammatory bowel disease. Moreover, the concentration of leukotriene B4 in acetic acid-treated mucosa was almost identical to that in human inflammatory bowel disease mucosa and was 50 times greater than that in normal rat colonic mucosa. These data indicate that lipoxygenase products, including leukotriene B4, may be important mediators of intestinal inflammation in a wide variety of inflammatory conditions. Moreover, the similarities in the metabolism of arachidonate by human inflammatory bowel disease and by acetic acid colitis may allow the use of this model, and perhaps other animal models of intestinal inflammation, in the screening of potential therapeutic agents for inflammatory bowel disease.

Acetates↗

PubMedDate not supplied

A report on efficacy and safety of azathioprine in a group of inflammatory bowel disease patients in northwest Greece.

BACKGROUND/AIMS: Inflammatory bowel disease has a variable severity and in a group of patients a second-line treatment with immunosuppressive agents, such as azathioprine is required. The aim of the present study was to determine the efficacy and safety of long-term azathioprine treatment in inflammatory bowel disease patients unresponsive to steroids. METHODOLOGY: We investigated the efficacy of azathioprine in controlling the disease relapse (in combination with other drugs) in 29 patients with inflammatory bowel disease (16 with ulcerative colitis and 13 with Crohn's disease). Patients, who were started on azathioprine in combination with steroids, were those who were resistant to steroids. After controlling the acute phase, steroids were discontinued or reduced in very low doses (up to 4 mg methylprednisone per day) and azathioprine was administered in combination with mesalamine for a period of 12-48 months. RESULTS: Azathioprine (in combination with 5-ASA products and steroids) succeeded in controlling the acute relapse in 24 of 29 patients [82.75%, 15/16 (93.7%) with ulcerative colitis and 9/13 (69.2%) with Crohn's disease]. Of the patients who achieved remission, this was maintained for 1 year at least. Only one case of pancreatitis and one with vomiting and diarrhea were noted a few months after the initiation of therapy and azathioprine was discontinued. CONCLUSIONS: Azathioprine is an effective agent which controls acute relapse of inflammatory bowel disease in many cases in combination with other drugs. Long-term remission can be achieved. Side effects are uncommon.

Azathioprine↗

PubMed2003

[Laboratory diagnosis in inflammatory bowel disease].

The assessment of disease activity in inflammatory bowel disease is done using clinical parameters and various biological disease markers. Classical disease markers including erythrocyte sedimentation rate, acute phase proteins, such as orosomucoid and CRP, leukocyte and platelet counts, play an important role in the monitoring of disease activity. Furthermore, the determination of zinc, iron, ferritin, vitamin B12, and folic acid is important to avoid deficiencies in patients with severe disease or after surgeries. Stool cultures are helpful to detect bacterial or parasitic infections mimicking inflammatory bowel disease. The detection of specific antibodies such as pANCA, PAB and ASCA is helpful for the differential diagnosis Crohn's disease--ulcerative colitis.

Acute-Phase Proteins↗

PubMed2005

[Probiotics and prebiotics for the treatment of inflammatory bowel disease].

Although the causes of inflammatory bowel disease including ulcerative colitis and Crohn's disease remain incompletely understood, increasing evidence implicates intestinal microflora in the pathogenesis of this disorder. Therefore, modulation of microflora with probiotics or prebiotics may offer a plausible therapeutic approach. While recent data support a potential therapeutic efficacy, such treatments need to be further assessed by large scale studies. A better understanding of the intestinal microflora and the mechanisms of their action may help us to develop more effective treatment for inflammatory bowel disease.

Bifidobacterium↗

PubMed1996

[Chronic inflammatory bowel diseases and nutrition].

The etiology of inflammatory bowel disease is still unknown. Several potential mechanisms are discussed. The etiological and therapeutic importance of nutrition is controversial. Though changes in dietary habits and incidence of inflammatory bowel disease during the last century were in parallel, no specific nutritional factor has been isolated. No dietary prophylaxis of inflammatory bowel disease is yet known; all dietary therapies in inflammatory bowel disease aim to improve nutritional support and to diminish inflammation by bowel rest. Children and adolescents gain in weight and height. Total parenteral nutrition will not substantially reduce disease activity and operation rates. Total parenteral nutrition can only be recommended in ulcerative colitis patients with severe disease in the initial phase and in Crohn's patients with severe malnutrition and intestinal complications. Enteral nutrition support is less effective in ulcerative colitis than in Crohn's disease. Reported remission rates on enteral nutrition are 25% for ulcerative colitis and up to 80% for Crohn. However, in active Crohn's disease enteral nutrition is less effective than standard therapy with methylprednisolone and sulfasalizine. It is generally believed that nutrition therapy in combination with drugs is the best treatment modality. There is no evidence to support the importance of any combination of the formula diets such as elemental, oligopeptide, or polymeric formulations. Administration of formula diets by nasogastric tubes all show similar remission rates. Whether newer diets supplemented with arginine, glutamine, omega-3-fatty acids or short chain fatty acids increase remission rates is not known. Further studies in this field are warranted.

Adolescent↗

PubMed1986

Indications for and results of operation in inflammatory bowel disease.

Of 363 patients with inflammatory bowel disease presenting between 1972 and 1983, 166 required definitive operation. A classification by histological type distinguishes Crohn's disease (CD) from ulcerative colitis (UC) and indeterminate inflammatory bowel disease. CD is divided into predominantly ileal disease (81), total or subtotal colonic disease (74) and distal disease (22), whilst UC is classified into colonic (95) or distal disease (63). Most patients with ileal disease required operation for chronic persistent symptoms. In patients with total colonic involvement a greater proportion of patients with CD than those with UC came to surgery. Very few patients with distal disease required surgery. After resection for ileal disease there was a low incidence of anastomotic leakage (3%) and no operative mortality. There was an overall operative mortality of 8% after colonic resection. This was much lower in the non-urgent cases but rose to 12% in urgent cases.

Colitis, Ulcerative↗

PubMed1997

Human colonic microvascular endothelial cells is a model of inflammatory bowel disease.

BACKGROUND: The pathophysiology of inflammatory bowel disease remains elusive primarily because of the limitations of the models available for study in the basic science laboratories. We propose a new model for the study of inflammatory bowel disease. DATA SOURCES: Research and review articles published in the English literature. CONCLUSIONS: The human colonic microvascular endothelial cell in culture is a legitimate model for the study of the human colon in the normal and diseased states.

Bradykinin↗

PubMed1997

Computed tomography in chronic inflammatory bowel disease.

In children with complicated inflammatory bowel disease, conventional ultrasound imaging may not define the extent of extraluminal disease and the involvement of other viscera. Three children with chronic inflammatory bowel disease are presented, where computed tomography was well tolerated and provided valuable information on extraluminal disease, involvement of other organs, and the state of the bowel wall and mesentery. In children in whom ultrasound examination is inconclusive or limited by gas or tenderness, computed tomography can provide important information that may determine clinical management.

Adolescent↗

PubMed2004

Characterization of colonic and mesenteric lymph node dendritic cell subpopulations in a murine adoptive transfer model of inflammatory bowel disease.

Ulcerative colitis and Crohn's disease, collectively termed inflammatory bowel diseases (IBD), are chronic inflammatory diseases of the intestine that afflict more than 4 million people worldwide. Intestinal inflammation is characterized by an abnormal mucosal immune response to normally harmless antigens in the gut flora. In Crohn's disease, the pathogenic mucosal immune response is a typical T helper (TH1) type cell response, whereas ulcerative colitis is predominantly associated with a TH2 response. We are interested in the role of dendritic cells in early immunologic events leading to T cell activation and chronic intestinal inflammation. Using a murine adoptive transfer model of IBD, we found an accumulation of dendritic cells in colon and mesenteric lymph nodes during the early stage of IBD before the appearance of epithelial lesions and tissue degradation. In situ immunostaining and flow-cytometric analysis revealed that approximately 50% of colonic dendritic cells were CD11b B220 myeloid dendritic cells and 50% expressed the CD11b B220 plasmacytoid phenotype. In corresponding mesenteric lymph nodes, approximately 16% were plasmacytoid dendritic cells. Colonic myeloid dendritic cells were shown to express the co-stimulatory molecule CD40. Both, colonic myeloid and plasmacytoid dendritic cells released interferon-alpha in situ and stimulated T cell proliferation ex vivo. Our results show that dendritic cells can mature in the intestine without migrating to mesenteric lymph nodes. Mature intestinal dendritic cells may form a nucleation site for a local T cell response and play an important role in the pathogenesis of IBD.

Animals↗

PubMed2006

Alterations of mesenchymal and endothelial cells in inflammatory bowel diseases.

The pathogenesis of complex chronic diseases like inflammatory bowel disease (IBD) can no longer be viewed as a one-way street in which classical immune cells have exclusive control over the initiation, duration and outcome of the disease. There is enough experimental evidence to demonstrate that nonimmune cells, among which are mucosal mesenchymal and endothelial cells, also play a decisive role by interacting with immune cells and establishing a two-way reciprocal exchange of signals and responses that dictate the ultimate outcome of inflammation. Smooth muscle cells and fibroblasts/myofibroblasts display a variety of immune functions and modulate the activity and survival of T-cells. Mucosal microvascular cells, through the expression of adhesion molecules and secretion of chemokines, regulate the quantity and quality of leukocytes transmigrating into the interstitial space. A number of receptor-ligand pairs are expressed by immune and nonimmune cells that control their functional interplay, but the CD40/CD40 ligand system may be the most effective because CD40 is expressed by activated muscle and endothelial cells, while the CD40 ligand is expressed by activated T-cells and platelets. The activation of this system in IBD can lead to the establishment of a continuous cycle of nonimmune cell-dependent, antigen-independent interactions that perpetuates gut inflammation.

Animals↗

PubMed2001

Seroprevalence of Schistosoma mansoni in Puerto Ricans with inflammatory bowel disease.

BACKGROUND: The etiology of Inflammatory Bowel Diseases, Crohn's disease (CD) and ulcerative colitis (UC), is unknown. These diseases have a higher incidence in industrialized countries and their pathogenesis involves an over-reaction of the immune system. A genetic factor is believed to predispose to the development of chronic inflammation in response to an unidentified stimulus. Exposure to infections in childhood may modulate future immune responses. Parasitosis, particularly Schistosomiasis, stimulate Th2 immune responses. It has been hypothesized that the absence of these parasitic infections, as seen in economically developed countries, favors a Th1 response that may result in the clinical appearance of Crohn's disease later in life. OBJECTIVE: To determine the prevalence of Schistosoma mansoni antibodies in Puerto Ricans with Inflammatory Bowel Disease and controls. METHODS: Serum from 92 Puerto Ricans with IBD and 106 controls was screened for S. mansoni adult microsomal antigens (MAMA) using the FAST:ELISA assay. Those positive were confirmed with an enzyme-linked immunoelectrotransfer blot test. RESULTS: Seven serum samples (3 UC and 4 controls) were positive for S. mansoni antibodies. There was no significant difference between groups in gender, municipality of origin or seroprevalence of Schistosomiasis. The control group was slightly older than the IBD group. CONCLUSIONS: Our study did not demonstrate an inverse relation between Schistosomiasis and IBD. However, the decreasing prevalence of Schistosomiasis in the general population of Puerto Rico may account for this result.

Adult↗

PubMed2003

Immune networks in animal models of inflammatory bowel disease.

The animal models of inflammatory bowel disease provide a framework to define the immunopathogenesis of intestinal inflammation. Studies in these models support the hypothesis that exaggerated immune responses to normal enteric microflora are involved in the initiation and perpetuation of chronic intestinal inflammation. A major pathway involves development of acquired immune responses by the interactions of CD4+ T-cell receptor alphabeta T cells with antigen-presenting cells (dendritic cells). Immunoregulatory cells, including Tr1 cells, Th3 cells, and CD4+ CD25+ T cells and B cells, directly or indirectly affect the T-cell receptor alphabeta T cell-induced immune responses and bridge innate and acquired immunity. The study of these complicated immune networks provides the rationale for the development of new therapeutic interventions in inflammatory bowel disease.

Animals↗

PubMedDate not supplied

Different distribution of mast cells and macrophages in colonic mucosa of patients with collagenous colitis and inflammatory bowel disease.

BACKGROUND/AIMS: Chronic inflammatory cells in colonic mucosa is a histopathologic feature in patients with collagenous colitis and inflammatory bowel disease. The aim of this study was to compare the distribution of mast cells and macrophages in the colonic mucosa of patients with collagenous colitis, Crohn's disease, and ulcerative colitis. METHODOLOGY: Patients with histologically confirmed collagenous colitis (n = 13), Crohn's disease (n = 20) or ulcerative colitis (n = 20) and normal control patients (n = 20) were included in this study. Biopsy specimens were obtained from the sigmoid colon of each patient, and immunostained using antibodies to tryptase (AA1) and CD68. The number of mast cells and macrophages located in upper and lower part of the lamina propria was determined. RESULTS: The number of mast cells in the upper part of lamina propria in patients with collagenous colitis (286 +/- 89/mm2, mean +/- SD), Crohn's disease (330 +/- 84/mm2) and ulcerative colitis (355 +/- 90/mm2), was higher than normal controls (201 +/- 44/mm2). The number of mast cells in the lower part of lamina propria in patients with Crohn's disease (345 +/- 87/mm2) and ulcerative colitis (363 +/- 86/mm2) was higher than collagenous colitis (266 +/- 63/mm2) and normal controls (309 +/- 60/mm2). The number of macrophages in the lower part of lamina propria in patients with Crohn's disease (330 +/- 63/mm2) and ulcerative colitis (301 +/- 60/mm2) was higher than in collagenous colitis (247 +/- 46/mm2) and normal controls (242 +/- 52/mm2), although there were no significant differences in the number of macrophages present in the upper part of the lamina propria among the four groups. CONCLUSIONS: Our data showed the presence of a different distribution of mast cells and macrophages in collagenous colitis and inflammatory bowel disease, and these suggest that because mucosal mast cells have been implicated in the development of Th2 response collagenous colitis is more of a Th2 type reaction rather than Th1.

Adult↗

PubMed2001

Inflammatory bowel disease and pregnancy.

Most women with inflammatory bowel disease who desire to become pregnant can expect to conceive successfully, carry to term, and deliver a healthy infant. However, the management of inflammatory bowel disease during pregnancy remains challenging, and some women with ulcerative colitis or Crohn's disease will have difficulty becoming pregnant or have increased disease symptoms while pregnant. Control of disease activity before conception and during pregnancy is critical to optimize both maternal and fetal health. The natural history of inflammatory bowel disease during pregnancy will be reviewed and the medical and surgical therapy discussed.

Adult↗

PubMed1990

Outpatient health care utilization of patients with inflammatory bowel disease.

On the basis of the normal life expectancy of inflammatory bowel disease patients, the early onset of their disease, and the variety of symptoms, inflammatory bowel disease patients were anticipated to be frequent users of outpatients services. This study assesses (1) the characteristics, (2) outpatient health care utilization, and (3) the degree of satisfaction with health care of inflammatory bowel disease patients compared to patients with other gastrointestinal disease. The study method was a secondary analysis of data collected on 395 patients attending the University of Calgary Gastroenterology Outpatient Clinic in 1988. Inflammatory bowel disease patients were significantly younger (P less than 0.001) and better educated (P less than 0.05) than other patients. During the past year inflammatory bowel disease patients consulted significantly more often with their gastroenterologist (P less than 0.001) and spent more time in hospital (P less than 0.05) than other patients. Inflammatory bowel disease patients also consulted more frequently with herbalists and naturopaths. Lastly, inflammatory bowel disease patients were as satisfied with the health care they received as other patients. These results provide information useful for health care planners as well as for those dealing directly with inflammatory bowel disease patients.

Adolescent↗

PubMed2006

Evaluation of short-term responsiveness and cutoff values of inflammatory bowel disease questionnaire in Crohn's disease.

BACKGROUND: The inflammatory bowel disease questionnaire (IBDQ) is a frequently used outcome parameter in clinical trials. Whereas the validity and reproducibility of the IBDQ have been extensively studied, there are limited data on its short-term responsiveness and cutoff values for remission and partial clinical response. METHODS: The IBDQ score and its bowel (BD), systemic (SysD), emotional (ED), and social (SocD) dimensions were tested for responsiveness in a cohort of 224 patients with Crohn's disease (CD) treated with infliximab for refractory luminal disease. Changes in the IBDQ score and its dimensions 4 weeks after therapy were analyzed and correlated with changes in the Crohn's Disease Activity Index (CDAI). The responsiveness ratios of the IBDQ and its dimensions were analyzed. Using regression line with DeltaCDAI, the cutoff values for the IBDQ remission and response were calculated. RESULTS: Overall, there was a good correlation between the CDAI and IBDQ at week 0 (correlation coefficient, 0.69; P < .001) and week 4 (-0.76; P < .001) and change after 4 weeks (0.74; P < .001). The correlation coefficients for DeltaCDAI and changes in BD, SysD, ED, and SocD were 0.753, 0.552, 0.620, and 0.631, respectively; all P < 0.001. The responsiveness ratios for DeltaIBDQ, BD, SysD, ED, and SocD were 2.6, 2.1, 1.9, 1.7, and 1.9, respectively. Regression line for the IBDQ (r = -0.76, P < .001) resulted in a cutoff value for remission of 168 points and for DeltaIBDQ resulted in a cutoff value of 22 and 27 points for clinical improvement based on DeltaCDAI > or = -70 and > or = -100 points. CONCLUSIONS: The IBDQ is a responsive instrument for reflecting quick change in the quality of life of patients with CD. Cutoff values for the IBDQ remission and partial response were 168 and > or = 27 points.

Adult↗