Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INFLAMMATORY BOWEL DISEASE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed2003

Homocysteine, cysteine, and glutathione in human colonic mucosa: elevated levels of homocysteine in patients with inflammatory bowel disease.

The present study was performed to evaluate the levels of the amino thiols cysteine, homocysteine, and glutathione in the colonic mucosa of patients with various intestinal diseases, especially chronic inflammatory bowel disease. Colonic biopsies of macroscopically normal mucosa out of a proximal and distal segment were collected from 187 patients with various intestinal diseases. Protein was assayed in duplicate by the method of Lowry et al (1951), using bovine serum albumin as standard. Total glutathione, cysteine, and homocysteine were quantified by high performance liquid chromatography (HPLC) with fluorescent detection. Only in patients with inflammatory bowel disease were the homocysteine levels in the large bowel mucosa significantly elevated compared with the concentrations in patients with normal mucosa. No significant differences were seen for glutathione and cysteine concentrations in colonic mucosa among the different groups of diseases. No correlation was found between the age of the patients and levels of the amino thiols investigated. GSH content and concentrations of cysteine and homocysteine were similar in male and female subjects. In our study markedly elevated concentrations of homocysteine in the colonic mucosa were observed in patients suffering from ulcerative colitis and Crohn's disease. This finding has been reported already in the literature for plasma homocysteine levels. Increased homocysteine levels in the colonic mucosa and plasma of patients with inflammatory bowel disease may play a role in the pathogenesis of Crohn's disease and ulcerative colitis.

Adolescent↗
PubMed1990

Inflammatory bowel disease and irritable bowel syndrome.

The irritable bowel syndrome accounts for 30 to 50 per cent of patients cared for by gastroenterology practices. Irritable bowel syndrome is more common than inflammatory bowel disease. Therefore, it should not be surprising that some patients with inflammatory bowel disease are initially told that they have irritable bowel syndrome before a diagnosis of inflammatory bowel disease is firmly established. This article contends that many people have both irritable bowel syndrome and inflammatory bowel disease.

Caffeine↗
PubMed1990

Advances in drug therapy for inflammatory bowel disease.

PURPOSE: To identify advances in drug therapy for inflammatory bowel disease, and to evaluate the effectiveness of the new agents in treating both ulcerative colitis and Crohn disease. DATA IDENTIFICATION: Studies published from January 1980 through June 1989 were identified using MEDLINE and through extensive hand searching of bibliographies in identified articles. STUDY SELECTION: One hundred and ten articles directly related to the topic were found and analyzed. Another 42 articles were relevant to the material reviewed. DATA EXTRACTION: Articles were selected on the basis of study quality and their significance with regard to treatment of inflammatory bowel disease. RESULTS OF DATA ANALYSIS: The aminosalicylates are emerging as effective and safe therapy for inflammatory bowel disease. Corticotropin can be considered the drug of choice for certain patients with severe ulcerative colitis, and new rapidly metabolized topical steroids appear to be as effective as traditional forms and have fewer side effects. Immunosuppressive agents, including 6-mercaptopurine and azathioprine, may be useful in treating difficult-to-manage patients with either Crohn disease or ulcerative colitis, whereas cyclosporine appears promising but should be reserved for patients in whom other measures have failed. Patients with refractory perineal Crohn disease and those with Crohn colitis may benefit from metronidazole. Many other drugs including clonidine, cromoglycate, chloroquine, fish oil, methotrexate, antituberculous agents, interferon, and superoxide dismutase have shown enough promise in preliminary studies to warrant controlled clinical trials. CONCLUSIONS: Drug therapy for inflammatory bowel disease, limited for many years to sulfasalazine and some corticosteroids, has been extended to include the aminosalicylates, rapidly metabolized topical steroids, immunosuppressive agents, and metronidazole. Potentially useful newer drugs await further study.

Administration, Oral↗
PubMed2001

Management issues in women with inflammatory bowel disease.

Medical practitioners caring for women with inflammatory bowel disease should recognize that gender may have a profound influence on patient perception of disease, body image, and clinical symptoms. These gender-related concerns as well as issues such as fertility and pregnancy increase the complexity of medical and surgical management of women with inflammatory bowel disease. This article reviews the important issues for practitioners to consider in taking care of women with ulcerative colitis and Crohn's disease, focusing especially on body image, fertility, management of disease during pregnancy, and osteoporosis.

Adult↗
PubMed2004

Colorectal cancer in inflammatory bowel disease.

PURPOSE OF REVIEW: Patients with inflammatory bowel disease, either Crohn disease or ulcerative colitis, are at an increased risk for developing colorectal carcinoma. RECENT FINDINGS: Surveillance colonoscopy, although never formally evaluated in a prospective controlled trial, is performed in an effort to reduce this risk. Novel methods of detecting dysplasia are constantly being evaluated, including chromoendoscopy and biomarkers of carcinoma, in an attempt to stratify patients who are at a higher risk of developing high-grade dysplasia or carcinoma. SUMMARY: Because of the potential impact on quality of life and life expectancy, an optimal strategy for reducing the risk of developing colorectal cancer in patients with inflammatory bowel disease needs to be defined.

Journal Article↗
PubMed2005

Risk factors for inflammatory bowel disease in the general population.

BACKGROUND: The aetiology of inflammatory bowel disease remains largely unknown. AIM: We performed a comprehensive assessment of potential risk factors associated with the occurrence of inflammatory bowel disease. METHODS: We identified a cohort of patients 20-84 years old between 1995 and 1997 registered in the General Practitioner Research Database in the UK. A total of 444 incident cases of IBD were ascertained and validated with the general practitioner. We performed a nested case-control analysis using all cases and a random sample of 10 000 frequency-matched controls. RESULTS: Incidence rates for ulcerative colitis, Crohn's disease, and indeterminate colitis were 11, 8, and 2 cases per 100 000 person-years, respectively. Among women, we found that long-term users of oral contraceptives were at increased risk of developing UC (OR: 2.35; 95% CI: 0.89-6.22) and CD (OR: 3.15; 95% CI: 1.24-7.99). Similarly, long-term users of HRT had an increased risk of CD (OR: 2.60; 95% CI: 1.04-6.49) but not UC. Current smokers experienced a reduced risk of UC along with an increased risk of CD. Prior appendectomy was associated with a decreased the risk of UC (OR: 0.37; 95% CI: 0.14-1.00). CONCLUSIONS: Our results support the hypothesis of an increased risk of inflammatory bowel disease associated with oral contraceptives use and suggest a similar effect of hormone replacement therapy on CD. We also confirmed the effects of smoking and appendectomy on inflammatory bowel disease.

Adult↗
PubMed1983

Surgical treatment, skin test reactivity, and lymphocytes in inflammatory bowel disease.

Sixty-three patients with inflammatory bowel disease were studied before and after bowel resection. Peripheral lymphocytes, T- and B-cell counts, and skin test reactivity to five recall antigens were determined before operation and 6 to 18 months postoperatively. Twenty-eight patients (44 percent) were unable to react to any skin test initially. Anergic patients had significantly lower lymphocyte and T- and B-cell counts. There was no difference in age, severity or duration of disease, or amount of weight loss between anergic patients and those who responded. Also, there was no difference between patients with ulcerative colitis and those with Crohn's disease. After surgery, 25 previously anergic patients became able to react to skin tests. They also showed a significant increase in T and B cells which did not occur in the previously reactive group. However, the overall peripheral lymphocyte and T- and B-cell counts remained well below those of the normal control subjects. Patients with inflammatory bowel disease that requires surgical treatment have significant immunologic abnormalities. Removal of the diseased bowel, weight gain, and cessation of steroid medication improves skin test reactivity but does not correct the depressed peripheral lymphocyte and especially T-cell counts.

Adult↗
PubMed1992

[Current insights on the pathogenesis of chronic inflammatory bowel diseases].

The pathogenesis and etiology of inflammatory bowel disease (IBD) is poorly understood. As a matter of fact, it is not even certain whether either one is a single entity with different forms of clinical manifestations, or whether each one represents a single clearly separable entity. Common features of both diseases are chronic persistence, recurrent exacerbation and remission, the production of autoantibodies, as well as the expression of aberrant HLA-class II molecules on the surface of epithelial cells on the site of inflammation gut. It is likely that these events involve a disturbed immunoregulatory function or autoimmune process. Since the beginning of investigation the cause of IBD, infectious agents (bacteria, virus, mycobacterium paratuberculosis and others) or bacterial products (endotoxin, peptidoglycans from the bacterial cell wall) have been considered as primary causes. Epidemiological studies showed a marked increase of the incidence rates of IBD in industrial countries leading to the hypothesis, that environmental factors could play a role in the pathogenesis of the disease. So far it is clear that the major identified risk factor for IBD is a genetic susceptibility confirmed by studies showing a positive family history.

Colitis, Ulcerative↗
PubMed1989

Beyond the scope: a nursing view of the extraintestinal manifestations of inflammatory bowel disease.

There are approximately 100 systemic complications of inflammatory bowel disease involving most organ systems of the body. A review of the nursing literature demonstrates a wealth of information on inflammatory bowel disease. Most of this literature, however, contains only a brief description of the extraintestinal manifestations of inflammatory bowel disease. It is the purpose of this manuscript to familiarize gastroenterology nurses with the major categories of extraintestinal manifestations seen in association with Crohn's disease and ulcerative colitis. An awareness of these manifestations will allow nursing to play a role in the assessment and care of a patient who demonstrates these conditions. The focus of this paper will be on the clinical presentation and medical management of these conditions along with implications for nursing and possible nursing interventions.

Humans↗
PubMed2002

Impact of a nurse-led counselling service on quality of life in patients with inflammatory bowel disease.

AIM: Health related quality of life is impaired in patients suffering from inflammatory bowel disease. Although counselling directed towards physical and psychological morbidity is assumed to improve health related quality of life, this has never been demonstrated. METHODS: Physical and psychological well-being were assessed using questionnaires administered to 100 out-patients in the United Kingdom suffering from inflammatory bowel disease, 50 subjects not suffering from inflammatory bowel disease and a disease control group comprising 28 patients with psoriatic arthritis. A specific nurse led counselling package was given to half the inflammatory bowel disease group and health related quality of life was assessed at baseline, 6 and 12 months. RESULTS: Inflammatory bowel disease and psoriatic arthritic patients had a range of physical disease activity, although none were severely ill during the course of the study. Medical therapy was similar in both groups throughout the duration of the trial. The mean Short Form 36 (SF-36) scores for mental health were low in inflammatory bowel disease patients; 62.9 +/- 9.1 (SD) in ulcerative colitis, 60 +/- 9.8 (SD) in Crohn's disease, compared with 72.4 +/- 7.2 (SD) in healthy controls (P < 0.05). Mean SF-36 scores for social function were also reduced in Crohn's disease patients; 68.4 +/- 10.1 (SD) in Crohn's disease, compared with 87 +/- 10.1 (SD) in healthy controls (P < 0.05). As expected, the mean SF-36 scores in psoriatic arthritic patients were significantly low 61.9 +/- 1.5 (SD) compared with 82.4 +/- 14 (SD) in healthy controls (P < 0.05). Crohn's disease patients were significantly more anxious than the other groups, mean HAD score was 10 +/- 3.7 (SD) in Crohn's disease patients and 6.86 +/- 3.5 (SD) in healthy volunteers (P < 0.05), although mean HAD scores for depression were similar in all groups. Maladaptive coping mechanisms were present in a significant proportion of Crohn's disease patients. At follow-up all aspects of psychological morbidity returned to the normal range in the Crohn's disease patients without significant change in the mean physical disease index. CONCLUSION: Health related quality of life can be improved over 6 months by provision of a nurse led counselling service but the effects are not sustained for 12 months.

Adaptation, Psychological↗
PubMed1999

Cytomegalovirus infection in patients with inflammatory bowel disease.

OBJECTIVE: It has been suggested that, in inflammatory bowel disease, cytomegalovirus behaves in the intestine as a nonpathogenic bystander, and even its finding in intestinal mucosa has unclear clinical relevance. We report our experience with a small series of patients with refractory inflammatory bowel disease and cytomegalovirus infection and their clinical outcome. METHODS AND RESULTS: Nine patients with moderate-severe attacks of inflammatory bowel disease did not respond to i.v. prednisone (1 mg/kg/day) for a mean of 24 days. Four of these patients were further treated with i.v. cyclosporine A (4 mg/kg/day). Cytomegalovirus infection was diagnosed in two patients after resection for treatment failure. In the remaining patients, cytomegalovirus infection was diagnosed in endoscopic mucosal biopsies and i.v. ganciclovir was then administered at a dose of 10 mg/kg/day for 2-3 wk. Five of these patients went into clinical remission, allowing corticosteroid and cyclosporine A discontinuation. Follow-up biopsies were performed and in all cases cytomegalovirus could not be detected in the colonic tissue. Two patients needed to be treated with intravenous cyclosporine A after antiviral therapy because of persistence of clinical symptoms despite the elimination of cytomegalovirus infection. CONCLUSIONS: Cytomegalovirus infection may play a role in the natural history of refractory inflammatory bowel disease and in some of its complications. The clearance of cytomegalovirus in colonic mucosa may lead some of these patients to remission.

Adult↗
PubMed2000

Anticipation in inflammatory bowel disease: a phenomenon caused by an accumulation of confounders.

Inflammatory bowel disease (IBD) has a definite genetic component as documented by epidemiological and linkage evidence. It shows an earlier onset of disease in children of affected patients than in their parents. This has lead to speculations about genetic anticipation in this disorder. 2,007 IBD patients with sporadic disease and 472 multiplex familial cases (including 103 affected parents and 99 children of affected patients) were evaluated with a multi-item questionnaire as part of a study of inflammatory bowel disease genetics. The Mann-Whitney U-test and the general linear model were used for analysis. Clinical characteristics such as presence of fistulae, stenoses, extraintestinal manifestations, and other parameters, which are related to the severity of the disease, were found to be similar between familial and sporadic cases of IBD (corrected P > or = 0.31 for all tests). The mean-age-of onset in children of affected patients was 19.4 years earlier than in their parents. However, the age of the parental cohort was significantly higher (27 years) and the diagnostic interval also longer (1.7 years). If these confounders are corrected in a general linear model, no significant difference is evident for the age-of-onset between the groups (P > or = 0.52). There is no evidence for genetic anticipation in inflammatory bowel disease. The absence of genetic anticipation is consistent with the clinical similarity of familial and sporadic inflammatory bowel disease. This finding justifies the primary genetic analysis of familial disease under the assumption that their genetic background will be representative for all presentations of IBD.

Adult↗
PubMed2006

Effects of changes in hemoglobin level on quality of life and cognitive function in inflammatory bowel disease patients.

BACKGROUND: Anemia commonly complicates inflammatory bowel disease (IBD). In patients with chronic renal failure, the treatment of anemia with iron+/-erythropoietin improves both quality of life (QOL) and cognitive function (CF). The same drugs are effective in treating severe anemia in IBD, but there is no evidence to direct the treatment of mild anemia. Concern exists that the use of iron may exacerbate inflammation in patients with IBD. The present study examined the association between changes in hemoglobin (Hb) in a population of IBD patients and changes in QOL and CF independent of change in disease activity (DA). Subsidiary aims were to assess whether the use of iron was associated with worsening DA. METHODS: A cohort of 50 patients with IBD (29 Crohn's disease and 21 ulcerative colitis) took part. Iron replacement was given to 21 patients with low Hb. Measures of QOL, CF, DA, and Hb were recorded at baseline and at 6 months. RESULTS: The iron-treated group had lower Hb and higher DA scores compared with the non-iron-treated group at baseline. In a hierarchical regression model, changes in DA accounted for 13% (P=0.17) and changes in Hb accounted for 18% (P=0.005) of the variance in change in SF-36 and 12% (P=0.23) and 17% (P=0.009) in the Inflammatory Bowel Disease Questionnaire. In this pilot study, although no associations were identified between changes in Hb or DA and CF, increases in Hb improved QOL scores in IBD patients independent of changes in DA. We found no similar effect with CF, but again, the sample size was small. We found no evidence that iron therapy causes worsening of DA. CONCLUSIONS: Treatment of IBD-associated anemia with iron may lead to improvement in patients' QOL.

Anemia, Iron-Deficiency↗
PubMed2000

Inhibition of platelet activation by 5-aminosalicylic acid in inflammatory bowel disease.

BACKGROUND: Platelets play an important role in inflammation and are activated in inflammatory bowel disease. Micro-vascular thrombosis in the gut wall leading to intestinal micro-infarction may be a pathogenic feature of Crohn's disease. 5-Aminosalicylic acid is an effective treatment for patients with inflammatory bowel disease. AIMS: To assess the effects of 5-aminosalicylic acid on platelet activation, when taken orally and in vitro by patients with inflammatory bowel disease. METHODS: Spontaneous and thrombin-induced platelet activation were studied using fluorescent antibodies to the activated platelet surface glycoprotein P-selectin and flow cytometry. RESULTS: Baseline platelet activation in inflammatory bowel disease was significantly greater than that in controls (P=0.0003). Independent of diagnosis or disease activity, spontaneous ex-vivo platelet activation was 50% lower in patients with inflammatory bowel disease taking 5-aminosalicylic acid orally than in those not on such treatment (P < 0.05). In vitro, 5-aminosalicylic acid significantly reduced both spontaneous (P < 0. 03 for >/=1 microM 5-aminosalicylic acid) and thrombin-induced platelet activation (P < 0.02 for >/= 1 microM 5-aminosalicylic acid). CONCLUSIONS: 5-Aminosalicylic acid given either orally or in vitro inhibits platelet activation. If this effect reflects an in vivo action in the gut, it could contribute to the beneficial actions of 5-aminosalicylic acid in inflammatory bowel disease.

Adult↗
PubMed1989

Immunosuppressive drugs in inflammatory bowel disease. A review of their mechanisms of efficacy and place in therapy.

Immune effector mechanisms are central to the disease process in inflammatory bowel disease, but it is not clear whether the mucosal or systemic immunological abnormalities are primary phenomena, or are secondary to disease activity. Corticosteroid drugs remain the most effective treatment for active disease, but there is no evidence that they are useful for maintenance therapy. Some patients, however, are dependent on low-dose corticosteroids, and relapse when the drug is withdrawn. These drugs have widespread actions on the immune response, and monocytes are particularly sensitive to corticosteroids. In contrast, sulphasalazine and 5-aminosalicylic acid are effective in maintenance therapy, but do not act primarily by immunosuppressive mechanisms. They are effective in maintenance therapy of ulcerative colitis, and mild relapses of ulcerative colitis and colonic Crohn's disease. New preparations of 5-aminosalicylic acid have reduced side effects, many of which are due to sulphapyridine. Azathioprine and 6-mercaptopurine are used less widely: in Crohn's disease there is reasonable evidence for benefit in chronic active disease unresponsive to corticosteroids, and maintenance of remission. In ulcerative colitis, the position is less clearcut. Overall, trials favour an effect in chronic active disease, and there are pointers to an effect in maintenance of remission. Because of their side effects, in particular marrow suppression, these drugs should be reserved for second-line therapy. Similarly, other cytotoxic drugs are not used because of their side effects. More recently, cyclosporin A, with its selective action on interleukin-2 release and/or synthesis, and inhibition of helper T cell function, has been shown to be helpful in Crohn's disease. At present it should only be used in controlled trials, for patients with unresponsive disease in whom surgery is contraindicated. Renal toxicity may limit long term use. There is little data for cyclosporin A in ulcerative colitis. On the basis that there may be an underlying immune defect in Crohn's disease leading to mucosal inflammation, immunostimulant therapy has been used, but there is no evidence for benefit from treatment with BCG or levamisole in active disease or in maintenance therapy. 7S-Immunoglobulin, plasmapheresis or T-lymphocyte apheresis have been used in acute relapse, but evidence is anecdotal, and does not support their use except as a desperate measure to avoid surgery. Further well-designed controlled trials are needed to define the role of all these drugs, and further research into the mechanism of action on the immune response may shed light on the pathogenesis of inflammatory bowel disease.

Clinical Trials as Topic↗
PubMed2004

[Inflammatory bowel diseases--pathogenesis and clinical symptoms].

The common factor of inflammatory bowel diseases is the unknown etiologic agent. It's suggested that it could be genetic predisposition, environment and immunologic factor. It seems probable that the etiology of these diseases has many sources but the pathogenesis is similar. Inflammatory bowel diseases etiology requires more research but the immunological system disturbances are out of the question. The most typical course of these diseases is the one with remissions and relapses. Clinical symptoms vary and depend on localization, phase and presence of complications. In this paper we present some basic information about epidemiology, pathogenesis and the clinical course of inflammatory bowel diseases.

Humans↗
PubMed2004

Key role of mast cells and their major secretory products in inflammatory bowel disease.

Historically, mast cells were known as a key cell type involved in type I hypersensitivity. Until last two decades, this cell type was recognized to be widely involved in a number of non-allergic diseases including inflammatory bowel disease (IBD). Markedly increased numbers of mast cells were observed in the mucosa of the ileum and colon of patients with IBD, which was accompanied by great changes of the content in mast cells such as dramatically increased expression of TNFalpha, IL-16 and substance P. The evidence of mast cell degranulation was found in the wall of intestine from patients with IBD with immunohistochemistry technique. The highly elevated histamine and tryptase levels were detected in mucosa of patients with IBD, strongly suggesting that mast cell degranulation is involved in the pathogenesis of IBD. However, little is known of the actions of histamine, tryptase, chymase and carboxypeptidase in IBD. Over the last decade, heparin has been used to treat IBD in clinical practice. The low molecular weight heparin (LMWH) was effective as adjuvant therapy, and the patients showed good clinical and laboratory response with no serious adverse effects. The roles of PGD2, LTC4, PAF and mast cell cytokines in IBD were also discussed. Recently, a series of experiments with dispersed colon mast cells suggested there should be at least two pathways in man for mast cells to amplify their own activation-degranulation signals in an autocrine or paracrine manner. The hypothesis is that mast cell secretogogues induce mast cell degranulation, release histamine, then stimulate the adjacent mast cells or positively feedback to further stimulate its host mast cells through H1 receptor. Whereas released tryptase acts similarly to histamine, but activates mast cells through its receptor PAR-2. The connections between current anti-IBD therapies or potential therapies for IBD with mast cells were discussed, implicating further that mast cell is a key cell type that is involved in the pathogenesis of IBD. In conclusion, while pathogenesis of IBD remains unclear, the key role of mast cells in this group of diseases demonstrated in the current review implicates strongly that IBD is a mast cell associated disease. Therefore, close attentions should be paid to the role of mast cells in IBD.

Cell Degranulation↗
PubMed1988

Narcotic dependence in inflammatory bowel disease.

Thirteen of 43 patients (30%) with inflammatory bowel disease referred for psychiatric consultation were found to be drug dependent, most commonly on oral narcotics. Drug dependence was more frequent in patients with Crohn's disease than ulcerative colitis and many had a borderline personality disorder. The study suggests that drug dependence is not recognized often enough in patients with inflammatory bowel disease and that patients with certain psychiatric disorders are at higher risk of developing it. Recognition of drug dependence is aided by interviewing family members. It is best prevented by seeking and treating the specific cause of pain and by having only one physician assigned to prescribe and manage narcotics.

Adult↗