PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Colitis, Ulcerative”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 91 records · Page 5Linked to original sources
PubMed1996

[Expression of Fas and Fas-ligand in epithelium of ulcerative colitis].

Ulcerative colitis (UC) is characterized by the loss of epithelium and inflammation of lamina propria. In normal colon, epithelial cells are eliminated by apoptosis at the luminal surface. The apoptotic cells recognized by their typical morphology and the presence of DNA breaks are also accompanied by Fas and Fas-ligand. It is thought when Fas-ligand bound the Fas, the cells bearing Fas will enter a path of apoptosis. On the other hand, in inflamed areas of UC and adjacent un-inflamed areas, the apoptosis of epithelial cells are recognized anywhere along crypts. These findings suggest that unscheduled apoptosis in the UC crypts takes place and the apoptosis is mediated by a auto- or paracrine Fas/Fas-ligand interaction.

Animals↗
PubMed1995

Surgical therapy for ulcerative colitis.

Ulcerative colitis is a curable disease. Despite newer medications, many patients either fail medical therapy or develop dysplasia or carcinoma requiring surgery. Surgical techniques have improved, and complication rates have declined. The functional results of ileoanal reservoir surgery are excellent in most patients, and most patients agree that a pouch is better than the disease. One must balance poor function secondary to disease, cancer risk, need for medication, and side effects of medication against surgical morbidity and postoperative function.

Carcinoma↗
PubMed1996

[Molecular pathoimmunology of ulcerative colitis].

Ulcerative colitis (UC) is a disease of acute on chronic at the active stage when lymphocytes, plasma cells as well as neutrophils and eosinophils infiltrate in the colonic mucosa. Molecular pathoimmunology of UC was discussed in this article from the viewpoint of disease susceptibility gene, immune activation gene of immunocompetent cells, molecular biology of cytokines, and molecular biology of colonic epithelial cells. HLA-DR2, DRB1* 1502, is the most susceptive gene for development and intractability of Japanese UC, and HLA-BW52 which was most frequently associated with Japanese UC and HLA-B35 which was also associated with Jewish UC were reported to have a common origin. Expression of IL-2 receptor and HLA-DR protein used as immune activation genes of lymphocytes was accelerated in UC. Overexpression of proinflammatory cytokines such as IL-1, IL-6 and IL-8 was found in the colonic mononuclear cells of UC, but IL-2 mRNA expression was not accelerated in UC. Therefore, immunological imbalance in the colonic mucosa may play an important role in the pathophysiology of UC.

Colitis, Ulcerative↗
PubMed1996

Usage of T cell receptor (TCR) V beta gene in ulcerative colitis.

Ulcerative colitis (UC) is an inflammatory disease of unknown etiology. In this study, the expression of TCRV beta gene in UC patients was examined. The present study included 11 consecutive Japanese patients with UC. The control group comprised 10 healthy people. The usage of T Cell Receptor (TCR) V beta chain gene segments in peripheral blood was examined using RT-PCR. In addition, HLA-DR DNA typing was performed for the 11 patients with UC. The average of the positive expression rates in the UC group was 0.617 +/- 0.126, which was significantly higher than that of the control group (0.829 +/- 0.080) (p < 0.01). In the UC group, the usage of V beta chain gene in the active phase was almost same as that in the inactive phase. No specific distribution of V beta repertoire was observed in the UC group. In UC patients, no distinct correlation was found between any certain HLA-DR type and TCRV B gene usage. UC patients had a significantly lower rate of the expression of TCR V beta genes compared to normal controls. There is a possibility that the restricted usage of TCR V beta repertoire is possibly related to the existence of oligoclonal TCR repertoire in UC patients.

Colitis, Ulcerative↗
PubMed1971

A clinico-immunological study of ulcerative colitis and ulcerative proctitis.

Fifteen patients with ulcerative colitis and 11 patients with ulcerative proctitis have been observed and studied for periods ranging from one to 15 years. It is suggested that the clinical course of the two disorders is quite distinct. Further, while the serum immunoglobulins were within normal limits in ulcerative proctitis, significant increases in the serum alpha(2)-, beta-, and gamma-globulins and in the IgA and IgG concentrations were found in ulcerative colitis. Despite total colectomy for ulcerative colitis, the serum IgG and IgA concentration remained high and even after subsequent rectal resection the relative IgA concentration continued to increase. The significance of these findings is discussed.

Adolescent↗
PubMed1991

Risk factors for extensive ulcerative colitis and ulcerative proctitis: a population based case-control study.

To examine socioeconomic factors, dietary and other personal habits, and medical history as risk factors for ulcerative colitis, we studied 167 (98%) of all prevalent cases of ulcerative colitis diagnosed in Uppsala county from 1945 to 1964 and 167 age and sex matched population controls. Ulcerative colitis patients were less likely than controls to be current cigarette, pipe, or cigar smokers (odds ratio (OR) = 0.44; 95% confidence limits (CL) = 0.25-0.78), but more likely to have symptoms induced by drinking milk (OR = 4.63; 95% CL = 2.15-9.93). Patients with ulcerative colitis do not differ in most of the socioeconomic, dietary and personal habits compared with the background population.

Adolescent↗
PubMed2004

Drug therapy for ulcerative colitis.

Ulcerative colitis (UC) is an inflammatory destructive disease of the large intestine occurred usually in the rectum and lower part of the colon as well as the entire colon. Drug therapy is not the only choice for UC treatment and medical management should be as a comprehensive whole. Azulfidine, Asacol, Pentasa, Dipentum, and Rowasa all contain 5-aminosalicylic acid (5-ASA), which is the topical anti-inflammatory ingredient. Pentasa is more commonly used in treating Crohn's ileitis because Pentasa capsules release more 5-ASA into the small intestine than Asacol tablets. Pentasa can also be used for treating mild to moderate UC. Rowasa enemas are safe and effective in treating ulcerative proctitis and proctosigmoiditis. The sulfa-free 5-ASA agents (Asacol, Pentasa, Dipentum and Rowasa) have fewer side effects than sulfa-containing Azulfidine. In UC patients with moderate to severe disease and in patients who failed to respond to 5-ASA compounds, systemic (oral) corticosteroids should be used. Systemic corticosteroids (prednisone, prednisolone, cortisone, etc.) are potent and fast-acting drugs for treating UC, Crohn's ileitis and ileocolitis. Systemic corticosteroids are not effective in maintaining remission in patients with UC. Serious side effects can result from prolonged corticosteroid treatment. To minimize side effects, corticosteroids should be gradually reduced as soon as the disease remission is achieved. In patients with corticosteroid-dependent or unresponsive to corticosteroid treatment, surgery or immunomodulator is considered. Immunomodulators used for treating severe UC include azathioprine/6-MP, methotrexate, and cyclosporine. Integrated traditional Chinese and Western medicine is safe and effective in maintaining remission in patients with UC.

Adrenal Cortex Hormones↗
PubMed2001

Ulcerative duodenitis accompanying ulcerative colitis.

Ulcerative colitis (UC) is a chronic inflammatory disease of the colon of unknown etiology. There are varied manifestations in the natural course of UC. However, duodenum is not generally considered a target organ of UC. Here, we report two patients with steroid-responsive ulcerative duodenitis with colitis that was consistent with UC, but not with Crohn's disease. We also reviewed six cases of ulcerative duodenitis with UC. Duodenal lesion with UC may be a more common phenomenon, although infrequently clinically manifested under steroid therapy. Upper gastrointestinal tract inflammation in UC warrants further studies to ascertain whether the duodenum is a target organ in UC, especially in steroid-free conditions.

Adult↗
PubMed2005

Molecular mimicry may contribute to pathogenesis of ulcerative colitis.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease with mucosal inflammation and ulceration of the colon. There seems to be no single etiological factor responsible for the onset of the disease. Autoimmunity has been emphasized in the pathogenesis of UC. Perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) are common in UC, and recently two major species of proteins immunoreactive to pANCA were detected in bacteria from the anaerobic libraries. This implicates colonic bacterial protein as a possible trigger for the disease-associated immune response. Autoantibodies and T-cell response against human tropomyosin isoform 5 (hTM5), an isoform predominantly expressed in colon epithelial cells, were demonstrated in patients with UC but not in Crohn's colitis. We identified two bacterial protein sequences in NCBI database that have regions of significant sequence homology with hTM5. Our hypothesis is that molecular mimicry may be responsible for the pathogenesis of UC.

Amino Acid Sequence↗
PubMed2007

Hypothesis about mechanisms through which nicotine might exert its effect on the interdependence of inflammation and gut barrier function in ulcerative colitis.

Ulcerative colitis (UC) is characterized by impairment of the epithelial barrier and the formation of ulcer-type lesions, which result in local leaks and generalized alterations of mucosal tight junctions. Ultimately, this results in increased basal permeability. Although disruption of the epithelial barrier in the gut is a hallmark of inflammatory bowel disease and intestinal infections, it remains unclear whether barrier breakdown is an initiating event of UC or rather a consequence of an underlying inflammation, evidenced by increased production of proinflammatory cytokines. UC is less common in smokers, suggesting that the nicotine in cigarettes may ameliorate disease severity. The mechanism behind this therapeutic effect is still not fully understood, and indeed it remains unclear if nicotine is the true protective agent in cigarettes. Nicotine is metabolized in the body into a variety of metabolites and can also be degraded to form various breakdown products. It is possible these metabolites or degradation products may be the true protective or curative agents. A greater understanding of the pharmacodynamics and kinetics of nicotine in relation to the immune system and enhanced knowledge of gut permeability defects in UC are required to establish the exact protective nature of nicotine and its metabolites in UC. This review suggests possible hypotheses for the protective mechanism of nicotine in UC, highlighting the relationship between gut permeability and inflammation, and indicates where in the pathogenesis of the disease nicotine may mediate its effect.

Colitis, Ulcerative↗
PubMedDate not supplied

High-iron diet: foe or feat in ulcerative colitis and ulcerative colitis-associated carcinogenesis.

Anemia associated with long-standing chronic inflammation and iron deficiency, and the increased risk for the development of dysplasia and carcinoma, are two of the most common complications in patients with ulcerative colitis (UC). Because of iron and nutrition deficiency, UC patients are encouraged to consume a high-protein and high-iron diet. The crucial clinical question is the effect of a high-iron diet on inflammation activity and inflammation-driven carcinogenesis. Is a high-iron diet a foe or a feat in UC and UC-associated carcinogenesis? This review updates the progress and information on (1) iron nutrition and iron-deficiency anemia in patients with UC, (2) experimental evidence of the exacerbating effect of a high-iron diet on UC and its associated carcinogenesis and the difference between a high-iron diet and parental iron supplementation, (3) the clinical efficacy of, and concerns about, oral and intravenous iron supplements in patients with inflammatory bowel disease and iron deficiency anemia, and (4) the clinical implications of long-term iron supplements and management of UC. These experimental findings from animal models provide evidence to warrant further consideration and clinical studies of iron nutrition, inflammation activity, and cancer development.

Administration, Oral↗
PubMed1987

Histopathology differentiates acute self-limited colitis from ulcerative colitis.

Acute self-limited colitis (ASLC) must be distinguished from chronic ulcerative colitis (CUC) for the proper early management of patients with the acute onset of bloody diarrhea. This study was undertaken to determine if any clinical, endoscopic, microbiologic, or histologic parameters can be used to make this distinction reliably and quickly. Forty-eight patients with ASLC, 36 patients with chronic ulcerative colitis during their first attack [CUC(F)], and 84 patients with recurrent flares of chronic ulcerative colitis [CUC(R)] were studied prospectively. The presence of fever (temperature greater than 100 degrees F), abdominal pain, or the time from onset of bloody diarrhea to presentation were not discriminatory. Overall clinical and endoscopic severity were identical among the three groups. Microbiologic studies identified an infectious agent in only 42% of patients with ASLC. Histopathologic features always distinguished patients with CUC from those with ASLC. No case of ASLC was misdiagnosed histologically as CUC or vice versa. Plasmacytosis in the lamina propria extending to the mucosal base and mucosal distortion were present in all cases of CUC(F) and CUC(R), but were absent in all cases of ASLC. The finding of focal cryptitis during the resolving phase of ASLC could be confused with similar lesions in biopsy specimens from patients with Crohn's disease and mandates clinical follow-up. Histopathology is thus the only reliable diagnostic tool for the rapid differentiation of ASLC from CUC. However, biopsy specimens are only diagnostic when obtained during the acute phase of illness; that is, usually within the first 4 days from the onset of symptoms.

Acute Disease↗
PubMed2006

Medical management of left-sided ulcerative colitis and ulcerative proctitis: critical evaluation of therapeutic trials.

BACKGROUND: The goal of this work was to critically evaluate the published studies on the treatment of ulcerative proctitis (UP) and left-sided ulcerative colitis (L-UC). The results of this review provided the content for the accompanying treatment guidelines, Clinical Guidelines for the Medical Management of Left-sided Ulcerative Colitis and Ulcerative Proctitis: Summary Statement. METHODS: All English language articles published between 1995 and September 2005 were identified through a comprehensive literature search using OVID and PubMed. The quality of the data supporting or rejecting the use of specific therapies was categorized by a data quality grading scale. An "A+" grade was assigned to treatment supported by multiple high-quality randomized controlled trials with consistent results, whereas a "D" grade was given to therapy supported only by expert opinion. The therapeutic efficacy of a treatment was defined by its success in treating UP and L-UC compared with placebo. A medication was ranked as "excellent" if it was specifically studied for UP and L-UC and had consistently positive results compared with placebo or another agent. Quality and efficacy scores were agreed on by author consensus. RESULTS: For the acute treatment of UP or L-UC, the rectally administered corticosteroids and mesalazine (5-ASA), either alone or in combination with oral 5-ASAs, are the most effective therapy: evidence quality, A+; efficacy, excellent. Only rectally administered 5-ASA received an A+/excellent rating for maintenance of remission. Infliximab received an A+ grade for induction and maintenance of remission but only a "good" rating because the studies were performed in all UC, not specifically UP or L-UC. CONCLUSIONS: This critical evaluation of treatment provides a "report card" on medications available for the management of patients with UP and L-UC. The guidelines should provide a useful reference and supplement for physicians treating UC patients.

Adrenal Cortex Hormones↗
PubMed1990

Lymphoid cell subsets in colonic mucosa and HLA-DR antigens on colonic epithelia in colitis excluding ulcerative colitis and Crohn's disease.

Lymphoid cell subsets, including T cells as well as Ig-containing cells in the colonic mucosa and HLA-DR antigens on colonic epithelia, were examined in non-IBD colitis (colitis excluding ulcerative colitis (UC) and Crohn's disease) by the indirect immunoperoxidase staining method. Mouse anti-CD5, CD8, CD4, IgG, IgA1, IgA2, IgM, IgD, IgE, HLA-DR, and NuIa monoclonal antibodies were used as the first antibody. The results were compared to those of the normal controls and UC. T cell subsets in non-IBD colitis were almost similar to those of the controls and UC. The number of Ig-containing cells of all classes, except for IgA, tended to be increased in non-IBD colitis. In particular, both IgG- and IgE-containing cells were significantly increased compared to those in the controls. Compared to UC, IgG-containing cells were decreased in non-IBD colitis. Namely, in non-IBD colitis, as well as in UC, the change of Ig-containing cells (B cell lineage) was more pronounced than that of T cells. The frequency of the expression of HLA-DR antigens on colonic epithelia in non-IBD colitis was 70%, which was significantly higher than that in controls (0%), but significantly lower than that in UC (100%). Whether the differences in the number of IgG-containing cells, and the frequency of epithelial HLA-DR expression between non-IBD colitis and UC was due to the differences of the degree of local inflammation or due to the differences of the nature of the two diseases was not elucidated in this study.

Colitis↗
PubMed1988

Differentiating Crohn's colitis from ulcerative colitis. A rundown of likenesses and dissimilarities.

Crohn's colitis and ulcerative colitis are two distinct clinical entities with differing clinical, pathologic, endoscopic, and radiographic findings. Because of distinct differences in their response to surgical and, in some instances, medical management, clinical separation of these two unique disease states is important. Although at times diagnostic confusion may persist, thorough clinical evaluation, including the judicious use of mucosal biopsy, yields the correct diagnosis in the majority of patients.

Colitis, Ulcerative↗
PubMed2003

Molecular underpinnings of cancer in ulcerative colitis.

Ulcerative colitis (UC) is a chronic inflammatory disease of the colon that can lead to cancer. Patients with UC have approximately 20% lifetime risk of colon cancer, with the risk increasing with the duration of disease. Why some patients develop colorectal cancer and others do not is not clearly understood. Evidence reveals that the UC patients who develop cancer have an underlying process of instability in the colonic mucosa as measured by DNA fingerprinting and fluorescent in situ hybridization techniques. The cause of instability may be shortened telomeres, the protective ends of chromosomes. Patients who progress to dysplasia and cancer have shorter telomeres, which become sticky and cause telomeric bridges to form, with subsequent chromosomal breakage. Thus, UC patients who have dysplasia and cancer appear to have a mutator phenotype present in the colonic mucosa that underlies the process of tumorigenesis.

Journal Article↗
PubMed1997

Nicotine: therapeutic potential for the treatment of ulcerative colitis.

Ulcerative colitis (UC) is predominantly a disease of non-smokers, and nicotine may be the agent responsible for this association. Transdermal nicotine has been shown to improve disease activity and sigmoidoscopic appearance in the active disease but in one study had no effect on maintenance of remission. Since side-effects with nicotine patches occur in up to two thirds of patients, attempts to reduce systemic levels and improve drug tolerance have been developed with colonic delivery systems of nicotine. Preliminary observations with nicotine enemas in UC have shown clinical benefit, but controlled trials are needed. Mechanisms responsible for the association of smoking with colitis and for the therapeutic effect of nicotine remain an enigma; possibilities include: modulation of the immune response, alterations of colonic mucus and eicosanoid production, changes in rectal blood flow, decreased intestinal permeability and the release of endogenous glucocorticoids. With current treatment for UC limited to corticosteroids and formulations of 5-aminosalicylic acid, alternative treatments are required and nicotine may fulfil this role.

Journal Article↗