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At least 253 records · Page 14Linked to original sources
PubMed2002

Etiology of nonresponsive celiac disease: results of a systematic approach.

OBJECTIVES: Nonresponse or relapse of symptoms is common in patients with celiac disease treated with gluten free diet. Refractory sprue (RS) is defined as initial or subsequent failure of a strict gluten-free diet to restore normal intestinal architecture and function in patients who have celiac-like enteropathy. The aims of this study were: 1) to identify causes of persistent symptoms in patients referred with presumed diagnosis of nonresponsive celiac disease (NCD); and 2) to characterize patients with true RS. METHODS: Patients were identified who had been systematically evaluated for NCD between January 1997, and May 2001. Patient records and small bowel biopsy results were reviewed. RESULTS: A total of 55 patients were referred with a presumed diagnosis of NCD. Six did not have celiac disease and had other diseases responsible for their symptoms. Diarrhea, abdominal pain, and weight loss were the most common reasons for evaluation in cases of NCD, whereas weight loss, steatorrhea, and diarrhea were the most common presenting features of RS (nine patients). Of the 49 patients with celiac disease, 25 were identified as having gluten contamination. Additional diagnoses accounting for persistent symptoms included: pancreatic insufficiency, irritable bowel syndrome, bacterial overgrowth, lymphocytic colitis, collagenous colitis, ulcerative jejunitis, T-cell lymphoma, pancreatic cancer, fructose intolerance, protein losing enteropathy, cavitating lymphadenopathy syndrome, and tropical sprue. CONCLUSIONS: Based on this study, we conclude the following: 1) gluten contamination is the leading reason for NCD; 2) of NCD cases, 18% are due to RS; and 3) alternative diseases or those coexistent with celiac disease and gluten contamination should be ruled out before a diagnosis of RS is made.

Adult↗
PubMed1995

Linear IgA disease (LAD): immunoglobulin deposition in oral and colonic lesions.

Two cases of adult linear IgA disease (LAD) with oral and colonic involvement are presented. Oral findings, for both patients, were of widespread painful ulceration present for two to three months and diagnosis was confirmed by biopsy and direct immunofluorescence. Colonic symptoms preceded oral symptoms in both cases and a number of investigations were undertaken, including routine histological examination, which suggested either lymphocytic colitis or Crohn's disease. Immunofluorescence studies showed linear IgA deposition confined to the distal colon. These cases highlight that large bowel involvement can be a feature of linear IgA disease and for the first time demonstrate IgA deposition at that site.

Aged↗
PubMed2003

Intestinal goblet cell autoantibody associated enteropathy.

This report describes a case of refractory enteropathy with circulating intestinal goblet cell autoantibodies (IGA). A 19 year old man with hyperthyroidism had suffered from protracted diarrhoea for nearly 10 years. Histological examination showed evidence of collagenous enterocolitis. The diarrhoea did not improve despite fasting under total parenteral nutrition. An immunofluorescence assay demonstrated IGA without anti-enterocyte autoantibodies, the hallmark of autoimmune enteropathy, although other criteria were fulfilled. None of 109 controls, including 55 cases of inflammatory bowel disease and one of lymphocytic colitis, had IGA. This case is considered to be a variant of autoimmune enteropathy, and might be a distinct entity.

Adult↗
PubMed2001

Ticlopidine-induced interstitial pulmonary disease: a case report.

We report a case of interstitial pulmonary disease that occurred together with lymphocytic colitis during treatment with ticlopidine. The drug was prescribed for transient ischemic cerebrovascular accidents. Ticlopidine treatment was stopped, and a prolonged course of prednisone was necessary to treat the pulmonary and intestinal symptoms. So far, few cases of pulmonary side effects caused by ticlopidine have been reported. This case is unique in that interstitial lung disease evolved in parallel with colitis and caused severe hypoxemia. Special care should be taken when pulmonary symptoms appear in association with ticlopidine treatment.

Aged↗
PubMed2003

An immunohistochemical study and review of potential markers of human intestinal M cells.

M cells are found in intestinal follicle associated epithelium. Studies into the physiological and pathological roles of human M cells have been hampered by the lack of well-substantiated, specific markers for these cells. A critical literature review suggests the following molecules may potentially serve as such markers: CK7, FcaR (CD89), S100, CD1a, CD21, CD23, sialyl Lewis A, and cathepsin E. Normal ileum, appendix and colorectum were studied using paraffin-embedded, formalin-fixed tissue and immunohistochemistry for these 8 markers. Cathepsin E immunohistochemistry was also performed on cases of colorectal adenocarcinoma, colorectal adenoma, colorectal hyperplastic/metaplastic polyp, lymphocytic colitis, collagenous colitis, pseudomembranous colitis and active ulcerative colitis. Of the 8 markers tested, only cathepsin E appeared to be specific to follicle associated epithelium (expressed by cells with and without M cell morphology) and follicular crypt epithelium; this specificity was limited to the colorectum. Focal epithelial expression of cathepsin E was seen in adenocarcinoma, adenoma, hyperplastic/metaplastic polyp, ulcerative colitis and pseudomembranous colitis. In conclusion, cathepsin E is a specific marker of normal colorectal follicle associated epithelium and follicular crypt epithelium though is not specific to M cells within these compartments. None of the other 7 markers studied is exclusively expressed by human M cells.

Adenocarcinoma↗
PubMed1995

Undefined malabsorption syndrome with villous atrophy successfully reversed by treatment with cyclosporine.

A 47-year-old man with a flat jejunal mucosa complicated by malabsorption, diarrhoea and lymphocytic colitis is presented. There was no response to gluten withdrawal alone, combination of a gluten-free diet and prednisone therapy, or total parenteral nutrition. Complete clinical remission was only achieved after simultaneous treatment with cyclosporine and a gluten-free diet. Rechallenge with a gluten-containing diet while cyclosporine treatment continued resulted in a relapse of diarrhoea and malabsorption. We conclude that cyclosporine may be an effective agent for the treatment of undefined, refractory forms of malabsorption.

Atrophy↗
PubMed1997

Analysis of intestinal lymphocytes in mouse colitis mediated by transfer of CD4+, CD45RBhigh T cells to SCID recipients.

Transfer of specific T lymphocyte subsets isolated from the spleens of healthy donor mice into immunodeficient SCID mice leads to chronic intestinal inflammation with characteristics similar to those of human inflammatory bowel disease (IBD). CD4+, CD45RBhigh cells cause disease, whereas CD4+, CD45RBlow and CD8+, CD45RBhigh cells do not. Despite this difference, we demonstrate that all three T cell populations reconstitute the intraepithelial and lamina propria compartments of both small and large intestines of SCID recipients. Therefore, infiltration of lymphocytes alone is not sufficient for disease development. CD4+ lymphocytes that have trafficked to the SCID intestine exhibit a phenotype characteristic of normal mucosal lymphocytes. This includes high expression of alpha E integrin and CD69, expression of CD8 alpha alpha homodimers in some of the intraepithelial lymphocytes, as well as low expression of CD62L and CD45RB. The phenotype of the infiltrating mucosal cells is indistinguishable, with respect to the cell surface markers tested, regardless of whether the starting donor population is CD45RBhigh or CD45RBlow. Severe inflammation is restricted primarily to the colon despite lymphocyte infiltration throughout the length of the intestine. This suggests that some property of the colon microenvironment contributes to inflammation. Consistent with this, transfer of CD4+, CD45RBhigh cells to SCID mice that have significantly reduced numbers of enteric flora results in attenuation of the wasting and colitis. Fewer numbers of donor lymphocytes are recovered from the intraepithelial and lamina propria compartments of reduced flora SCID mice. We hypothesize that the ability of pathogenic cells to traffic to the intestine and mediate colitis may be driven by T cell reactivity to bacteria or bacterial products.

Adoptive Transfer↗
PubMed1991

Flow cytometric analysis of peripheral blood lymphocytes in ulcerative colitis and Crohn's disease.

Using two colour immunofluorescence with fluorescein isothiocyanate and phycoerythrin labelled monoclonal antibodies, multi-parameter flow cytometry was used to examine the antigenic characteristics of peripheral blood lymphocytes in whole blood of patients with ulcerative colitis and Crohn's disease who were not taking immunosuppressive drugs. The numbers of CD4+ and CD8+ lymphocytes in patients with ulcerative colitis and Crohn's disease remained unchanged so that the CD4/CD8 ratio was the same as that of normal control subjects. In Crohn's disease there were many activated T cells (CD3+, CD25+). Although natural killer cells in active Crohn's disease were lower than in normal control subjects, cytotoxic T lymphocytes, as defined by CD3+, CD16+, did not differ in patients with inflammatory bowel disease compared with normal control subjects. For B cell subsets, there were differences in Leu-1+ B cells, Leu-8+ B cells, Fc epsilon R+B cells (Leu-16+, Leu-20+), and activated B cells (Leu-12+, Leu-21+) between patients with inflammatory bowel disease and normal control subjects. These differences are compatible with local activation of B cells in the inflamed colon.

Adolescent↗
PubMed1989

Colonic mucosal T lymphocytes in ulcerative colitis: expression of CD7 antigen in relation to MHC class II (HLA-D) antigens.

T-cell subsets and their activation state were examined by double-label immunofluorescence of cryostat tissue sections of the colon from 21 patients with ulcerative colitis (UC) and 30 histologically normal controls. Expression of MHC class I (HLA-A, B, C) and class II (HLA-D) antigens was studied in parallel. In the normal colonic mucosa, the CD4:CD8 ratio in the epithelial compartment approximated 1:1, and in the lamina propria, 2.55:1. Of the CD8+ (cytotoxic/suppressor) subset, approximately half did not express the CD5 "pan-T" marker in either compartment. Virtually no Leu8+ cells were observed, implying that the CD4+ subset consisted of helper, rather than suppressor-inducer cells. Classical markers of T-cell activation (CD25, HLA-D) and proliferation were absent, and strong expression of the CD7 "immunostimulation" marker was approximately equal in both CD4 and CD8 subsets. The epithelium was uniformly negative for class II antigens, but positive for class I. In UC, there were no significant alterations in CD4:CD8 ratios in either compartment, and there were no changes with respect to phenotype of the subsets. In 11 of 19 patients (mainly with total colitis), enterocytes were HLA-D+. In this HLA-D+ group, there was an increase in the percentage of CD4+ cells coexpressing CD7; this difference was significant (P less than 0.02) in the lamina propria. Increased expression of CD7 was also found by the CD6+ T cell subset (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

[Studies on the cytotoxicity of lymphocytes in ulcerative colitis].

Cytotoxic action was examined with 51 Cr labelled fetal human colon epithelial cell cultures -- using lymphocytes of healthy test persons and of patients suffering from ulcerous colitis and colon carcinoma. There was no significant difference as to the cytotoxic action of the lymphocytes between the three above-mentioned groups; these results are in contrast to those obtained by previous research. This fact is considered to be due to the different methods applied. In the cases with ulcerous colitis E. coli or E. coli with CEA together formed the antigen against which complex immuno-processes are generated.

Antibodies↗
PubMed2003

Effect of dietary pectin on the production of immunoglobulins and cytokines by mesenteric lymph node lymphocytes in mouse colitis induced with dextran sulfate sodium.

The present study explores the dietary effect of pectin on the MLN lymphocyte functions of mice with dextran sulfate sodium (DS)-induced colitis. We found that the immunoglobulin (Ig)A level in mesenteric lymph node (MLN) lymphocytes was high, while the IgE level was lower, in mice fed with pectin than in those fed with cellulose. Interestingly, the fecal IgA concentration of the pectin-fed mice was significantly higher than that of the cellulose-fed mice. The concentrations of interferon-gamma and interleukin (IL)-2 treated with concanavalin A (ConA) were significantly higher in the pectin-fed group than in the cellulose-fed group. Although dietary pectin did not affect the IL-4 and IL-10 levels, the activation-induced IL-4 and IL-10 secretion was lower in MLN cells of the pectin-fed mice than of the cellulose-fed mice following DS-induced colitis. Based on these findings, we propose that the effect of dietary pectin on mice with DS-induced colitis is mediated by the manipulation of Th1 cells. Furthermore, the inhibitory effect of IL-4 and IL-10 by dietary pectin may play an important role in promoting a change in Th1/Th2 balance toward Th1-dominant immunity.

Animals↗
PubMed1984

Altered blood lymphocyte subclasses in patients with ulcerative colitis.

Peripheral blood lymphocytes were studied by flow cytofluorimetry and monoclonal antibody techniques in 107 patients with ulcerative colitis and in 20 healthy controls of similar ages. Total T, T helper (TH), and T cytotoxic/suppressor (TC/S) lymphocytes were defined by the monoclonal antibodies OKT3, OKT4 and OKT8, respectively, while B lymphocytes were defined by surface immunoglobulin. Patients had a significantly (P less than 0.05) lower proportion of TC/S lymphocytes than the controls, and patients with quiescent disease had a reduced proportion of B lymphocytes compared to controls and those with active disease. Patients with marked mucosal dysplasia had a significantly (P less than 0.025) lower proportion of TH lymphocytes and a higher (P less than 0.01) proportion of B lymphocytes than those without dysplasia. There were no significant associations between lymphocyte levels and any other clinicopathological features assessed.

Adult↗
PubMed1992

[Immunohistochemical analysis of colonic mucosa with ulcerative colitis--activation of lymphocytes and expression of ICAM-1 by lamina propria dendritic cells and macrophages].

The colonic mucosa of 30 patients with ulcerative colitis was analyzed by an immunohistochemical technique. A quantitative evaluation for lymphocyte subsets show significantly increased numbers of CD3+, CD4+, CD8+, and CD28+ cells in ulcerative colitis cases of histological grades 3, 4 and 5 by Matts' classification comparing to normal control cases. CD4/CD8 ratio in each histological grade of ulcerative colitis was not significantly different from those in normal controls and disease controls (infectious colitis cases). However, CD28/CD3 ratio was increased significantly in ulcerative colitis cases of histological grades 3, 4 and 5 comparing to control cases. Most of the lymphocytes were positive for lymphocyte function-associated antigen-1 alpha (LFA-1 alpha). There were increased numbers of S100-beta + dendritic cells and CD68+ macrophages in the luminal area of the lamina propria. Moreover double stainings revealed that most of the S100-beta + dendritic cells and CD68+ macrophages were intercellular adhesion molecule-1 (ICAM-1, a ligand for LFA-1) positive. These findings suggested that the expression of ICAM1 on S100-beta + dendritic cells and CD68+ macrophages is important by the interaction with T cells and T cell antigen recognition.

CD4-CD8 Ratio↗
PubMed1982

Abnormalities of T cells in patients with ulcerative colitis. FACS analysis of peripheral lymphocytes.

Heterologous antisera against human brain tissue and human embryonal thymocytes were used to distinguish the changes in lymphocyte subpopulations accompanying ulcerative colitis. Peripheral lymphocytes from normal individuals and from patients with ulcerative colitis were reacted with these heterologous antibodies, stained with fluoresceinated rabbit anti-human immunoglobulins, and analyzed by fluorescence-activated cell sorter. All of the fluorescence profiles of T cells in ulcerative colitis showed shifts with a marked increase in the population that had high fluorescence intensity. Time-course analysis by fluorescence-activated cell sorter revealed that the grade of fluorescence profile shift varied in accordance with the activity of the disease. Natural T-cell toxic autoantibody was found in 27 of the 35 patients with ulcerative colitis. Natural T-cell toxic autoantibodies from these patients reacted with 20% of peripheral T cells without Fc receptors. The abnormality of peripheral blood lymphocytes in ulcerative colitis may be caused by the production of autoantibodies.

Antigens, Surface↗