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PubMed2003

Collagenous gastritis in a young Japanese woman.

Collagenous gastritis, a counterpart of collagenous colitis, is a rare disorder with less than 20 cases reported in the literature. A case of collagenous gastritis in a Japanese woman in her early 20s who had been receiving treatment for atopic dermatitis and bronchial asthma is reported. The patient complained of repeated epigastric pain, and endoscopy revealed multifocal atrophic areas and scars in the gastric body. Biopsy specimens showed a thickened eosinophilic band-like structure with entrapped capillaries approximately 30-70 micro m thick beneath the surface epithelium. It was regarded as a collagen band because it was positive on Azan staining but negative on amyloid staining. This finding was accompanied by marked infiltration of mononuclear cells and eosinophils in the lamina propria; however, no evidence of lymphocytic gastritis was found. Helicobacter pylori infection was not detected and inflammatory cell infiltration was minimal in the mucosa without the collagen band. Immunohistochemical analysis revealed that the band was positive for type III and type VI collagen. The size of the collagen band did not change for 2 years. These findings suggest that subepithelial collagen deposition was due to an abnormal local immune response based on generalized allergic disorder.

Adult↗
PubMed1998

[Drug-associated hemorrhagic enteritis].

Drug-associated hemorrhagic colitis are divided into antibiotic associated hemorrhagic colitis (AAHC) and other drug associated hemorrhagic colitis. AAHC are mainly caused by oral usage of Ampicillin and its derivatives (85%). Initially AAHC are believed to be caused by Klebsiella oxytoca overgrowth. However, these organisum has no exotoxin like Clostridium difficile and pathogenesis of AAHC are still unresolved. Typical AAHC are diagnosed by colonoscopy with diffuse hemorrhage and edema mainly found in descending colon and transverse colon. NSAIDs are also the cause of hemorrhagic colitis like AAHC. Mephenamic acid are famous for this complication. Diarrhea is one of the main complication of oral 5-fluorouracil administration and even causes hemorrhagic colitis. Its histology are characteristic in gland atrophy. Gold colitis are reported 36 cases in rheumatoid arthritis patients. Exact mechanism of bleeding are not understood. NSAIDs may cause collagenous colitis and or lymphocytic colitis in RA patients. Other rare hemorrhagic colitis are associated with azathioprine, methyl dopa, interferon alfa etc. NSAIDs and anticoagulants are well known drugs for complication of GI bleeding making hemorrhagic enteritis.

Ampicillin↗
PubMed1990

Antireticulin antibodies in collagenous and lymphocytic (microscopic) colitis.

Serum antireticulin antibodies (ARAs) are often present in patients with dermatitis herpetiformis and celiac disease (CD), especially before instituting a gluten-free diet. In both collagenous colitis (CC) and lymphocytic (microscopic) colitis (LC) the colorectal mucosa shows surface epithelial damage with intraepithelial lymphocytes that is strikingly comparable to the small intestinal findings in CD. Also, CD may show subepithelial collagen deposition resembling that seen in CC. Because of these similarities, ARAs were measured in sera from patients with biopsy-proven CC and LC and compared with sera tested from CD patients. Antibody binding to reticulin was detected in frozen sections of rat liver and kidney by indirect immunofluorescent techniques. Whereas five of 14 CD patients (35.7%) had ARAs, only one of 29 CC patients (3.4%) (P = 0.010 versus CD) and none of 17 LC patients (0%) (P = 0.012 versus CD) had ARAs. The positive CC patient had IgA ARA titers of 1:20 noted in two sera taken 2 mo apart. The five positive CD patients had IgA ARA titers ranging from 1:20 to 1:320. The rare presence of ARAs noted in collagenous colitis and lymphocytic colitis was similar to its occurrence in normals, whereas the frequency of ARAs found in celiac disease (35.7%) was within the range reported for that disorder. Therefore, ARAs do not appear to be associated with CC or LC despite the morphologic similarities to CD.

Adult↗
PubMed1988

Diffuse excess mucosal collagen in rectal biopsies facilitates differential diagnosis of solitary rectal ulcer syndrome from other inflammatory bowel diseases.

Solitary rectal ulcer syndrome (SRUS) is sufficiently uncommon that the clinician or general pathologist may lack familiarity with the disorder and may confuse it with other inflammatory bowel diseases. To evaluate the role of collagen staining in facilitating the differential diagnosis of SRUS, an initial open review was undertaken on 1672 consecutive patients whose 4780 colorectal biopsies were stained with H&E with added saffron to demonstrate collagen. Excess mucosal collagen was present in 39 (2.3%) of these patients. Twenty patients with a diffuse excess of mucosal collagen in biopsies from rectal ulcer margins or from otherwise abnormal rectal mucosa had SRUS; in the remaining 19 patients, excess mucosal collagen was focal (seven ischemic colitis, five collagenous colitis, three adenocarcinoma, and four chronic idiopathic ulcerative colitis). Diffuse excess mucosal collagen never was seen in idiopathic inflammatory bowel disease (128 Crohn's colitis and 446 ulcerative colitis). Blinded reviews then were performed on rectal biopsies from 33 patients with a variety of diagnoses (14 SRUS and 19 controls). Diffuse excess collagen by saffron staining was consistently observed in SRUS but was absent in all 19 controls. Additional blinded reviews were carried out because the collagen staining pattern in ischemic colitis, although focal, could potentially be confused with SRUS. It was possible to differentiate these two diseases blindly from one another by using additional histologic criteria (14 SRUS and 12 ischemic colitis). We conclude that the demonstration of a diffuse excess of mucosal collagen in rectal biopsies facilitates the diagnosis of SRUS and differentiates it from idiopathic ulcerative colitis and Crohn's disease, with which SRUS is often confused, and other inflammatory bowl diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1993

[Side effects of non-steroidal antirheumatic agents in the lower intestinal tract].

Side effects of non-steroid anti-inflammatory drugs (NSAIDs) on the lower intestinal tract are reviewed. NSAID use may exacerbate or reactivate quiescent inflammatory bowel disease. There are distinct types of NSAID-induced enterocolitis: ulcerative colitis, Crohn's disease, and necrotizing enterocolitis in premature infants. It is also suggested that NSAIDs may play an etiological role in collagenous colitis. Furthermore, NSAIDs may induce ulcerations, perforations and strictures in the small as well as large bowel. Occult and severe blood loss from lower intestinal tract under treatment with NSAIDs should be kept in mind.

Adolescent↗
PubMed2001

Collagenous gastritis associated with lymphocytic gastritis and celiac disease.

Collagenous gastritis is a rare disorder, with only 8 cases reported in the literature, 2 in children and 6 in adults. We report an additional case of collagenous gastritis in a 42-year-old man with celiac disease. A thickened (>10 microm) subepithelial collagen band with entrapped capillaries, fibroblasts, and inflammatory cells was seen in the stomach, associated with lymphocytic gastritis. The duodenal mucosa showed severe villous atrophy but no subepithelial collagen deposition. No evidence of lymphocytic or collagenous colitis was found in the colon. The patient became symptom-free on a gluten exclusion diet and showed partial improvement of histopathologic findings after 3 months. Collagenous gastritis is a rare disease, but a wider recognition of its histopathologic features and clinical associations may bring more cases to light and provide additional clues in determining its etiology and pathogenesis.

Adult↗
PubMed1991

Anti-neutrophil cytoplasmic antibodies in ulcerative colitis. Comparison with other colitides/diarrheal illnesses.

Previous studies from this laboratory showed that serum anti-neutrophil cytoplasmic antibodies, distinct from those associated with active Wegener's granulomatosis, are present in the majority of patients with ulcerative colitis. In this study, the specificity of anti-neutrophil cytoplasmic antibodies for ulcerative colitis as compared with other colitides and diarrheal illness was determined. In a blinded study, test samples of serum were screened for anti-neutrophil immunoglobulin G in a fixed neutrophil enzyme-linked immunosorbent assay. Levels of neutrophil binding by immunoglobulin G and titers of anti-neutrophil immunoglobulin G in sera from patients with ulcerative colitis and patients with ulcerative colitis post colectomy were each significantly greater than the levels and titers for normal controls and patients with a variety of other colitides and diarrheal illnesses. Levels of neutrophil binding for colonic Crohn's disease, bacterial/amoebic colitis, the irritable bowel syndrome with diarrhea, and other miscellaneous diarrheal illnesses were not significantly different than the levels for normal controls. Although the levels of binding for collagenous colitis were significantly less than the levels for ulcerative colitis, they were significantly greater than the levels for normal controls. Patterns of neutrophil binding by serum samples that were positive in the enzyme-linked immunosorbent assay were determined by indirect immunofluorescence. Perinuclear staining was the predominant pattern shown by sera from patients with ulcerative colitis. The combination of a positive value in the enzyme-linked immunosorbent assay and a perinuclear immunofluorescence pattern was 60% sensitive and 94% specific for ulcerative colitis. It is concluded that anti-neutrophil cytoplasmic antibodies in ulcerative colitis are not simply an epiphenomenon related to inflammation of the colon. Identification of the antigen(s) to which these autoantibodies are directed may facilitate understanding of the underlying immune response and may allow development of an assay that is more sensitive and specific for ulcerative colitis.

Adult↗
PubMed2002

[Microscopic colitis].

Microscopic colitis is an umbrella term for a newly described group of colitides, belonging to the inflammatory bowel diseases, which are only diagnosable by microscopic evaluation of a macroscopically normal colon mucosa. Collagenous colitis and lymphocytic colitis are the most common of these colitides. Microscopic colitis is characterised clinically by chronic non-bloody watery diarrhoea. Crampy abdominal pain, nocturnal diarrhoea, urgency, and initial weight loss are usual. Concomitant diseases of autoimmune origin and arthralgia are commonly seen. Treatment of microscopic colitis follows the guidelines for treatment of other inflammatory bowel diseases, but a substantial part of the patients with microscopic colitis enter spontaneous remission after some years. A minor part, however, have very troublesome symptoms and are almost refractory to treatment. Microscopic colitis has apparently no malignant potential.

Chronic Disease↗
PubMed2001

Neutrophil transmigration in inflammatory bowel disease is associated with differential expression of epithelial intercellular junction proteins.

Inflammatory bowel disease (IBD) consisting of ulcerative colitis (UC) and Crohn's (CD) typically displays a waxing and waning course punctuated by disease flares that are characterized by transepithelial migration of neutrophils (PMN) and altered barrier function. Since epithelial barrier function is primarily regulated by the apical most intercellular junction referred to as the tight junction (TJ), our aim was to examine expression of TJ and adherens junction (AJ) proteins in relation to PMN infiltration in mucosal tissue samples from patients with active IBD. Expression of epithelial intercellular TJ proteins (occludin, ZO-1, claudin-1, and JAM) and subjacent AJ (beta-catenin and E-cadherin) proteins were examined by immunoflourescence/confocal microscopy, immunohistochemistry, and Western blotting. Colonic mucosa from patients with UC revealed dramatic, global down-regulation of the key TJ transmembrane protein occludin in regions of actively transmigrating PMN and in quiescent areas in the biopsy samples. Significant decreases in occludin expression were observed at the protein and mRNA levels by Western and Northern blotting. In contrast, expression of other TJ and AJ proteins such as ZO-1, claudin-1, JAM, beta-catenin, and E-cadherin were down-regulated only in epithelial cells immediately adjacent to transmigrating PMN. Analysis of inflamed mucosa from Crohn's disease patients mirrored the results obtained with UC patients. No change in TJ and AJ protein expression was observed in colonic epithelium from patients with collagenous colitis or lymphocytic colitis that are respectively characterized by a thickened subepithelial collagen plate and increased intraepithelial lymphocytes. These results suggest that occludin expression is diminished in IBD by mechanisms distinct from those regulating expression of other intercellular junction proteins. We speculate that down-regulation of epithelial occludin may play a role in enhanced paracellular permeability and PMN transmigration that is observed in active inflammatory bowel disease.

Adherens Junctions↗
PubMed1994

Unusual colitides.

Colitis is an important cause of abdominal pain and diarrhoea and is the main cause of blood and mucus in the stool. The inflammation can be due to infectious or to non-infectious causes, most commonly ulcerative colitis and Crohn's disease. However, a wide variety of rarer causes of colitis also present in childhood. These include colitis or enterocolitis secondary to Hirschsprung's disease and metabolic disorders (which include Hermansky-Pudlak syndrome, glycogen storage disease type 1b and pellagra). Primary inflammation of the colon is seen in microscopic and collagenous colitis, ulcerating enterocolitis of infancy, allergic colitis and autoimmune enteropathy. The histological pattern of each of these diseases has a characteristic picture and separates them from each other from ulcerative colitis and Crohn's disease. The pathophysiology of these rare forms of colitis in childhood is not clear; but in the future they may give us an insight into the pathogenesis of large bowel inflammation, particularly when the colitis occurs secondary to an established disease.

Child↗
PubMed2001

[Therapeutic principles for chronic inflammatory bowel disease].

Whereas the incidence of ulcerative colitis has remained stable at around 8-9/10(5), the incidence of Crohn's disease has increased from below 1 to more than 5/10(5) per year during the last three decades. The new disease entities, collagenous colitis and lymphocytic colitis, are now covered by the term, chronic inflammatory bowel disease. The general principles of treatment of these diseases are to induce remission of outbreaks and to prevent outbreaks during remission. Available pharmaceutical products are 5-aminosalicylic acid preparations, with different delivery profiles in the gastrointestinal tract, glucocorticoids, and other immunosuppressants, especially azathioprine. New immunomodulating agents, with a specific effect on intracellular processes in the inflammatory cascade are now being developed, and infliximab, a TNF-alpha antibody, is now an accepted agent for use in severe, treatment-resistant cases of fistulising Crohn's disease. When medical treatment fails, surgical treatment is an option. In ulcerative colitis, colectomy is, in principle, curative, but it leaves the patient with either a permanent ileostomy or an ileal pouch, which serves as an artificial rectum after ileoanal anastomosis. This latter procedure has the obvious advantage of giving the patient a normal bowel continuity, but complications in the form of intractable "pouchitis" have been experienced in a small number of patients, thus necessitating removal of the pouch. Patients with Crohn's disease, who do not respond to medical treatment or present signs of stenosis in either the small or the large bowel, must be given surgical treatment, although an operation is less curative than in ulcerative colitis. Surgical resections for Crohn's disease must therefore be more conservative, so as to preserve the bowel and only remove macroscopically affected tissue.

Adjuvants, Immunologic↗
PubMed1999

[Chronic diarrhea due to lymphocytic colitis treated with piroxicam beta cyclodextrin].

BACKGROUND: Lymphocytic colitis is a chronic diarrhea syndrome with no endoscopically detectable anomaly and histological colonic lesions. CASE REPORT: A 52-year-old woman was hospitalized for chronic diarrhea. She experienced 10 to 30 liquid bowel movements per day. Symptoms had begun 8 days after taking piroxicam fl-cyclodextrin. Intraepithelial cell counts on rectum and colon endoscopic biopsies showed more than 20% lymphocytes, giving the diagnosis of lymphocytic colitis. The patient was given 5ASA 3 g/24 h. Symptoms regressed in less than one week. DISCUSSION: Lymphocytic colitis is uncommon. The cause remains unknown but a secondary autoimmune mechanism triggered by drugs has been suggested. This case would implicate nonsteroidal antiinflammatory drugs. Certain authors have demonstrated that they can be involved in the development of collagen colitis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2004

[Microscopic colitis. A possible diagnosis in secretory diarrhea].

The colitis microscopic was characterized by chronic watery diarrhea accompanied or not of abdominal pain. Present in patients of median age and the diagnosis was realized by means of the microscopic finds of a mucus of colon with an aspect macroscopic normal. They exist 2 types microscopically distinct, the collagenous colitis and the lymphocytic colitis. We referred 2 cases of each one of the types of microscopic colitis, whose manifestation clinic in common was the chronic watery diarrhea.

Abdominal Pain↗
PubMed1996

The differential expression of a novel intestinal epithelial glycoprotein in various forms of inflammatory bowel disease.

A13D8 is a monoclonal IgM antibody that identifies an as yet unknown antigen that is expressed intensely and ubiquitously in enterocytes. Immunohistochemically, it was shown that A13D8 has a granular supranuclear staining pattern in columnar epithelial cells of normal small intestine and the colon. In ulcerative colitis, this staining pattern was retained. However, during active inflammation, staining also was evident in goblet cells. To test whether this feature of goblet cell staining was unique to ulcerative colitis, tissue sections from a variety of colitides were examined. Crohn's disease, infectious colitis, and ischemic colitis had similar staining patterns to that seen with ulcerative colitis. There was significantly more inflammation in the biopsies from patients with ulcerative colitis and Crohn's disease with positive goblet cell staining than in the biopsies from those patients with negative goblet cell staining. Almost all positive goblet cell staining in ulcerative colitis and Crohn's disease occurred in biopsies that were actively inflamed, whereas there was rare staining in biopsies that were noninflamed (regardless of whether or not there was active inflammation elsewhere in the colon). Ileal goblet cells stained positively with A13D8 only in cases of active ileitis. In cases of collagenous colitis, with comparable degrees of inflammation to that seen in ulcerative colitis and Crohn's disease, there was rarely goblet cell staining and in graft-versus-host disease goblet cell staining of A13D8 was not observed. The binding of A13D8 to tissue sections was completely inhibited by N-acetyl-D-galactosamine. These results, in conjunction with immunochemical studies, suggest that the antibody recognizes an N-acetyl-D galactosamine-containing epitope on a glycoprotein(s). In conclusion, these data suggest that A13D8 recognizes a glycoprotein expressed by intestinal columnar epithelial cells and during specific inflammatory states, particularly those associated with a neutrophilic infiltrate, becomes evident in goblet cells. Further work is required to establish the exact nature of this molecule and whether it is a pro- or anti-inflammatory factor.

Antibodies, Monoclonal↗
PubMed2002

Microscopic colitis: the tip of the iceberg?

OBJECTIVES: The aims were to determine whether a wide variation exists between hospitals in the diagnosis of microscopic colitis and to assimilate clinical data. DESIGN: Retrospective study of 90 patients with microscopic colitis aged between 16 and 92 years from 11 hospitals in south-east England. METHODS: A questionnaire was designed to collect relevant data from all patients in whom a new diagnosis of microscopic colitis had been made at the source hospital between January 1990 and December 1996. The inclusion criteria were presentation with watery diarrhoea, a normal endoscopy and a histological report of microscopic colitis. Histology slides were then requested and reviewed. Clinical data were analysed with reference to the confirmed diagnosis. RESULTS: The number of patients diagnosed at each hospital ranged between zero and 30, with a median of six. Sixty-eight patients had histological slides reviewed. The numbers of patients with a final reviewed diagnosis of collagenous colitis, lymphocytic colitis and microscopic colitis, type undesignated, were 37, 18 and seven respectively. In thirty-one patients (34%) there was a recent history of the use of non-steroidal anti-inflammatory drugs. CONCLUSIONS: These data confirm that there is wide hospital variation in the diagnosis of microscopic colitis. Furthermore, the small group with the undesignated type may be associated with the use of non-steroidal anti-inflammatory drugs.

Adolescent↗
PubMed1991

[Prerequisites for therapy of inflammatory bowel diseases. Pathophysiology--symptomatology--diagnosis].

The etiology of the idiopathic chronic inflammatory bowel diseases Crohn's disease and ulcerative colitis remains unclear. Differences in prognosis, medical and surgical treatment, and the nature of expected complications require not only a differential diagnosis vis-a-vis other disorders, but also the correct diagnosis of these two diseases. Symptomatology and clinical presentation can be mimicked both by infectious, ischemic and other chronic bowel diseases such as collagenous colitis, eosinophilic colitis, and Behçet's disease. This means that, in the absence of pathognomonic changes, the correct diagnosis can be established only on the basis of all the findings (laboratory, endoscopy, X-rays), and sometimes only on the basis of the course of the condition. The most important differential diagnostic procedure has proved to be ileocolonoscopy, since in addition to gross evaluation of the mucosa, targeted removal of biopsy specimens is also possible.

Colitis, Ulcerative↗
PubMed2001

[Collagen gastritis, an unusual cause of anemia in children. Report of 2 cases].

UNLABELLED: When a child presents a severe anemia or resistant to iron supplementation, an upper gastrointestinal endoscopy has to be realized to find special causes. CASE REPORTS: We report observations of two patients, respectively 11 and 12 years old, who were admitted to hospital for a severe microcytic, hypochromic, aregenerative anemia (hemoglobin less than 50 g/L) due to an iron deficiency. The two children's history did not reveal a deficient diet, gastrointestinal tract disorder, ingested toxic or gastrotoxic drugs, or exteriorized hemorrhage. Upper gastrointestinal endoscopy showed a macroscopic pattern of gastritis. The stomach biopsies revealed subepithelial collagenous deposits. CONCLUSION: The collagenous gastritis involves lesions similar to those described in the small intestine (collagenous sprue) and colon (collagenous colitis). The pathogenic factors of the three entities are presently unknown, but they are often associated with autoimmune pathology. These two observations are the third and the fourth pediatric cases described.

Anemia↗
PubMed1987

Is biopsy necessary if colonoscopy is normal?

Multiple endoscopic biopsies were taken from 100 consecutive patients who had a macroscopically normal colon at colonoscopy. Of these, 78 were regarded as histologically normal; 13 cases of melanosis coli, 7 cases of intestinal spirochetosis, and 2 cases of collagenous colitis were identified. In no cases was there histologic evidence of inflammatory bowel disease. Histologic abnormality could not be predicted by retrospective analysis of various clinical, hematologic and biochemical data. In individual subjects the microscopic abnormality was present to a varying degree in all biopsies, except in intestinal spirochetosis where patchy distribution occurred in some subjects. It is therefore concluded that significant pathology may be missed without biopsy of the apparently normal colon, but in order to reduce the workload of pathology departments and shorten the duration of the examination two biopsies from the hepatic flexure and sigmoid colon may be adequate.

Adolescent↗