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[Collagenous colitis. Morphologic and immunohistochemical study].

Collagenous colitis is a clinico-pathological entity characterized by chronic diarrhoeas and deposition of collagen beneath the epithelium surface of large bowel. We revised 265 endoscopy biopsy specimens of the large bowel from 198 consecutive patients with "aspecific chronic colitis". Morphometric study showed that were not significant differences among various tracts in the same patients regarding to the thickness of basament membrane. It was more than 11.9 +/- 0.49 mu only in 13 pts (6.6%), while it was 3.96 +/- 1.4 mu in the others. Immunohistochemistry study confirmed the normality of subepithelial basement membrane and the below deposition of the large quantity of collagen IV.

Aged↗

PubMed2004

Collagenous colitis: implications for the role of vascular endothelial growth factor in repair mechanisms.

OBJECTIVES: Collagenous colitis is a chronic inflammatory bowel disease with a band-like subepithelial deposition of immature extracellular matrix. Because the extracellular matrix deposition is potentially reversible, an imbalance between fibrogenesis and fibrolysis with reduced matrix degradation has been suspected. Vascular endothelial growth factor plays a central role in extracellular matrix degradation. Therefore, we investigated the expression of vascular endothelial growth factor in the colonic mucosa of patients with collagenous colitis before and after long-term treatment with oral budesonide. METHOD: A quantitative immunohistochemical method was used to measure the amount of immunoreactive vascular endothelial growth factor, tenascin and leucocyte common antigen within the epithelium and the lamina propria of colonic biopsies by area morphometry. RESULTS: Strong immunostaining for vascular endothelial growth factor within the epithelium and the lamina propria, and for tenascin, was seen in patients with collagenous colitis compared with normal controls. The enhanced immunostaining for vascular endothelial growth factor within the lamina propria was accompanied by the accumulation of leucocytes, detected by staining for leucocyte common antigen. After long-term treatment with oral budesonide, the amount of immunostaining for leucocyte-derived vascular endothelial growth factor within the lamina propria decreased significantly to normal levels. In contrast, staining for vascular endothelial growth factor within the epithelium remained significantly increased. CONCLUSIONS: Our data suggest an important role of vascular endothelial growth factor in counteracting the local imbalance of fibrogenesis and fibrolysis, leading to an accumulation of immature subepithelial matrix in collagenous colitis.

Administration, Oral↗

PubMed2001

Evidence of local eosinophil activation and altered mucosal permeability in collagenous colitis.

The local release of the inflammatory mediators eosinophil cationic protein and myeloperoxidase and the permeability marker albumin was studied in collagenous colitis using a new technique for segmental perfusion of the rectum and descending colon. Perfusion of both segments was successful in 19/25 (76%) of patients with collagenous colitis and controls with noninflammatory conditions. The concentration of myeloperoxidase was increased in the perfusion fluids from both segments in only one patient with collagenous colitis and in none of the controls. On the other hand, concentrations of eosinophil cationic protein and albumin in the perfusate from the rectum were significantly increased in collagenous colitis compared with controls, and similar trends were seen in the perfusates from the descending colon. Furthermore, there was a significant correlation between the increased concentrations of eosinophil cationic protein and albumin, indicating a possible relation between eosinophil activation and disturbed mucosal permeability in collagenous colitis.

Adult↗

PubMed1996

Collagenous colitis: a retrospective study of clinical presentation and treatment in 163 patients.

BACKGROUND: Data on collagenous colitis have been based on a limited number of patients. AIMS: To obtain more information on this disease from a register set up at Orebro Medical Center Hospital. PATIENTS AND METHODS: Twenty five Swedish hospitals have contributed to this patient register, which comprises 163 histopathologically verified cases. Clinical data were retrospectively analysed. RESULTS: Collagenous colitis followed a chronic intermittent course in most cases (85%) with a sudden onset in 42%. Symptoms were chronic watery diarrhoea, often nocturnal (27%), abdominal pain (41%), and weight loss (42%). Sixty six patients (40%) had one or more associated diseases. Routine laboratory data were mostly normal. The median age at diagnosis was 55 (range 16-86) years, but 25% of the patients were younger than 45 years. Seven patients died of unrelated diseases. The response rate for sulphasalazine was 59%, and 50% and 40% for mesalazine and olsalazine. Prednisolone was most effective with a response rate of 82%, but the required dose was often high and the effect was not sustained after withdrawal. Antibiotics were efficient in 63%. Cholestyramine and loperamide had response rates of 59% and 71% respectively. CONCLUSIONS: Collagenous colitis follows a chronic continuous course. Symptoms can be socially disabling, but the disease does not seem to have a malignant potential. A plan for the treatment of a newly diagnosed patient with collagenous colitis is proposed.

Adolescent↗

PubMed1988

Collagenous colitis with rapid response to sulphasalazine.

A case of collagenous colitis in a young female with a rapid response to sulphasalazine both symptomatically and histologically is reported. This is only the third such response to be reported. In most published accounts, collagenous colitis fails to respond to treatment and runs a very prolonged course.

Adult↗

PubMed1996

Lymphocytic and collagenous colitis: an immunohistochemical study.

OBJECTIVES: An increase of intraepithelial lymphocytes (IEL) is commonly found in lymphocytic colitis (LC) and collagenous colitis (CC), and has also been observed in the colonic mucosa of some patients with celiac disease or celiac-like disease. Thus, a similar mechanism could play a role in these apparently different entities. The aim of this work was to determine the phenotype of IEL and of lamina propria lymphocytes in the setting of LC and CC. METHODS: Biopsies were taken from all segments of the large bowel and from the ileon of eight patients with CC, four patients with LC, and 10 controls. An immunohistochemical study using monoclonal antibodies directed against IEL, T-cells, helper T-cells, suppressor/cytotoxic T-cells, HLA DR antigens, T-cell-bearing T-cell receptor (TcR) alpha beta, and TcR gamma delta was carried out. RESULTS: There was an increased in mean numbers of IELs in both LC and CC, with significantly more CD 8 IELs than CD 4 IELs. Most IELs were bearing TcR alpha beta; TcR gamma delta-bearing cells were not increased in CC or LC. CD 4+ helper T-cells predominated in the lamina propria. Epithelial cells of colonic mucosa abnormally expressed HLA DR antigens. There were no significant differences between findings in LC and CC. CONCLUSION: This study suggests that the immune abnormalities are similar in LC and CC and that a MHC-restricted immune mechanism could be involved in both diseases. Evidence for this includes: 1) the accumulation of CD 4+ T-cells within the lamina propria, 2) epithelial damage closely related to the increase of CD 8 TcR alpha beta IELs, and 3) abnormal class II MHC molecule expression on epithelial cells of colonic mucosa. Furthermore, the results suggest that the putative immune mechanisms underlying LC or CC are probably different from those that are incriminated in celiac disease.

Adult↗

PubMed1999

Fibrogenesis and fibrolysis in collagenous colitis. Patterns of procollagen types I and IV, matrix-metalloproteinase-1 and -13, and TIMP-1 gene expression.

Collagenous colitis is characterized by the deposition of a superficial subepithelial collagenous layer, the pathogenesis of which is unknown. Because the excess matrix deposition is potentially reversible, a labile imbalance between fibrogenesis and fibrolysis may be suspected. Expression of procollagen alpha1(I) and alpha1(IV), matrix-metalloproteinase (MMP)-1 and -13, and tissue inhibitor of metalloproteinase (TIMP)-1 genes was semiquantitated by in situ hybridization on serial biopsies of 12 patients with collagenous colitis and compared to controls. Collagen types I, III, IV, and VI, tenascin, undulin/collagen XIV, and alpha-actin were localized by immunohistology. The superficial collagen layer stained strongly for collagen types I, III, and VI, and particularly for tenascin, but not for undulin. Elevated procollagen alpha1(I), procollagen alpha1(IV), and TIMP-1 transcript levels were found in alpha-actin-positive cells with linear distribution underneath the superficial collagenous layer, whereas MMP-1 RNA expression was variable and restricted to cell clusters. MMP-13 expression was undetectable. The patterns of procollagen alpha1(I)- and alpha1(IV)-specific labeling, combined with an intense tenascin- but absent undulin-specific staining, indicate deposition of an immature interstitial matrix that may be susceptible to degradation. The restricted MMP-1 RNA expression, counteracted by increased TIMP-1 expression, suggests locally impaired fibrolysis as a relevant factor in the pathogenesis of collagenous colitis.

Adult↗

PubMed1998

Collagenous colitis in a patient with Addison's disease: a case report.

Diarrhea is a non-specific symptom which may be associated with Addison's disease and several causes had been demonstrated in the aetiology. We describe a patient with Addison's disease who was suffering from chronic diarrhea for three months. She was diagnosed as having collagenous colitis and successfully treated with Sulphasalazine, 2 g/day. Collagenous colitis is an uncommon cause of chronic diarrhea and the association of collagenous colitis with Addison's disease has not previously been described. We think that collagenous colitis may play a role in the aetiology of diarrhea in patients with Addison's disease and therefore we suggest a full colonoscopic examination in other patients with Addison's disease and diarrhea to determine the incidence of collagenous colitis in the aetiology of diarrhea.

Addison Disease↗

PubMed1991

Collagenous colitis: report of nine cases and review of the literature.

Collagenous colitis is characterized clinically by chronic watery diarrhea and pathologically by a distinctive band of collagen deposited below the colonic epithelium and an inflammatory cell infiltrate of the lamina propria. Since 1976, more than 100 cases have been described. We report an additional nine cases occurring in five women and four men ranging in age from 18 to 80 years. Diarrhea was present before diagnosis for 2 to 4 months in four cases and for 1 to 25 years in another four cases. One patient did not have diarrhea. Results of radiologic and stool studies were normal in all cases. All patients had flexible sigmoidoscopy or colonoscopy. Microscopic examination of biopsy material was interpreted as characteristic of collagenous colitis. Two cases resolved with psyllium mucilloid therapy alone. Of the five patients treated with azulfidine, three had marked improvement, one had partial response, and one had no change.

Adolescent↗

PubMed1981

[Collagen colitis. A new disease picture or merely a histological abnormality?].

"Collagenous colitis" has been recently defined as a new entity characterized by protracted diarrhoea, associated with subepithelial broadening of the collagen layer. A report is presented on two patients fulfilling the above criteria. Based on a critical analysis of these two cases and on prospective study of biopsies in 50 consecutive coloscopies it is concluded that a causal relationship between the enlarged collagen layer and the diarrhoea cannot be unequivocally established and hence "collagenous colitis" should not yet be considered a new entity.

Adult↗

PubMed2004

Collagenous colitis with spondyloarthropathy presenting as fibromyalgia syndrome.

Collagenous colitis is a newly recognized clinicopathologic entity that presents with diarrhea and weight loss. In some patients arthropathy may be a concomitant feature. We describe a patient whose initial presentation masqueraded as fibromyalgia with associated bowel symptoms, but who was finally diagnosed as having collagenous colitis and inflammatory spondyloarthropathy.

Colitis↗

PubMed1995

Collagenous colitis: mucosal biopsies and association with fecal leukocytes.

OBJECTIVE: To determine the frequency of patchy colonic involvement, fecal leukocytosis, and association with celiac sprue in a large cohort of patients with collagenous colitis. DESIGN: We conducted a retrospective review of the medical records of 172 consecutive Mayo Clinic patients in whom collagenous colitis had been diagnosed between 1982 and 1993. METHODS: For each of the 172 patients, the medical record was reviewed to determine the frequency of (1) fecal leukocytosis; (2) characteristic histologic findings in the rectum and the sigmoid, descending, and ascending colon; and (3) small bowel biopsy findings consistent with celiac sprue. RESULTS: The presence of fecal leukocytes was noted in 64 of 116 patients (55%) who had undergone assessment for fecal leukocytosis. On analysis of histologic findings, 113 of 123 rectal, 116 of 121 sigmoid, and 68 of 70 descending colon biopsy specimens were diagnostic of collagenous colitis. Small bowel biopsies were performed in 45 patients who did not have a history of small intestinal disease: 1 had celiac sprue and 44 had normal findings. Two other patients had previously diagnosed celiac sprue. CONCLUSION: The finding of fecal leukocytes in 55% of patients with collagenous colitis confirms the inflammatory basis of this disease. Biopsy specimens obtained by flexible sigmoidoscopy seem sufficient to establish the diagnosis in most patients, and colonoscopic biopsy of the more proximal area of the colon is usually unnecessary. Celiac sprue infrequently accompanies collagenous colitis; thus, routine small bowel biopsy is not warranted.

Adolescent↗

PubMed1988

Collagenous enterocolitis: a case of collagenous colitis with involvement of the small intestine.

A 78-yr-old previously well caucasian female presented with a 6-wk history of profuse watery diarrhea and weight loss. Clinical investigation showed evidence of mild malabsorption. Multiple biopsies of colonic mucosa revealed a wide subepithelial band of collagen typical of collagenous colitis. Duodenal biopsies showed similar collagen deposition and partial villous atrophy. Some amelioration of symptoms occurred with sulfasalazine therapy. This is the first reported case of collagenous colitis with histological evidence of small intestinal involvement. At least in some patients, collagenous colitis and collagenous sprue appear to be manifestations of a single disease. For such cases, the term collagenous enterocolitis is suggested.

Aged↗

PubMed2004

Effect of intravenous L-NMMA on nitric oxide production in collagenous colitis.

BACKGROUND: Nitric oxide (NO) is greatly increased in the colon of patients with inflammatory bowel disease of different aetiology, including collagenous colitis. In man, NO can be generated from NO synthases as well as from non-enzymatic sources. The source of the NO found in luminal intestinal gas has not been exactly pinpointed. We investigated the effect of the NO synthase inhibitor L-NMMA on intestinal concentrations of NO in patients with clinically active collagenous colitis. In addition, we measured NO levels from the respiratory tract. METHODS: Ten patients with active collagenous colitis were studied. NO levels were measured from the respiratory tract and in the rectum before and after i.v. administration of L-NMMA (7.5 mg/kg) using a chemiluminescence method. RESULTS: Airway NO release decreased markedly, and mean arterial blood pressure increased in all patients following L-NMMA treatment. Basal rectal NO levels were high (median > 10000 ppb) and decreased markedly in 5 patients after L-NMMA. In contrast, NO levels remained completely unchanged or even increased in the other 5 patients. CONCLUSION: Rectal levels of NO are greatly increased in patients with symptomatic collagenous colitis. Intravenous administration of an NO synthase inhibitor reduced rectal NO only in half of the patients despite clear evidence of effective systemic NO synthase inhibition. This could indicate alternative NOS-independent sources of intestinal NO in this disease.

Adult↗

PubMed1987

Collagenous colitis and rheumatoid arthritis with response to sulfasalazine. A case report and review of the literature.

Collagenous colitis has been associated with rheumatoid arthritis in only a few cases. We describe a 76-year-old man with chronic rheumatoid arthritis whose diarrhea and abdominal pain came from collagenous colitis. He had a good clinical response to sulfasalazine. We review the clinical and histopathological features of collagenous colitis, together with the different therapeutic approaches.

Aged↗

PubMed1989

Collagenous colitis, enteropathic arthritis, and autoimmune diseases: results of a patient survey.

We surveyed all patients with collagenous colitis seen at Johns Hopkins over a 4-year period, using a standardized, previously validated telephone questionnaire. Of 29 patients, 2(7%), including the index case, had monoarticular reactive arthritis. Five additional patients (17%) had a coexisting autoimmune illness. Collagenous colitis should be added to the list of causes of enteropathic arthritis. In addition, collagenous colitis should be considered in the differential diagnosis of diarrhea occurring in patients with known autoimmune diseases.

Aged↗

PubMed1992

Non-steroidal anti-inflammatory drugs as a possible cause of collagenous colitis: a case-control study.

The use of oral non-steroidal anti-inflammatory drugs (NSAIDs) in 31 patients with collagenous colitis and in 31 matched control patients with irritable bowel syndrome or colonic diverticular disease who had also undergone colonoscopy and biopsy was investigated. The long term use (greater than 6 months) of NSAIDs was significantly commoner in the study group (19/31) than in the control group (4/31) (p less than 0.02), even assuming the most adverse drug history in six patients in whom this could not be established. In all patients with collagenous colitis taking NSAIDs, diarrhoea followed the use of these drugs, and by a mean (SD) of 5.5 (4.4) years (range 0.5 to 15 years). In three patients with collagenous colitis, diarrhoea improved after withdrawing NSAIDs; rechallenge in one was followed by a recurrence of diarrhoea, which improved after withdrawing the drug again. It is suggested that NSAIDs may play an aetiological role in the diarrhoea and thickened collagen band in some patients with collagenous colitis.

Adult↗

PubMed2003

Pyoderma gangrenosum in a patient with collagenous colitis.

The association between pyoderma gangrenosum and inflammatory bowel disease is well established. Collagenous colitis is one of the microscopic colitides, which are thought to be on the same spectrum of disease as Crohn's disease and ulcerative colitis. Before this study there had been no reported cases of pyoderma gangrenosum in the setting of collagenous colitis. We report a case of a 79-year-old woman with symptomatic collagenous colitis and refractory pyoderma gangrenosum.

Administration, Oral↗