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[Collagenous colitis: clinicopathologic study of 6 new cases].

Collagenous colitis (CC) is a newly recognized entity characterized clinically by chronic watery diarrhoea and pathologically by epithelial inflammatory injury and the presence of a thickened collagen band beneath the surface epithelium of the colon. Clinical and pathological data of six patients (5 women and 1 man, mean age 54 years) with this diagnosis have been reviewed. Chronic watery diarrhoea was the main symptom in all cases, ranging from 2 to 12 bowel movements a day (mean +/- SD, 5.5 +/- 2.3) lasting from 8 months to 19 years (mean +/- SD, 6.6 +/- 5.9 years). Laboratory, barium and endoscopic studies showed unspecific findings. Rheumatic and thyroid diseases as well as drug allergies were found in five cases. The cause of collagenous colitis and the mechanism of diarrhoea remains undefined, being the inflammatory and autoimmune hypothesis the most likely. Diagnosis was made by multiple rectal and colonic biopsies. Pathologic findings characteristic of CC were more prominent in proximal than in distal colonic specimens. Different treatments were applied and diverse clinic responses were obtained. A review of the literature is made.

Adult↗

Budesonide treatment for collagenous colitis: a randomized, double-blind, placebo-controlled, multicenter trial.

BACKGROUND & AIMS: Collagenous colitis is an idiopathic microscopic colitis characterized by chronic watery diarrhea, a typical subepithelial collagen layer, and lymphoplasmacellular infiltration. We investigated the effect of budesonide on symptoms and histology in patients with collagenous colitis in a randomized, double-blind, placebo-controlled multicenter trial. METHODS: Patients with chronic diarrhea and histologically proven collagenous colitis were randomized to receive either oral budesonide (Entocort capsules; AstraZeneca, Sodertalje, Sweden) 9 mg/day for 6 weeks or placebo. Complete colonoscopy was performed before and after treatment. Histopathology was assessed by a single pathologist blinded to the patients' treatment. Clinical symptoms were assessed by standardized questionnaires. RESULTS: Fifty-one patients were randomized; 45 patients were available for per protocol analysis. The rate of clinical remission was significantly higher (P < 0.001) in the budesonide group than in the placebo group (per protocol 86.9% vs. 13.6%, respectively; intention-to-treat 76.9% vs. 12.0%, respectively). Histologic improvement was observed in 14 patients of the budesonide group (60.9%) and in 1 patient of the placebo group (4.5%; P < 0.001). Two patients in the budesonide group (7.7%) and 1 patient in the placebo group (4.0%) discontinued treatment prematurely because of side effects. CONCLUSIONS: Oral budesonide (Entocort capsules) is an effective and safe treatment modality for patients with collagenous colitis. Long-term follow-up of these patients is necessary to investigate whether clinical and histologic remission is sustained.

Administration, Oral↗

Collagenous colitis and cutaneous polyarteritis nodosa in the same patient.

Collagenous colitis is associated with chronic diarrhoea and inflammatory changes detected by colonic biopsy, but no endoscopic abnormalities. Cutaneous polyarteritis nodosa shows the same histopathology as systemic polyarteritis nodosa, but is limited to the skin. Both diseases are rare and of unknown aetiology. Collagenous colitis has been described in association with different autoimmune disorders. We report on a case of collagenous colitis and cutaneous polyarteritis nodosa. To our knowledge, this association has not been reported previously.

Colitis↗

[Collagen colitis: separate illness or syndrome?].

Six patients with collagenous colitis are described and the literature is reviewed. Collagenous colitis is not a rare disease. Its most prominent feature is profuse watery diarrhoea. Although the endoscopic picture of the mucosa is usually normal, there is a microscopic thickening of the (subepithelial) basement membrane. For diagnostic purposes, multiple colon biopsies are warranted in patients with chronic or relapsing diarrhoea. There is no established therapy for this disease.

Adult↗

Collagenous colitis: physiologic and histopathologic studies in seven patients.

Collagenous colitis is a clinicopathologic syndrome with chronic watery diarrhea, diffuse colitis with surface epithelial injury, and a distinctive collagen band beneath the surface epithelium especially in the proximal colon. The cases of seven patients (including six middle-aged women) with chronic, watery, noninfectious diarrhea were studied. Roentgenographic and endoscopic findings were not diagnostic. Two patients had rectal mucosal inflammation but sparing of the distal colon from subepithelial collagen. Other findings included thyroid disease (four patients), urethral fibrosis (three), elevated erythrocyte sedimentation rate (six), and eosinophilia (three). The colon was thought to be the main source of diarrheal fluid, but bile salt malabsorption, steatorrhea, and net small-bowel secretion were additive factors in some patients. With antiinflammatory treatment the diarrhea abated, the surface epithelial injury decreased, and the subepithelial collagen resolved (two patients), but lamina propria inflammation persisted. Collagenous colitis seems to be a chronic systemic, and perhaps autoimmune, disorder.

Adult↗

[Collagenous colitis: an entity with diverse therapeutic options].

Collagenous colitis is a disorder which has been diagnosed with increasing frequency in the last few years, probably due to the routine obtention of colon biopsy specimens in the study of patients with chronic diarrhoea. Good responses have been reported with a number of therapies, although only a scarce number of clinical trials have been performed, partly because of the small number of patients studied. Two cases of collagenous colitis with different therapeutic approaches are here reported. All medical therapy options for this interesting disorder are reviewed.

Administration, Topical↗

Enhanced histamine metabolism: a comparative analysis of collagenous colitis and food allergy with respect to the role of diet and NSAID use.

OBJECTIVES AND DESIGN: To compare clinical data and histamine metabolism of patients with collagenous colitis with those of food allergy. METHODS: In 17 patients with collagenous colitis, clinical findings (diarrhoea, abdominal pain) were recorded. Plasma (for histamine) and 12-h-urine (for histamine and n-methylhistamine, all measured by RIA) were collected during two days with an unrestricted diet followed by two days with an hypoallergenic. The clinical data and measured values were compared with those from patients with confirmed food allergy (n = 21) and controls (n = 41). RESULTS: Patients with collagenous colitis were found to present with significantly more liquid stools than patients with food allergy (p < 0.001) during both types of diet, but they did not experience more abdominal pain. N-methylhistamine in 12-h-urine was significantly increased during both types of diet in patients with collagenous colitis and food allergy when compared with controls (p < 0.001 for all). Patients with food allergy--but not those with collagenous colitis--showed a significant decrease of severity of pain (p < 0.05) when the diet was changed to the elimination protocol. CONCLUSION: Histamine is extensively produced and metabolised in patients with collagenous colitis. In contrast to food allergy, the allergenic potency of the administered food seems not to influence histamine production in collagenous colitis. However, histamine metabolism corresponds with the clinical activity in both patients with food allergy and collagenous colitis.

Aged↗

[Are lymphocytic and collagenous colitis two forms of a single disease? Arguments taken from a biopsy quantitative study].

Collagenous colitis and lymphocytic colitis are defined by a clinicopathologic syndrome with chronic watery diarrhea, microscopic lesions of colonic biopsies, and normal barium enema and colonoscopy. A histopathological study was performed on multiple colorectal biopsies to compare 12 cases of collagenous colitis (defined by a subepithelial collagen thicker than 10 microns) and 7 cases of lymphocytic colitis (defined by a number of intraepithelial lymphocytes more than 20 per 100 epithelial cells at least in one biopsied site). The study included a semiquantitative analysis of inflammatory infiltrate in the lamina propria, crypts distortion and epithelial detachment. The number of intraepithelial lymphocytes per 100 epithelial cells was determined in surface epithelium and crypts. The subepithelial collagen thickening was studied by computerised morphometry. The intraepithelial lymphocytes, villous atrophy and thickness of the subepithelial collagen were also determined in gastric and duodenal biopsies. In collagenous colitis, the subepithelial collagenous thickness ranged from 10 to 40 microns in the colon (median 20.99 microns). In 4 cases of collagenous colitis, no thickening of the collagen plate was seen in the rectum. We found constant epithelial detachment and mucosal distortion. In lymphocytic colitis, the thickness of the subepithelial collagen ranged from 6 to 10 microns in 4 cases and was less than 6 microns in 3 cases (median 6.24 microns). The median number of intraepithelial lymphocytes in surface epithelium was 22.35 (range 18.2 to 40) in lymphocytic colitis versus 12.22 (range 4.6 to 24.4) in collagenous colitis. In conclusion, we observed an overlap of both the collagenous plate thickness and the number of intraepithelial lymphocytes in collagenous colitis and lymphocytic colitis. This result favours a unified histogenesis for these two entities.

Colitis↗

Collagenous colitis in Orebro, Sweden, an epidemiological study 1984-1993.

The incidence and prevalence of collagenous colitis are unknown. An epidemiological study was undertaken between 1984-93. All patients living in the immediate catchment area of Orebro Medical Center Hospital with the diagnosis collagenous colitis were identified. Biopsy specimens classified as unspecific intestinal fibrosis were re-examined to identify cases not correctly diagnosed at first. Medical records were scrutinised and colorectal biopsy specimens re-evaluated. Thirty patients with collagenous colitis were diagnosed during the study period. The female:male ratio was 9:1. The median age at diagnosis was 64 (28-78) years. The prevalence at 31 December 1993, was 15.7/10(5) inhabitants (95% CI; 9.8 to 21.6/10(5)). The mean annual incidence during the period 1984-93 was 1.8/10(5) inhabitants (95% CI; 1.2 to 2.4/10(5)). A peak incidence was found in women 70-79 years old. Collagenous colitis occurs mainly in middle aged women, and the frequency is higher than earlier anticipated. The prevalence and incidence is similar to primary biliary cirrhosis. In women 70-79 years of age, the incidence for collagenous colitis approaches the incidence for ulcerative colitis.

Adult↗

Collagenous colitis: a disease of pericryptal fibroblast sheath?

Mucosal biopsies from four women with collagenous colitis and ten controls were studied. By light microscopy the cells of the pericryptal fibroblast sheath appeared diminished in number but increased in size in collagenous colitis. Electron optically in the controls the pericryptal fibroblasts were in intimate contact with the epithelial basal lamina in the crypts. On the free surface the fibroblasts maintained contact with the epithelial cells by attenuated cell processes. In collagenous colitis, in the middle and upper thirds of the crypts the fibroblasts sheath was separated from the epithelium and the fibroblasts assumed the characteristics of myofibroblasts. The separation was accentuated towards the mouths of the crypts. Beneath the surface epithelium the attenuated fibroblast cell processes seen in normal colon were grossly deficient. The basal lamina was also deficient focally and the surface epithelial cells were resting directly on a thickened collagen table. In collagenous colitis the excess collagen appeared to be secreted by the activated myofibroblasts of the pericryptal sheath.

Adult↗

Tenascin labelling in colorectal biopsies: a useful marker in the diagnosis of collagenous colitis.

AIMS: This study was undertaken to clarify whether immunohistological detection of tenascin (TN), an extracellular matrix glycoprotein that is expressed during stromal remodelling, may allow a more precise diagnosis of collagenous colitis. METHODS AND RESULTS: We studied multiple colorectal biopsies specimens from 15 patients with clinically suspected collagenous colitis for TN expression by using a monoclonal antibody. Biopsies from further 15 patients without symptoms and signs of collagenous colitis served as controls. In seven of the 15 cases with clinically suspected collagenous colitis a prominent and selective subepithelial tenascin expression was identified. The TN expression pattern closely correlated with the conventional detection of a subepithelial collagen band diagnostic of collagenous colitis. The immunohistological labelling for TN allowed a quicker and more precise measurement of the thickness of the diagnostic collagen deposits than conventional staining. By this approach one further case could be reclassified as collagenous colitis. CONCLUSIONS: Our data show that immunohistological detection of TN allows a more correct and easy diagnosis of collagenous colitis.

Adult↗

Collagenous gastroduodenitis on collagenous colitis.

We report on a case of collagenous gastroduodenitis with concomitant collagenous colitis in a 75-year-old woman with watery diarrhea of approximately six months' standing. The step biopsy material obtained from the colon revealed continuous collagenous colitis with thickening of the basal membrane to 30 microns. The biopsies taken from the stomach and duodenum also revealed a band-like deposition of collagen in the duodenum (bulb and proximal portion of the descending portion) along the basal membrane of the lining epithelium, associated with partial atrophy of the villi. In the stomach, this band of collagen was located, parallel to the mucosal surface, at the level of the floor of the foveolae.

Aged↗

Collagenous colitis in Spain: a report of nine new cases.

BACKGROUND: collagenous colitis is a clinicopathological entity that causes chronic watery diarrhea. The patients are predominantly women in the sixth or seventh decade of life. Radiological and endoscopic studies are usually normal or nonspecific. It is diagnosed by the presence in colonic biopsies of a thickened subepithelial band of collagen and an inflammatory infiltrate in the mucosa. METHODS: 9 cases diagnosed in our hospital and 18 previously described in Spain have been reviewed. RESULTS: all the cases showed chronic watery diarrhea. In 17 patients symptoms were present since at least one year before diagnosis. Five of the 27 patients had been taking nonsteroidal antiinflammatory drugs. Rheumatological and autoimmune diseases were found in 6 patients. Colonoscopy was normal or showed nonspecific findings except in one of our patients, in which aphthous ulcers and pseudomembranes were found. Different treatments had been employed, including antidiarrheal agents, sulfasalazine, 5-ASA and omeprazole. CONCLUSIONS: collagenous colitis is uncommon but should be considered in patients with long-standing chronic watery, nonbloody diarrhea. Collagenous colitis is probably more common than we think, as biopsies are not usually taken in cases of chronic diarrhea with normal endoscopic findings.

Adult↗

Collagenous colitis: are bacterial cytotoxins responsible?

In a case of collagenous colitis, cholestyramine treatment resulted in symptomatic and histological normalization. After discontinuation of cholestyramine, collagenous colitis relapsed. At this time fecal cytotoxic activity was demonstrated in McCoy cell lines. Symptoms, histologic changes, and cytotoxicity disappeared when cholestyramine treatment was reinstituted. We hypothesize that a bacterial toxin is responsible for the development of collagenous colitis.

Aged↗

Concurrent collagenous colitis and multiple ileal carcinoids.

A case of collagenous colitis in a patient with ileal carcinoid is described. Considerable fibrofatty thickening of the small bowel mesentery was present. The association of these findings appears to be unprecedented. Further observations are required to ascertain that collagenous colitis is one of the protean manifestations of carcinoid tumor.

Carcinoid Tumor↗

Distribution of collagenous colitis: utility of flexible sigmoidoscopy.

We investigated the distribution of the collagen band in 33 patients with collagenous colitis to estimate the likelihood of the disease being diagnosed in biopsy specimens from the left side of the colon, such as those obtained using flexible sigmoidoscopy. To be included in this study patients had a subepithelial collagen band greater than or equal to 10 microns, an increase in chronic inflammatory cells in the same specimen, and diarrhoea for which there was no other apparent cause. In 17 patients undergoing full colonoscopy with a thickened collagen band, collagenous colitis was frequently patchy, even though overall the thickened collagen band was almost equally distributed throughout the colon. Rectal biopsy specimens showed a normal collagen band in 73% of patients, while a thickened collagen band was found in 82% of patients in at least one specimen from the left side of the colon. Three patients had a thickened collagen band only in the caecum. In three of eight rectal biopsy specimens with a normal collagen band there was no mucosal inflammation to raise the possibility of proximal disease, although all but one specimen with a normal collagen band from the sigmoid and descending colon were inflamed. Rectal biopsy alone is therefore a relatively poor method of making the diagnosis. Flexible sigmoidoscopy with multiple biopsy specimens from several sites is a reasonable initial investigation but not sufficient to exclude collagenous colitis when based on the presence of a thickened collagen band alone. Should left sided biopsy specimens show a normal collagen band but an inflamed mucosa, total colonoscopy with multiple specimens including the caecum may be required to establish the diagnosis.

Adolescent↗

Collagenous colitis as the presenting feature of biopsy-defined celiac disease.

BACKGROUND: Prior case reports have linked celiac disease with collagenous colitis, but serological and retrospective pathologic survey studies of small intestinal biopsies have produced conflicting results. METHODS: In this report, consecutive patients with chronic diarrhea and the initial finding of collagenous colitis were evaluated to determine if occult celiac disease was also present. All 36 patients with no exclusions were offered upper endoscopy and biopsies. If the changes of untreated celiac disease were detected in the small intestinal biopsies, then a gluten-free diet was instituted. Diet response was based on resolution of diarrhea and normalization of repeated small intestinal biopsies. RESULTS: Eight patients, or over 20%, had severely abnormal small bowel biopsy changes characteristic of untreated celiac disease. In some, lymphocytic or collagenous gastritis were also detected with or without celiac disease. All 8 patients were treated with a gluten-free diet alone and, in all, diarrhea improved and small intestinal biopsies normalized. In 5, however, repeated colonic biopsies showed persistent collagen deposits. Autoimmune thyroid disease or neoplastic diseases, like lymphoma known to be associated with celiac disease were also noted in this cohort with collagenous colitis, often in the absence of celiac disease. CONCLUSIONS: This study indicates that collagenous colitis may be the presenting clinical and pathologic feature of celiac disease. Diagnosis of collagenous colitis should lead the clinician to consider exclusion of underlying occult celiac disease.

Adult↗

[Collagen colitis and lymphocytic (microscopic) colitis: different or common origin?].

Collagenous and lymphocytic colitis are two chronic inflammatory colonic diseases characterized by chronic watery diarrhea. They can only be diagnosed by histological examination of colonic biopsies. The pathogenesis is unknown, but may be of an inflammatory possibly autoimmune nature. Others hypothesize that a bacterial toxin or another noxious luminal factor is responsible for the development of the microscopic colitis syndrome. Some studies suggest that NSAIDs may be an etiologic factor in collagenous colitis in a subgroup of patients with this disease. These disorders may be different entities, although some data support the possibility that they are only different manifestations of the same disease. Therapy with 5-aminosalicylate and in severe cases corticosteroids, is successful in most patients. The course of these chronic diseases is commonly benign and is characterized by periods of spontaneous remissions and relapses, but clinical and histopathological resolutions are occasionally seen. On the basis of our own two cases and the literature, these two diseases will be discussed. These patients were admitted to our hospital within a month of each other due to therapy-refractive chronic watery diarrhea. A 70-year-old woman had been suffering from diarrhea for more than ten years. The histological examination produced a diagnosis of collagenous colitis. Lymphocytic colitis was diagnosed from a histological examination in a 30-year-old man who had been suffering from diarrhea for six months. Both received a therapy of mesalazine and the symptoms disappeared within three weeks.

Adult↗