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We report the case of a female patient who suffered from collagenous colitis for 13 years, the complications of which may have contributed to her death. The disease was associated with seropositive rheumatoid arthritis and Sjögren's syndrome. Cases of collagenous colitis with a course leading to death have not been reported in the literature, to the best of our knowledge.
We examined 129 colonic biopsies from 21 patients with collagenous colitis, most of whom presented with diarrhoea. Morphometric measurements gave a mean thickness of the subepithelial collagen deposit of 19.5 mu +/- 5.1. The trapped fusiform and/or stellate cells within the deposits were identified immunohistochemically as myoid cells, being positive with antibody against smooth muscle cell alpha-actin. Ultrastructurally, these cells have all the characteristic features of myofibroblasts. Similar cells are also present along the crypts, where they were formerly referred to as pericryptal fibroblasts. Although there is still much debate as to the pathogenesis of this condition, we would like to suggest that collagenous colitis is a disease of pericryptal myofibroblasts. During their migration and maturation into the subepithelial region they may synthesize an excess of collagen, under some yet unknown or undefined stimulus/stimuli.
OBJECTIVES: To conduct a systematic review to determine effective treatments for patients with clinically active collagenous colitis. METHODS: Relevant articles were identified via the MEDLINE, PUBMED, and Cochrane Collaboration databases, manual searches of the references of identified articles, and review articles on collagenous or microscopic colitis, as well as searches of abstracts from major gastroenterological meetings. RESULTS: Five randomized trials assessing treatments for collagenous colitis were identified. One trial studying bismuth subsalicylate (nine 262 mg tablets daily for 8 wk) included 9 patients. Patients who received the bismuth preparation were more likely to have clinical (p= 0.003) and histological (p= 0.003) improvement than those who received placebo. In a trial comparing prednisolone (50 mg daily for 2 wk) to a placebo in 11 patients, a trend toward clinical response in patients on prednisone was reported (p= 0.064). The effect of prednisolone on histological improvement was not studied. A total of 94 patients were enrolled in three trials studying budesonide (9 mg daily or in a tapering schedule for 6-8 wk). The pooled odds ratio for clinical response to treatment with budesonide was 12.32 (95% CI: 5.53-27.46). The NNT (number of patients needed to treat with budesonide to achieve 1 improved patient) was 2 patients. This therapy was well tolerated. There was significant histological improvement with treatment in all three trials studying budesonide therapy. CONCLUSIONS: There is strong evidence that budesonide is effective and well tolerated for the treatment of collagenous colitis. The evidence for benefit with bismuth subsalicylate or prednisolone is weaker. It is not clear that any of these agents produce actual remission, as opposed to clinical and histological improvement of the disease.
In a 37-year-old woman with chronic watery diarrhea of three years duration, the diagnostic of collagenous colitis was established by optical and ultrastructural examination of rectal and colonic biopsies. No other cause of diarrhea could be found. Moreover, this patient had also selective IgA deficiency, Grave's disease and chronic atrophic gastritis of auto-immune type. Sequential treatments with loperamide, cholestyramine and antibiotics did not modified diarrhea which improved with salazosulfapyridine and betamethasone enemas. These observations suggest that collagenous colitis might be a part of the spectrum of enteropathies associated with immunoglobulin deficiencies.
A 37-year-old woman presented with an acute abdomen following the onset of watery diarrhea. Spontaneous peritonitis was detected, along with evidence of a focal sigmoid colon perforation. Subsequent postoperative colonoscopic studies revealed collagenous colitis with a focal, deep, nongranulomatous ulcer in the sigmoid colon. Although the literature suggests that collagenous colitis tends to have a relatively 'benign' clinical course characterized by chronic or episodic watery diarrhea. Potentially serious and life- threatening complications may occur in this microscopic form of inflammatory bowel disease.
A patient with rheumatoid arthritis and collagenous colitis apparently responding to sulfasalazine and prednisolone enemas is reported. It is suggested that this form of therapy should be considered in patients with this rare disorder not only as a short-term measure but also, in the case of sulfasalazine, as long-term treatment in patients with chronic symptoms.
We report the first case of coexisting progressive systemic sclerosis and collagenous colitis in a 12-year-old girl.
We present the case of a 45-yr-old female patient with a 23 yr history of interstitial cystitis that multiple surgical procedures, including a ceco-cystoplasty, were unable to cure. After a cystectomy was performed, histological examination of the bladder showed the development of collagenous colitis. Although the etiology of both interstitial cystitis and collagenous colitis is unknown, this report postulates an association between these two conditions.
Patients with symptomatic collagenous-lymphocytic colitis should eliminate dietary secretagogues such as caffeine- or lactose-containing food from their diet. When possible, use of nonsteroidal anti-inflammatory drugs should be discontinued. If steatorrhea is documented, a low-fat diet may be helpful. In the presence of bile salt malabsorption, binding resins such as cholestyramine might be useful. Nonspecific diarrheal agents such as loperamide hydrochloride, diphenoxylate hydrochloride and atropine, deodorized tincture of opium, or codeine might prove effective in some patients. Antibacterial agents such as bismuth subsalicylate (8 chewable 262-mg tablets daily) have been effective in symptom control. Metronidazole and erythromycin achieve response rates of 60%. Sulfasalazine, at the usual dose of 2 to 4 g daily, used in collagenous-lymphocytic colitis, demonstrated cessation of diarrhea in 1 to 2 weeks for 50% of patients. Other 5-aminosalicylic (5-ASA) compounds are preferred for patients with a history of sulfa allergy, and those who experience adverse reactions to sulfasalazine. Adrenocorticoid medication is reserved for patients whose conventional treatment with sulfasalazine or 5-ASA has failed. Resolution of diarrhea has been documented in 80% to 90% of patients within 1 week of treatment, however, in most patients, long-term therapy is required. Surgical management is reserved for those patients with disease refractory to medical therapy. Colectomy with ileostomy resulted in clinical and histologic resolution in small case series. If there is no abatement of symptoms, rule out other etiologies of diarrhea such as thyroid dysfunction, celiac disease, or bacterial overgrowth.
We report a case of a 62-year-old man who developed watery diarrhoea after starting treatment with cimetidine for dyspepsia. Macroscopically, sigmoidoscopy and colonoscopy were normal. Histology revealed features consistent with a diagnosis of collagenous colitis. The diarrhoea is responding to treatment with prednisolone and withdrawal of cimetidine. We conclude that the collagenous colitis may have been drug induced.
When the usual workup for chronic diarrhea fails to provide a diagnosis and the endoscopic findings are normal, alternative etiologies must be considered. This case of collagenous colitis represents such an alternative diagnosis. The patient is a 65-year-old woman who complained of abdominal cramps and watery diarrhea for an 8-month span. The key element to her diagnosis was subepithelial collagen deposits of the mucosa of the colon. Her symptoms were resolved with supportive care, diet, and diphenoxylate. Essential features and treatment of collagenous colitis are reviewed.
The present report describes the morphologic findings in sequential colorectal biopsy specimens obtained from 2 patients who within 1.5-2.5 yr developed collagenous colitis. The initial biopsy specimens revealed an acute nonspecific inflammatory reaction in the colorectal mucosa. An intermediate stage, characterized by edema and slight fibrosis in the subepithelial region of the colorectal mucosa, preceded the final development of collagenous colitis. We suggest that the mechanism that leads to the formation of a thick, bandlike subepithelial collagenous deposit in the colorectal mucosa may be triggered off by some inflammatory or toxic stimulus.
A middle-aged female with chronic, watery diarrhea was diagnosed after extensive evaluation as having collagenous colitis. The clinical, histological, and pathological findings of our case and those previously reported are reviewed. The diagnostic importance of total colonoscopy with biopsy in a normal-appearing colon in a patient with chronic, undiagnosed, watery diarrhea is discussed.
BACKGROUND AND AIMS: Luminal nitric oxide (NO) is greatly increased in the colon of patients with collagenous and ulcerative colitis. To define the source and consequence of enhanced NO production we have studied expression of NO synthase (NOS) isoforms and nitrotyrosine in mucosal biopsies from these patients. In addition, effects on colonic fluid transfer caused by manipulating the substrate of NOS were studied in patients with collagenous colitis. PATIENTS: Eight patients with collagenous colitis, nine with active ulcerative colitis, and 10 with uninflamed bowel were included. METHODS: Expression of NOS isoforms was quantified by western blotting. Inducible NOS (iNOS) and nitrotyrosine were localised by immunohistochemistry. Modulation of NOS activity by topical N(G)-monomethyl-L-arginine (L-NMMA) or L-arginine was assessed during perfusion of whole colon. Plasma and perfusate nitrite/nitrate (NOx) was measured by Griess' reaction. RESULTS: Both in collagenous and ulcerative colitis, expression of iNOS was 10(2)-10(3) higher (p<0.001) than in uninflamed bowel and localised primarily to the epithelium. Endothelial NOS was evenly expressed in all groups while neuronal NOS was undetectable. Nitrotyrosine was markedly expressed in active ulcerative colitis but rarely detected in collagenous colitis and never in uninflamed bowel. In collagenous colitis, the output of NOx was markedly increased compared with uninflamed bowel (283 (58) v <37 nmol/min; p<0.01) and fluid was net secreted. L-NMMA reduced the output of NOx by 13-66% (95% confidence intervals) and secretion of fluid by 25-109% whereas L-arginine increased the output of NOx by 3-39% and secretion of fluid by 15-93%. CONCLUSIONS: In collagenous colitis, as opposed to ulcerative colitis, upregulation of iNOS occurs in the absence of nitrotyrosine formation and mucosal damage. Excess generation of NO may be the primary cause of diarrhoea in this condition.
The condensed article reports the results of 40 women and 16 men with a mean age of 59 +/- 2.6 years diagnosed with collagenous colitis between 1980 and 1993 at the UCLA Medical Center. Diarrheal symptoms lasted from 3 months to 15 years and a total of 291 biopsies were obtained from four sites in the large intestine (rectum and sigmoid colon, n = 141; descending colon, n = 60; transverse colon, n = 46; cecum and ascending colon, n = 44). Fifty randomly selected specimens from 30 patients were independently investigated to test concordance of histopathologic interpretation. Thickness of collagen band, inflammatory cells, and epithelium were assessed by grading with H&E stained sections; measurement of the subepithelial collagen band on trichrome-stained sections was compared with the subjective grading. The results of the study appeal both to endoscopists and histologists: 1) If sigmoidoscopy is applied in the differential diagnosis of diarrhea, biopsies including the most proximal extent visualized, are mandatory. 2) Inflammatory changes parallel the collagen deposition. 3) Subjective sensitivity in the estimation of collagen thickness in H&E stained slides is low. 4) Collagenous colitis without increase of inflammatory cells and a special type of collagen deposition is doubtful.
Pyoderma gangrenosum is a reactive inflammatory dermatosis which belongs to the spectrum of neutrophilic dermatoses. Due to a lack of diagnostic criteria, pyoderma gangrenosum is mainly a diagnosis of exclusion. It is rarely observed on the perineum, and vulvar involvement is even less frequent. Collagenous colitis is an idiopathic inflammatory colonic disease that is included in the microscopic colitides. The colonic mucosa and the crypt architecture are preserved but histologic alterations are found. We describe a case of collagenous colitis associated with vulvar pyoderma gangrenosum that improved spectacularly with cyclosporine 3 mg/kg/day and the twice-daily application of topical tacrolimus 0.1%.
A case of collagenous colitis is reported in an 86 year old man who presented with watery diarrhea. This case differs from previous reports in that five of the six reported cases involved women, mostly in their mid-forties, and that previously the collagenous band has been demonstrated in the mucosa of the left side of the colon only. This case is the first report to demonstrate the collagenous band in the right side of the colon as well as the left, and is the thickest band reported to date. In keeping with the two reported cases with follow-up, the subepithelial collagenous band was shown to have disappeared three months after the initial biopsy with a corresponding clinical improvement after symptomatic treatment only. The diagnosis needs to be considered in all patients presenting with watery diarrhea, and can only be confirmed after rectal or colonic biopsy.
AIM: To study the effect of oral steroids upon clinical response and rectal mucosa secretion of eosinophil cationic protein (ECP), myeloperoxidase (MPO), basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and albumin in patients with collagenous colitis (CC). METHODS: A segmental perfusion technique was used to collect perfusates from rectum of CC patients once before and twice (one and four weeks) after the start of steroid treatment. Clinical data was monitored and ECP, MPO, bFGF, VEGF and albumin concentrations were analyzed by immunochemical methods in perfusates and in serum. RESULTS: Steroids reduced the number of bowel movements by more than five times within one week and all patients reported improved subjective well-being at wk 1 and 4. At the same time, the median concentrations of ECP, bFGF, VEGF and albumin in rectal perfusates decreased significantly. MPO values were above the detection limit in only 3 patients before treatment and in none during treatment. VEGF, bFGF, ECP and albumin concentrations correlated with each other with the exception of ECP and albumin. A decrease of serum ECP and VEGF concentrations was also seen even if the overtime reduction was not significant. CONCLUSION: Oral steroid treatment in CC patients induced a simultaneous reduction of bowel movements and rectal release of ECP, bFGF, VEGF and albumin, suggesting that these polypeptides and increased mucosal permeability are important components of the pathophysiology in collagenous colitis.