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PubMed1984

Lymphocytic-plasmacytic colitis in the cat.

Lymphocytic-plasmacytic colitis was diagnosed in 6 cats. Owners sought veterinary care because of semiformed -to-liquid feces, tenesmus , fresh blood and/or mucus in the feces, or increased frequency of defecation in their cats. Lymphocytic, plasmacytic infiltration in the colonic lamina propria was found on colon biopsies. Clinical signs resolved in all 6 cats after dietary management, utilizing lamb and rice, horsemeat , or a feline prescription diet. Clinical improvement also occurred in 1 cat following sulfasalazine therapy.

Animals↗

PubMed1995

Microscopic colitis syndrome.

The colorectal biopsy specimens from 30 patients with chronic watery diarrhoea but normal endoscopic and radiographic findings were studied by light microscopy, morphometry, immunohistochemistry, and two patients with electron microscopy. The histological changes in the colorectum were originally diagnosed in six patients as lymphocytic colitis and in 24 patients as collagenous colitis. The analysis of the specimens for this study could delineate three distinct groups of microscopic colitis: lymphocytic colitis (six patients), collagenous colitis without lymphocytic attack on the surface epithelium (seven patients), and a mixed form presenting with both thickening of the collagen plate and increased number of intraepithelial lymphocytes (17 patients). No transformation was seen from one type to another during follow up of six patients for four to seven years. Increased numbers of active pericryptal myofibroblasts were found with the electron microscope in one patient with mixed microscopic colitis showing also myofibroblasts entrapped within the collagen layer. Hitherto undescribed flat mucosa of the ileum was found in one patient with lymphocytic colitis and both flat mucosa and thickening of the collagen plate in the ileum were seen in one patient with the mixed form of the disease. In another patient with mixed microscopic colitis, normalisation of the colorectal morphology occurred after temporary loop ileostomy, followed by the reappearance of both diarrhoea, inflammation, and thickening of the collagen plate after the ileostomy was reversed. No association was found between non-steroid anti-inflammatory drug (NSAID) consumption and collagenous or mixed microscopic colitis. The primary cause of microscopic colitis is probably an immunological reaction to luminal antigen/s, perhaps of ileal origin. The engagement of the pericryptal myofibroblasts in the disease process might result in the development of the various forms of microscopic colitis. An inverse relation between intraepithelial lymphocyte count and collagen thickness may indicate that microscopic colitis is a spectral disease.

Adult↗

PubMed2001

Bile acid malabsorption in microscopic colitis and in previously unexplained functional chronic diarrhea.

Bile acid malabsorption (BAM) has been described in patients with collagenous colitis. There are no similar studies in lymphocytic colitis. The possibility that BAM might not necessarily be part of the microscopic colitis process and that both entities could simply be concomitant has not been evaluated. Our aim was to assess the frequency and severity of BAM in patients with microscopic colitis as well as in patients with previously unexplained functional chronic diarrhea. Likewise, we wanted to investigate the effect of cholestyramine on the induction and maintenance of remission of these conditions. A [75Se]HCAT abdominal retention test was performed in 26 patients with collagenous colitis, 25 with lymphocytic colitis, and 32 with previously unexplained functional chronic diarrhea. Patients with microscopic colitis who had BAM as well as a subgroup of eight collagenous colitis patients without BAM received treatment with cholestyramine. All patients with previously unexplained chronic diarrhea who had BAM were treated with cholestyramine. Twenty-two (43.1%) patients with microscopic colitis and 24 (75%) patients with previously unexplained functional chronic diarrhea presented with BAM. The frequency of BAM was higher in lymphocytic colitis than in collagenous colitis (60% vs 27%; P = 0.025). Cholestyramine induced clinical remission in 19 of 22 patients with microscopic colitis and BAM, none of eight patients with collagenous colitis without BAM, and all patients with previously unexplained chronic diarrhea and BAM. In conclusion, BAM seems to be common in patients with microscopic colitis-mainly in lymphocytic colitis-and in those with previously unexplained functional chronic diarrhea, suggesting that idiopathic BAM and microscopic colitis are often concomitant conditions. In this setting, cholestyramine seems to be highly effective in stopping diarrhea.

Aged↗

PubMed2001

[Evolution and treatment response in microscopic colitis].

AIM: To study the clinical characteristics, treatment response and evolution in patients with microscopic colitis. MATERIAL AND METHODS: We performed a retrospective analysis of 24 patients (15 with collagenous colitis and 9 with lymphocytic colitis). Clinical and diagnostic features, treatment response and evolution according to the presence of maintenance therapy were evaluated. RESULTS: The mean age of the patients was 59.7 years and most were male. Nine patients took non-steroidal anti-inflammatory drugs (NSAID). No significant association was found with other drugs. Four patients presented associated rheumatological disease. Most patients presented insidious-onset diarrhea without pathological products, which was frequently associated with other symptoms (abdominal pain, bloating, weight loss, asthenia, tenesmus, and incontinence). Seven patients showed a slight increase in globular sedimentation rate. Fat in stools and radiological investigations (transit and opaque enema) were normal in patients who underwent these tests. Endoscopy revealed non-specific alterations in 42% of the patients while results were normal in the remaining patients. One patient showed clinical improvement on withdrawal of NSAIDs and 4 patients improved spontaneously. Clinical response was achieved in 7 of 13 patients treated with antimotility drugs, in 8 of 9 patients treated with salicylates, in 3 treated with oral corticoids, in 1 treated with cholestyramine and in 1 treated with topical budesonide. Nineteen patients required no maintenance therapy, 4 were administered salicylates and 1 was administered cholestyramine. After a mean follow-up of 42 months, evolution was chronic and intermittent in 14 patients and chronic and continuous in 1; 9 patients presented a single episode. No significant differences were found between patients administered maintenance therapy and those who were not or between collagenous colitis and lymphocytic colitis in the parameters analyzed. CONCLUSIONS: Microscopic colitis constitutes a group of diseases characterized by chronic diarrhea, few systemic effects and minimal radiological and/or endoscopic alterations. Evolution is characterized by recurrent episodes, with good response to treatment with cholestyramine, salicylates or corticoids when required.

Adult↗

PubMedDate not supplied

[Microscopic colitis--more common cause of diarrhea than believed. Biopsies are the only way to diagnosis, drug treatment is effective].

Microscopic colitis, encompassing collagenous and lymphocytic colitis, is a fairly common cause of chronic watery diarrhoea, especially in elderly women. In recent epidemiological studies the annual incidence of each disorder was 4-6/100.000 inhabitants. The aetiology is unknown. The main clinical symptoms are watery diarrhoea, weight loss and abdominal pain. Laboratory analyses are nondiagnostic, and the diagnoses rely on histopathological examination of colonic mucosal biopsies. There is an association to autoimmune diseases such as thyroid disorders, diabetes mellitus, celiac disease and arthritis. Budesonide is the best-documented treatment of collagenous colitis. It is superior to placebo in short-term therapy, but the long-term efficacy is not well studied. The evidence for other therapeutic alternatives such as loperamide, cholestyramine, bismuth subsalicylate, or 5-aminosalicylates is weak. In unresponsive severe disease azathioprine or methotrexate may be tried. There are at present no controlled data on the treatment of lymphocytic colitis. The long-term prognosis of microscopic colitis is good, serious complications are rare and there is no increased mortality.

Age Factors↗

PubMed2002

Increased colonic intraepithelial lymphocytes in patients with Hashimoto's thyroiditis.

BACKGROUND: Hashimoto's thyroiditis is an autoimmune thyroid disorder. Lymphocytic colitis and collagenous colitis are characterized by diarrhea with normal endoscopic findings. Autoimmune disorders are common in Hashimoto's thyroiditis and lymphocytic colitis. The aim of this study was to investigate the incidence of lymphocytic colitis in patients with Hashimoto's thyroiditis. STUDY: Fifty patients with well-documented Hashimoto's thyroiditis were included. Twenty patients with nonulcer dyspepsia served as a control group. Five of 50 patients with Hashimoto's thyroiditis reported intermittent diarrhea, whereas no patients had diarrhea in the control group. All patients and the control group underwent total colonoscopy, and multiple colonoscopic biopsies were performed. RESULTS: We found that 40% (20 of 50) of Patients with Hashimoto's thyroiditis had histologic findings consistent with lymphocytic colitis, and one patient in the control group had lymphocytic colitis (p < 0.01). The mean number of intraepithelial lymphocytes was 34.4/100 epithelial cells in these 20 patients, whereas the mean number of intraepithelial lymphocytes was 12.3/100 epithelial cells in the other 30 patients with Hashimoto's thyroiditis (p < 0.05). CONCLUSIONS: There was a higher incidence of histologic findings of lymphocytic colitis in patients with Hashimoto's thyroiditis, although most of the patients were clinically asymptomatic. This finding suggests that lymphocytic colitis may have an asymptomatic clinical course and should encourage further clinical investigations to better anticipate the relationship between autoimmune disorders.

Adult↗

PubMed2006

Drug consumption and the risk of microscopic colitis.

BACKGROUND: Microscopic colitis is a rare disease of unknown etiology. It has been described that some drugs could cause or worsen the disease; however, the scientific evidence is limited. AIM: To investigate the possible association of chronic drug consumption with microscopic colitis. METHODS: This was a case-control study in which groups of cases were: Group 1-39 patients with collagenous colitis; Group 2-39 patients with lymphocytic colitis; and Group 3-52 patients with chronic watery diarrhea of functional characteristics. 103 subjects formed the control group. At diagnosis, a drug consumption history of at least 2-wk duration was registered. An age- and sex-adjusted logistic regression analysis was used, and the odds ratio (OR, 95% CI) was calculated. RESULTS: Drug consumption was more frequent in lymphocytic colitis than in the control group (92.3%vs 76.3%, P < 0.05). The mean daily number of drugs by person was also higher in lymphocytic colitis (3.79 +/- 0.44 vs 2.13 +/- 0.22, P= 0.04). The following associations as compared with the control group were observed: Group 1-Consumption of NSAIDs (46.2%vs 23%, OR 2.9, 1.3-6.4), selective serotonin reuptake inhibitors (SSRIs) (18%vs 1%, OR 21, 2.5-177), specifically, sertraline (15.4%vs 0%, P < 0.0005); Group 2-SSRIs (28%vs 1%, OR 37.7, 4.7-304), beta-blockers (13 vs 3%, OR 4.79, 1.04-20), statins (13%vs 3%, OR 4.6, 1.04-20), biphosphonates (8%vs 0%, P= 0.022); Group 3-SSRIs (15%vs 1%, OR 16.2, 2-135), statins (11.5%vs 3%, OR 5.4, 1.2-24). As compared with the chronic diarrhea group, a significant association with the usage of sertraline in LC (P= 0.005) and a trend for NSAIDs in CC (P= 0.057) were found. CONCLUSIONS: Drug consumption increases the risk of microscopic colitis. Some drugs might be trigger factors of colonic inflammation in predisposed hosts, and others might only worsen self-evolving microscopic colitis.

Aged↗

PubMed2006

The epidemiology of microscopic colitis: a population based study in Olmsted County, Minnesota.

OBJECTIVE: Although the epidemiology of microscopic colitis has been described in Europe, no such data exist from North America. We studied the incidence, prevalence and temporal trends of microscopic colitis in a geographically defined US population. DESIGN AND SETTING: In this population based cohort study, residents of Olmsted County, Minnesota, with a new diagnosis of microscopic colitis, and all who had colon biopsies for evaluation of diarrhoea, between 1 January 1985 and 31 December 2001 were identified. Biopsies were reviewed for confirmation (cases) and to identify missed cases (diarrhoea biopsies). MAIN OUTCOME MEASURES: Incidence rates, age and sex adjusted to the 2000 US white population. Poisson regression assessed the association of calendar period, age and sex with incidence. RESULTS: We identified 130 incident cases for an overall rate of 8.6 cases per 100,000 person-years. There was a significant secular trend, with incidence increasing from 1.1 per 100,000 early in the study to 19.6 per 100,000 by the end (p<0.001). Rates increased with age (p<0.001). By subtype, the incidence was 3.1 per 100,000 for collagenous colitis and 5.5 per 100,000 for lymphocytic colitis. Collagenous colitis was associated with female sex (p<0.001) but lymphocytic colitis was not. Prevalence (per 100,000 persons) on 31 December 2001 was 103.0 (39.3 for collagenous colitis and 63.7 for lymphocytic colitis). CONCLUSIONS: The incidence of microscopic colitis has increased significantly over time, and by the end of the study, the incidence and prevalence were significantly higher than reported previously. Microscopic colitis is associated with older age, and collagenous colitis is associated with female sex.

Adult↗

PubMed2006

Autoantibody profiles in microscopic colitis.

OBJECTIVE: The etiology of microscopic colitis is unclear; an autoimmune response and pharmacological induction have been proposed as possible mechanisms. We conducted a multicentre cross-sectional study to compare the antibody profiles of patients with collagenous and lymphocytic colitis with those of a control group. METHODS: The medical histories and antibody profiles of 26 patients with collagenous and 16 patients with lymphocytic colitis were compared with the corresponding data of 43 controls without gastroenterological disease. Antibodies to the following structures were determined: intestinal goblet cells, antinuclear antibodies (ANA), antineutrophil cytoplasmic antibodies, anti-Saccharomyces cerevisiae antibody (ASCA), tissue transglutaminase, gliadin, pancreatic acini, glutamate decarboxylase, tyrosine phosphatase IA-2 and thyroid (microsomal anitbodies, MAB). RESULTS: Patients with collagenous and lymphocytic colitis had been treated significantly more often with H(2)-receptor antagonists and non-steroidal anti-inflammatory drugs (P = 0.026 and 0.014, respectively). Additional diseases of presumed autoimmune etiology were present in 43% (18/42) of patients. Comparison with the controls showed significantly more positive findings for ANA immunoglobulin G (IgG), gliadin immunoglobulin A (IgA) and ASCA (IgA and IgG) in patients with collagenous colitis but not in those with lymphocytic colitis. Collagenous colitis was associated with positive ASCA in 15% of patients and lymphocytic colitis in 13%. CONCLUSIONS: The autoantibodies investigated are of no diagnostic relevance to microscopic colitis. Positive ANA and strong associations with other autoimmune diseases point to an autoimmune etiology. H(2)-receptor antagonists and non-steroidal anti-inflammatory drugs might also be of pathogenetic significance.

Adult↗

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↗

PubMed1996

Colonic epithelial lymphocytosis associated with an epidemic of chronic diarrhea.

The term Brainerd diarrhea has been applied to outbreaks of chronic watery diarrhea of unknown etiology characterized by acute onset and prolonged duration. Our aim was to describe the histologic changes in gastrointestinal biopsy specimens from patients with Brainerd diarrhea. We examined 52 colonic and 12 small bowel biopsy specimens from 22 patients who were involved in an outbreak of Brainerd diarrhea that was linked to the water supply of a cruise ship visiting the Galapagos Islands. Small bowel biopsy specimens from seven patients were histologically normal. One patient had a duodenal biopsy specimen that resembled celiac sprue. Colonic biopsy specimens from 20 patients revealed surface epithelial lymphocytosis without distortion of mucosal architecture, surface degenerative changes, or thickened subepithelial collagen plates. The degree of surface epithelial lymphocytosis was greater than that seen in control groups of persons with normal colons, acute colitis, and ulcerative colitis (p < 0.001), similar to that seen with collagenous colitis, and less than that seen with lymphocytic colitis (p < 0.001). Three patients showed focal active colitis similar to that described in acute infectious-type colitis in addition to the epithelial lymphocytosis. Two patients had colonic biopsy specimens that were histologically normal. In summary, histologic abnormalities in the small bowel are generally absent in Brainerd diarrhea. Colonic biopsy specimens in Brainerd diarrhea frequently show epithelial lymphocytosis similar to that seen in collagenous and lymphocytic colitis. Although currently Brainerd diarrhea can be diagnosed only with epidemiologic data indicating an epidemic and a point source, the lack of surface degenerative changes and the relatively lower lymphocyte counts seen in our cases of Brainerd diarrhea may serve to distinguish it from lymphocytic colitis, and the lack of a thickened subepithelial collagen plate distinguishes it from collagenous colitis.

Adult↗

PubMed2005

Microscopic colitis: a report of two cases.

Microscopic colitis is characterized by chronic, watery, secretory diarrhea, with a normal or near-normal gross appearance of the colonic mucosa. Biopsy is diagnostic and usually reveals either lymphocytic colitis or collagenous colitis. The symptoms of collagenous colitis appear most commonly in the sixth decade. With collagenous colitis, the major microscopic characteristic is a thickened collagen layer beneath the colonic mucosa, and with lymphocytic colitis, an increase number of intraepithelial lymphocytes. Clinically, collagenous colitis is characterized by long-standing diarrhea. In patients with lymphocytic colitis, the duration of diarrhea is usually shorter and female predominance is less apparent. We report two cases of lymphocytic colitis in elderly women. Both presented with watery diarrhea of two month duration and weight loss. Extensive investigations were done and several medications failed to stop their diarrhea. Biopsy revealed lymphocytic colitis. Their diarrhea responded well to cholestyramine.

Aged↗

PubMed2003

Subepithelial myofibroblasts and tenascin expression in microscopic colitis.

AIMS: To assess differences in the pattern of subepithelial myofibroblasts and the expression of tenascin as a marker of extracellular matrix production in collagenous and lymphocytic colitis. METHODS AND RESULTS: Colorectal biopsies were studied from 122 patients with chronic diarrhoea and normal colonoscopy. The pathological diagnoses were collagenous colitis (n = 35), lymphocytic colitis (n = 37), mild non-specific chronic inflammation (n = 28) and normal mucosa (n = 18). Four cases showed features of collagenous colitis but with collagen bands <10 micro m thick. Normal mucosa from 14 patients without diarrhoea served as healthy control tissue. Immunohistochemical expression of alpha-smooth muscle actin (myofibroblast marker) and tenascin was evaluated in well-orientated sections. The expression of alpha-smooth muscle actin was significantly increased in collagenous colitis compared with all the other groups. Strong tenascin subepithelial expression was seen in all cases of collagenous colitis, including the four without full-blown features. The mean thickness of tenascin bands was greater than that obtained by conventional stains. CONCLUSIONS: There are clear differences, with respect to extracellular matrix remodelling, between collagenous and lymphocytic colitis. These results support the theory of matrix overproduction in the genesis of collagenous colitis.

Actins↗

PubMed1989

Immunohistochemical study of lymphoplasmacytic infiltrate and epithelial HLA-DR expression in the rectal and colonic mucosae of children with ulcerative colitis.

Lymphocyte subpopulations, plasma cells in the lamina propria, and the expression of HLA-DR antigens on the epithelium of the rectal and colonic mucosae were studied in eight children with ulcerative colitis and 12 control subjects using a panel of monoclonal antisera and the peroxidase technique before any treatment and 3 months later (four patients). The numbers of intraepithelial lymphocytes were similar in specimens from patients and controls. The majority of these cells (on average, 73% in the patients and 84% in the controls) were mature CD3+ T cells; among them, CD8+ suppressor-cytotoxic cells were preponderant. In both untreated and treated patients, the numbers of mature T cells in the rectal mucosae were supranormal (1,870 +/- 205 cells/mm2, p less than 0.01 and 1,537 +/- 214 cells/mm2, p less than 0.05, respectively; controls, 1,105 +/- 214 cells/mm2). In rectal specimens from untreated patients, the number of helper T (CD4+) cells was increased (1,094 +/- 74 versus 801 +/- 74 cells/mm2, p less than 0.05); the same specimens had more B-1-positive (CD20+) B cells and pre-B cells (122 +/- 21 versus 71 +/- 17 cells/mm2, p less than 0.05). The number of IgG-containing cells was significantly greater than in the controls (1,058 +/- 263 versus 359 +/- 64 cells/mm2, p less than 0.01), and the commonest isotype in the plasma cells of patients was IgG. The number of IgE-containing cells was also significantly elevated (230 +/- 40 versus 95 +/- 16 cells/mm2, p less than 0.01). The numbers of IgA- and IgM-containing cells were similar in patients and controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2005

Irritable bowel syndrome and inflammatory bowel disease: interrelated diseases?

In the past inflammatory bowel disease (IBD), celiac disease and irritable bowel syndrome (IBS) were regarded as completely separate disorders. Now, with the description of inflammation, albeit low-grade, in IBS, and of symptom overlap between IBS and celiac disease, this contention has come under question. Is there true overlap between these disorders? Despite the limitations of available data one cannot but be struck by some areas of apparent convergence: IBD and celiac disease in remission, lymphocytic colitis and microscopic inflammation in IBS, in general, and, especially, in the post-infectious IBS category. The convergence between latent celiac disease and sub-clinical IBD, on the one hand, and IBS, on the other, appears, based on available evidence, to be somewhat spurious and may largely relate to misdiagnosis, a phenomenon which may also explain the apparent evolution of IBS into IBD in some studies. Similarities between IBS and lymphocytic colitis are more striking and less readily dismissed; as for IBS, well documented instances of progression of lymphocytic colitis to full-blown IBD are infrequent, suggesting a true separation between this disorder and classical IBD. Do IBS and lymphocytic colitis represent different responses to similar triggers? Will some of the 'inflamed' IBS subgroup be reclassified as part of the spectrum of lymphocytic colitis in the future? Will inflammation emerge as a common underlying factor in the pathogenesis of IBS? The answer to these and many questions must await further study of this fascinating area.

Environment↗

PubMed1991

Collagenous colitis: pathophysiologic considerations.

Collagenous colitis, a cause of watery diarrhea characterized by a distinctive band of collagen under the surface epithelium of the colon, has been recognized with increasing frequency in recent years. The pathophysiology of collagenous colitis remains obscure. The thickening of the subepithelial collagen layer may be a response to chronic inflammation or a local abnormality of collagen synthesis. The precise mechanism of the diarrhea in collagenous colitis is also unclear, and it has not been possible to link the diarrhea directly to the excess collagen deposition. The relationship between collagenous colitis and lymphocytic colitis, another type of microscopic colitis, remains to be defined; elucidating the relationship between the two disorders may provide clues to the pathophysiology of both.

Colitis↗

PubMed2006

Colon lesions: pathology specific to women.

Lymphocytic colitis and collagenous colitis represent two conditions that fall under the category of microscopic abnormalities within the lamina propria of the colon. Patients are predominantly women in the sixth decade of life who present with non-bloody watery diarrhea. Few other symptoms exist. Diagnosis is based upon finding characteristic abnormalities in the colonic mucosa, more likely to be found on the right side of the colon than the left. Treatment is symptomatic, although some newer therapies suggest regression of the lesion. Other autoimmune associations have been described, including celiac disease, and appropriate work-up for this condition should be considered for the patient who has seemingly refractory colitis. The natural history is benign, and most patients experience resolution of their symptoms.

Colitis, Collagenous↗

PubMed2002

Microscopic colitis.

Microscopic colitis is an umbrella term used to include two idiopathic inflammatory bowel disorders that present with chronic watery diarrhea, normal endoscopic findings and characteristic inflammatory changes on histology. Collagenous colitis and lymphocytic colitis are distinguished by the presence of a thickened subepithelial collagen table. It is likely that they are a spectrum of one disease, but this is yet to be proven. The majority of cases tend to undergo spontaneous remission within a few years of onset, and their clinical course is benign, with no increase in risk of colorectal cancer. Sufficient evidence exists to suggest that microscopic colitis occurs as a response to one or more luminal antigens. A variety of medications have been reported in the treatment of this condition, but only colloidal bismuth and budesonide have thus far been shown to be effective in randomized controlled trials.

Anti-Inflammatory Agents↗