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PubMed1990

A grading system for lymphocytic plasmacytic colitis in dogs.

Colonic mucosal samples were obtained every 4 weeks for 13 months from 6 clinically normal dogs and from 47 dogs with a clinical diagnosis of chronic inflammatory bowel disease. All samples were graded on a scale of 0-5, based upon the quantity of lymphocytes and plasma cells in the lamina propria, epithelial changes, and the presence of ulcers and erosions. A grade of less than or equal to 2.0 was considered normal and was assigned to 77 of 78 samples from clinically normal dogs and 28 of 48 samples from dogs with diarrhea. A transient increase in cellularity was noted in 1 sample from 1 control dog. Nineteen dogs with clinical disease had obvious histologic abnormalities. The grading scheme described provides the pathologist with an objective criterion for the microscopic evaluation of colonic mucosal samples obtained by endoscopic techniques and offers clinicians a method of assessing the dog's progress and response to therapy.

Animals↗
PubMed2003

Histopathological features of the terminal ileum in lymphocytic and collagenous colitis: a study of 32 cases and review of literature.

Biopsy specimens from the terminal ileum of 32 patients with the histopathological diagnosis of lymphocytic colitis or collagenous colitis and 11 control individuals were evaluated for the presence or absence of ileal mucosal abnormalities and for the number of intraepithelial lymphocytes, assessed by immunohistochemical stains for the pan T-cell marker, CD3. We found that the mean CD3 counts in patients with lymphocytic/collagenous colitis were significantly higher than those in the control group. Seven of 14 patients with collagenous colitis and 14 of 18 patients with lymphocytic colitis revealed an increase in intraepithelial T lymphocytes when compared with the control group (P =.001). Other notable changes included ileal villous atrophy in one case of lymphocytic colitis and in three cases of collagenous colitis and epithelial damage with thickened subepithelial collagen in two cases of collagenous colitis.

Adult↗
PubMed1990

Colonic lymphocytosis in patients with celiac sprue.

We examined colonic biopsies from 39 patients with clinical and small bowel biopsy changes of celiac sprue. In 12 of 39 patients (31%), striking lymphocytic infiltration of the superficial colonic epithelium and chronic inflammation of the lamina propria were identified. These 12 cases had a mean of 30.4 lymphocytes per 100 superficial colonic epithelial cells, compared with means of 8.4 in sprue cases without colonic epithelial lymphocytosis, 4.8 in normal controls, and 32.4 in nine cases of lymphocytic colitis without concurrent celiac sprue. No case showed subepithelial collagen layer thickening. Four patients with celiac sprue and colonic lymphocytosis also had gastric biopsies; two showed gastric lymphocytosis. Intraepithelial lymphocytes at all sites were positive for the T-cell marker MT-1. These findings indicate that sprue-associated colonic lymphocytosis and lymphocytic colitis are histologically, quantitatively, and immunohistochemically indistinguishable, that the epithelial T-cell infiltration of celiac sprue occurs in glandular mucosa at all levels of the gastrointestinal tract, and that colonic subepithelial collagen deposition in patients with celiac sprue is an infrequent occurrence. These findings also suggest that gastrointestinal epithelial T-cell infiltration may be an immunologic response that is common in individuals sensitized to absorbed lumenal antigens, and that colonic lymphocytosis may occur as a response to a number of antigens, including gluten.

Celiac Disease↗
PubMed1996

Microscopic colitis is a cause of large bowel diarrhea in Northern India.

Chronic diarrhea is a common clinical problem. To determine the possible causes in North India, we studied prospectively 71 patients with chronic diarrhea of the large bowel type. A definite diagnosis could be established in 70 patients. Ulcerative colitis was found in 18 patients, colorectal malignancies in three, colonic polyps in three, and irritable bowel syndrome in 32. In addition, seven patients with seronegative polyarthritis and chronic diarrhea were found to have chronic inflammation of the colon on histology. Two patients had pseudodiarrhea, and no diagnosis could be established in one patient. The remaining five patients with chronic diarrhea showed histologic evidence of chronic colonic inflammation with predominantly mononuclear cell infiltration of the lamina propria and increased intraepithelial lymphocytes, but results of their radiologic and endoscopic studies were normal. These five patients were classified as having microscopic (lymphocytic) colitis. We conclude that the causes of chronic diarrhea in North India patients are similar to a large extent to those seen in Western populations. Microscopic (lymphocytic) colitis is a definite clinicopathologic entity that should be considered in the differential diagnosis of chronic diarrhea.

Adolescent↗
PubMed2005

Predisposing HLA-DQ2 and HLA-DQ8 haplotypes of coeliac disease and associated enteropathy in microscopic colitis.

OBJECTIVE: To assess the presence of both genetic and serological markers of coeliac disease in patients with microscopic colitis, and whether there was associated enteropathy. METHODS: HLA-DQ2, HLA-DQ8, serum immunoglobulin A-antiendomysial and immunoglobulin A-anti-tissue transglutaminase antibodies were investigated in 59 patients with microscopic colitis. Seventy healthy subjects acted as the control group. Endoscopic biopsies from the distal duodenum were obtained in DQ2-positive or DQ8-positive patients. Patients with histological changes compatible with gluten-sensitive enteropathy were started on a gluten-free diet. RESULTS: Seventeen of 70 (24.3%) healthy controls were DQ2-positive. Twelve of 25 (48%) patients with lymphocytic colitis (P = 0.027 versus controls), and 11 of 34 (32.3%) with collagenous colitis (P = 0.38 versus controls) were DQ2-positive. There were no differences in the frequency of DQ8-positivity. The coeliac serology was positive in one patient. Duodenal biopsies were performed in 23 DQ2-positive and/or DQ8-positive patients. None had villous atrophy (Marsh III lesion) (0%; 95% confidence interval, 0-6.1). A Marsh type I lesion was found in four patients. Three of these patients were put on a gluten-free diet with disappearance of diarrhoea. CONCLUSIONS: The results suggest that there is an association of lymphocytic colitis with HLA-DQ2 genes, which might be relevant in the pathogenesis of this disease. The association of microscopic colitis with Marsh type III coeliac disease seems to be rare, making it unnecessary to routinely screen for coeliac disease in microscopic colitis patients.

Aged↗
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↗
PubMed1992

Pericrypt eosinophilic enterocolitis and chronic diarrhea.

An unusual pattern of eosinophilic infiltration around intestinal crypts was detected in mucosal biopsy specimens of 10 patients with chronic diarrhea, half of whom had evidence of systemic connective tissue disease. The median duration of symptoms was 11 months, and no other explanation for diarrhea could be determined in any case. The cellular infiltrate on biopsy specimens was present deep in the mucosa of small and large intestinal specimens, separating crypt bases from the muscularis mucosae and penetrating the latter. Consistent with the microscopic findings, surface mucosal appearance by endoscopy was uniformly normal. These histological features of colonic biopsy specimens were statistically differentiated from those of asymptomatic subjects (n = 8), subjects with diarrhea-predominant irritable bowel syndrome (n = 6), and subjects with collagenous colitis (n = 7) or lymphocytic colitis (n = 5). Diarrhea improved in five of seven subjects treated with oral prednisone or prednisone in conjunction with azathioprine (median follow-up period, 2.2 years). Histological changes on subsequent biopsy specimens correlated closely with symptomatic status. These findings strongly suggest that chronic diarrhea is related to this pericrypt eosinophilic enterocolitis, a pathological lesion often associated with features of systemic connective tissue disease. The disorder appears responsive to corticosteroid therapy in some cases.

Adrenal Cortex Hormones↗
PubMed2003

Incomplete remission with short-term prednisolone treatment in collagenous colitis: a randomized study.

BACKGROUND: Microscopic colitis is a disease of unknown aetiology characterized by chronic watery diarrhoea and diarrhoea can be eliminated by budesonide but frequently recurs when budesonide is stopped. We studied whether prednisolone could induce remission in patients with disabling, chronic diarrhoea due to microscopic colitis. METHODS: A double-blind, randomized (3:1) trial of oral prednisolone 50 mg daily or placebo for 2 weeks. Remission was defined as stool weight < or = 200 g/day or frequency < or = 2/day; effect was defined as > 50% reduction of either stool frequency or weight. Six centres screened 31 consecutive patients and included 11 with collagenous colitis and 1 with lymphocytic colitis. Median duration of diarrhoea was 9 months. Patients had a normal colonoscopy, and no evidence of coeliac disease, bile acid or lactose malabsorption. Patients with gastrointestinal infection, previous gastrointestinal surgery, abnormal biochemical screening or recent treatment with immunosuppressive agents were excluded. RESULTS: Stool weight (grams) declined in 7 of 9 patients given prednisolone and in 1 of 3 receiving placebo; changes in median weight were from 430 to 278 and from 825 to 489, respectively. Stool frequency (per day) declined from 6 to 3 and from 8 to 5. Remission was obtained in 2 and 0, and effect in 5 and 0, respectively (NS; Fisher exact test). CONCLUSIONS: Prednisolone 50 mg daily for 2 weeks induces incomplete remission in patients with chronic diarrhoea due to collagenous colitis.

Adult↗
PubMed1999

Biopsy diagnosis of colitis: possibilities and pitfalls.

The histopathologic diagnosis of inflammation is common in colorectal biopsies but is of limited value, if not further specified. We reviewed 280 endoscopic colorectal biopsy specimens for nonneoplastic disease from 100 consecutive patients in order to assess (a) the frequency of inflammation in excess of the physiologic infiltrate, (b) the frequency with which the cause of the inflammation could be specified, and (c) the interobserver variability in diagnosing inflammation. Based on the reviewers' impression, each case was classified into one of three categories: (I) normal or nonspecific change, (II) nonspecific inflammation, and (III) inflammation suggestive or diagnostic of specific cause. Inflammation was diagnosed in 68% of cases. The majority of these cases (75%) showed features typically associated with specific types of colitis, including Crohn's disease (n = 16), ulcerative colitis (n = 13), inflammatory bowel disease not otherwise specified (n = 5), infectious colitis (n = 6), ischemic colitis (n = 4), solitary rectal ulcer syndrome (n = 3), radiation colitis (n = 2), and lymphocytic colitis (n = 2). Interobserver variability was greatest in biopsy specimens interpreted by the reviewers as normal or showing nonspecific changes, most of which had been diagnosed as mild inflammation by the original pathologists. Etiologic classification of colitis was lacking in 59% of the cases interpreted by the reviewers as suggestive or diagnostic of a specific cause. We conclude that (a) the majority of colorectal biopsy specimens from patients with nonneoplastic disease in this series show inflammation, (b) the majority of such cases allow a specific cause of colitis to be suggested or firmly diagnosed, and (c) pathologists tend to overdiagnose the physiologic inflammatory infiltrate as evidence of colitis and underdiagnose specific etiologic types of colitis.

Adult↗
PubMed2002

Lansoprazole-associated microscopic colitis: a case series.

Lansoprazole is a potent proton pump inhibitor that has been well tolerated with minimal serious adverse events. One of the most commonly reported side effects is diarrhea in 3-8% of study patients. During 1997, approximately 850 veterans at our institution had their proton pump inhibitor converted from omeprazole to lansoprazole because of a formulary change. A number of patients subsequently developed chronic watery diarrhea. While evaluating six of these patients, we discovered microscopic colitis that resolved with discontinuation of lansoprazole. The diarrhea was described as three to 10 loose, nonbloody bowel movements per day with some abdominal cramping. Colonoscopy in five patients and flexible sigmoidoscopy in one patient revealed normal colonic mucosa, but random biopsies all supported microscopic colitis (five cases of lymphocytic colitis and one case of collagenous colitis). Complete symptom resolution occurred in all patients within 4 to 10 days of discontinuing lansoprazole. In all patients, follow-up biopsies demonstrated normalization of the colonic histology. This is the first published case series of patients with microscopic colitis that correlated clinically and histologically with the initiation and discontinuation of lansoprazole.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

[Functional diarrheas are not, in most cases, minor clinical forms of lymphocytic or collagenous colitis].

AIM: The aim of the study was to test the hypothesis that some patients with functional diarrhea could actually suffer from a mild clinical pattern of collagenous or lymphocytic colitis. PATIENTS AND METHODS: Twenty consecutive patients with chronic diarrhea were included in the study if the colonic mucosa appeared normal during colonoscopy. From multiple colonic biopsies were established a conventional histological diagnosis and a quantitative histological diagnosis. This latter diagnosis was based on the semiquantitative evaluation of epithelial morphological alterations and lamina propria monocellular infiltration, and on the determination of both intraepithelial lymphocyte count and subepithelial collagen layer thickness. Multiple colonic biopsies from 12 control patients without diarrhea were analyzed according to the same protocol. RESULTS: Among the 20 patients with diarrhea, the quantitative diagnosis of collagenous colitis was made in 3 patients (thickness of the collagen band between 11 and 26 microns) and the diagnosis of lymphocytic colitis in one (21% of intraepithelial lymphocytes). The percentage of intraepithelial lymphocytes did not differ between the 16 remaining patients and the controls (12 +/- 5% and 9 +/- 4%, respectively). Similarly, the score of surface epithelial damage and the score of lamina propria infiltration in patients with diarrhea (1.2 +/- 1.0 et 1.7 +/- 1.5) were not different from the values in the control group (1.3 +/- 1.3 et 1.5 +/- 1.2). The mean fecal weight in patients with diarrhea but without colitis was 161 +/- 130 g/d. All the values of fecal weight were below 300 g/d, except in one patient with a past history of truncular vagotomy. CONCLUSIONS: These results suggest that most of the patients with functional diarrhea do not suffer from mild clinical patterns of collagenous or lymphocytic colitis.

Adult↗
PubMed1996

Microscopic colitis progressed to collagenous colitis: a morphometric study.

Microscopic (also called lymphocytic) colitis and collagenous colitis are two newly recognised clinicopathologic entities of unknown aetiology presenting with chronic watery diarrhoea. In both conditions, the colon appears normal by barium enema and colonoscopy, however, colonic biopsies reveal infiltration of plasma cells and neutrophils within the lamina propria and increased intraepithelial lymphocytes within the surface epithelium. Lack of a thickened collagen band beneath the surface epithelium histologically differentiates microscopic from collagenous colitis. The exact relationship between the two disorders is as yet unknown. The two entities may be variants of the same spectrum of disease or distinct conditions with and without collagen table thickening. The present case report shows progression of microscopic colitis to collagenous colitis in sequential colonic biopsies taken from a patient during a 7-year endoscopic follow-up suggesting that progression of microscopic to collagenous colitis is a possibility and the two diseases are likely to represent variants of the same condition.

Adult↗
PubMed1999

Review article: the potential role of nitric oxide in chronic inflammatory bowel disorders.

The aetiology of the chronic inflammatory bowel diseases-ulcerative colitis and Crohn's disease-as well as 'microscopic colitis'-both collagenous (COC) and lymphocytic colitis (LC)-remains unknown. Autoimmune mechanisms, cytokine polymorphism, commensal bacteria, infectious agents and vascular impairment have all been proposed as playing important roles in the pathogenesis of this spectrum of diseases. A variety of proinflammatory mediators, including tumour necrosis factor alpha, interleukin-1beta, interferon gamma, leukotriene B4 and platelet activating factor, promote the adherence of phagocytes to the venular endothelium and extravasation of these cells into the colonic mucosa. In addition to large amounts of nitric oxide (NO), injurious peroxynitrite may be formed in the epithelium by the inducible nitric oxide synthase (iNOS), which is considered to elicit cytotoxicity by the generation of superoxide with reduced L-arginine availability. In active ulcerative colitis, and to a lesser extent in Crohn's disease, a greatly increased production of NO has been demonstrated by indirect and direct measurements. Surprisingly, even higher rates of production have been observed in COC-a condition which is never associated with injurious inflammation. The latter observation favours the notion that NO promotes mucosal integrity. Further evidence for a protective role of NO in chronic inflammatory bowel disorders is provided by the observation of increased susceptibility to the induction of experi mental colitis in 'knock-out' mice deficient in iNOS. Selective inhibitors of iNOS activity, as well as topical L-arginine, may therefore prove beneficial in inflammatory bowel disease by reducing the production of superoxide by iNOS, while only the former option may be expected to reduce diarrhoea in chronic inflammatory bowel disorders. Clearly, further experimental work needs to be done before testing topical L-arginine in human inflammatory bowel disease.

Animals↗
PubMed1999

Colonic epithelial lymphocytosis without a thickened subepithelial collagen table: a clinicopathologic study of 40 cases supporting a heterogeneous entity.

Lymphocytic colitis (LC) is classically described as a triad of chronic nonbloody, watery diarrhea, normal or nearly normal endoscopy findings, and colonic epithelial lymphocytosis without a thickened subepithelial collagen table (SECT). It is unknown how often patients with colonic epithelial lymphocytosis without a thickened SECT actually present with this classic triad. Cases diagnosed histologically as lymphocytic or microscopic colitis were reviewed. Criteria for inclusion were the presence of at least 15 surface lymphocytes per 100 epithelial cells and the absence of a thickened SECT (<12 microm). Clinical features and course were recorded by chart review and telephone follow-up. Forty patients met the inclusion criteria, including 25 women and 15 men with a mean age of 63.2 years (range, 25-83 years). Twenty-eight patients had the classic triad and were designated as having classic LC. The other 12 patients fulfilled the histologic criteria but not the clinical or endoscopic criteria for classic LC and were classified as having atypical LC (constipation, five patients; macroscopic colitis at endoscopy, five patients; hematochezia, one patient; and incidental finding, one patient). Clinically, patients with classic LC were predominantly women and had a higher incidence of autoimmune disease (p = 0.03) than did those with atypical LC. Histologically, surface eosinophilia was significantly greater in patients with classic LC (p = 0.04). Twenty patients were using nonsteroidal antiinflammatory drugs at the time of their colonic biopsy. Surface epithelial lymphocyte counts were higher in these patients, particularly in the distal sigmoid colon (p = 0.02). Fourteen patients had associated autoimmune disease, including three patients with sprue diagnosed by small bowel biopsy, all of whom responded to gluten withdrawal. Diarrhea present in 25 patients, without documented evidence of celiac sprue, was self-limited in five, resolved with treatment in three, required intermittent treatment in eight, daily treatment in five, and was refractory to treatment in four. All eight patients who experienced spontaneous or treatment-related symptom resolution had classic LC. No histologic feature correlated with clinical course. In conclusion, our study shows that colonic epithelial lymphocytosis without a thickened SECT is a histologic finding seen in a heterogeneous group of patients. Within this heterogeneous group is a distinct subset of patients who have the classic clinicopathologic triad of LC. This subset of patients has striking similarities to patients with collagenous colitis, lending further support to a close relationship between these two entities. Atypical LC comprises a heterogeneous group and includes patients with idiopathic constipation, coexisting LC and inflammatory bowel disease, and possibly infectious colitides. Because of the clinical heterogeneity among our study population, the descriptive term colonic epithelial lymphocytosis may be a more prudent diagnosis than lymphocytic colitis in the absence of adequate clinical information.

Adult↗
PubMed1971

Electron microscopy in Crohn's disease.

An electron microscopic study of Crohn's disease of the colon is presented. The positive findings that supplement those obtained by light microscopy are: a prominent nucleolus is more common in the lymphocytes of Crohn's disease than in normal lymphocytes or those found in cases of ulcerative colitis; lymphocytes are often observed close to macrophages and epithelioid cells; the epithelioid cells are metabolically active, and have vesicles which contain acid phosphatase but little visible debris; intramural bacteria were identified in six of the 11 specimens of colon with intact epithelia and minimal inflammatory changes. The possible significance of these findings for the pathogenesis of the disease is discussed.

Acid Phosphatase↗
PubMed2001

Familial occurrence of microscopic colitis: a report on five families.

BACKGROUND: The etiology and pathogenesis of microscopic colitis is unknown. Whether genetic predisposition is of importance, as in many other gastrointestinal diseases, is unknown. Familial occurrence of collagenous colitis has earlier been reported only in two families. METHODS: Familial occurrence of microscopic colitis was searched for in a Swedish national microscopic colitis register. RESULTS: Familial occurrence of microscopic colitis was identified in five families. In all families a sister-sister relationship was found. Two sisters with collagenous colitis had been living apart in different Nordic countries for many years before developing the disease. In one pair, the smoking sister had collagenous colitis and the never smoking sister had lymphocytic colitis. CONCLUSIONS: Considering the relative rarity of microscopic colitis, these findings indicate that a genetic predisposition may be of importance.

Adult↗
PubMedDate not supplied

Chronic colitis in baboons: similarities with chronic colitis in humans.

In recent years, a substantial number of baboons died at the Southwest Foundation for Biomedical Research following protracted intractable diarrheas. The histopathologic diagnosis at autopsy was chronic colitis. The diarrhea could last for more than one year and occurred in infants, juveniles or young adult baboons, i.e. < or = 8 years of age (a healthy baboon may live up to 27 years). The aim was to assess the histopathologic subtype of chronic colitis in a relatively large number of colonic specimens obtained at autopsy (n = 132). In 88 out of 132 baboons with chronic diarrhea, the colonic mucosa was well preserved for histological examination. At review, various histological phenotypes of chronic colitis were disclosed in 86 of the 88 baboons. Chronic lymphocytic-plasmacytic colitis was found in 54.6% (47 out of 86), chronic ulcerative colitis in 15.1% (13 out of 86), Crohn's colitis in 12.8% (11 out of 86), superficial lymphocytic colitis in 10.5% (9 out of 86), cryptal lymphocytic colitis in 5.8% (5 out of 86) and collagenous colitis in 1.2% (1 out of 86). Chronic ulcerative colitis, Crohn's colitis, superficial lymphocytic colitis and collagenous colitis in baboons closely mimic corresponding histological phenotypes of chronic colitis in humans. Recently, cryptal lymphocytic colitis has also been found in humans. The awareness that chronic colitis in baboons is not one disease but a series oi chronic inflammatory changes, having common clinical symptoms and similar gross appearance, may lead to the correct diagnosis of the subtype of the disease. Only then would it be feasible to systematically initiate the search for the corresponding etiologic agent(s), aiming to tailor specific therapeutic strategies in those animals.

Animals↗