Microscopic Colitis Patients Research Articles

Human leucocyte antigen and TNFα polymorphism association in microscopic colitis

Coeliac disease (CD) is common in patients with microscopic colitis (MC). The human leucocyte antigen (HLA)-DR3-DQ2 haplotype is strongly associated with CD, and there is evidence for an association with MC. We analysed the genetic background of MC by assessing the haplotypes of HLA-DR3-DQ2 and HLA-DR4-DQ8. In addition, TNFalpha gene polymorphism (-308) associated with susceptibility to several autoimmune diseases was studied. Eighty patients with MC including 29 with collagenous colitis (CC) and 51 with lymphocytic colitis (LC) were typed for HLA-DR3-DQ2, and HLA-DR4-DQ8 molecule encoding genes using either an allele-specific PCR, or hybridization with sequence-specific oligonucleotides. Duodenal biopsies (N=78) confirmed the diagnosis of CD in 15 (18.8%) patients. TNFalpha(308) alleles were analyzed in 78 patients with MC (27 with CC and 51 with LC). A control group of 3627 patients was used in the HLA study and 178 patients in the TNFalpha study. HLA-DR3-DQ2 haplotype was more frequent in patients with MC (43.8%) including both subgroups (LC, 44.8%; CC, 43.1%; P<0.001), and MC with CD (86.7%; P<0.001) and without CD (33.3%; P=0.003), compared with the controls (18.1%). Similarly, the TNF2 carrier rate was higher in MC (46.2%; P<0.001) including both CC (44.4%; P=0.031) and LC (47.1%; P=0.001), and both MC patients with CD (66.7%; P=0.001) and without CD (39.3%; P=0.019), compared with the controls (23%). Both CC and LC are associated with the HLA-DR3-DQ2 haplotype and with TNF2 allele carriage. These associations are present also in MC patients without CD. The shared predisposing HLA-DR3-DQ2 haplotype and the high prevalence of CD in patients with MC suggest an epidemiological overlap, and probably some similarities in the pathogenesis of CD and MC.

Budesonide in the treatment of inflammatory bowel disease: The first year of experience in clinical practice

Delayed release budesonide was approved by the FDA for the treatment of mildly to moderately active Crohn's disease involving the ileum and ascending colon. Controlled trials have demonstrated that budesonide is effective in inducing remission and for maintenance of remission, with less frequent steroid side effects than conventional steroids. We sought to determine the benefit of this medication in clinical practice and to identify any non-FDA-approved uses that may warrant further study. Patients in whom oral budesonide was prescribed between November 1, 2001 and October 31, 2002, were identified and medical records were reviewed. Patients were categorized by indication for therapy: ileocolonic Crohn's disease (group 1), Crohn's disease elsewhere (group 2), and other conditions (group 3). A total of 225 patients were identified (108 in group 1, 62 in group 2, and 55 in group 3). Group 3 included patients with microscopic colitis (n = 28), pouchitis (n = 13), ulcerative colitis (n = 12), and celiac disease (n = 2). A favorable outcome occurred in 61% of group 1 patients but only 24% of patients in group 2. In group 3, only microscopic colitis patients and pouchitis patients experienced response rates >50% (77% and 60%, respectively). Budesonide is effective in a majority of patients with ileocolonic Crohn's disease and microscopic colitis, which is consistent with results reported from clinical trials. A majority of patients with pouchitis also benefit from budesonide therapy, but prospective controlled trials are necessary to clarify the benefit in this group.

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

To assess the presence of both genetic and serological markers of coeliac disease in patients with microscopic colitis, and whether there was associated enteropathy. 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. 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. 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.

Microscopic colitis: A retrospective study of clinical presentation in 53 patients

To evaluate the relationship between symptoms and microscopic colitis (MC) subtypes: to test whether collagenous colitis (CC) and/or lymphocytic colitis (LC) might be related to both constipation and diarrhea. A cohort of patients with independently confirmed typical histopathological changes was investigated. Fifty-three patients with histologically proved MC (46 with CC, 7 with LC) were included. The existence of diarrhea or constipation and the co-existence of autoimmune diseases were also investigated and all data were retrospectively analyzed. Twenty-three (43.39%) of MC patients had chronic constipation (20 in CC, 3 in LC patients). Twenty-four (45.28%) of MC patients had autoimmune disease and the diagnosis of autoimmune disease was always prior to MC. Sjögren's syndrome was associated only with the constipation subgroup. The Janus face of MC resembles the subgroups of irritable bowel syndrome. The co-existence of autoimmune diseases and MC is confirmed in both the constipation and diarrhea subgroups.

Genetic background of lactose intolerance and implications for diagnosis

with both CC and LC, and if there was associated entempathy. Methods: 32 patients with microscopic colitis (17 CC, 15 LC) diagnosed using objective histological criteria were included. Serum IgA-antiendomysial (AEA) and lgA-human tissue antitransglutaminase (AtTG) antibodies (IIF and ELISA assays, respectively) were investigated, after ruling-out lgA deficiency. The DQ2 hapforype (DQAI*0501 + DQBI*0201) was deterrmned by PCRSSP. This method detects the presence or absence of at least one copy of the haplotype. HLA-DQ2 was also assayed in 50 healthy controls from the general population. Endoscopic biopsies from 2d-3rd portions of duodenum were obtained in DQ2 + patients. The number of intraepithefial lymphocytes (IEL) (N<8 x 20 epithelial cells), their distribution pattern, and the architecture of villi were assessed. Results: 13 of 32 (40.6%) patients with microscopic colitis and 9 of 50 (18%) controls had DQ2 + (p = 0.025). There were no differences between CC and LC (35.3 vs 47%). A LC patient had positive AEA and AtTG, and biopsy with IEL increase (11x20 epithelial cells) without atrophy (Marsh 1); she was diagnosed of CS and a gluten-free diet was started. In the other 30 patients, AEMAtTG were negative. In 7 DQ2 + patients the number of [EL was normal and there was no villous atrophy (in 5 patients endoscopic biopsies were not available). Conclusions: in the present series, the frequency of CS in microscopic colitis patients was 3.2%, lower than that previously described, but higher than that observed in the general population in our country (0.03%). The high frequency of DQ2 haplotype observed in patients with CC/LC confirms the existence of a high genetic susceptibility to CS in these patients, and suggests that class II HLA genes might be implicated in the pathogenesis of microscopic colitis.