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Inflammatory Bowel Disease (inflammatory + bowel_disease)
Kinds of Inflammatory Bowel Disease Terms modified by Inflammatory Bowel Disease Selected AbstractsGIANT PSEUDOPOLYPOSIS IN INFLAMMATORY BOWEL DISEASEANZ JOURNAL OF SURGERY, Issue 5 2000Boon-Swee Ooi First page of article [source] Course and treatment of perianal disease in children newly diagnosed with Crohn's diseaseINFLAMMATORY BOWEL DISEASES, Issue 3 2009David J. Keljo MD Abstract Background: We sought to characterize perianal disease and its treatment in pediatric patients newly diagnosed with Crohn's disease. Methods: Data were obtained from the Pediatric Inflammatory Bowel Disease (IBD) Collaborative Group Registry, a prospective, multicenter observational registry recording clinical and laboratory outcomes in children under 16 years of age newly diagnosed with IBD. Patients with Crohn's disease were selected who had data on perianal disease and at least 24 months of follow-up. The records of patients with a Pediatric Crohn's Disease Activity Index perianal subscore greater than 0 were reviewed, and patients with abscesses or fistulas were selected. The therapies used and the course of their perianal disease were then assessed. Results: Of the 276 patients identified, 41 had perianal lesions within 30 days of diagnosis. Thirteen of these had skin tags and fissures only, whereas 28 had fistulas and/or abscesses. The latter lesions resolved by 1 year in 20 patients, and 8 had chronic/recurrent perianal disease persisting for more than 1 year following diagnosis. Patients with fistulizing disease were much more likely to be treated and were treated earlier with antibiotics, infliximab, and immunomodulators than were nonfistulizing patients. Patients who developed chronic perianal disease were more likely to have low body mass indices and required more perianal surgery than did patients whose perianal disease resolved. Conclusions: Approximately 10% of newly diagnosed pediatric patients with Crohn's disease will have perianal fistulas and/or abscesses at the time of diagnosis. Most of these will resolve within a year with medical therapy alone. (Inflamm Bowel Dis 2008) [source] Incidence and Prognosis of Colorectal Dysplasia in Inflammatory Bowel Disease: A Population-based Study from Olmsted County, Minnesota,INFLAMMATORY BOWEL DISEASES, Issue 8 2006Tine Jess MD Abstract Background and Aims: The risk, fate, and ideal management of colorectal dysplasia in inflammatory bowel disease (IBD) remain debated. We estimated the incidence, long-term outcome, and risk factors for progression of colorectal dysplasia (adenomas [adenoma-associated lesions or masses (ALMs)], flat dysplasia, and dysplasia-associated lesions or masses [DALMs]) in a population-based IBD cohort from Olmsted County, Minnesota. Materials and Methods: The Rochester Epidemiology Project was used to identify cohort patients with colorectal dysplasia. Medical records were reviewed for demographic and clinical characteristics. Histology slides were reviewed by a pathologist blinded to previous pathology reports. The cumulative incidence of dysplasia was estimated, and the association between patient characteristics and recurrence/progression of dysplasia was assessed using proportional hazards regression. Results: Twenty-nine (4%) IBD patients developed flat dysplasia (n = 8), DALMs (n = 1), ALMs in areas of IBD (n = 18), or ALMs outside areas of IBD (n = 2). Among 6 patients with flat low-grade dysplasia (fLGD) who did not undergo colectomy, none progressed during a median of 17.8 (range 6,21) years of observation with a median of 3 (range 0,12) surveillance colonoscopies. Four (22%) patients with ALMs in areas of IBD who did not undergo surgery developed LGD or DALMs. Primary sclerosing cholangitis and dysplasia located proximal to the splenic flexure were significantly associated with risk for recurrence/progression of dysplasia. Conclusions: This population-based cohort study from Olmsted County, Minnesota did not confirm an increased risk of cancer related to fLGD, whereas 22% of patients with ALMs in areas of IBD developed fLGD or DALMs. [source] Inflammatory Bowel Disease in Returning TravelersJOURNAL OF TRAVEL MEDICINE, Issue 6 2000Daphne Yanai-Kopelman No abstract is available for this article. [source] Comparison of Oral Prednisone and Prednisone Combined with Metronidazole for Induction Therapy of Canine Inflammatory Bowel Disease: A Randomized-Controlled TrialJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2010A.E. Jergens Background: Although prednisone and metronidazole are commonly used to treat canine inflammatory bowel disease (IBD), no randomized-controlled trials have been performed. Hypothesis: Combination drug therapy with prednisone and metronidazole will be more effective than prednisone alone for treatment of canine IBD. Reduction in disease severity will be accompanied by decreased canine IBD activity index (CIBDAI) scores and serum C-reactive protein (CRP) concentrations. Animals: Fifty-four pet dogs diagnosed with IBD of varying severity. Methods: Dogs were randomized to receive oral prednisone (1 mg/kg; n = 25) or prednisone and metronidazole (10 mg/kg; n = 29) twice daily for 21 days. Clinical (CIBDAI) scores and serum CRP were determined at diagnosis and after 21 days of drug therapy. The primary efficacy measure was remission at 21 days, defined as a 75% or greater reduction in baseline CIBDAI score. Results: Differences between treatments in the rate of remission (both exceeding 80%) or the magnitude of its change over time were not observed. CRP concentrations in prednisone-treated dogs were increased because of many dogs having active disease. Both treatments reduced CRP in comparison with pretreatment concentrations. An interaction between CIBDAI and CRP was identified in 42 of 54 dogs (78%), whereas 8 of 54 dogs (15%) showed disagreement between these indices. Conclusions and Clinical Importance: Prednisone is as effective as combined treatment with prednisone and metronidazole for induction therapy of canine IBD. CRP may be normal or increased in dogs with IBD and may be useful in assessing the response of individual dogs to treatment along with changes in the CIBDAI. [source] Perinuclear Antineutrophilic Cytoplasmic Antibody and Response to Treatment in Diarrheic Dogs with Food Responsive Disease or Inflammatory Bowel DiseaseJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2006Nicole Luckschander The goal of this study was to investigate the correlation between perinuclear antineutrophilic cytoplasmic antibody (pANCA) and clinical scores before and after treatment in diarrheic dogs with food-responsive disease (FRD) or inflammatory bowel disease (IBD). pANCA serology was evaluated prospectively by indirect immunofluorescence in 65 dogs with signs of gastrointestinal disease, and if positive, pANCA antibody titers were determined. Thirty-nine dogs with FRD responded to a novel diet, and 26 dogs with IBD were treated with corticosteroids. The severity of clinical signs was scored by means of a canine IBD activity index (CIBDAI). At initial examination, a significantly (P= .002) higher percentage of dogs were pANCA-positive in the FRD group (62%) compared with the IBD group (23%). pANCA titers were significantly higher (P=.003) before treatment in the FRD group (median titer 100) compared with the IBD group (median titer 1). However, there was no difference in pANCA titers between the groups after respective treatments because dogs in the IBD group had a significant increase in pANCA titer after treatment. The CIBDAI score decreased significantly (P <.001) after treatment in both groups (74% moderate to severe in FRD dogs before versus 8% after treatment; 85% moderate to severe in IBD dogs before versus 32% after treatment). There was no correlation between pANCA status in FRD or IBD dogs before treatment and scores for CIBDAI, endoscopy, or histopathology before or after treatment, except for the endoscopic duodenal score in dogs with FRD after treatment (P= .03). A positive pANCA test before therapy may aid in the diagnosis of FRD. [source] Influence of Dietary Fiber on Inflammatory Bowel Disease and Colon Cancer: Importance of Fermentation PatternNUTRITION REVIEWS, Issue 2 2007Devin J. Rose MS The benefits of dietary fiber on inflammatory bowel disease may be related to the fermentative production of butyrate in the colon, which appears to decrease the inflammatory response. The benefits of dietary fiber against colon cancer may be related to both fermentative and non-fermentative processes, although poorly fermentable fibers appear more influential. Dietary fiber fermentation profiles are important in determining optimal fibers for colonic health, and may be a function of structure, processing conditions, and other food components. A greater understanding of the relationships between fermentation rate and dietary fiber structure would allow for development of dietary fibers for optimum colonic health. [source] Effect of Different Doses of Thalidomide in Experimentally Induced Inflammatory Bowel Disease in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2008Om Prakash Adult Wistar rats of either sex were used (n = 36). Colitis was induced by a single intra-colonic application of 20 mg 2,4,6-trinitrobenzene sulfonic acid (TNBS) dissolved in 35% ethanol into the descending colon. Rats were divided into six groups (n = 6). Animals were treated with vehicle (ethanol), TNBS dissolved in 35% ethanol, thalidomide (with different doses of 50, 100 and 150 mg/kg body weight), and sulfasalazine (360 mg/kg body weight) for 14 days. After completion of 14 days of treatment, animals were killed and the following parameters were assessed: morphological score, histological score and biochemical parameters (myeloperoxidase, malondialdehyde and tumour necrosis factor-,). Results showed thalidomide with different doses provided protection against TNBS-induced colonic damage. There was significant protection with thalidomide 150 mg/kg body weight compared to controls (P < 0.001). All the biochemical parameters were highly reduced in the entire thalidomide-treated group compared to controls particularly with thalidomide 150 mg/kg body weight (P < 0.001). Treatment with thalidomide restored malondialdehyde as well as reduction of myeloperoxidase and tumour necrosis factor-, towards normal levels. Morphological and histological score were significantly reduced in all the treated groups with significant effect found with 150 mg/kg (P < 0.001). Our results indicate efficacy of thalidomide in TNBS induce experimental colitis model in rats but present findings requires further investigation to establish the real safety and efficacy in human beings. [source] Abstracts from the 2009 Advances in Inflammatory Bowel Diseases, Crohn's & Colitis Foundation's National Clinical & Research ConferenceINFLAMMATORY BOWEL DISEASES, Issue S2 2009Article first published online: 16 NOV 200 First page of article [source] Abstracts from the 2008 Advances in Inflammatory Bowel Diseases, Crohn's & Colitis Foundation's National Clinical & Research ConferenceINFLAMMATORY BOWEL DISEASES, Issue S3 2008Article first published online: 26 NOV 200 First page of article [source] Abstracts from the 2007 CCFA National Research and Clinical Conference, 6th Annual Advances in the Inflammatory Bowel DiseasesINFLAMMATORY BOWEL DISEASES, Issue S1 2008Article first published online: 10 DEC 200 First page of article [source] Abstracts from the 2006 CCFA National Research and Clinical Conference, 5th Annual Advances in the Inflammatory Bowel Diseases, Dec. 1-3, 2006, Miami, FLINFLAMMATORY BOWEL DISEASES, Issue S5 2007Article first published online: 6 APR 200 First page of article [source] Increased prevalence of burnout symptoms in parents of chronically ill childrenACTA PAEDIATRICA, Issue 3 2010C Lindström Abstract Aim:, To examine the prevalence of burnout symptoms in the context of parenting a chronically ill child. Methods:, A total of 252 parents of children with Type 1 Diabetes Mellitus and 38 parents of children with Inflammatory Bowel Diseases participated in a population-based study. A control group consisted of 124 randomly selected parents of healthy children. We used self-report questionnaires to assess symptoms of burnout. Results:, The main finding was that significantly more parents of children with chronic diseases (36%) scored for clinical burnout, compared with parents of healthy children (20%). Burnout symptoms were most prominent among mothers of children with diabetes, although fathers of children with diabetes and mothers and fathers of children with inflammatory bowel diseases also reported higher levels of various burnout symptoms. Conclusion:, Burnout may be a useful model for understanding long-term parental responses and should be acknowledged among the different types of psychological consequences of the multi-faceted experience of parenting a child with chronic illness. Gender seems to influence the risk of burnout symptoms. Continued research about other background factors, and how the parents' situation changes over time are warranted. In the clinic, we need to draw attention to the group of parents who may suffer from burnout. [source] Advances in the management of inflammatory bowel diseaseFUTURE PRESCRIBER, Issue 2 2007James Jupp BM MRCP Specialist Registrar in Gastroenterology Inflammatory bowel disease is a common and complicated disorder that has a great impact on the lives of those affected. This review discusses the properties and uses of the treatments available and possible future advances in therapy. Copyright © 2007 Wiley Interface Ltd [source] Preliminary evidence supporting a framework of psychological adjustment to inflammatory bowel disease,INFLAMMATORY BOWEL DISEASES, Issue 10 2010Jennifer L. Kiebles PhD Abstract Background: Adjustment to chronic disease is a multidimensional construct described as successful adaptation to disease-specific demands, preservation of psychological well-being, functional status, and quality of life. Inflammatory bowel disease (IBD) can be particularly challenging due to the unpredictable, relapsing and remitting course of the disease. Methods: All participants were patients being treated in an outpatient gastroenterology clinic at a university medical center. Participants completed a survey of questionnaires assessing illness perceptions, stress, emotional functioning, disease acceptance, coping, disease impact, and disease-specific and health-related quality of life. Adjustment was measured as a composite of perceived disability, psychological functioning, and disease-specific and health-related quality of life. Results: Participants were 38 adults with a diagnosis of either Crohn's disease (45%) or ulcerative colitis (55%). We observed that our defined adjustment variables were strongly correlated with disease characteristics (r = 0.33,0.80, all P < 0.05), an emotional representation of illness (r = 0.44,0.58, P < 0.01), disease acceptance (r = 0.34,0.74, P < 0.05), coping (r = 0.33,0.60, P < 0.05), and frequency of gastroenterologist visits (r = 0.39,0.70, P < 0.05). Better adjustment was associated with greater bowel and systemic health, increased activities engagement and symptom tolerance, less pain, less perceived stress, and fewer gastroenterologist visits. All adjustment variables were highly correlated (r = 0.40,0.84, P < 0.05) and demonstrated a cohesive composite. Conclusions: The framework presented and results of this study underscore the importance of considering complementary pathways of disease management including cognitive, emotional, and behavioral factors beyond the traditional medical and psychological (depression and anxiety) components. (Inflamm Bowel Dis 2010) [source] Inflammatory bowel disease in young people: The case for transitional clinicsINFLAMMATORY BOWEL DISEASES, Issue 6 2010J. Goodhand MRCP Abstract Background: The incidence of inflammatory bowel disease (IBD) is increasing among adolescents. In all, 25% of patients are diagnosed before the age of 16, when they are traditionally transferred from the pediatric to the adult service. Methods: We conducted a retrospective case-controlled study to characterize patients treated in a novel transitional adolescent,young adult IBD clinic. This compared disease extent, radiation exposure, therapeutic strategy, and requirement for surgery in 100 adolescents with controls from our adult IBD clinic matched for disease duration. Results: The median (range) ages for the adolescent and adult population was 19 (16,28) and 43 (24,84), with a median age at diagnosis of 15 (3,26) and 39 (13,82) respectively (P < 0.001). Crohn's disease was significantly more common in the adolescents. Disease distribution was ileocolonic in 69% of adolescents and 28% of adults, restricted to the ileum in 20% of adolescents and 47% of adults, and colonic only in 11% and 22%, respectively. Upper gastrointestinal involvement occurred in 23% of adolescents, but was not seen in adults (P < 0.01). Total ulcerative colitis was seen in 67% of adolescents and 44% of adults (P < 0.01). Contrary to previous data adolescents did not receive more ionizing radiation than adults. Requirement for immunosuppressive therapy was higher in the adolescent group (53% versus 31%, respectively, P < 0.01). Likewise, 20% of adolescents had required biological therapy compared to only 8% in the adult cohort (P < 0.05). Conclusions: Gastroenterologists should recognize that IBD is more complex when presenting in adolescence and our data support the creation of specific adolescent transitional clinics. Inflamm Bowel Dis 2009 [source] CXCL12 Is a constitutive and inflammatory chemokine in the intestinal immune systemINFLAMMATORY BOWEL DISEASES, Issue 4 2010Iris Dotan MD Abstract Background: Inflammatory bowel disease (IBD) is characterized by increased lymphocytic infiltrate to the lamina propria (LP) and upregulation of inflammatory chemokines and receptors. CXCL12 is a constitutive chemokine involved in lung, brain, and joint inflammation. We hypothesized that CXCL12 and its receptor, CXCR4, would have a constitutive and inflammatory role in the gut. Methods: Intestinal epithelial cells (IECs) and T lymphocytes were isolated from intestinal mucosa of IBD and control patients undergoing bowel resection. Autologous T cells were isolated from peripheral blood (PB). CXCL12 and CXCR4 expression by IECs was assessed by polymerase chain reaction and immunohistochemistry, lymphocyte phenotype by flow cytometry, and migration by Transwells. Results: IECs expressed CXCL12 and expression was increased and more diffuse in IBD compared to normal crypts (ulcerative colitis [UC] > Crohn's disease [CD], inflamed > noninflamed). CXCR4 was expressed by IECs, LP T cells (LPTs), and PB T cells (PBTs), and CXCR4+ cells were increased in IBD LP in situ. PBTs and LPTs from all patients had a high and comparable migration toward CXCL12 (P < 0.0001 and P < 0.05 vs. medium, respectively). Migration toward IBD-IEC-derived supernatant was significantly higher compared to normal. Antibodies against CXCR4 and CXCL12 blocked migration. Conclusions: CXCL12 is expressed by normal IECs and upregulated and differentially distributed in IBD IECs. CXCR4 is expressed by IECs and LPTs, and CXCR4+ cells are significantly increased in IBD LP. CXCL12 is chemotactic for both PBTs and LPTs. Thus, CXCL12 and CXCR4 have a constitutive and inflammatory role in the intestinal mucosa and their selective therapeutic manipulation may be considered in IBD management. (Inflamm Bowel Dis 2009;) [source] World Gastroenterology Organization Practice Guidelines for the Diagnosis and Management of IBD in 2010INFLAMMATORY BOWEL DISEASES, Issue 1 2010Dr. Charles N. Bernstein Chairman Abstract Inflammatory bowel disease (IBD) represents a group of idiopathic, chronic, inflammatory intestinal conditions. Its two main disease categories are: Crohn's disease (CD) and ulcerative colitis (UC), which feature both overlapping and distinct clinical and pathological features. While these diseases have, in the past, been most evident in the developed world, their prevalence in the developing world has been gradually increasing in recent decades. This poses unique issues in diagnosis and management which have been scarcely addressed in the literature or in extant guidelines. Depending on the nature of the complaints, investigations to diagnose either form of IBD or to assess disease activity will vary and will also be influenced by geographic variations in other conditions that might mimic IBD. Similarly, therapy varies depending on the phenotype of the disease being treated and available resources. The World Gastroenterology Organization has, accordingly, developed guidelines for diagnosing and treating IBD using a cascade approach to account for variability in resources in countries around the world. Inflamm Bowel Dis 2010 [source] Inflammatory bowel disease in the setting of autoimmune pancreatitis,INFLAMMATORY BOWEL DISEASES, Issue 9 2009Karthik Ravi MD Abstract Background: Despite scattered case reports, the prevalence of inflammatory bowel disease (IBD) in patients with autoimmune pancreatitis (AIP) is unknown. We sought to better characterize the putative association between the conditions. Methods: Medical records of 71 patients meeting accepted criteria for AIP were reviewed to identify those with endoscopic and histological evidence of IBD. Colon samples in patients with both AIP and IBD were immunostained to identify IgG4-positive cells. Results: Four patients with AIP (5.6%) had a diagnosis of IBD: 3 had ulcerative colitis (UC) and 1 had Crohn's disease (CD). The diagnosis of IBD preceded or was simultaneous to that of AIP. Two AIP-UC patients treated for AIP with prednisone had a recurrence of AIP, and 1 required 6-mercaptopurine for long-term corticosteroid-sparing treatment. Two AIP-IBD patients underwent Whipple resections, and 1 had recurrent AIP. All 3 patients with UC presented with pancolitis, and 2 required colectomy. Colon samples from 1 patient with UC and 1 patient with CD were available for review. Increased numbers of IgG4-positive cells (10 per high-power field) were noted on the colon sample from the patient with UC. Conclusions: Almost 6% of patients with proven AIP had a diagnosis of IBD, compared to a prevalence of ,0.4%,0.5% in the general population, potentially implying a 12,15-fold increase in risk. Patients with both AIP and IBD may have increased extent and severity of IBD. The finding of IgG4-positive cells on colon biopsy suggests that IBD may represent an extrapancreatic manifestation of AIP. (Inflamm Bowel Dis 2009) [source] Runt-related transcription factor 3 is associated with ulcerative colitis and shows epistasis with solute carrier family 22, members 4 and 5INFLAMMATORY BOWEL DISEASES, Issue 12 2008Rinse K. Weersma MD Abstract Background: Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), are intestinal inflammatory disorders with a complex genetic background. Mice deficient for the runt-domain-transcription-factor3 (Runx3) develop spontaneous colitis. Human RUNX3 resides in an IBD-susceptibility locus. We studied the association of RUNX3 in a cohort of IBD patients and analyzed the interaction with SLC22A4/5. RUNX3 and OCTN1 mRNA expression was assessed in inflamed and noninflamed mucosa from patients and controls. Methods: 543 IBD patients (309 CD / 234 UC) and 296 controls were included. Four single nucleotide polymorphisms (SNPs) and 4 microsatellite markers were studied for RUNX3. Five SNPs (including SNP-207G,C and SNP1672C,T) were analyzed for SLC22A4/5. RUNX3, and OCTN1 expression in mucosal tissue from 30 patients (14 UC / 16 CD) and 6 controls were determined by quantitative polymerase chain reaction. Results: A significant association between RUNX3 -SNP rs2236851 and UC (OR 1.61; 95% confidence interval [CI] 1.11,2.32, P = 0.020) was found. Carriership is associated with pancolitis (odds ratio [OR] 1.86; 95% CI 1.08,3.21). SLC22A4/5 -SNPs rs272893 and rs273900 are associated with CD (OR 2.16; 95% CI 1.21,3.59 and OR 2.40; 95% CI 1.43,4.05). We found epistasis for carriership of a risk-associated allele in RUNX3 and SLC22A4/5 for UC patients versus CD patients (OR 3.83; 95% CI 1.26,11.67). RUNX3 mRNA expression is increased (P = 0.01) in inflamed colonic mucosa of UC patients compared to noninflamed mucosa and controls. Conclusions: We provide evidence for the genetic association of RUNX3 with UC and for CD with the IBD5 locus including SLC22A4/5. An epistatic effect of RUNX3 and SLC22A4 was associated with an increased risk for UC. Our data suggest a role for RUNX3 in UC susceptibility. (Inflamm Bowel Dis 2008) [source] Nationwide prevalence and prognostic significance of clinically diagnosable protein-calorie malnutrition in hospitalized inflammatory bowel disease patientsINFLAMMATORY BOWEL DISEASES, Issue 8 2008Geoffrey C. Nguyen MD Abstract Background Inflammatory bowel disease (IBD) patients are at increased risk of protein-calorie malnutrition. We sought to determine the prevalence of clinically diagnosable malnutrition among those hospitalized for IBD throughout the United States and whether this malnutrition influenced health outcomes. Methods We queried the Nationwide Inpatient Sample between 1998 and 2004 to identify admissions for Crohn's disease (CD) or ulcerative colitis (UC) and a representative sample of non-IBD discharges. We assessed the prevalence and predictors of malnutrition and its association with in-hospital mortality and resource utilization. Results The prevalence of malnutrition was greater in CD and UC patients than in non-IBD patients (6.1% and 7.2% versus 1.8%, P < 0.0001). The adjusted odds ratio for malnutrition among IBD admissions compared with non-IBD admissions was 5.57 [95% confidence interval (CI): 5.29,5.86]. More IBD discharges than non-IBD discharges with malnutrition received parenteral nutrition (26% versus 6%, P < 0.0001). There was increased likelihood of malnutrition among those with fistulizing CD (OR 1.65; 95% CI: 1.50,1.82) and among those who had undergone bowel resection (OR 1.37; 95% CI: 1.27,1.48). Malnutrition was associated with increased in-hospital mortality 3.49 (95% CI: 2.89,4.23), length of stay (11.9 days versus 5.8 days, P < 0.00001), and total charges ($45,188 versus $20,295, P < 0.0001). Conclusions Clinically apparent malnutrition is more frequent among IBD admissions than among non-IBD admissions. Its association with greater mortality and resource utilization may reflect more severe underlying disease that can lead to both malnutrition and worse outcomes. Nonetheless, diagnosable malnutrition may serve as a clinical marker of poor IBD prognosis in hospitalized patients. (Inflamm Bowel Dis 2008) [source] Abnormal Pap smears in inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 8 2008Sunanda Kane MD Abstract Inflammatory bowel disease (IBD) is a chronic inflammatory condition that is frequently treated with immunomodulators. Previous work has demonstrated an increased risk for abnormal cervical cytology in women treated with chronic immunosuppression, due mainly to human papillomavirus. This review summarizes the data known for this relationship in women with IBD, and management strategies for patients found to have abnormal cervical cytology. (Inflamm Bowel Dis 2008) [source] Inflammatory bowel disease and African Americans: A systematic reviewINFLAMMATORY BOWEL DISEASES, Issue 7 2008Suhal S. Mahid MRCS Abstract Background: Inflammatory bowel disease (IBD) is comprised of Crohn's disease (CD) and ulcerative colitis (UC). There are conflicting reports on whether African Americans have a more severe disease course, presentation, and more frequent extraintestinal manifestations (EIM). We examined the precise nature of this relationship by conducting a systematic review. Methods: Using predefined inclusion criteria we searched multiple healthcare databases and Grey literature. Eight reports met the inclusion criteria. Using the parameters as defined in the Montreal classification and the presence or absence of EIM, we compared IBD in African Americans and Caucasians. Results: Over 2000 IBD cases were pooled from 8 reports with African Americans comprising 17%. African Americans and Caucasians had similar distribution of types of IBD, with CD being more common than UC in both groups (CD 76% versus 68% and UC 24% versus 32%, respectively). With respect to CD, both groups presented with nonstricturing and nonpenetrating disease behavior (55% versus 41%) more frequently and had similar rates of ileocolonic disease location (42% versus 38%), and presence of perianal disease (26% versus 29%). In UC patients, proctitis was the most frequent initial presentation in both races. Joint complications were the most frequent EIM in both African Americans (52%) and Caucasians (60%). Conclusions: This study dispels the commonly held views that African Americans with IBD generally have more colonic disease, more severe disease behavior, and more perianal disease than Caucasians. African Americans also have similar variety and frequency of EIMs as compared to Caucasians. (Inflamm Bowel Dis 2008) [source] TNFSF15 is an ethnic-specific IBD geneINFLAMMATORY BOWEL DISEASES, Issue 11 2007Yoana Picornell BS Abstract Background: Inflammatory bowel disease (IBD) is a clinically and, likely, genetically heterogeneous group of disorders. A recent report suggests that genetic variations in the TNFSF15 gene contribute to the susceptibility of IBD in both Japanese and Caucasian populations. The aim was to confirm the association between TNFSF15 high- and low-risk haplotypes and IBD in a Caucasian population. Methods: Five single-nucleotide polymorphisms (SNPs) that comprise the 2 common haplotypes were genotyped in 599 Caucasian patients with Crohn's disease (CD), 382 Caucasian patients with ulcerative colitis (UC), and 230 ethnically matched healthy controls, including both Jews and non-Jews. Results: The previously reported ,risk' haplotype was not associated with CD or UC (88.2% in CD cases versus 88.3% in controls, P = 0.96; 88.1% in UC cases versus 88.3% in controls, P = 0.78). We did, however, observe an increased frequency of the "protective" haplotype in non-Jewish controls for both CD and UC (38.8% CD cases versus 50% controls, P = 0.01; 37.3% UC cases versus 50% controls, P = 0.01) with no such effect observed in the Jewish samples. There was an interactive effect between ethnicity and the protective haplotype in CD (P = 0.04). Conclusions: We observed a protective haplotype, consisting of the minor alleles for all 5 markers, to have a higher frequency in the non-Jewish controls than in CD and UC. Of further interest, the haplotype frequency was in the opposite direction in our Jewish case-control panels (both CD and UC), leading us to conclude 1) that TNFSF15 is indeed an IBD susceptibility gene, and 2) the disease susceptibility is ethnic-specific. (Inflamm Bowel Dis 2007) [source] Microbial diversity of inflamed and noninflamed gut biopsy tissues in inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 6 2007Shadi Sepehri MD Abstract Background: Inflammatory bowel disease (IBD) is a chronic gastrointestinal condition without any known cause or cure. An imbalance in normal gut biota has been identified as an important factor in the inflammatory process. Methods: Fifty-eight biopsies from Crohn's disease (CD, n = 10), ulcerative colitis (UC, n = 15), and healthy controls (n = 16) were taken from a population-based case-control study. Automated ribosomal intergenic spacer analysis (ARISA) and terminal restriction fragment length polymorphisms (T-RFLP) were used as molecular tools to investigate the intestinal microbiota in these biopsies. Results: ARISA and T-RFLP data did not allow a high level of clustering based on disease designation. However, if clustering was done based on the inflammation criteria, the majority of biopsies grouped either into inflamed or noninflamed groups. We conducted statistical analyses using incidence-based species richness and diversity as well as the similarity measures. These indices suggested that the noninflamed tissues form an intermediate population between controls and inflamed tissue for both CD and UC. Of particular interest was that species richness increased from control to noninflamed tissue, and then declined in fully inflamed tissue. Conclusions: We hypothesize that there is a recruitment phase in which potentially pathogenic bacteria colonize tissue, and once the inflammation sets in, a decline in diversity occurs that may be a byproduct of the inflammatory process. Furthermore, we suspect that a better knowledge of the microbial species in the noninflamed tissue, thus before inflammation sets in, holds the clues to the microbial pathogenesis of IBD. (Inflamm Bowel Dis 2007) [source] Inflammatory bowel disease: Epidemiology, pathogenesis, and therapeutic opportunitiesINFLAMMATORY BOWEL DISEASES, Issue 5 2006Stephen B Hanauer MD Abstract Ulcerative colitis (UC) and Crohn's disease (CD), the primary constituents of inflammatory bowel disease (IBD), are precipitated by a complex interaction of environmental, genetic, and immunoregulatory factors. Higher rates of IBD are seen in northern, industrialized countries, with greater prevalence among Caucasians and Ashkenazic Jews. Racial gaps are closing, indicating that environmental factors may play a role. IBD is multigenic, with the most clearly established genetic link between certain NOD2 variants and CD. Regardless of the underlying genetic predisposition, a growing body of data implicates a dysfunctional mucosal immune response to commensal bacteria in the pathogenesis of IBD, especially CD. Possible triggers include a chronic inflammatory response precipitated by infection with a particular pathogen or virus or a defective mucosal barrier. The characteristic inflammatory response begins with an infiltration of neutrophils and macrophages, which then release chemokines and cytokines. These in turn exacerbate the dysfunctional immune response and activate either TH1 or TH2 cells in the gut mucosa, respectively associated with CD and, less conclusively, with UC. Elucidation of immunological and genetic factors indicate multiple points at which the inflammatory cascade may be interrupted, yielding the possibility of precise, targeted therapies for IBD. [source] Inflammatory bowel disease in patients with celiac diseaseINFLAMMATORY BOWEL DISEASES, Issue 6 2005Alice Yang MD Abstract Background: Several case reports and series report an association between celiac disease and inflammatory bowel disease (IBD); however, there is no current data assessing this association. We therefore studied the occurrence of these conditions in a cohort of patients with celiac disease seen at a referral center. Methods: A database of patients with celiac disease seen between 1981 and 2002 was analyzed. Only biopsy-proven adults were included. Patients who had endoscopic and pathologic evidence of IBD were identified, and their pathology was reviewed. Age- and sex-adjusted prevalence rate ratios were determined by comparing results with population-based prevalence data. Results: Among 455 patients with celiac disease, IBD was identified in 10 (5 had ulcerative colitis and 5 had Crohn's disease). This represented an age- and sex-adjusted prevalence rate ratio for ulcerative colitis of 3.56 (95% confidence interval, 1.48-8.56) and for Crohn's disease of 8.49 (95% confidence interval, 3.53-20.42). Conclusion: Within our cohort of patients with celiac disease, IBD was significantly more common than in the general population. [source] Impairment of health-related quality of life in patients with inflammatory bowel disease: A Spanish multicenter studyINFLAMMATORY BOWEL DISEASES, Issue 5 2005Dr. F Casellas PhD Abstract Background: Inflammatory bowel disease impairs patients' perception of health and has a negative impact on health-related quality of life (HRQOL). Most studies include patients from a single hospital. This may bias limit results through the use of small patient samples and/or samples within a restricted disease spectrum. Methods: HRQOL was measured in patients with ulcerative colitis (UC) and Crohn's disease (CD) from 9 hospitals located in different geographical areas in Spain using 2 questionnaires: the Spanish version of the Inflammatory Bowel Disease Questionnaire (IBDQ) and the EuroQol. Results are expressed as medians. Results: The study included 1156 patients (528 patients with UC and 628 with CD; median age, 35 yr; slight predominance of women, 617 versus 539). HRQOL worsened in parallel with disease severity to a similar extent in both UC (IBDQ scores of 6.1, 4.7, and 4.0 for the 3 disease severity groups, respectively) and CD (IBDQ scores of 6.1, 5.0, and 4.1, respectively). A similar inverse relation between clinical activity and quality of life was observed when EuroQol preference values were used. All 5 dimensions of the IBDQ showed significantly lower scores in patients with active UC and CD than in patients in remission. The pattern of scores by IBDQ dimensions differed between patients in relapse (who scored worse on the digestive symptoms dimension) and patients in remission. Variables related with disease activity, time of evolution since diagnosis and female sex, were significantly associated with having a worse perception of HRQOL. The type of disease or geographical area of residence did not influence results on the IBDQ. Conclusions: UC and CD impair patients' HRQOL, and the degree of impairment depends on disease activity but is independent of the type of disease and place of residence. [source] Inflammatory bowel disease is linked to 19p13 and associated with ICAM-1INFLAMMATORY BOWEL DISEASES, Issue 3 2004Jin Hong Low Abstract Genome-wide scans have implicated several susceptibility loci, but linkage of 19p13 (IBD6) to Crohn's disease (CD) has not been fully replicated. We report a replication study of IBD6 in a UK Caucasian population. Two hundred eighty-four affected sibling pairs from 234 families were used for the linkage study. Linkage between IBD6 linkage and CD was replicated (LOD score = 1.59). Two candidate genes (DDXL and ICAM-1) within the IBD6 locus were examined in a case/control study with a total of 228 CD and 243 ulcerative colitis (UC) patients and 407 healthy controls. No association to either UC or CD was found in three novel intronic single nucleotide polymorphisms (SNPs) in DDXL. For ICAM-1, a significant association was found between K469 homozygosity and CD overall (39.9% vs 29.4%; Pc = 0.0096) and between E469 and fistulating disease (21.8% vs 10.0%, Pc = 0.030). In the UC group, limited disease extent was associated with homozygosity of the G241 allele (82.7% vs 64.7%, Pc = 0.0040). These data support linkage for CD at 19p13 and suggest that the amino acid polymorphisms in ICAM-1 may be associated with IBD. [source] Assessing health-related quality of life in patients with inflammatory bowel disease in Zhejiang, ChinaJOURNAL OF CLINICAL NURSING, Issue 1-2 2010Yunxian Zhou Aims., The aim of this study was to assess health-related quality of life in patients with inflammatory bowel disease in Zhejiang, Mainland China. Background., The incidence of inflammatory bowel disease in China is believed to be low but has been increasing in the past decade. The quality of life of Chinese patients with inflammatory bowel disease is unknown. Design., A cross-sectional study. Methods., The study was conducted in 92 patients with inflammatory bowel disease in Zhejiang, China, 52 with ulcerative colitis and 40 with Crohn's disease. Health-related quality of life was measured by the Chinese version of the Inflammatory Bowel Disease Questionnaire and Short Form-36, respectively. Disease activity was assessed by the Walmsley and Harvey,Bradshaw simple indices for ulcerative colitis and Crohn's disease, respectively. Demographic and clinical variables were also recorded. Short Form-36 data from the study sample were compared with a reference population of 1688 Chinese people residing in Hangzhou, Zhejiang, China. Results., No significant health-related quality of life differences were found between patients with ulcerative colitis and Crohn's disease (p > 0·05). Pooled data showed that inflammatory bowel disease patients with active disease had significantly lower scores for all eight dimensions of Short Form-36 compared to those in remission (p < 0·01); those with active disease scored significantly lower than population norms in all dimensions of Short Form-36 except mental health (p < 0·05); whereas those in remission scored significantly lower than population norms in role physical (p < 0·01) and general health dimensions (p < 0·05). The regression analyses identified only disease activity index and employment status to explain variations in health-related quality of life (p < 0·01). Conclusions., Inflammatory bowel disease similarly impairs health-related quality of life in patients with both ulcerative colitis and Crohn's disease. Relevance to clinical practice., The results suggest that any interventions that produce a stable clinical remission, whether medical or surgical, allowing patients to return to their usual work position can decrease the disease impact on their daily lives. [source] | ||||||||||||||||||||||||||||||||||