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PubMed2006

The nature of inflammatory bowel disease in patients with coexistent colonic diverticulosis.

GOALS/BACKGROUND: Reports of segmental colitis with diverticula regard this entity as a local disease. Our goal was to reexamine the association of diverticula to colitis and question the relationship of colonic diverticulosis with generalized inflammatory bowel disease (IBD). STUDY: A retrospective database review of more than 1,600 patients matched 100 cases with IBD and colonic diverticulosis with a control group of 100 patients with IBD without diverticulosis. Patients were matched by gender, IBD diagnosis, and date of birth. Variables examined included disease distribution, strictures, fistulae, extraintestinal manifestations (EIMs), family history, and age at IBD diagnosis. RESULTS: For all IBD diagnoses, more sigmoid inflammation occurred in cases with diverticular disease: 82% versus 65% for controls (P = 0.005), and in the rectum: 85% versus 69% for controls (P = 0.005). In the Crohn's disease with diverticulosis subset, sigmoid inflammation was more common: 70% versus 42% for controls (P = 0.007), and in the rectum: 70% versus 46% for controls (P = 0.02). Disease distribution was otherwise similar throughout the colon, ileum, and jejunum. The incidence of strictures (P = 0.99) and fistulae (P = 0.69) was similar. EIMs were more frequent in cases with diverticulosis: 28% versus 16% (P = 0.05). Family history of IBD was similar: 26% for cases and 16% for controls (P = 0.12). Age at IBD diagnosis was significantly greater in diverticulosis cases compared with controls: 51.5 years (+/-17.6) versus 42.8 years (+/- 17.5) (P < 0.001), respectively. CONCLUSIONS: We observed an increased frequency of sigmoid and rectal inflammation, EIMs, and an older age of IBD onset in cases with diverticulosis. This suggests a role for diverticula in IBD beyond that of a mere coincidental finding.

Adult↗
PubMed2001

Use of pharmaceuticals by inflammatory bowel disease patients: a population-based study.

OBJECTIVES: In 1996 we created the population-based University of Manitoba Inflammatory Bowel Disease (IBD) Database. In 1994, Manitoba Health established the Drug Program Information Network (DPIN), which identified all ambulatory prescription drugs dispensed to each individual resident of the province. All residents have a personal health identification number, and use of this number allowed linkage of the IBD database with the DPIN database. Our aim was to use the linkage of these databases to describe prescription drug use by patients with IBD in Manitoba in 1997. METHODS: We analyzed all prescriptions and costs for fiscal year 1997, and stratified our analysis by age, sex, urban versus nonurban residence, income, and disease (Crohn's disease vs ulcerative colitis). We also extracted all subjects diagnosed with IBD in 1984-1987 and those diagnosed in 1994-97 and compared any differences in prescribing patterns in 1997 for these two cohorts. RESULTS: A total of 87.5% of IBD subjects received prescriptions in 1997. There was a direct, significant relationship between increasing age and number of different prescriptions per IBD drug user and total prescription costs per IBD drug user (in adults only), particularly for alimentary drugs. Female patients used a greater number of different prescriptions, but there was no difference between sexes in costs per user. Only 7.8% of patients used immunomodulatory drugs, but these accounted for the greatest cost ($1404) per user. Patients whose disease was diagnosed in 1994-1997 were significantly more likely to be prescribed oral or rectal 5-aminosalicylic acid and steroids than were those whose disease was diagnosed in 1984-1987. In addition, prescriptions for rectal 5-aminosalicylic acid were significantly increased in those patients whose diagnoses were made later over those whose diagnoses were made earlier. Male patients and Crohn's disease patients were more likely to use oral steroids and immunomodulatory medications. Based on the decade of diagnosis, there was no difference in prescribing patterns for immunomodulatory medications. CONCLUSIONS: The linkage of the University of Manitoba IBD Database and the Manitoba DPIN Database allowed a description of patterns of prescription use in a population-based sample of IBD patients. Among the important findings are the lack of effect of gender and urban residence on prescription use in IBD patients; however the decade of diagnosis did affect prescribing patterns. Furthermore, only 7.8% overall receive immunomodulatory medications, but this was independent of the decade of diagnosis.

Adjuvants, Immunologic↗
PubMed2002

Lamina propria and circulating interleukin-6 in newly diagnosed pediatric inflammatory bowel disease patients.

OBJECTIVES: Understanding cytokine production patterns in early mucosal lesions of pediatric patients newly diagnosed with inflammatory bowel disease (IBD) may be critical to understanding IBD pathogenesis. Interleukin-6 (IL-6) has a central role in a multitude of immune system reactions; however, inconsistent lamina propria and serum IL-6 has been reported in IBD patients. Newly diagnosed pediatric IBD patients have not previously been evaluated for lamina propria or serum IL-6. METHODS: Serum and intestinal lamina propria biopsy whole organ culture supernatants were evaluated by ELISA for IL-6 obtained from newly diagnosed IBD patients, before initiation of immunomodulatory therapies. RESULTS: Levels of lamina propria IL-6 demonstrated significant correlation with graded severity of histological inflammation (p < 0.001). Log-transformed serum and organ culture IL-6 levels demonstrated significant correlation (p < 0.0001, R2 = 0.6226). Assigning a demarcation level of >400 pg/ml, serum IL-6 concentrations were a superior marker for the presence of microscopic intestinal inflammation than erythrocyte sedimentation rate (ESR), with a sensitivity of 82%, specificity of 100%, positive predictive value of 100%, and negative predictive value of 82%. When evaluating subtypes of IBD, serum IL-6 levels were correlated more significantly with active disease in ulcerative colitis patients (p = 0.01, R2 = 0.74) than in Crohn's disease patients (p = 0.21, R2 = 0.33). CONCLUSIONS: This study outlines graded production of IL-6 in intestinal lamina propria and serum of newly diagnosed pediatric IBD patients, confirming the presence of IL-6 in early IBD patients. In addition, serum IL-6 may be a good predictor of IBD in pediatric patients with suspected or newly diagnosed IBD.

Adolescent↗
PubMed2003

Work losses related to inflammatory bowel disease in the United States: results from the National Health Interview Survey.

BACKGROUND: U.S. studies using varying methodologies have reported different estimates for the indirect, or nonmedical cost per person with inflammatory bowel disease (IBD). Our analysis contributes to this literature by using the 1999 sample of the National Health Interview Survey (NHIS) to estimate the work-loss effect of IBD on work in the United States and the associated cost to society. METHODS: A weighted logistic regression model was used to estimate the OR of being out of the labor force as determined by predictive variables, including having been diagnosed with IBD, with or without symptoms. Controls included health status indicators and demographic variables. For those people in the labor force, a second analysis was performed to determine the relative influence of the same variables on working less than 12 months versus the entire year. SUDAAN 8.0 was used to generate population estimates, systematically correcting for survey design. RESULTS: Of IBD patients who had experienced symptoms in the past 12 months, 31.5% reported being out of the labor force (OR = 2.14, relative to the non-IBD group). We estimated the excess in the nonparticipation rate attributable to IBD with symptoms in the past 12 months in the United States to be 12.3%. Based on this, the indirect cost of nonparticipation attributable to IBD in 1998/1999 was more than $3.6 billion U.S. dollars (USD) or $5228 USD per person with IBD and symptoms. According to the second weighted logistic regression, for those who are in the labor force, having IBD had no association with the duration of work. CONCLUSIONS: By using directly observed data in our analysis, this method of estimation can be used to predict the overall paid-employment burden of IBD.

Absenteeism↗
PubMed2004

Assessment of thrombin-activatable fibrinolysis inhibitor (TAFI) plasma levels in inflammatory bowel diseases.

OBJECTIVES: Hypofibrinolysis has been proposed as a possible mechanism underlying the known risk of thrombosis observed in patients with inflammatory bowel diseases (IBD). Thrombin-activatable fibrinolysis inhibitor (TAFI) is a recently described inhibitor of fibrinolysis. Increased TAFI plasma levels are associated with a risk for venous thrombosis. The objective was to evaluate TAFI plasma levels and their possible correlations with clinical features and acute-phase reactants in IBD patients. METHODS: Eighty-one IBD patients (47 Crohn's disease and 34 ulcerative colitis) and 81 sex- and age-matched healthy controls were enrolled in the study; moreover, we studied 30 inflammatory controls (13 Reiter's syndrome, 4 Behçet's syndrome, and 13 patients with newly diagnosed celiac disease). TAFI plasma levels were assessed by means of a commercially available ELISA kit. Erythrocytes sedimentation rate, C-reactive protein, and alpha1-acid glycoprotein were measured as acute-phase reactants. Statistical analysis was performed by means of nonparametric tests and Fisher's exact test and chi(2) test for independence. RESULTS: Median TAFI plasma levels were significantly higher in IBD patients (116.0%, range: 39.0-232.0%) and in inflammatory controls (176.0%, 50.0-435.0%) than in healthy controls (99.0%, 40.0-170.0%) (p< or = 0.05 and p< or = 0.001, respectively). TAFI plasma levels higher than the 95th percentile of control values were significantly more frequent in IBD patients (19.7%) and in inflammatory controls (53.3%) than in healthy controls (4.9%) (p< or = 0.008 and p< or = 0.0001, respectively) and more frequent in clinically active IBD than in clinically quiescent IBD (31.4%vs 10.9%, p< or = 0.03). Finally, in IBD, significant correlations were observed between TAFI plasma levels and erythrocytes sedimentation rate (p< or = 0.02), C-reactive protein (p< or = 0.001), and alpha1-acid glycoprotein (p< or = 0.05). CONCLUSIONS: TAFI plasma levels are increased in IBD patients and correlate with acute-phase reactants. Increased TAFI plasma levels might contribute to the prothrombotic state observed in IBD through the induction of hypofibrinolysis.

Adult↗
PubMed2005

Thrombosis in inflammatory bowel diseases: role of inherited thrombophilia.

BACKGROUND: Inflammatory bowel diseases (IBD) are characterized by an increased risk for venous and arterial thrombosis. Although the pathogenetic mechanisms of this predisposition are unclear, a possible role of inherited risk factors for thrombosis in determining this predisposition has been suggested. AIM: To evaluate the role of factor V Leiden (G1691A) and G20210A prothrombin gene mutations in determining the occurrence of thrombosis in IBD patients. PATIENTS AND METHODS: Forty-seven IBD patients (30 ulcerative colitis and 17 Crohn's disease) with a positive history for thrombosis (9 at arterial sites and 38 at venous sites) were enrolled in the study. For each patient, two non-IBD subjects matched for sex and age, type, and site of thrombosis were used as controls. Peripheral blood DNA specimens were amplified by PCR using appropriate primers and analyzed by restriction analysis on agarose gel electrophoresis. Statistical analysis was performed by means of Fisher's exact test. RESULTS: The total number of subjects with one or both mutations was significantly lower in IBD patients with thrombosis than in control subjects (12.8%vs 29.8%, respectively; p= 0.035, OR = 0.34, 95% CI 0.13-0.90). The total frequency of the mutated alleles was also significantly lower in IBD than in controls (7.4%vs 16.5%, respectively; p= 0.041, OR = 0.40, 95% CI 0.17-0.96). Prothrombotic mutations were particularly unfrequent in IBD patients with active disease at the time of thrombosis compared with patients with quiescent disease (8.0%vs 36.4%, respectively; p= 0.057, OR = 0.15, 95% CI 0.02-1.01). CONCLUSIONS: The major inherited risk factors for thrombosis are significantly less frequent in thrombotic IBD patients than in thrombotic non-IBD subjects, suggesting that acquired risk factors play the most relevant role in determining thromboembolic events observed in IBD patients, particularly during active phases of the disease.

Adult↗
PubMed2006

Genetic polymorphisms associated with inflammatory bowel disease do not confer risk for primary sclerosing cholangitis.

OBJECTIVES: Approximately 80% of patients with primary sclerosing cholangitis (PSC) of Northern European origin have concurrent inflammatory bowel disease (IBD). The majority have ulcerative colitis, but there is also an association with Crohn's colitis. The pathogenetic link between PSC and IBD is unknown. We aimed to assess whether genetic risk factors in PSC can be identified on the basis of known IBD susceptibility genes and the shared PSC-IBD phenotype. METHODS: IBD-associated polymorphisms in the CARD15, TLR-4, CARD4, SLC22A4, SLC22A5, DLG5, and MDR1 genes were genotyped in a large cohort of 365 Scandinavian PSC patients and 368 healthy controls using TaqMan technology. RESULTS: No significant association between any of the investigated genetic IBD risk variants and overall susceptibility to PSC was observed. Apart from a tendency toward an increased carrier frequency of the mutant CARD15 alleles in PSC patients with concurrent Crohn's disease as compared with healthy controls (15.6%vs 9.0%, P = 0.22), no association with any of the polymorphisms investigated was evident even when considering only PSC patients with concurrent IBD. CONCLUSION: It seems unlikely that IBD-associated polymorphisms in the CARD15, TLR-4, CARD4, SLC22A4, SLC22A5, DLG5, and MDR1 genes confer susceptibility to PSC. The current knowledge of genetic risk factors in IBD may not contribute to our understanding of molecular mechanisms involved in the pathogenesis of PSC or the IBD phenotype in PSC.

Adolescent↗
PubMed2001

Duck hepatitis B virus replication in primary bile duct epithelial cells.

Primary cultures of intrahepatic bile duct epithelial (IBDE) cells isolated from duckling livers were successfully grown for studies of duck hepatitis B virus (DHBV). The primary IBDE cells were characterized by immunohistochemistry using CAM 5.2, a cytokeratin marker which was shown to react specifically to IBDE cells in duck liver tissue sections and in primary cultures of total duck liver cells. Immunofluorescence assay using anti-duck albumin, a marker for hepatocytes, revealed that these IBDE cultures did not appear to contain hepatocytes. A striking feature of these cultures was the duct-like structures present within each cell colony of multilayered IBDE cells. Normal duck serum in the growth medium was found to be essential for the development of these cells into duct-like structures. When the primary cultures of duck IBDE cells were acutely infected with DHBV, dual-labeled confocal microscopy using a combination of anti-DHBV core proteins and CAM 5.2 or a combination of anti-pre-S1 proteins and CAM 5.2 revealed that the IBDE cell colonies contained DHBV proteins. Immunoblot analysis of these cells showed that the DHBV pre-S1 and core proteins were similar to their counterparts in infected primary duck hepatocyte cultures. Southern blot analysis of infected IBDE preparations using a digoxigenin-labeled positive-sense DHBV riboprobe revealed the presence of hepadnavirus covalently closed circular (CCC) DNA, minus-sense single-stranded (SS) DNA, double-stranded linear DNA, and relaxed circular DNA. The presence of minus-sense SS DNA in the acutely infected IBDE cultures is indicative of DHBV reverse transcriptase activity, while the establishment of a pool of viral CCC DNA reveals the ability of these cells to maintain persistent infection. Taken collectively, the results from this study demonstrated that primary duck IBDE cells supported hepadnavirus replication as shown by the de novo synthesis of DHBV proteins and DNA replicative intermediates.

Animals↗
PubMed2006

A meta-analysis on the influence of inflammatory bowel disease on pregnancy.

BACKGROUND: Inflammatory bowel disease (IBD) has a typical onset during the peak reproductive years. Evidence of the risk of adverse pregnancy outcomes in IBD is important for the management of pregnancy to assist in its management. AIM: To provide a clear assessment of risk of adverse outcomes during pregnancy in women with IBD. DESIGN: The Medline literature was searched to identify studies reporting outcomes of pregnancy in patients with IBD. Random-effect meta-analysis was used to compare outcomes between women with IBD and normal controls. PATIENTS AND SETTING: A total of 3907 patients with IBD (Crohn's disease 1952 (63%), ulcerative colitis 1113 (36%)) and 320 531 controls were reported in 12 studies that satisfied the inclusion criteria. RESULTS: For women with IBD, there was a 1.87-fold increase in incidence of prematurity (<37 weeks gestation; 95% CI 1.52 to 2.31; p<0.001) compared with controls. The incidence of low birth weight (<2500 g) was over twice that of normal controls (95% CI 1.38 to 3.19; p<0.001). Women with IBD were 1.5 times more likely to undergo caesarean section (95% CI 1.26 to 1.79; p<0.001), and the risk of congenital abnormalities was found to be 2.37-fold increased (95% CI 1.47 to 3.82; p<0.001). CONCLUSION: The study has shown a higher incidence of adverse pregnancy outcomes in patients with IBD. Further studies are required to clarify which women are at higher risk, as this was not determined in the present study. This has an effect on the management of patients with IBD during pregnancy, who should be treated as a potentially high-risk group.

Birth Weight↗
PubMed2003

Insurance problems among inflammatory bowel disease patients: results of a Dutch population based study.

BACKGROUND AND AIMS: The majority of patients with inflammatory bowel disease (IBD) have a normal life expectancy and therefore should not be weighted when applying for life assurance. There is scant literature on this topic. In this study our aim was to document and compare the incidence of difficulties in application for life and medical insurance in a population based cohort of IBD patients and matched population controls. METHODS: A population based case control study of 1126 IBD patients and 1723 controls. Based on a detailed questionnaire, the frequency and type of difficulties encountered when applying for life and medical insurance in matched IBD and control populations were appraised. RESULTS: In comparison with controls, IBD patients had an 87-fold increased risk of encountering difficulties when applying for life assurance (odds ratio (OR) 87 (95% confidence interval (CI) 31-246)), with a heavily weighted premium being the most common problem. Patients of high educational status, with continuous disease activity, and who smoked had the highest odds of encountering such problems. Medical insurance difficulties were fivefold more common in IBD patients compared with controls (OR 5.4 (95% CI 2.3-13)) although no specific disease or patient characteristics were identified as associated with such difficulties. CONCLUSIONS: This is the first detailed case control study that has investigated insurance difficulties among IBD patients. Acquiring life and medical insurance constituted a major problem for IBD patients in this study. These results are likely to be more widely representative given that most insurance companies use international guidelines for risk assessment. In view of the recent advances in therapy and promising survival data on IBD patients, evidence based guidelines for risk assessment of IBD patients by insurance companies should be drawn up to prevent possible discriminatory practices.

Adolescent↗
PubMed2024

Risk relationship between inflammatory bowel disease and urolithiasis: A two-sample Mendelian randomization study.

BACKGROUND: The causal genetic relationship between common parenteral manifestations of inflammatory bowel disease (IBD) and urolithiasis remains unclear because their timing is difficult to determine. This study investigated the causal genetic association between IBD and urolithiasis using Mendelian randomization (MR) based on data from large population-based genome-wide association studies (GWASs). METHODS: A two-sample MR analysis was performed to assess the potential relationship between IBD and urolithiasis. Specific single nucleotide polymorphism data were obtained from GWASs, including IBD (n = 59957) and its main subtypes, Crohn's disease (CD) (n = 40266) and ulcerative colitis (UC) (n = 45975). Summarized data on urolithiasis (n = 218792) were obtained from different GWAS studies. A random-effects model was analyzed using inverse-variance weighting, MR-Egger, and weighted medians. RESULTS: Genetic predisposition to IBD and the risk of urolithiasis were significantly associated [odds ratio (OR), 1.04 (95% confidence interval [CI], 1.00-.08), P = 0.01]. Consistently, the weighted median method yielded similar results [OR, 1.06 (95% CI, 1.00-1.12), P = 0.02]. The MR-Egger method also demonstrated comparable findings [OR, 1.02 (95% CI, 0.96-1.08), P = 0.45]. Both funnel plots and MR-Egger intercepts indicated no directional pleiotropic effects between IBD and urolithiasis. CD was strongly associated with it in its subtype analysis [OR, 1.04 (95% CI, 1.01-1.07), P = 0.01], and UC was also causally associated with urolithiasis, although the association was not significant [OR, 0.99 (95% CI, 0.95-1.03), P = 0.71]. CONCLUSION: A unidirectional positive causal correlation was identified between IBD and urolithiasis, with varying degrees of association observed among the different subtypes of IBD. Recognizing the increased incidence of urolithiasis in patients with IBD is crucial in clinical practice. Early detection and surveillance of IBD, improved patient awareness, adoption of preventive strategies, and promotion of collaborative efforts among healthcare providers regarding treatment methodologies are vital for improving patient outcomes.

Humans↗
PubMed2001

Measles vaccination and inflammatory bowel disease: controversy laid to rest?

The increasing incidence of Crohn's disease has lead to speculation about changes in exposures to environmental or infectious agents. Considerable attention has focused on the role of measles infection and/or vaccination in the pathogenesis of Crohn's disease and ulcerative colitis. Current evidence regarding the association between measles vaccination and inflammatory bowel disease (IBD) comprises analytic epidemiological studies, a case-series report and ecological studies. The first of these, a 1995 cohort study, found an association between measles vaccination and Crohn's disease and ulcerative colitis, but was widely questioned on methodological grounds. This was followed by a 1997 case-control study showing no association between measles vaccination and IBD. In 1998, public concern was rekindled by a report of 12 children with nonspecific colitis, ileal-lymphoid-nodular hyperplasia, and developmental disorders largely attributed to measles-mumps-rubella vaccine, but the nature of the report limited its scientific conclusions. Two additional studies, one case-control and one cohort, then followed and neither found an association with measles vaccination. Of the several ecological studies of measles vaccine coverage or measles schedule changes, none found an association with rates of IBD. The role of measles infection in IBD has been examined more extensively with studies of in utero measles exposure, measles infection early in life, and laboratory based investigations. An initial report of high rates of Crohn's disease among pregnancies affected by measles infection was followed by negative studies. Numerous case-control and ecological studies of children with measles infections early in life have also had discordant findings. Of three recent cohort studies, two showed no relationship between infection with early measles exposure and risk for IBD, while one found an approximate 3-fold elevation in risk. Laboratory investigations into persistent measles infection and IBD have been contentious. While some investigators have claimed to find persistent measles infection among patients with IBD, others, using highly sensitive polymerase chain reaction techniques, have not been able to replicate the findings. Recent controversy has centred on whether there is any evidence for molecular mimicry in the pathogenesis of IBD. In summary, available evidence does not support an association between measles-containing vaccines and risk of IBD, nor between measles infection and IBD. While further research is necessary into the causal factors underlying Crohn's disease and ulcerative colitis, continued public education efforts are needed to reassure the public about vaccine safety and to prevent declines in vaccine coverage.

Adult↗
PubMed2003

Progress in searching for susceptibility gene for inflammatory bowel disease by positional cloning.

Inflammatory bowel disease (IBD) includes two clinical subtypes: Crohn disease (CD) and ulcerative colitis (UC). The general prevalence is about 1.0-2.0 % in Western countries. It is predominantly regarded as a multifactorial disorder involving environmental factors and polygenic defects. The view was confirmed by a lot of evidences from clinical attributions and animal models, especially from epidemiological investigations. So the etiological study of IBD has been focused on searching for susceptibility genes by positional cloning, which consists of two steps: linkage analysis and association analysis. Linkage analysis has been an important method of searching for susceptibility genes to polygenic diseases as well as single-gene disorders. IBD, as a polygenic disease, has been widely investigated by linkage analysis for susceptibility gene since 1996. The paper reviewed 38 articles, which covered almost all original researches in relation to IBD and linkage analysis. So far, several loci, such as 16q, 12q, 6p and 3p, have been identified by the studies. The most striking is 16q12 (IBD1), which linked only with CD not UC in the majority of studies. Association analysis, as one essential step for positional cloning, is usually carried out by genotyping candidate genes selected by means of linkage analysis or other methods, for figuring out the frequencies of alleles and comparing the frequencies between IBD group and healthy control group to identify the specific allele. It has been established that IBD is implicated in immune disorder. So the studies were centered on the genes of NOD2/CARD15, HLA-II, cytokine, cytokine receptor and adhesion molecule. This paper reviewed 14 original articles on association between NOD2 and IBD that have been published since 2001. All results, with the exception of one report from a Japanese group, provide evidences that the three kinds of variants of NOD2 are susceptibility factors for IBD. This article also comprehensively analyzed 18 original researches of HLA gene polymorphism in IBD. We found extensive discrepancy among the conclusions and a novel hypothesis was put forward to explain the discordance. Most studies published recently on association between IBD and cytokine gene polymorphism were reviewed.

Carrier Proteins↗
PubMed1995

Tumour necrosis factor-alpha and microalbuminuria in patients with inflammatory bowel disease.

OBJECTIVE: To determine whether tumour necrosis factor-alpha (TNF-alpha) is important in the pathogenesis of microalbuminuria in patients with inflammatory bowel disease (IBD). PATIENTS AND METHODS: We measured serum TNF-alpha, interleukin (IL)-6, the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) levels and microalbuminuria in 48 patients with IBD. Serum TNF-alpha was measured by enzyme-linked immunosorbent assay and microalbuminuria was measured using an immunoturbiditimetric method. Clinical disease activity was quantified using the simple index of Harvey and Bradshaw. RESULTS: Microalbuminuria was more severe in patients with IBD than in controls, and in patients with active versus inactive disease. TNF-alpha levels were higher in patients with IBD than in controls (mean +/- SE 16.4 +/- 1.4 versus 6.6 +/- 1.3 pg/ml, respectively; P < 0.01) and in patients with active versus inactive IBD (means +/- SE 20.1 +/- 2 versus 12.8 +/- 2.7 pg/ml; respectively P = 0.056). Microalbuminuria correlated strongly with TNF-alpha (r = 0.60; P < 0.009), ESR (r = 0.67, P < 0.02) and CRP levels (r = 0.935, P < 0.001). TNF-alpha correlated significantly with CRP (r = 0.54, P < 0.01). IL-6 levels were raised significantly in patients with IBD (7 +/- 4 pg/ml, controls undetectable; P < 0.05). Patients with active IBD had higher IL-6 levels than those with inactive IBD (mean +/- SE 13 +/- 8 versus 0.90 +/- 0.35 pg/ml, respectively; P < 0.05). However, IL-6 levels did not correlate with microalbuminuria in patients with IBD (r = 0.105, P = 0.256). CONCLUSIONS: Our findings suggest that TNF-alpha may be important in the pathogenesis of microalbuminuria in patients with IBD, possibly through TNF-induced damage to the glomerular basement membrane. The mechanism for this has not been defined but may relate to TNF-induced disruption of sulphated glycosaminoglycans.

Adolescent↗
PubMedDate not supplied

HNPCC-Lynch syndrome and idiopathic inflammatory bowel disease. A hypothesis on sharing of genes.

Colon cancer occurring in patients with Lynch Syndrome and in Inflammatory Bowel Disease (IBD) share many features. There is some evidence to support the assumption that multiple genetic factors play an important role in the pathogenesis of idiopathic IBD and Lynch Syndrome. In our previous study, providing detailed medical, genetic and pathologic findings on 202 hereditary non polyposis colorectal cancer (HNPCC) relatives we found in the colonic mucosa features indicating an IBD though all the screened subjects of the family denied symptoms of IBD. Some studies have reported that the rate of undetected IBD ranges from 27 to 38%. Finally, a member of this family, considered not at risk for cancer by genetic analysis results, developed a clinically manifested IBD. The morphological aspects of the disease were not discussed in our previous study. It is possible that many members of this family inherit a major gene giving liability to the disease and are carriers of a subclinical form of IBD with a minimal morphological marker which becomes manifest in some members when other factors intervene. A possible genetic model linking the two diseases can be suggested: IBD needs two major genes for susceptibility (s) and clinical development (D). Both can be present in IBD and Lynch Syndrome, but in the latter a third gene plays a suppressor role on the development gene (D). In conclusion, we hypothesize that the IBD developing gene may be considered as protective against HNPCC, and this condition may result in a selective genetic advantage.

Colorectal Neoplasms, Hereditary Nonpolyposis↗
PubMedDate not supplied

[Association of risk factors for cerebral atherosclerosis in patients with acute ischemic brain disease].

Atherosclerosis is the primary disease in the majority of patients with ischemic brain disease (IBD). Etiopathogenesis of atherosclerosis has not been more precisely defined, but risk factors significant for its generation and development, so as for IBD development, have been identified. They were designated as risk factors for brain atherosclerosis (RFBA). The aim of this study was to establish the frequency and significance of RFBA association in the patients with acute IBD in relation to IBD severity. The investigation included 60 patients with AIBD. RFBA were: arterial hypertension, dyslipoproteinemia, diabetes and smoking. For all the patients included in the study detailed history was noted, daily glycemia profile was done, blood pressure was measured 3 times a day and parameters of lipid status with counting of LDL/HDL indices and Apo A1/Apo B were determined. IBD was confirmed by computerized tomography of brain. The degree of IBD severity was determined in all the patients by Grotta's scale. After the statistical processing, the results of the research showed that in the patients with IBD the most frequent were arterial hypertension, then smoking, dyslipoproteinemia and diabetes. In significant number of patients existed association of several factors, which was in significant positive correlation with the degree of IBD severity. It was concluded that risk factors for atherosclerosis were simultaneously risk factors for IBD. IBD is the most severe, final stage in evolution of brain atherosclerosis.

Acute Disease↗
PubMed2006

DLG5 variants contribute to Crohn disease risk in a Canadian population.

Variants in the gene encoding the DLG5 scaffolding protein have been reported to be associated with increased risk of inflammatory bowel disease (IBD) and particularly Crohn's disease (Crohn disease; CD). These findings have not been uniformly replicated in follow-up studies. In this study we genotyped a cohort of 402 Canadian CD and 179 ulcerative colitis (UC) patients and 537 healthy controls for three IBD/CD-associated DLG5 variants. Our data reveal that the common DLG5 haplotype (A), which was previously considered protective for IBD, is associated with modest increases in risk for IBD (P=0.02) and CD (P=0.04). The effects of haplotype copy number on risk for IBD were minor, with the odds ratio (ORs) being 1.37 for the heterozygous risk genotype and 1.7 for the homozygous risk genotype. While we were unable to replicate the proposed association between the DLG5 c.113G>A variant and IBD, an association of IBD (P=0.02) and CD (P=0.04) with the rarer c.4136C>A variant was replicated in this cohort. These associations were restricted to the non-Jewish subjects in this cohort and were not detected in the Ashkenazi Jewish population studied here. Within the non-Jewish group, no associations were detected between the DLG5 variants and specific phenotypic features, such as site of disease, and there was no evidence of epistasis between DLG5 and any of the CD-associated CARD15 or SLC22A4/A5 gene variants. Together, the results indicate a role for DLG5 variants in IBD susceptibility and suggest that further studies are warranted to evaluate this role in different IBD populations and to determine the functional pathways that couple DLG5 variants to IBD.

Adult↗
PubMed2002

The impact of helical computed tomography on the diagnosis of unsuspected inflammatory bowel disease in the large bowel.

Inflammatory bowel diseases (IBD) are diagnoses that can be easily overlooked clinically. The aim of this study was to investigate if CT is able to make a contribution to the identification of previously unsuspected cases of IBD. We retrospectively identified cases in which the possibility of an IBD was raised in CT reports (over a 4-year period), by utilising a keyword search of the radiology database. Cases with a previously known or suspected IBD were rigorously excluded by review of case notes, and endoscopic, radiological, histological and microbiological findings. The CT images of the identified cases were reviewed by a blinded observer to document the extent of bowel wall thickening, the location of lesion(s), and presence of peri-colic fat abnormality, ascites and/or collections. The observer also attempted to corroborate the presence, and to identify the type, of IBD based on the CT appearances alone. Thirty-five cases (out of approximately 19,000 body CTs performed) of clinically unsuspected IBD were identified, of which 27 underwent further investigation. An IBD was confirmed in 48% (13 of 27): Crohn's disease (n=6), ulcerative colitis (n=2), pseudomembranous colitis (n=3) and other (n=2), of which 70% (9 of 13) were correctly typed by the reviewer. Inflammatory bowel disease was not substantiated in the remainder (14 of 27), although 7 of these had other bowel pathologies: diverticular disease (n=4); and carcinoma (n=3). Prospectively determining the presence, and furthermore type, of IBD on CT is challenging largely because of the considerable overlap in the appearances of the individual IBDs and indeed of normality. Nevertheless, CT is able to identify clinically unsuspected cases and radiologists should be alert to this treatable and not infrequently elusive diagnosis.

Adult↗