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PubMed2000

Inflammatory bowel disease promotes venous thrombosis earlier in life.

BACKGROUND: Patients with inflammatory bowel disease (IBD) may be at increased risk of having venous thromboembolism. METHODS: Medical records from 1,253 IBD patients attending hospital care during the years 1987-97 were studied. These patients were recruited from a population of 340,000 inhabitants. Patients with verified venous thrombosis were characterized clinically, and blood samples were examined for coagulopathy including analyses of antithrombin, plasminogen, protein C, protein S, factor V, and prothrombin mutations. As control groups we used 99 patients with verified venous thrombosis and no history of IBD and 288 volunteers with no history of thrombosis. RESULTS: The incidence of venous thrombosis was 1.5/1,000 IBD patients per year, which is comparable to the background population. The mean age was significantly lower in IBD patients than in non-IBD patients (53 versus 64 years, P= 0.0225). We found one patient with antithrombin deficiency but none with protein C, protein S, or plasminogen deficiency. Factor V mutation was as prevalent in IBD patients with thrombosis as in thrombotic non-IBD patients (27% versus 28%) and 3.0 times (95% confidence interval, 0.8-11.9) more frequent in IBD patients with thrombosis than in healthy controls. Prothrombin mutation was not detected in IBD patients with venous thrombosis. CONCLUSION: We found no increased incidence of venous thrombosis in IBD patients compared with a background population. However, IBD patients had venous thrombosis earlier in life than non-IBD patients. Although factor V mutation may contribute to thrombosis, IBD acts as a trigger through mechanisms that still remain unexplained.

Adolescent↗
PubMed2006

High incidence of Crohn's disease in Canterbury, New Zealand: results of an epidemiologic study.

BACKGROUND: Inflammatory bowel disease (IBD) has increased exponentially in industrialized nations over the last 50 years. Previous New Zealand studies have shown that IBD is less common than in other countries; however, clinical observations suggested a high incidence and prevalence of IBD in Canterbury, particularly Crohn's disease (CD). AIM: This study aimed to determine the descriptive epidemiology of IBD in Canterbury. METHODS: Canterbury IBD patients, recruited using multiple strategies, gave informed consent, permission for clinical record review, completed a questionnaire, and were bled for DNA extraction as part of the Canterbury IBD Project. Cases were confirmed using standard criteria, and completeness of recruitment was validated using capture-recapture methods. Demographic and phenotypic data were extracted from case notes. One thousand four hundred twenty patients (715 CD, 668 ulcerative colitis [UC]) were recruited (> 91% of Canterbury IBD patients). RESULTS: In 2004, age-standardized (World Health Organization World Standard Population) IBD, CD, and UC incidence rates were 25.2, 16.5, and 7.6/100,000/year, respectively. The IBD, CD, and UC point prevalences on 1 June, 2005 were 308.3, 155.2, and 145.0/100,000, respectively. CD patients were more likely than UC patients to be female (61.4% vs. 47.1%) and to be younger (median age, 39.9 years vs. 43.7 years). The percent of IBD patients who were white was 97.5%. CONCLUSION: IBD is at least as common in Canterbury as in other western regions. CD incidence and prevalence are amongst the highest ever reported and are higher than for UC. IBD population characteristics are otherwise similar to other countries. The Canterbury IBD Project will be a valuable tool for future population-based IBD epidemiology and genetics research.

Adolescent↗
PubMed2004

Key role of mast cells and their major secretory products in inflammatory bowel disease.

Historically, mast cells were known as a key cell type involved in type I hypersensitivity. Until last two decades, this cell type was recognized to be widely involved in a number of non-allergic diseases including inflammatory bowel disease (IBD). Markedly increased numbers of mast cells were observed in the mucosa of the ileum and colon of patients with IBD, which was accompanied by great changes of the content in mast cells such as dramatically increased expression of TNFalpha, IL-16 and substance P. The evidence of mast cell degranulation was found in the wall of intestine from patients with IBD with immunohistochemistry technique. The highly elevated histamine and tryptase levels were detected in mucosa of patients with IBD, strongly suggesting that mast cell degranulation is involved in the pathogenesis of IBD. However, little is known of the actions of histamine, tryptase, chymase and carboxypeptidase in IBD. Over the last decade, heparin has been used to treat IBD in clinical practice. The low molecular weight heparin (LMWH) was effective as adjuvant therapy, and the patients showed good clinical and laboratory response with no serious adverse effects. The roles of PGD2, LTC4, PAF and mast cell cytokines in IBD were also discussed. Recently, a series of experiments with dispersed colon mast cells suggested there should be at least two pathways in man for mast cells to amplify their own activation-degranulation signals in an autocrine or paracrine manner. The hypothesis is that mast cell secretogogues induce mast cell degranulation, release histamine, then stimulate the adjacent mast cells or positively feedback to further stimulate its host mast cells through H1 receptor. Whereas released tryptase acts similarly to histamine, but activates mast cells through its receptor PAR-2. The connections between current anti-IBD therapies or potential therapies for IBD with mast cells were discussed, implicating further that mast cell is a key cell type that is involved in the pathogenesis of IBD. In conclusion, while pathogenesis of IBD remains unclear, the key role of mast cells in this group of diseases demonstrated in the current review implicates strongly that IBD is a mast cell associated disease. Therefore, close attentions should be paid to the role of mast cells in IBD.

Cell Degranulation↗
PubMed1993

First attack of inflammatory bowel disease and infectious colitis. A clinical, histological and microbiological study with special reference to early diagnosis.

To investigate the possibilities of differentiating between inflammatory bowel disease (IBD) and infectious colitis on clinical, microbiological, laboratory and histological grounds, a prospective study of 105 patients with a first attack of colitis was undertaken. Rectal biopsy was performed on four occasions during 1 year. In 56% of the patients who proved to have IBD, the mode of onset of diarrhoeal symptoms was insidious and in 44% it was more acute, while in 81% of those who proved to have infectious colitis the onset was acute. Most patients with infectious colitis presented within 1 week, had early fever, and did not show any histological features characteristic of IBD. In most IBD patients with a non-insidious onset there were clinical warning signs of IBD, such as slight previous bowel symptoms, a late presentation time (> 1 week) and absence of early fever, or histological features characteristic of IBD. Moreover, 62% of the IBD patients with a non-insidious onset fell ill in connection with travelling abroad, gastrointestinal infection or treatment with antibiotics. Travel abroad seemed to be associated with an increased risk of developing IBD. The strongest histological predictor of IBD was basal plasmocytosis, followed by more than two vertical crypt branches/MPF, crypt distortion, villous mucosa, mucosal atrophy, epithelioid granulomas and Paneth cell metaplasia. These signs were rarely or never found among patients with infectious colitis. Their frequency increased with the interval between the initial symptoms and the first biopsy. The presence of focal basal plasmocytosis seems to be the earliest sign of IBD. The frequency of histological signs indicating IBD was maximal (88%) at the 1-week biopsy. During treatment the basal plasmocytosis and villous mucosa decreased, while crypt distortion and mucosal atrophy remained unchanged. Early treatment did not prevent the appearance of any feature. Nor did it prevent relapse. In 21% of the IBD patients microbial findings were positive. The findings consisted in known colitis-causing agents in 14% and other agents, such as viruses, in another 7%. In 78% of the patients with non-relapsing colitis (NRC), colitis-causing agents were found. Haemolytic strains of E. coli were detected more often in IBD. Among the IBD patients, 65% showed positive immunofluorescence reactivity to neutrophil granulocytes, indicating the presence of antineutrophil antibodies (ANCA). The corresponding figure for NRC patients was 5%. Antibodies against beta-glucuronidase were found in 42% of the patients with granulocyte reactivity.

Acute Disease↗
PubMed1994

Long-term monitoring of psychosocial stress and symptomatology in inflammatory bowel disease.

Eleven subjects with inflammatory bowel disease (IBD) participated in a longterm self-monitoring investigation of the relationship between psychosocial stress and IBD symptomatology. Two measurement instruments, the IBD Symptom Diary and the Psychosocial Stress Diary, were completed by each subject for 7 consecutive days each month for one year. Pooled time-series analysis of the influence of daily stress on IBD activity revealed a significant effect. A positive concurrent relationship was found between both daily and monthly psychosocial stress and IBD activity. Investigations of temporal relationship among variables revealed a negative effect of previous month stress on IBD. Results suggest a monthly rebound effect whereby IBD symptom severity is negatively responsive to the severity of the previous month stress. The effects of stress upon IBD were not found to be modified by behavioral coping strategies. These results support the prevailing impression that psychosocial stress contributes to the clinical course of IBD, and specifically suggest an influential role of daily and monthly stress. A pattern matching IBD's characteristic waxing and waning clinical course emerges when the association between stress and IBD is examined from a monthly viewpoint. Refinement of our knowledge of the IBD-stress model calls for replication and explanation of the monthly rebound effect as well as investigations into type of stressor and coping strategy that may influence IBD activity.

Adaptation, Psychological↗
PubMed2000

Detection of Listeria monocytogenes by polymerase chain reaction in intestinal mucosal biopsies from patients with inflammatory bowel disease and controls.

BACKGROUND AND AIMS: Components of the intestinal microflora are believed to play an important role in the pathogenesis of inflammatory bowel disease (IBD) in genetically susceptible hosts acting either as a non-specific antigenic stimulus or as a specific pathogen. Listeria monocytogenes has been suggested as an organism with the potential to cause IBD. The objective of the present study was to investigate the prevalence of L. monocytogenes DNA in intestinal biopsies from patients with IBD and from non-IBD controls by using nested polymerase chain reaction (PCR). METHODS: The DNA was extracted from 274 colonoscopic biopsies, which were obtained from 23 patients with Crohn's disease (CD), 28 with ulcerative colitis (UC) and 39 non-IBD control patients. Nested PCR amplification was used to detect the presence of the L. monocytogenes listeriolysin O (hly) gene. The sequences of positive PCR products were determined and compared with databases. RESULTS: The sensitivity of our nested PCR was 10 fg L. monocytogenes DNA. Overall, L. monocytogenes DNA was detected in 13.0% patients with CD, 17.9% patients with UC and 25.6% non-IBD control patients or in 29 of 274 (10.6%) endoscopic biopsies. Among them, L. monocytogenes DNA was detected in four of 67 (6%) biopsies from patients with CD, five of 94 (5.3%) biopsies from patients with UC and 20 of 113 biopsies (17.7%) from non-IBD control patients. Sequence analysis of positive PCR products demonstrated more than 95% similarity to the hly gene sequence of L. monocytogenes, confirming the authenticity of our PCR products. CONCLUSION: Listeria monocytogenes DNA was detected in the intestine of both patients with IBD and in non-IBD control patients, probably reflecting the widespread presence of this organism in the environment. The low yield of positive biopsies in our IBD patients (5-6%) and the fact that the detection rate of L. monocytogenes DNA was similar in endoscopic biopsies from IBD patients and non-IBD controls does not support a direct role for L. monocytogenes in the pathogenesis of IBD, at least in New Zealand patients.

Adolescent↗
PubMed2006

Change of diagnosis during the first five years after onset of inflammatory bowel disease: results of a prospective follow-up study (the IBSEN Study).

OBJECTIVE: An exact diagnosis of inflammatory bowel disease (IBD) and further subclassification may be difficult even after clinical, radiological and histological examinations. A correct subclassification is important for the success of both medical and surgical therapeutic strategies, but there is a dearth of information available on the frequency of changes in diagnosis in population-based studies. The objective of this work was prospectively to re-evaluate the diagnosis in an unselected cohort of IBD patients during the first five years after the initial diagnosis. MATERIAL AND METHODS: Patients classified as IBD or possible IBD in the period 1990-94 (the IBSEN cohort) had their diagnosis re-evaluated after 1 and 5 years. Initially, the patients were classified as ulcerative colitis (UC), Crohn's disease (CD), indeterminate colitis (IC) or possible IBD. At the 5-year visit, patients were classified as UC, CD or non-IBD. RESULTS: A total of 843 patients (518 UC, 221 CD, 40 IC and 64 possible IBD) were identified. Clinical information was available for 94% of the patients who survived after 5 years. A change in diagnosis was found in 9% of the patients initially classified as UC or CD. A change to non-IBD was more frequent than a change between UC and CD. A large proportion of patients initially classified as IC or possible IBD were diagnosed as non-IBD after 5 years (22.5% versus 50%). When IBD was confirmed in these groups, UC was more frequent than CD. Two changes in diagnosis during follow-up were observed in 2.8% of the patients; this was more frequent in patients initially classified as IC or possible IBD. CONCLUSIONS: There are obvious diagnostic problems in a minority of patients with IBD; a systematic follow-up is therefore important in these patients.

Adolescent↗
PubMed2003

Haemostasis in inflammatory bowel diseases: clinical relevance.

BACKGROUND: In inflammatory bowel disease (IBD), many alterations of haemostasis have been reported. Furthermore. IBD is associated with thromboembolic disease. METHODS: Literature on new insights into the physiology of haemostasis. the interaction between haemostasis and inflammation, plasmatic and mucosal changes in haemostasis in IBD, and haemostasis-interfering therapy in patients with IBD are reviewed. RESULTS: Haemostasis is a vascular-bed-specific, locally regulated, physiological phenomenon aimed at the maintenance of fluidity of blood, and not a simple cascade-shaped chain of reactions. Coagulation activation is part of the inflammatory response, but coagulation activation induces pro-inflammatory effects at the same time. Coagulation and fibrinolysis are activated in the course of IBD. but sometimes in a misbalanced way. Overall, this may induce a state of plasmatic hypercoagulation, irrespective of disease activity. Thromboembolic disease is a common extra-intestinal manifestation of IBD. Established treatment of thromboembolism is similarly useful in IBD patients: concurrent aggressive treatment of exacerbations is recommended. Intractable gastrointestinal bleeding seldom occurs, and has mainly been reported in patients with untreated active IBD. Thrombophilic genetic background does not seem to be responsible for either the increased risk of thromboembolism, or the prevalence of IBD. Haemostasis-interfering therapy to alter the course of IBD is experimental. CONCLUSION: Thromboembolism is an extraintestinal manifestation of IBD, partly because of the associated state of plasmatic hypercoagulation. Thrombophilic genetic background does not contribute to prevalence or course of IBD: genetic investigations may be restricted to patients with clinically proven thrombophilia. Anticoagulant therapy can normally be given to patients. but not as an established therapy against IBD.

Anticoagulants↗
PubMed1985

The use in practice of inactivated oil emulsion vaccine against infectious bursal disease in broiler breeders and its influence on the progeny: a comparative field trial.

Field trials were conducted to establish the effect of the use of an inactivated oil emulsion vaccine against Infectious Bursal Disease (IBD OEV) in broiler breeder hens, and its effects on their progeny. The performance of 18 broiler flocks, which were the progeny of the IBD OEV vaccinated breeder hens, but which were not vaccinated with a live vaccine against IBD, was equal to that of broiler flocks which were vaccinated with a live IBD vaccine and originated from parent stock that had been vaccinated only against IBD with a live vaccine. In none of the 18 flocks, progeny of IBD OEV vaccinated parents, was IBD diagnosed. In a second stage, 15 broiler flocks were included in the trial: these were derived partly from IBD OEV vaccinated parents, and partly from parents that received only live IBD vaccine at 8-10 days of age. No cases of IBD occurred and all flocks were positive for IBD precipitins at slaughter age. Vaccination with a live vaccine against IBD at the age of 8-10 days had no influence on NCD antibody development after a NCD vaccination at 7 days. No immunosuppressive effect from this type of live live IBD vaccine could be determined under field conditions.

Animals↗
PubMed2002

Lactase deficiency: not more common in pediatric patients with inflammatory bowel disease than in patients with chronic abdominal pain.

OBJECTIVE: Lactase deficiency is commonly found in adults with inflammatory bowel disease (IBD). Our aim was to determine its prevalence in children with IBD. METHODS: We conducted a retrospective and descriptive analysis of patients with symptomatic IBD whose mucosal lactase activity was measured on duodenal biopsies obtained during gastrointestinal endoscopic evaluations. Age- and gender-matched controls were chosen randomly from a group with chronic abdominal pain. RESULTS: One hundred twelve patients with IBD were identified from January 1994 to December 2000. Seventy-nine (71%) had Crohn disease, and 33 (29%) had ulcerative colitis. Forty-five (40%) of all IBD patients (29 with Crohn disease and 16 with ulcerative colitis) had low lactase activity levels (< 15 microM/min/gm). The prevalence of lactase deficiency in patients with IBD was 37% (38 of 103) in white patients and 78% (7 of 9) in blacks. Thirty-four of 112 controls (30%) had lactase deficiency. IBD patients were more likely to be lactase deficient than the controls, but the difference was not statistically significant ( = 0.162). Normal duodenal histology was found in 67% of lactase-deficient IBD patients compared with 82% in lactase-sufficient IBD patients. The frequency of duodenal inflammation did not differ significantly between lactase-deficient and -sufficient patients with IBD ( = 0.068). CONCLUSIONS: More than one third of pediatric patients with IBD have lactase deficiency, which is not significantly different from non-IBD patients with chronic abdominal pain. The majority of lactase-deficient patients with IBD have normal duodenal biopsy results. Lactase activity from small bowel biopsy specimens can be measured at the time of initial endoscopy. Reevaluation, either by small bowel biopsy or the breath hydrogen test, may then be considered during follow-up of symptomatic patients.

Abdominal Pain↗
PubMed2006

Do patients with inflammatory bowel disease want genetic testing?

BACKGROUND: Inflammatory bowel disease (IBD) is a complex genetic disorder characterized by nonmendelian inheritance, incomplete penetrance, and disease susceptibility but not disease certainty. Genotype and phenotype associations are described, but the level of interest of patients with IBD in genetic testing for themselves or at-risk family members remains unknown. Thus, the goal of this study was to assess the interest of patients with IBD in genetic testing and their willingness to accept the uncertainty inherent in complex genetics. MATERIALS AND METHODS: Consecutive outpatients with IBD were recruited to complete a 57-item self-administered survey. The survey included a layperson explanation of the limits of IBD genetics. A 5-point Likert scale was used to determine willingness to undergo genetic testing to determine diagnosis, prognosis, and treatment; to help their family; and to advance medical knowledge. The IBD Questionnaire, a validated measure of the health status attitudes of patients with IBD, was used. To determine limits of patient interest in testing family members, the standard reference gamble paradigm was used. Patients were presented with situations for the genetic test with various levels of certainty in 10% decrements starting with 100%. They indicated the lowest degree of certainty that they would accept to test their family member. RESULTS: One hundred fourteen patients (mean age 38.4 years; 48.2% women) completed the survey. Of these 114, 71.9% (82) had Crohn's disease. Among the patients who answered questions on self-willingness, 76.8% (86 of 112) would undergo testing for diagnostic confirmation, 81.3% (91 of 112) for prognostic value, 88.4% (99 of 112) for therapeutic decision making, and 85.0% (96 of 113) for advancement of medical knowledge. We found that 28.1% of patients (32 of 114) had a first-degree relative with IBD. Those patients with a first-degree relative with IBD were more willing to undergo genetic testing than those without a first-degree relative with IBD (raw score on self-willingness 4.62 vs 4.36; P=0.026). There was no significant association between patients' health status and their willingness to undergo genetic testing (IBD Questionnaire score and raw score on self-willingness; Spearman's correlation coefficient -0.06; P=0.51). We also found that 88.6% of patients (93 of 105) indicated an interest in testing family members if the test provided absolute certainty of future disease. The average lowest level of certainty these patients were willing to accept was 42.2%. CONCLUSIONS: Despite the complexity of IBD genetics, most patients with IBD are interested in testing and willing to accept a variable degree of uncertainty about the results. An important minority of patients does not wish to be tested. Future work should better identify the reasons for these different attitudes. This information should be factored into plans for widespread clinical testing.

Adult↗
PubMed2006

Familial occurrence of inflammatory bowel disease in Korea.

BACKGROUND: Little information is available about the familial aggregation of inflammatory bowel disease (IBD) in Asian populations. We therefore determined the risk of familial aggregation of IBD among first-degree relatives of patients with ulcerative colitis (UC) or Crohn's disease (CD) in an ethnically distinct Korean population. METHODS: Familial aggregation of IBD was evaluated in terms of family history, prevalence, lifetime risk, and population relative risk in first-degree relatives of 1440 unrelated patients with UC (n = 1043) or CD (n = 397). RESULTS: A positive first-degree family history of IBD was observed in 27 probands (1.88%): 21 of 1043 (2.01%) with UC and 6 of 397 (1.51%) with CD. The crude prevalence of IBD in first-degree relatives of probands with IBD was 0.31%. The lifetime risk of IBD was 0.54% in all first-degree relatives of IBD probands, 0.52% in UC probands, and 0.67% in CD probands, with overall lifetime relative risks of 0.12% in parents, 0.79% in siblings, and 1.43% in offspring. The age- and sex-adjusted population relative risk of IBD was 13.8 in first-degree relatives of probands with IBD. CONCLUSIONS: Although a positive family history, prevalence, and lifetime risk of IBD among first-degree relatives of Korean IBD patients are much lower than among relatives of Western patients, the population relative risk in first-degree relatives is about equal in Koreans and Westerners. This finding indicates that a positive family history is an important risk factor for IBD in Koreans and in Westerners.

Adolescent↗
PubMed2006

The prevalence of long bone fractures in pediatric inflammatory bowel disease.

INTRODUCTION: The association of inflammatory bowel disease (IBD) with decreased bone mineral density is well recognized. In the adult population, up to 50% of IBD patients are reported to have osteopenia, correlating with an increase in the incidence of fractures as compared with controls. The aim of this study was to determine the prevalence of fractures in a pediatric population with IBD as compared with healthy sibling controls (SC). PATIENTS AND METHODS: The families of 209 patients with IBD were sent a questionnaire asking them to compare their children with IBD to a healthy sibling (non-IBD). RESULTS: Surveys were returned by 132 of the 209 families (63%). The sample characteristics of this sample closely resembled the overall clinic population for age (mean 14.3 vs 14.7 years), gender (53% vs 59% male) and diagnosis (58.1 vs 57.8 Crohn disease). Completed surveys described 263 children. Of the 132 with IBD 73 (55%) had Crohn disease, 52 (39%) had ulcerative colitis and 7 (6%) had indeterminate colitis. There were 76/132 males (age range, 4-18 years) with IBD and 64/131 males (age range, 1-26 years) in the sibling controls. Mean ages of the IBD sample 14.3 +/-.3 was compared with 13.9 +/- in SC. Of the total group, 73/263 (28%) reported ever having a fracture, 44 (60%) were siblings (SC), and 29 (40%) had IBD. Of the 29 children with IBD, 17 (59%) reported having a fracture after diagnosis including 2 who had fractures both before and after diagnosis. The total number of fractures reported was 96 (55 SC:41 IBD). CONCLUSION: In this survey, we found no statistically significant difference in the prevalence of fracture in IBD patients compared with their normal siblings.

Adolescent↗
PubMed2003

Work losses related to inflammatory bowel disease in Canada: results from a National Population Health Survey.

OBJECTIVE: Few studies have assessed the influence of inflammatory bowel disease (IBD) on work loss or estimated the costs related to work loss. Our analysis reports the employment effects related to IBD as based on the 1998 sample of the Canadian National Population Health Survey (NPHS). METHODS: Our predictive analysis adapts the theory of labor supply to a health context. Respondents between the ages of 20 and 64 who reported that they had been diagnosed by a health professional to have "a bowel disorder such as Crohn's disease or colitis" were distinguished from the other respondents. A logistic regression model was used to estimate the OR for labor force nonparticipation and variables predictive of it in the case of IBD. For those people in the labor force, the Cox proportional hazard model was used to determine whether having IBD and similar bowel disorders had an effect on the number of months of continuous employment. RESULTS: Of the IBD patients 28.9% reported labor force nonparticipation, which was a greater proportion than the non-IBD respondents (18.5% nonparticipation). The OR was 1.20 (95% CI = 1.19-1.21) for nonparticipation of IBD patients versus non-IBD patients controlling for potentially confounding factors. We estimated the excess nonparticipation attributable to IBD and similar bowel disorders in Canada to be 2.9%. Based on this, the indirect cost of nonparticipation attributable to IBD in 1998 was >$104.2 million Canadian dollars. According to the second regression using the Cox proportional hazard model, IBD and similar bowel disorders were not significantly related to the number of months worked until a break in employment was reported. Thus, there was no excess work loss among those who were employed that was associated with IBD. CONCLUSIONS: By using directly observed data in our analysis, this method of estimation can predict the overall burden of IBD and similar bowel disorders, controlling for the effect of other potentially influential characteristics.

Adult↗
PubMed1997

Mast cell mediated ion transport in intestine from patients with and without inflammatory bowel disease.

BACKGROUND: Mast cells have been shown to regulate intestinal ion transport in animal models and normal human colon but their physiological role in human intestinal inflammatory disorders is unknown. AIMS: To examine mast cell regulation of ion transport in inflammatory bowel disease (IBD). SUBJECTS AND METHODS: Small and large intestine was obtained from patients with and without IBD undergoing surgical resection. Short circuit current (Isc) responses to rabbit antihuman IgE, histamine, and electrical stimulation were measured in Ussing chambers. Specimens were also examined for mast cell numbers and degree of inflammation. RESULTS: Isc responses to anti-IgE and histamine were smaller in magnitude in IBD compared with non-IBD tissues. In all tissues, anti-IgE Isc responses were reduced by about 80% in chloride free buffer. The histamine H1 receptor antagonist, pyrilamine, decreased anti-IgE responses in non-IBD tissues. Greater inhibition with pyrilamine was seen in IBD small intestine but its effect was less in IBD colon. Histamine pretreatment of non-IBD control tissues reduced anti-IgE responses to levels seen in IBD colon but had no effect in small intestine. Mast cell numbers were greater in IBD compared with non-IBD small intestine while no differences were observed between the colonic groups. Isc responses to anti-IgE were not correlated with the degree of mucosal inflammation. CONCLUSIONS: This study provides further evidence that mast cells are capable of mediating alterations of ion transport in human gut but that this regulatory role may be altered in IBD. The data suggest that prior activation of mast cells with release of histamine may account for the reduced secretory response to anti-IgE observed in IBD colonic tissues.

Animals↗
PubMed2005

Optimal haplotype structure for linkage disequilibrium-based fine mapping of quantitative trait loci using identity by descent.

A linkage disequilibrium-based method for fine mapping quantitative trait loci (QTL) has been described that uses similarity between individuals' marker haplotypes to determine if QTL alleles are identical by descent (IBD) to model covariances among individuals' QTL alleles for a mixed linear model. Mapping accuracy with this method was found to be sensitive to the number of linked markers that was included in the haplotype when fitting the model at a putative position of the QTL. The objective of this study was to determine the optimal haplotype structure for this IBD-based method for fine mapping a QTL in a previously identified QTL region. Haplotypes consisting of 1, 2, 4, 6, or all 10 available markers were fit as a "sliding window" across the QTL region under ideal and nonideal simulated population conditions. It was found that using haplotypes of 4 or 6 markers as a sliding "window" resulted in the greatest mapping accuracy under nearly all conditions, although the true IBD state at a putative QTL position was most accurately predicted by IBD probabilities obtained using all markers. Using 4 or 6 markers resulted in greater discrimination of IBD probabilities between positions while maintaining sufficient accuracy of IBD probabilities to detect the QTL. Fitting IBD probabilities on the basis of a single marker resulted in the worst mapping accuracy under all conditions because it resulted in poor accuracy of IBD probabilities. In conclusion, for fine mapping using IBD methods, marker information must be used in a manner that results in sensitivity of IBD probabilities to the putative position of the QTL while maintaining sufficient accuracy of IBD probabilities to detect the QTL. Contrary to expectation, use of haplotypes of 4-6 markers to derive IBD probabilities, rather than all available markers, best fits these criteria. Thus for populations similar to those simulated here, optimal mapping accuracy for this IBD-based fine-mapping method is obtained with a haplotype structure including a subset of all available markers.

Crosses, Genetic↗
PubMed2005

Risk factors for thromboembolic complications in inflammatory bowel disease: the role of hyperhomocysteinaemia.

Inflammatory bowel disease (IBD) is associated with an increased risk for thromboembolic events. Aim of this study was to examine the relationship of hyperhomocysteinemia and thrombosis in IBD patients and to assess the role of this factor in addition to other known prothrombotic abnormalities. IBD patients with a history of thrombosis (n = 22) and sex-, age-, and diagnosis-matched IBD controls (n = 23) were studied. Homocysteine (tHcy) was assessed before and after methionine loading. Plasma levels of protein C, protein S, antithrombin III, and fibrinogen and the presence of anticardiolipin and antiphospholipid antibodies were determined and genetic testing for factor V Leiden and the prothrombin gene mutation was performed. Results showed that fasting homocysteine levels in IBD patients with a history of arterial or venous thrombosis tended to be higher than in IBD controls, although not significantly. The increase in homocysteine levels after methionine loading was significantly higher in IBD patients in the arterial thrombosis group than in IBD controls (40.9 +/- 17.7 vs. 27.2 +/- 9.9 microM; P < 0.05). Among the other prothrombotic factors, only factor V Leiden was significantly associated with a history of venous thrombosis (20 vs. 0%). At least one risk factor was found in 64% of the IBD patients with previous thromboembolic complications. We conclude that there is an association between hyperhomocysteinemia and a history of arterial thrombosis in IBD patients. We confirm the high prevalence of factor V Leiden in IBD patients with a history of venous thrombosis. In the majority of IBD patients with previous thromboembolic complications, at least one prothrombotic risk factor is detected.

Adult↗
PubMed1991

Frequency of inflammatory bowel disease in offspring of couples both presenting with inflammatory bowel disease.

A private practice was surveyed for prevalence of inflammatory bowel disease (IBD) in husband-wife partners and in their children. Among approximately 2500 patients with IBD in our files, 19 couples were identified. They were subdivided into group A (n = 5) in which both partners had symptoms of IBD before marriage; group B (n = 7) in which only one spouse had IBD before marriage and the other partner experienced symptoms afterwards; and group C (n = 7) in which neither spouse had symptoms before marriage but IBD subsequently developed in both. In group B, the disease developed in the second spouse 2-16 years after marriage (mean, 6.4 years). In group C, IBD developed in the first spouse 0.3-41 years after marriage and in the second spouse 1-14 years after the first spouse (mean, 6.8 years). Thirty-five children have been born to 16 of the couples. Two children died before age 20. Of the surviving 33 children, IBD has already developed in 12 (36%). Among the other 21 unaffected children, 1 had uveitis at age 9 and 10 are still under the age of 21, perhaps too young to have yet developed IBD. The frequency of IBD in children was slightly higher if both parents had already developed IBD at the time of conception (67%) compared with when only 1 parent (50%) or neither parent (50%) had developed IBD when conception occurred. Although these data do not distinguish genetic from environmental factors, they show a higher risk of IBD in children when both parents have this illness.

Adult↗