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Billy Bourke

Publications and source records attributed to Billy Bourke.

15 recordsLinked to original sources
PubMed2026

Transitioning to adult care for patients with IBD: the impact of a structured IBD transition program on service engagement.

BACKGROUND AND AIMS: The British Society of Gastroenterology recommend use of structured transition programs to improve control of chronic gastrointestinal disease in adolescents. We sought to determine the impact of attending a structured transition program on engagement of patients with inflammatory bowel disease (IBD) services and disease outcomes. METHODS: We performed a retrospective multicenter study of patients with IBD prior to and post-transfer to adult services. Patients were grouped into those who attended a structured transition program and those who received standard care, transferred with a referral letter. RESULTS: A total of 282 patients were included: 155 patients in our structured transition program cohort and 127 patients in the standard care cohort. Patients who took part in a structured transition program had significantly better engagement with adult IBD services with significantly lower rates of nonattendance at outpatient clinics 1-year post-transfer (12.3% vs 27.2%, P = .002) and significantly lower rates of disengagement with services (4.2% vs 13.1%, P = .015). There were no significant differences seen in rates of biologic failure, need for steroid/surgery or median fecal calprotectin levels between either group. Attending a structured transition program was the only factor that positively impacted engagement with IBD services in a multivariate analysis (OR 4.08, confidence interval 1.41-11.91, P = .01). CONCLUSION: Structured transition programs in IBD can improve engagement of patients with IBD services with significantly lower rates of disengagement with IBD services seen in our study. Large prospective studies are needed in this field to further investigate this and the impact of these programs on disease outcomes.

Humans↗
PubMed2006

Age-specific incidence of Helicobacter pylori.

BACKGROUND & AIMS: Helicobacter pylori is most likely acquired in childhood, but the incidence of infection has not been determined prospectively by using an appropriate noninvasive test. The aim of this study was to determine the age-specific incidence of Helicobacter pylori infection in children and the risk factors for infection. METHODS: Three hundred twenty-seven healthy index children between 24 and 48 months of age were enrolled over 15 months. At baseline, the Helicobacter pylori infection status of each index child and his or her older siblings and parents was assessed by using the carbon 13-urea breath test. All noninfected index children were then followed up with an annual carbon 13-urea breath test for 4 years to determine whether they became infected with Helicobacter pylori and, if so, the age at first infection. Information on potential risk factors was collected at baseline and each subsequent visit. RESULTS: At baseline assessment, 28 of 327 (8.6%) index children were infected with Helicobacter pylori. The mean age of the 28 infected children was 32.78 months (SD, 5.14 months). Over the next 4 years, 279 index children not infected at baseline contributed 970 person-years of follow-up to the study. During this time, 20 children became infected with Helicobacter pylori. The rate of infection per 100 person-years of follow-up was highest in the 2-3-year age group (5.05 per 100 person-years of follow-up (95% confidence interval, 1.64-11.78) and declined progressively as children aged. Only 1 child became infected after 5 years of age. Having an infected mother, an infected older sibling, and delayed weaning from a feeding bottle (ie, after 24 months of age) were all risk factors for infection. CONCLUSIONS: Children who become infected with Helicobacter pylori are infected at a very young age, and the risk of infection declines rapidly after 5 years of age. These findings have important implications for studies on the mode of transmission of infection.

Age of Onset↗
PubMed2006

Interaction of Cryptosporidium hominis and Cryptosporidium parvum with primary human and bovine intestinal cells.

Cryptosporidiosis in humans is caused by the zoonotic pathogen Cryptosporidium parvum and the anthroponotic pathogen Cryptosporidium hominis. To what extent the recently recognized C. hominis species differs from C. parvum is unknown. In this study we compared the mechanisms of C. parvum and C. hominis invasion using a primary cell model of infection. Cultured primary bovine and human epithelial intestinal cells were infected with C. parvum or C. hominis. The effects of the carbohydrate lectin galactose-N-acetylgalactosamine (Gal/GalNAc) and inhibitors of cytoskeletal function and signal transduction mechanisms on entry of the parasites into host cells were tested. HCT-8 cells (human ileocecal adenocarcinoma cells) were used for the purpose of comparison. Pretreatment of parasites with Gal/GalNAc inhibited entry of C. parvum into HCT-8 cells and primary bovine cells but had no effect on entry of either C. parvum or C. hominis into primary human cells or on entry of C. hominis into HCT-8 cells. Both Cryptosporidium species entered primary cells by a protein kinase C (PKC)- and actin-dependent mechanism. Staurosporine, in particular, attenuated infection, likely through a combination of PKC inhibition and induction of apoptosis. Diversity in the mechanisms used by Cryptosporidium species to infect cells of different origins has important implications for understanding the relevance of in vitro studies of Cryptosporidium pathogenesis.

Animals↗
PubMed2005

A prospective study of the oral manifestations of Crohn's disease.

BACKGROUND & AIMS: Recent studies suggest that the mouth may be involved frequently in patients with Crohn's disease (CD). The aim of this study was to document prospectively the proportion of children with oral lesions at diagnosis of CD, to describe the type of lesions found, and to examine the ability of gastroenterologists to identify correctly oral Crohn's manifestations. METHODS: In a prospective 3-year study, systematic dental examinations were performed on all children with suspected inflammatory bowel disease. Each child underwent upper endoscopy, colonoscopy, and barium follow-through radiography. RESULTS: Forty-eight of 49 children with CD were examined by the dentist. Oral CD was found in 20 patients (41.7%). Oral findings included mucogingivitis (12 patients), mucosal tags (4 patients), deep ulceration (4 patients), cobblestoning (3 patients), lip swelling (3 patients), and pyostomatitis vegetans (1 patient). Noncaseating granulomas were found in all 8 oral biopsy specimens from oral CD lesions (100%). Two patients with granulomas in oral biopsy specimens had no granulomas found in any other biopsy specimens. The presence of oral manifestations was associated with perianal disease. In only 9 patients (45%) with oral CD was the mouth found to be abnormal by the consultant gastroenterologists. Only nonspecific oral changes were seen in children with ulcerative colitis and indeterminate colitis. CONCLUSIONS: More than one third of all children presenting with CD had involvement of the mouth. The ability of physicians to recognize oral lesions was poor. Expert dental evaluation may be useful during the investigation of patients with suspected inflammatory bowel disease.

Adolescent↗
PubMed2005

Will treatment of Helicobacter pylori infection in childhood alter the risk of developing gastric cancer?

Helicobacter pylori has been classified as a group 1 carcinogen for gastric cancer. It is estimated that there is between a two- and sixfold increase in the risk of developing gastric cancer among infected patients. Among different populations, the risk of H. pylori-infected individuals developing gastric cancer varies greatly. However, on a worldwide scale, gastric cancer is the second most common cause of cancer-related death. Therefore, H. pylori eradication could help prevent up to three to four million gastric cancer deaths per year. H. pylori is usually acquired in childhood. Because infected children have not harboured the organism for long enough to have developed precancerous lesions, childhood is theoretically an attractive time for H. pylori eradication and, thus, could help prevent gastric cancer later in life. However, as H. pylori prevalence and the incidence of gastric cancer are falling rapidly in developed nations, widespread population screening programs aimed at the eradication of H. pylori in these countries would be enormously expensive. Therefore, except in groups with a high risk for development of gastric cancer (eg, Japanese or those with a strong positive family history of gastric cancer), a population-based test-and-treat policy is not justified.

Asian People↗
PubMed2005

Canadian Helicobacter Study Group Consensus Conference: Update on the approach to Helicobacter pylori infection in children and adolescents--an evidence-based evaluation.

As an update to previously published recommendations for the management of Helicobacter pylori infection, an evidence-based appraisal of 14 topics was undertaken in a consensus conference sponsored by the Canadian Helicobacter Study Group. The goal was to update guidelines based on the best available evidence using an established and uniform methodology to address and formulate recommendations for each topic. The degree of consensus for each recommendation is also presented. The clinical issues addressed and recommendations made were: population-based screening for H. pylori in asymptomatic children to prevent gastric cancer is not warranted; testing for H. pylori in children should be considered if there is a family history of gastric cancer; the goal of diagnostic interventions should be to determine the cause of presenting gastrointestinal symptoms and not the presence of H. pylori infection; recurrent abdominal pain of childhood is not an indication to test for H. pylori infection; H. pylori testing is not required in patients with newly diagnosed gastroesophageal reflux disease; H. pylori testing may be considered before the use of long-term proton pump inhibitor therapy; testing for H. pylori infection should be considered in children with refractory iron deficiency anemia when no other cause has been found; when investigation of pediatric patients with persistent or severe upper abdominal symptoms is indicated, upper endoscopy with biopsy is the investigation of choice; the 13C-urea breath test is currently the best noninvasive diagnostic test for H. pylori infection in children; there is currently insufficient evidence to recommend stool antigen tests as acceptable diagnostic tools for H. pylori infection; serological antibody tests are not recommended as diagnostic tools for H. pylori infection in children; first-line therapy for H. pylori infection in children is a twice-daily, triple-drug regimen comprised of a proton pump inhibitor plus two antibiotics (clarithromycin plus amoxicillin or metronidazole); the optimal treatment period for H. pylori infection in children is 14 days; and H. pylori culture and antibiotic sensitivity testing should be made available to monitor population antibiotic resistance and manage treatment failures.

Adolescent↗
PubMed2004

Cystic fibrosis-associated liver disease: a population-based study.

OBJECTIVES: The aim of this study was to explore the clinical factors associated with the development of cystic fibrosis-associated liver disease (CFALD). STUDY DESIGN: This was a case-control study of all children (age 5-18 years) with established CFALD in the Republic of Ireland between January 1999 and June 2000. Each child was pair matched for age and sex with a patient with cystic fibrosis (CF) without evidence of liver disease. Only children with clinically overt liver disease were enrolled in the disease group. RESULTS: Patients with established CFALD (n = 42; 26 boys) were enrolled. Children with CFALD had worse forced expiratory volume in 1 second values than those without CFALD. However, chest radiography and clinical scores did not differ between groups. Height (mean difference, -4.2 cm [95% confidence interval [CI], -7.41 to -0.90], P =.014), weight (mean difference, -3.21 kg [95% CI, -6.03 to -0.40], P =.026), and mid-upper arm circumference (mean difference, -1.23 cm [95% CI, -2.35 to -0.12], P =.031) were significantly lower among children with CFALD. Children with CFALD were given diagnoses of CF later than children without liver disease. There were more children with meconium ileus in the control group (14 vs 4) than among those with CFALD. CONCLUSIONS: Children with established CFALD have impaired growth and nutrition, altered body composition, and worse forced expiratory volume in 1 second values. CFALD is associated with later age of diagnosis of CF.

Adolescent↗
PubMed2004

Host cell tropism underlies species restriction of human and bovine Cryptosporidium parvum genotypes.

It has been recognized recently that human cryptosporidiosis is usually caused by Cryptosporidium parvum genotype I ("human" C. parvum), which is not found in animals. Compared to C. parvum genotype II, little is known of the biology of invasion of the human-restricted C. parvum genotype I. The aims of the present study were (i) to explore and compare with genotype II the pathogenesis of C. parvum genotype I infection by using an established in vitro model of infection and (ii) to examine the possibility that host-specific cell tropism determines species restriction among C. parvum genotypes by using a novel ex vivo small intestinal primary cell model of infection. Oocysts of C. parvum genotypes I and II were used to infect HCT-8 cells and primary intestinal epithelial cells in vitro. Primary cells were harvested from human endoscopic small-bowel biopsies and from bovine duodenum postmortem. C. parvum genotype I infected HCT-8 cells with lower efficiency than C. parvum genotype II. Actin colocalization at the host parasite interface and reduction in levels of invasion after treatment with microfilament inhibitors (cytochalasin B and cytochalasin D) were observed for both genotypes. C. parvum genotype II invaded primary intestinal epithelial cells, regardless of the species of origin. In contrast, C. parvum genotype I invaded only human small-bowel cells. The pathogenesis of C. parvum genotype I differs from C. parvum genotype II. C parvum genotype I does not enter primary bovine intestinal cells, suggesting that the species restriction of this genotype is due to host tissue tropism of the infecting isolate.

Actins↗
PubMed2003

Enteric campylobacter: purging its secrets?

Campylobacterial infections are the most common cause of bacterial enterocolitis in humans. Among children, especially in developing countries, Campylobacter infections can cause severe life-threatening diarrheal disease. Although usually associated with a benign outcome in the developed world, the burden of illness posed by Campylobacter infections is enormous, and serious neurologic sequelae also can occur. For a variety of reasons our understanding of the molecular and cellular pathogenesis of Campylobacter infection has lagged far behind that of other enteric pathogens. However, recent completion of the genome sequence of Campylobacter jejuni promises to open up the Campylobacter research field with the prospect of developing novel therapeutic and preventive strategies.

Campylobacter Infections↗
PubMed2003

Invasion of human epithelial cells by Campylobacter upsaliensis.

Few data exist on the interaction of Campylobacter upsaliensis with host cells, and the potential for this emerging enteropathogen to invade epithelial cells has not been explored. We have characterized the ability of C. upsaliensis to invade both cultured epithelial cell lines and primary human small intestinal cells. Epithelial cell lines of intestinal origin appeared to be more susceptible to invasion than non-intestinal-derived cells. Of three bacterial isolates studied, a human clinical isolate, CU1887, entered cells most efficiently. Although there was a trend towards more efficient invasion of Caco-2 cells by C. upsaliensis CU1887 at lower initial inocula, actual numbers of intracellular organisms increased with increasing multiplicity of infection and with prolonged incubation period. Confocal microscopy revealed C. upsaliensis within primary human small intestinal cells. Both Caco-2 and primary cells in non-confluent areas of the infected monolayers were substantially more susceptible to infection than confluent cells. The specific cytoskeletal inhibitors cytochalasin B, cytochalasin D and vinblastine attenuated invasion of Caco-2 cells in a concentration-dependent manner, providing evidence for both microtubule- and microfilament-dependent uptake of C. upsaliensis. Electron microscopy revealed the presence of organisms within Caco-2 cell cytoplasmic vacuoles. C. upsaliensis is capable of invading epithelial cells and appears to interact with host cell cytoskeletal structures in order to gain entry to the intracellular environment. Entry into cultured primary intestinal cells ex vivo provides strong support for the role of host cell invasion during human enteric C. upsaliensis infection.

Antineoplastic Agents, Phytogenic↗
PubMed2003

Importance of parental conceptual model of illness in severe recurrent abdominal pain.

OBJECTIVES: Recurrent abdominal pain (RAP) affects up to 15% of children. A biopsychosocial approach to the treatment of children with RAP has been proposed as an alternative to the traditional medical model. The aim of this study was to examine whether the parental conceptual model of illness is a factor in the long-term outcome of children with severe RAP. METHODS: The study was undertaken in 2 parts: 1) a review of the medical and psychiatric records (including Child Behavior Checklist [CBCL]) of all children with RAP of sufficient severity to necessitate hospitalization during a 5-year period and 2) a structured telephone interview to collect information on ongoing abdominal pain, other somatic symptoms, school attendance, and the parents' opinion as to the cause of the child's pain. RESULTS: Twenty-eight of 30 children who were identified were available for follow-up. Twenty-three (82%) were tertiary referrals from other pediatric services, and 20 had pain for >6 months. On admission 7 (25%) of 28 had a depressive disorder, and 8 (29%) had an anxiety/depressive disorder. Twenty-one of 28 parents completed the CBCL, and on analysis of the CBCL, 11 (52%) children had scores in the clinical range (>65). At follow-up (mean: 3.56 years; standard deviation: 1.59), 14 (50%) of 28 continued to complain of pain. These children also complained of multiple other somatic complaints and had repeated school absences. Only 1 (7%) of 14 parents of children with ongoing pain believed that there was a psychological cause for their child's pain, whereas 11 (78%) of 14 parents of the children who had recovered believed that the cause was attributable to psychological factors (odds ratio: 47.67; 95% confidence interval: 3.56-1511.6). CONCLUSIONS: The acceptance by parents of a biopsychosocial model of illness is important for the resolution of recurrent abdominal pain in children.

Abdominal Pain↗
PubMed2002

Campylobacter infection: small bowel and colon.

The important contribution of Campylobacter infections to human enteric disease is well established. Recent completion of the genomic sequence of a Campylobacter jejuni strain has heralded a renaissance in the field of Campylobacter pathogenesis research. With the application of novel, powerful technologies, our understanding of how these organisms mediate disease is set to evolve rapidly from its current, relatively neglected status.

Journal Article↗