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Biomedical subjects

B Drumm

Publications and source records attributed to B Drumm.

At least 19 recordsLinked to original sources
PubMed2001

The oral cavity in Crohn's disease.

We assessed the utility of expert oral examination as a part of the diagnostic evaluation of patients with suspected Crohn's disease. Of 45 patients with newly diagnosed CD, 25 had been examined by a dentist. Twelve (48%) of these had oral CD lesions. Mucosal tags constituted the most frequent form of oral lesion (8/12). Of 8 oral biopsy specimens, 6 (75%) contained non-caseating granulomas. Patients with oral CD had more oral symptoms, presented for diagnosis sooner, and were more likely to have other upper gastrointestinal inflammation than those without oral lesions. Oral manifestations of CD are common in children; therefore, expert oral examination may be useful during diagnostic evaluation of children with suspected inflammatory bowel disease.

Adolescent↗
PubMed2001

Antigastric autoantibodies in ferrets naturally infected with Helicobacter mustelae.

Infection with Helicobacter pylori has been associated with induction of autoantibodies that cross-react with the gastric mucosa. There have been discordant reports as to whether or not these autoantibodies arise due to molecular mimicry between H. pylori and host cell antigens on parietal cells. In this study, we investigated whether molecular mimicry by H. mustelae causes autoantibodies in infected ferrets. Serum from H. mustelae-infected ferrets reacted with parietal cells in the ferret gastric mucosa but not with duodenal or colonic mucosa. These sera did not react with the blood group A epitope on erythrocytes or H. mustelae lipopolysaccharide, and absorption with H. mustelae whole cells or red blood cells did not remove autoantibodies. In conclusion, ferrets naturally infected with H. mustelae generate antibodies that react with parietal cells, but these autoantibodies are not due to molecular mimicry.

ABO Blood-Group System↗
PubMed2001

A new polymorphism for the RI22H mutation in hereditary pancreatitis.

BACKGROUND AND AIMS: Hereditary pancreatitis (HP) is a rare form of recurrent acute and chronic pancreatitis. Mutations in the cationic trypsinogen (protease serine 1, PRSS1) gene have been identified as causing HP. The R122H (previously known as R117H) mutation is the commonest and can be detected by a single and rapid polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP) based technique using the AflIII enzyme. This test however may give a false negative result in the presence of a neutral polymorphism within the enzyme recognition site. The frequency of this event was examined by sequencing studies in patients with HP and in healthy controls. METHODS: Of 60 families identified by the UK and Ireland consortium of EUROPAC (European Registry for Hereditary Pancreatitis and Familial Pancreatic Cancer), 51 were screened for R122H, N29I, and A16V mutations using standard techniques, and by sequencing of all five exons of cationic trypsinogen. RESULTS: Twelve families had the N29I mutation, one family had A16V and, on standard testing, 15 families had the R122H mutation. An additional family with the R122H mutation was found on direct sequencing. The false negative result was due to a neutral polymorphism C-->T at the third base of the codon, not affecting the amino acid coded for, destroying the AflIII restriction site. This polymorphism was not observed in 50 DNA specimens (100 chromosomes) from controls nor from 50 individuals from PRSS1 mutation negative HP families. A novel mutation specific PCR was developed to avoid this pitfall. CONCLUSIONS: One of the 16 families with HP and an R122H mutation contained a polymorphism affecting the AflIII restriction site. Adoption of an alternative R122H assay is important for genetic studies in individuals with apparent HP.

Acute Disease↗
PubMed2001

Is Helicobacter pylori infection in childhood a risk factor for gastric cancer?

Helicobacter pylori infection is associated with chronic gastritis and peptic ulcer disease. Furthermore, the World Health Organization has classified this organism as a carcinogen for gastric cancer. H pylori infection is mainly acquired in childhood. Children with H pylori infection are asymptomatic except for a very small number that develop peptic ulcer disease. However, if H pylori gastritis is associated with gastric cancer, do pediatricians need to screen children for this infection and treat those who are infected? In an attempt to determine the significance of the association between H pylori and gastric cancer, we have reviewed all of the English language literature on this topic. H pylori infection seems to be associated with an increased risk of developing gastric cancer. However, only a small number of infected individuals (~1%) will develop gastric cancer. Furthermore, there are potential cofactors other than H pylori that could be equally important. The effect of the eradication of H pylori alone on the development of gastric cancer is unknown. Based on our knowledge to date, we suggest that it is not indicated to treat all children with H pylori infection because of the risk of developing gastric cancer or to institute a screening and treatment program.

Adenocarcinoma↗
PubMed2000

Adherence of isogenic flagellum-negative mutants of Helicobacter pylori and Helicobacter mustelae to human and ferret gastric epithelial cells.

Isogenic flagellum-negative mutants of Helicobacter pylori and Helicobacter mustelae were screened for their ability to adhere to primary human and ferret gastric epithelial cells, respectively. We also evaluated the adherence of an H. pylori strain with a mutation in the flbA gene, a homologue of the flbF/lcrD family of genes known to be involved in the regulation of H. pylori flagellar biosynthesis. H. pylori and H. mustelae mutants deficient in production of FlaA or FlaB and mutants deficient in the production of both FlaA and FlaB showed no reduction in adherence to primary human or ferret gastric epithelial cells compared with the wild-type parental strains. However, adherence of the H. pylori flbA mutant to human gastric cells was significantly reduced compared to the adherence of the wild-type strain. These results show that flagella do not play a direct role in promoting adherence of H. pylori or H. mustelae to gastric epithelial cells. However, genes involved in the regulation of H. pylori flagellar biosynthesis may also regulate the production of an adhesin.

Adhesins, Bacterial↗
PubMed1999

Fine-resolution mapping by haplotype evaluation: the examples of PFIC1 and BRIC.

Loci for two inherited liver diseases, benign recurrent intrahepatic cholestasis (BRIC) and progressive familial intrahepatic cholestasis type 1 (PFIC1), have previously been mapped to 18q21 by a search for shared haplotypes in patients in two isolated populations. This paper describes the use of further haplotype evaluation with a larger sample of patients for both disorders, drawn from several different populations. Our assessment places both loci in the same interval of less than 1 cM and has led to the discovery of the PFIC1/BRIC gene, FIC1; this discovery permits retrospective examination of the general utility of haplotype evaluation and highlights possible caveats regarding this method of genetic mapping.

Cholestasis, Intrahepatic↗
PubMed1999

Low rates of Helicobacter pylori reinfection in children.

BACKGROUND & AIMS: Reinfection after treatment for Helicobacter pylori is uncommon in adults. It is more likely to occur in children because they acquire primary infection. The aim of this study was to determine whether children are likely to become reinfected with H. pylori and if there are any risk factors for reinfection. METHODS: A prospective study of children who had documented evidence of successful treatment for H. pylori infection was performed. Sixty children were eligible for inclusion; results for 52 are presented. Children, parents, and siblings underwent [(13)C]urea breath tests. Details of family size and socioeconomic status were documented. Cox logistic regression analysis was used to determine the risk factors for reinfection. RESULTS: The duration of follow-up was 103.8 patient-years (mean +/- SD, 24 +/-14.0 months). Forty-six (88.5%) of the index children remained clear of infection, and 6 (11.5%) children were reinfected. The mean age of those who became reinfected was 5.8 +/- 5.6 years compared with 12.3 +/- 3.0 years for those who remained clear of infection (P = 0.00001). Only 2 of 46 (4.3%) children older than 5 years of age were reinfected, although 80.8% had 1 infected parent and 65% of siblings were infected. Reinfection rate was 2.0% per person per year in children older than 5 years. Living with infected parents and siblings and low socioeconomic status were not risk factors for reinfection. In logistic regression analysis, age was the only risk factor for reinfection. CONCLUSIONS: Reinfection with H. pylori occurs rarely in children older than 5 years of age regardless of socioeconomic group or number of infected family members. These findings also indicate that it is not necessary to treat all family members to achieve long-term eradication of H. pylori.

Adolescent↗
PubMed1999

How should Helicobacter pylori infected children be managed?

It is now recognised that Helicobacter pylori, like most enteric infections, is mainly acquired in childhood. Adults rarely become infected, with seroconversion rates varying between 0.33and 0.5% per person year. The age at which children are most likely to become infected is still unclear, but findings in a number of cross-sectional studies suggest that infection is acquired before the age of five. The prevalence of infection is highest in children in the developing world where up to 75% of children may be infected by the age of 10. In the developed world the prevalence of infection is noticeably increased among socially deprived children. The diagnosis of H pylori infection in childhood is most often made at endoscopy, for which there are many indications. Symptoms such as abdominal pain, vomiting, and haematemesis may be associated with duodenal ulcer and H pylori infection. However, in the case of children undergoing endoscopy for assessment of oesophagitis, failure to thrive, coeliac disease, Crohn's disease, or portal hypertension, the finding of H pylori infection is likely to be incidental. How should we manage these children with a diagnosis of H pylori infection? Currently, there are no consensus guidelines for the management of H pylori infected children. In 1994 the National Institutes of Health consensus statement recommended that adults with gastric or duodenal ulcer disease, who are infected with H pylori, should receive antimicrobial treatment. The European Maastricht Consensus Report suggested broader indications for treatment of infected adults. It states that treatment is advisable for all H pylori infected dyspeptic patients diagnosed non-invasively under 45 years of age at a primary care level. Patients older than 45 years with dyspeptic symptoms should be treated for H pylori infection but only after endoscopy to rule out any other underlying pathology. The European guidelines also recommend treatment for infected patients with mucosa associated lymphoid tissue lymphoma and patients who are found to have intestinal metaplasia and gastric atrophy.

Anti-Bacterial Agents↗
PubMed1999

Pancreatic duct stenting as a treatment for hereditary pancreatitis.

Hereditary pancreatitis is a genetically transmitted condition usually presenting in childhood or adolescence. The natural history of the condition is that recurrent episodes of pancreatitis may be followed by the development of pancreatic exocrine and endocrine failure. Treatment options are limited, usually consisting of surgical drainage procedures whose efficacy is uncertain and whose effect on disease progression is unknown. We report a child with hereditary pancreatitis treated by means of a pancreatic duct stent placed via endoscopic retrograde cholangiopanctreatography resulting in long-term control of symptoms and speculate that earlier intervention may alter the disease course.

Child, Preschool↗
PubMed1998

Molecular mimicry of ferret gastric epithelial blood group antigen A by Helicobacter mustelae.

BACKGROUND & AIMS: Molecular mimicry of Lewis blood group antigens by Helicobacter pylori may be involved in immune evasion by the bacteria and in the pathogenesis of chronic atrophic gastritis. Helicobacter mustelae infects ferrets naturally, causing gastritis, and may be involved in ulcerogenesis. The aim of this study was to determine if H. mustelae shows a similar form of molecular mimicry. METHODS: Antibodies raised against H. mustelae were used to stain ferret gastric tissue by immunoblotting, immunohistochemistry, and flow cytometry. Epitopes recognized by cross-reactivity were characterized by proteinase K and sodium metaperiodate treatment. RESULTS: H. mustelae antiserum reacted with H. mustelae and with ferret gastric tissue. Absorption of the antiserum with H. mustelae or ferret and rabbit gastric tissue removed the cross-reactive antibodies. Antibodies reacted with a blood group antigen A-like structure on ferret gastric epithelial cells and H. mustelae lipopolysaccharide. CONCLUSIONS: H. mustelae expresses a blood group-like antigen as part of its lipopolysaccharide that may be used as a method of immune evasion by mimicry of gastric epithelial cells. The cross-reactivity shown by H. mustelae-specific antibodies with gastric mucosa may suggest a role for autoantibodies in the pathogenesis of H. mustelae-induced gastritis in ferrets.

ABO Blood-Group System↗
PubMed1998

Clinical significance of Helicobacter infection in children.

Helicobacter pylori infection of the gastric mucosa causes chronic gastritis and is associated with peptic ulcer disease and gastric carcinoma. These are conditions which usually occur in adult life. However, H. pylori is an infection which is mainly acquired in childhood. The overall prevalence of H. pylori in children is 10% in developed countries but can be as high as 30-40% in children from lower socio-economic groups. In developing countries, the prevalence of H. pylori in children ranges from 80-100%. H. pylori gastritis does not appear to be associated with symptoms in children in the absence of duodenal ulcer disease. H. pylori infection is present in the vast majority of children with duodenal ulcer disease and, as in adults, eradication of the organism results in long-term healing of duodenal ulceration. H. pylori infection acquired in childhood is now considered to be a significant risk factor for the development of gastric carcinoma. The World Health Organization has classified H. pylori as a Group 1 carcinogen. Specific epidemiological questions which need to be answered in children include the age at which infection is acquired, specific risk factors for infection, the mode of transmission and the risk of reinfection following treatment. Recently, a one week treatment regimen using colloidal bismuth subcitrate, metronidazole and clarithromycin has been shown to be effective in treating children, but compliance is important. Currently there are no guidelines on the need to treat children and a consensus is urgently required on this issue.

Adolescent↗
PubMed1998

Effect of Helicobacter pylori eradication on the natural history of duodenal ulcer disease.

BACKGROUND: Duodenal ulcer disease is strongly associated with Helicobacter pylori infection of the gastric mucosa. Eradication of H pylori from the gastric mucosa in adults is associated with long term healing of ulcers. AIMS: To follow a cohort of children with duodenal ulcer disease for a minimum of two years after the eradication of H pylori. PATIENTS AND METHODS: Over a three year period, all children diagnosed with duodenal ulcer disease had their symptoms documented and their H pylori status evaluated. The histories of these children were carefully screened to determine previous symptoms and to document previous treatment regimens. RESULTS: Sixteen children were diagnosed with ulcers and 15 were available for treatment and long term follow up. The median age at which symptoms first occurred was 10.5 years (range, 6-14) and the median duration of symptoms was 24 months (range, 2-60). Ten of the children had been treated with H2 receptor antagonists for a median of 3.5 months (range, 1-60). Duodenal ulcers healed in all children after eradication of H pylori and all children have remained asymptomatic for a median of 37 months (range, 26-62). No child has required subsequent admission to hospital. CONCLUSION: Eradication of H pylori is very effective in the long term healing of duodenal ulcer disease. H pylori eradication should be the standard treatment for all infected children who present with duodenal ulcer disease.

Adolescent↗
PubMed1998

Colonoscopy under general anesthesia in children.

OBJECTIVE: In children, colonoscopy is usually performed using deep sedation that may be associated with significant risks. The purpose of this study was to evaluate the safety of colonoscopy performed under general anesthesia. METHODS: All patients undergoing colonoscopy during a 3-year period were reviewed for the study. One hundred and thirty-six procedures were performed. Colonoscopies were performed by a pediatric gastroenterologist. Anesthesia was administered by a pediatric anesthetist in a gastroenterology procedure room, adjacent to the operating recovery area. RESULTS: Three patients had significant abdominal pain and tenderness after the procedure, 1 of whom suffered a perforation of the sigmoid colon. This patient had severe ulcerative colitis. The gastrointestinal complication rate was no higher than reported in adult patients undergoing colonoscopy under sedation. No significant complications relating to the administration of anesthesia were encountered. CONCLUSION: We conclude that colonoscopy performed under general anesthesia in children is a very safe procedure. It is superior to the use of sedation because the child is not placed at risk of respiratory compromise. Furthermore, the procedure is less worrisome for children when performed under a general anesthetic.

Abdominal Pain↗