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Biomedical subjects

B Drumm

Publications and source records attributed to B Drumm.

At least 19 recordsLinked to original sources
PubMed2002

Focally enhanced gastritis in children with Crohn's disease and ulcerative colitis.

OBJECTIVES: Focally enhanced gastritis (FEG) has been suggested as a specific diagnostic marker for patients with Crohn's disease. However, the utility of FEG for distinguishing Crohn's disease from ulcerative colitis is uncertain in adults, and the occurrence of this lesion in children has not been defined. The aim of this study was to evaluate the occurrence of FEG and other gastric histological abnormalities in children with inflammatory bowel disease (IBD) and to examine the utility of FEG in discriminating between ulcerative colitis and Crohn's disease. METHODS: This is a retrospective, case-controlled study of upper GI histopathological findings in children with IBD. Gastric histopathology was defined and graded according to the Updated Sydney System. RESULTS: FEG was present in 28 of 43 (65.1%) children with Crohn's disease and five of 24 (20.8%) children with ulcerative colitis, compared to three of 132 (2.3%) children without IBD or one of 39 (2.6%) children with Helicobacter pylori infection. There were no differences between those with and without FEG with regard to upper GI symptoms or previous anti-inflammatory drug ingestion (5-aminosalicylic acid compounds or steroids). All patients with H. pylori infection had chronic antral gastritis, but only one child with H. pylori had FEG. In addition, mild to moderate chronic gastritis was present in 15 of 43 (34.9%) children with Crohn's disease and in 12 of 24 (50%) patients with ulcerative colitis. CONCLUSIONS: The presence of FEG suggests underlying IBD. Although FEG is particularly common in children with Crohn's disease, it does not reliably differentiate between Crohn's disease and ulcerative colitis.

Case-Control Studies↗
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

Limitations to carbon 13-labeled urea breath testing for Helicobacter pylori in infants.

We determined the validity of the carbon 13-labeled urea breath test in young children. We found that although the 13C-labeled urea breath test had a specificity greater than 90%, borderline or false positive results occurred more frequently in children younger than 2 years compared with older children. False positive results may be caused by oral-urease-producing organisms because direct intragastric administration of 13C urea reduced the excess delta 13CO2. Care is urged in interpreting one positive 13C-labeled urea breath test in children younger than 2 years.

Breath Tests↗
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↗