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Biomedical subjects

B Drumm

Publications and source records attributed to B Drumm.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1997

Absence of effect of Lewis A and Lewis B expression on adherence of Helicobacter pylori to human gastric cells.

BACKGROUND & AIMS: Lewis b blood group antigen and antibodies to Lewis b inhibit the binding of stationary-phase Helicobacter pylori organisms to fixed sections of gastric tissue. The aim of this study was to determine the effect of expression of Lewis a and Lewis b on binding of H. pylori to primary gastric cells. METHODS: ABO and Lewis blood types were determined for 13 individuals. Cells were isolated from gastric biopsy specimens by collagenase digestion. Lewis antigen expression and adherence of H. pylori to the cells were quantitated using flow cytometry. RESULTS: Two of the three nonsecretors were found to express Lewis b on their cells. Nineteen of 19 individuals expressed Lewis a on their cells and 18 of 19 expressed Lewis b. The percentage of cells expressing Lewis antigens varied from individual to individual. H. pylori binding was independent of expression of Lewis antigens. Preincubation of cells with antibodies to Lewis antigens did not inhibit the adherence. CONCLUSIONS: H. pylori adheres to isolated human gastric cells in a manner that is not dependent on Lewis antigen expression on these cells, and expression of Lewis antigens on the surface of gastric cells is not dependent on Lewis antigen expression on erythrocytes.

Bacterial Adhesion↗
PubMed1997

Carbon 13-labeled urea breath test for the diagnosis of Helicobacter pylori infection in children.

Helicobacter pylori infection is mainly acquired in childhood, and studies on the epidemiology of this infection depend on the availability of a noninvasive diagnostic test for use in children. The aim of this study was to determine whether the carbon 13-labeled urea breath test (UBT) can be used in children by evaluating: (1) its sensitivity and specificity compared with either culture or both rapid urease test and histologic examination, (2) whether a test meal or a prolonged fast is required, (3) the usefulness after treatment for H. pylori. Eighty-eight children (mean age, 10.6 +/- 4.19 years) who were undergoing upper endoscopy were studied while fasting, not fasting, and after treatment. Children were given 50 mg of 13C-urea if they weighed less than 50 kg or 75 mg of 13C-urea if they weighed more than 50 kg with 50 mg of a glucose polymer solution in 7.5 ml of water. Breath samples were collected at baseline and at 15, 30, 45, and 60 minutes. In 63 fasting children the UBT was 100% sensitive and 97.6% specific at 30 minutes with a cutoff value of 3.5 delta 13CO2 per mil. Nonfasting tests in 23 children, performed between 1 and 2 hours after their usual meal, were 100% sensitive and 91.6% specific. In 13 children fed directly before the UBT, the sensitivity of the test was reduced to 50%. Thirty minutes was the optimal sampling time. There was a significant decrease in specificity when samples were obtained at 15 minutes, possibly caused by the interference of oral urease-producing organisms. The test was 100% sensitive and specific in 20 children after treatment for H. pylori infection. The UBT is a highly sensitive and specific test for the diagnosis of H. pylori infection in children. Neither a prolonged fast nor a test meal is required.

Adolescent↗
PubMed1997

Helicobacter pylori: challenges for the paediatrician.

During the last 15 years, a great body of knowledge about Helicobacter pylori has been accumulated. Much, however, remains to be studied, particularly in relation to children. The vast majority of infections occur in childhood. It is towards children that any widespread screening, prevention or treatment strategies would need to be aimed. In this annotation, we discuss the epidemiology, symptomatology, diagnosis and treatment of H. pylori in children.

Anti-Bacterial Agents↗
PubMed1997

One week treatment for Helicobacter pylori infection.

Helicobacter pylori is associated with primary antral gastritis, duodenal ulceration, and gastric cancer. Current regimens for treating infection in children using bismuth and antibiotics for two to six weeks are cumbersome. The aim of this study was to evaluate a one week course of treatment. All children undergoing endoscopy were assessed for the presence of H pylori by culture, histology, rapid urease test, and 13C urea breath test. Infected children received a one week course of colloidal bismuth subcitrate 480 mg/1.73 m2/day (maximum 120 mg four times a day), combined with metronidazole 20 mg/kg/day (maximum 200 mg three times a day), and clarithromycin 15 mg/kg/day (maximum 250 mg twice a day). To optimise compliance, drugs were dispensed in a 'Redidose' box containing a compartment for each day, and subcompartments marked 'breakfast', 'lunch', 'dinner', and 'bedtime'. Compliance and side effects were assessed immediately after treatment. A urea breath test was performed at least one month after treatment. Twenty two children infected with H pylori were entered into the study; 20 of these took all doses; two children suffered significant side effects (diarrhoea and vomiting). H pylori was eradicated in 21 of the 22 children (95.45%; 95% confidence interval 77% to 100%). This study shows that H pylori infection in children can be cleared by a one week course of treatment.

Adolescent↗
PubMed1997

In vitro evaluation of the role of antibodies against Helicobacter pylori in inhibiting adherence of the organism to gastric cells.

BACKGROUND: Once Helicobacter pylori infection is established, it is difficult to eradicate despite a persistent systemic and local immune response. It is not known whether immunisation can be used to prevent H pylori infection in humans. AIMS: To evaluate the effect of the human immune response on adherence of H pylori to gastric cells. METHODS: Human milk from a woman infected with H pylori and milk from a non-infected woman were each fractionated by chromatography on DEAE cellulose. Bacteria were incubated with either serum, human milk, human milk fractions, or secretory IgA before incubation with Kato III cells (cells from a gastric adenocarcinoma cell line). Bacterial adherence to the cells was assessed using flow cytometry. RESULTS: Serum from both the H pylori infected and non-infected women killed H pylori. This resulted from the action of complement as heating the serum to 56 degrees C for 30 minutes abolished the bactericidal activity. Immunoglobulin fractions from serum of both infected and non-infected women did not inhibit H pylori adherence to Kato III cells. Human milk from the woman infected with H pylori and from the non-infected woman inhibited binding of H pylori to Kato III cells by 50 to 70%. Secretory IgA isolated from human milk had minimal inhibitory effect on adherence and this was notably less than the inhibitory effect of whole human milk. CONCLUSIONS: Human milk inhibits adherence of H pylori to Kato III cells and this inhibition is independent of whether or not the donor is infected with H pylori. Secretory IgA has minimal inhibitory effect on H pylori adherence.

Antibodies, Bacterial↗
PubMed1997

Adherence of Helicobacter pylori to the gastric mucosa.

Bacterial adhesion to the intestinal epithelium is a critical initial step in the pathogenesis of many enteric diseases. Helicobacter pylori is a duodenal pathogen that adheres to the gastric epithelium and causes gastritis and peptic ulceration. The mechanism by which H pylori causes disease has not been elucidated but adherence to the gastric mucosa is thought to be an important virulence determinant of the organism. What is known about adherence of H pylori to the gastric mucosa is summarized. Topics discussed are the mechanism of H pylori adherence; in vitro and in vivo models of H pylori infection; and adherence and potential adhesins and receptors for H pylori.

Adhesins, Bacterial↗
PubMed1996

Cell envelope characteristics of Helicobacter pylori: their role in adherence to mucosal surfaces and virulence.

Helicobacter pylori colonises the gastric mucosa of humans and causes both antral gastritis and duodenal ulcer disease. Exactly how H. pylori causes disease is not known but several pathogenic determinants have been proposed for the organism. These include adhesins, cytotoxins and a range of different enzymes including urease, catalase and superoxide dismutase. Surface molecules of H. pylori such as flagella, lipopolysaccharide, the urease enzyme and outer membrane proteins are putative adhesin molecules. While phosphatidylethanolamine and the Lewis(b) blood group antigen have been proposed as receptor molecules for the organism the exact mechanism by which H. pylori adheres to the gastric mucosa has still to be identified. Characterisation of the adhesins of H. pylori could lead to the development of adhesin analogues for use in the inhibition of colonisation and improved therapy for ulcer disease. In vivo studies with isogenic mutants which are incapable of adhering to the gastric mucosa would greatly clarify the significance of adherence. Such mutants could possibly be useful as a vaccine against infection with wild-type organisms.

Adhesins, Bacterial↗
PubMed1996

The urease enzyme of Helicobacter pylori does not function as an adhesin.

Helicobacter pylori urease is essential for colonization of the gastric mucosa irrespective of whether the stomach is acidic or hypochlorhydric. It has therefore been speculated that the enzyme functions as an adhesin. The aim of this study was to compare the adherence of H. pylori N6 with the adherence of an isogenic urease-negative mutant, strain N6(ureB::TnKm), to gastric cells. Strain N6 originated from a patient with gastritis. Strain N6(ureB::TnKm) is specifically modified in the gene which encodes the large subunit of urease, UreB, and hence does not form a UreA-UreB enzyme complex. We have used flow cytometry to assess the adherence of H. pylori to the cells. We have also used phase-contrast microscopy to assess the adherence of the organism to Kato III cells. In the absence of urea both strains bound to Kato III cells and to primary gastric cells. Binding of both strains to the cells occurred rapidly. The presence of urea in the incubation medium decreased the binding of strain N6 to the cells. This was due to a rise in the pH of the incubation medium, which caused loss of viability of the organism. Urea had no effect on the adherence of strain N6(ureB::TnKm). We conclude that the urease of H. pylori does not play a role in the adherence of the organism to gastric cells.

Adhesins, Bacterial↗
PubMed1996

Byler-like familial cholestasis in an extended kindred.

Progressive familial intrahepatic cholestasis (PFIC) occurs in many communities and races. A form of PFIC in five children from two consanguineous marriages in an Irish kindred is described. In addition, a review of clinical information from the records of three deceased members of the kindred strongly implies that they also suffered from PFIC. The children had a history of neonatal diarrhoea, sepsis, and intermittent jaundice that ultimately became permanent. They suffered intractable pruritus and growth retardation. Despite evidence of severe cholestasis, serum gamma-glutamyl transferase and cholesterol were normal in these children. Sweat sodium concentration were raised in three children. Liver histology showed severe intrahepatic cholestasis and hepatocellular injury. Urinary bile acid analysis revealed a non-specific pattern consistent with chronic cholestasis. These children suffer from a form of PFIC remarkably similar to that occurring in members of the Byler kindred.

Bile Acids and Salts↗
PubMed1996

Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori.

BACKGROUND: Helicobacter pylori infection of the gastric mucosa is vital in the pathogenesis of duodenal ulcer disease. H pylori will only colonise gastric epithelium and its association with duodenal disease is therefore not easily explained. AIMS: To determine if gastric metaplasia in the duodenum increases the risk of duodenal ulcer disease in children infected with H pylori. PATIENTS: All children undergoing upper endoscopy over a 20 month period in a children's hospital in Ireland. METHODS: Two biopsy specimens were obtained from the antral mucosa and two from the first part of the duodenum. One antral biopsy specimen was used in a rapid urease test (Clo Test). Biopsy sections were stained with haematoxylin and eosin and also with cresyl violet for identification of H pylori. Periodic acid Schiff (PAS) stain was performed to identify areas of gastric metaplasia. RESULTS: Gastric and duodenal biopsy specimens were obtained from 148 patients (M:F 1:2:1). Twenty five children (17%) had H pylori positive gastritis. Thirty four children (23%) had gastric metaplasia in the duodenum. Nine per cent of children under the age of 8 years had gastric metaplasia compared with 38% in those 12 years of age or over (p < 0.005). Seven children had duodenal ulcer disease. Gastric metaplasia was present in six of seven (86%) children with duodenal ulcer disease compared with 28 of 141 (20%) without ulceration (p < 0.001). While both H pylori and gastric metaplasia were each significant risk factors for duodenal ulcer disease, the combined presence of both factors was associated with a pronounced increase in duodenal ulcer disease. Duodenal ulcer disease occurred in over 50% of children with both H pylori infection and gastric metaplasia. In contrast duodenal disease did not occur in children (0 of 100) when both were absent. CONCLUSION: The presence of gastric metaplasia in the duodenum is the major risk factor for duodenal ulcer disease in patients colonised by H pylori.

Adolescent↗
PubMed1995

Isolated cerebral thrombo-embolism and Crohn disease.

Arterial thrombo-embolism is an unusual complication in inflammatory bowel disease in adults and children. Cerebral arterial disease has been reported on only a few occasions. There are only two previous case reports of arterial disease occurring in a child with Crohn disease. However in both instances the arterial disease was part of a generalised Takayasu arteritis which resulted in multi-organ involvement. This report describes a 14-year-old boy who developed seizures before a histological diagnosis of Crohn disease was made. These seizures were the result of a vascular lesion which was confined to the right middle cerebral artery. CONCLUSION. Crohn disease as well as ulcerative colitis should be considered as a possible cause of cerebrovascular accidents in children.

Adolescent↗
PubMed1995

Acute cytomegalovirus infection in a child with Ménétrier's disease.

The cause of Ménétrier's disease is unknown, although allergic, autoimmune, and infectious, particularly viral, causes have been postulated. This case report describes a 3-year-old child with Ménétrier's disease in whom evidence of acute cytomegalovirus (CMV) infection was found. To our knowledge, this is the first case with evidence of acute infection, indicated by the presence of CMV-specific immunoglobulin M antibody in the acute serum as well as a seroconversion to CMV. CMV was also found in a gastric mucosal biopsy specimen using monoclonal antibodies to the early antigen of CMV.

Acute Disease↗