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Biomedical subjects

B D Gold

Publications and source records attributed to B D Gold.

At least 19 recordsLinked to original sources
PubMed2001

New approaches to Helicobacter pylori infection in children.

Helicobacter pylori infection is usually acquired during childhood, and evidence-based guidelines regarding diagnosis and treatment of infected children have been recently published. Diseases associated with H. pylori infection are gastritis, duodenal ulcers, mucosal-associated lymphoid-type (MALT) lymphoma, and gastric adenocarcinoma. The association of specific symptoms with H. pylori infection in children and adults (ie, recurrent abdominal pain and nonulcer dyspepsia) remains controversial. Additionally, the role of H. pylori in gastroesophageal reflux disease or in extra-gastrointestinal diseases (ie, coronary artery disease) lacks sufficient evidence to demonstrate causality. The diagnosis of H. pylori-associated diseases in children can reliably be made through gastroduodenal endoscopy with biopsies. Clinical trials are underway for the validation of noninvasive diagnostic tests for the H. pylori-infected child, and current guidelines recommend eradication therapy for infected children with duodenal and gastric ulcer, gastric lymphoma, and atrophic gastritis with intestinal metaplasia. The natural history of childhood H. pylori infection is poorly described. Moreover, rational approaches to the prevention and control of childhood H. pylori infection are critically needed, requiring characterization of the determinants for acquisition and persistence and the disease outcomes following eradication.

Child↗
PubMed2001

Characteristics of Helicobacter pylori infection in Jamaican adults with gastrointestinal symptoms.

Helicobacter pylori infection is common in Jamaica. Describing its epidemiology in a population-based study depends largely on serology, but serologic assays have not been validated in this population. To address this issue, we examined the presence of H. pylori infection in 30 sequential adult patients with gastroduodenal symptoms by three biopsy-based methods (rapid urease test, histology, and culture) as well as by one research and two commercial enzyme-linked immunosorbent assays (ELISAs). A patient was considered H. pylori positive if the organism was detected by at least one biopsy-based method. Eighteen (60%) of the 30 patients were H. pylori positive by these criteria, whereas 21 (70%) were seropositive for H. pylori immunoglobulin G by our research ELISA. The presence of H. pylori infection in patients with gastric cancer and those with chronic gastritis was missed by biopsy-based methods but was detected by serologic assays. This observation indicates that serologic assays may be better suited for the detection of this infection in a population in which H. pylori-associated pathology is prevalent. The performance of our research ELISA in detecting biopsy-based H. pylori-positive cases was excellent, with a sensitivity and specificity of 100% and 75%, respectively. Molecular genotyping of the isolates revealed that the predominant H. pylori genotypes in this cohort of Jamaicans were cagA(+) vacA slb-m1, and iceA2. The validated serologic assay enables us to interpret epidemiologic data from population-based studies in Jamaica by comparison to those from other populations.

Adult↗
PubMed2001

Genotypic, clinical, and demographic characteristics of children infected with Helicobacter pylori.

Helicobacter pylori isolates vary between geographic regions. Certain H. pylori genotypes may be associated with disease outcome. Thirty-eight children underwent diagnostic upper endoscopy at four medical centers and were retrospectively analyzed to determine if H. pylori virulence genes were associated with endoscopic disease severity, histologic parameters, and host demographics. The H. pylori virulence genotype was analyzed by a reverse hybridization line probe assay and type-specific PCR. Endoscopic ulcers or erosions were found in 17 (45%) patients, with 13 (34%) of these patients having antral nodularity. Histological gastritis, of varying severity, was present in all children. Four patients harbored more than one H. pylori strain: one subject had both cagA(+) and cagA-negative strains, while three patients harbored either two different cagA-negative strains (two children) or two cagA(+) strains (one child). There were 28 (74%) cagA(+) isolates; 19 were associated with the vacA s1b genotype, 7 were associated with the vacA s1a genotype, 1 was associated with the vacA s1c genotype, and 1 was associated with the s2 genotype. Of 14 cagA-negative isolates, 6 were vacA s2 genotype, 4 were vacA s1b, 3 were vacA s1a, and 1 was vacA s1c. Nine of ten (90%) Hispanics had similar H. pylori strains (vacA s1b,m1), and all Asian-Canadian children were infected by strains with vacA s1c genotype. No correlation between H. pylori strain and endoscopic or histopathologic abnormalities was found. This study provides a baseline framework of North American children and their H. pylori strains, serving as a powerful epidemiological tool for prospective investigations to better understand the transmission and evolution of diverse disease outcomes.

Adolescent↗
PubMed2000

Increased macrophage infiltration of gastric mucosa in Helicobacter pylori-infected children.

The purpose of the study was to quantify gastric mucosal macrophages and define their association with the histopathologic features of stomach biopsies obtained from Helicobacter pylori-infected and uninfected children. Endoscopically obtained gastric biopsies from symptomatic children were independently evaluated by two groups of pathologists. Thirty children were evaluated; 14 were H. pylori-infected. H. pylori positivity was determined by hematoxylin and eosin (H&E), Giemsa, Warthin-Starry and an H. pylori-specific immunoperoxidase stain. A macrophage-specific, KP-1, immunoperoxidase stain was used to quantify positive cells. Inflammatory cell infiltrates were graded by severity with scores of mild to severe. Increased numbers of gastric mucosal macrophages were observed in biopsies of H. pylori-infected versus uninfected children (P < 0.05) and correlated with gastritis severity. The role of this inflammatory cell the in persistence of gastric mucosal inflammation in H. pylori infection warrants further study to develop targeted immunotherapeutic strategies.

Adolescent↗
PubMed2000

Helicobacter pylori gastritis in children and adults: comparative histopathologic study.

The inflammatory response to Helicobacter pylori in adults has been well characterized. In children, studies of H. pylori gastritis have been based on small numbers of patients and have used loose definitions of the inflammatory components. Comparative study of the inflammatory response to H. pylori in children and adults can help our understanding of the natural history of this infection. Using the Updated Sydney Classification, we performed a retrospective, blinded pathology review of gastric biopsy specimens from 42 children and 40 adults with H. pylori infection, and we quantified each inflammatory cell separately (neutrophils, lymphocytes, plasma cells, and eosinophils). Differences in inflammatory cell components of children and adults were assessed by logistic regression analysis. More children had marked amounts of H. pylori (P = .05) and mild degree of neutrophils (P = .02), plasma cells (P = .005), and eosinophils (P = .0001) compared with adults. No differences existed when quantifying mononuclear cells or atrophy. Ulcers and intestinal metaplasia were present only in adults. We found that the numbers of inflammatory cells present in H. pylori-infected biopsy specimens is different in children and adults. We hypothesize that these differences demonstrate how H. pylori infection evolves from an acute childhood infection to an adult chronic disease.

Adolescent↗
PubMed2000

Seroprevalence of Helicobacter pylori infection in cystic fibrosis and its cross-reactivity with anti-pseudomonas antibodies.

BACKGROUND: The prevalence of Helicobacter pylori infection and its role in gastroduodenal disease in cystic fibrosis (CF) are controversial. Additionally, serologic determination of infection in this population may be inaccurate because of cross-reactivity with other bacterial species. The seroprevalence of H. pylori in a cohort of patients with CF and its cross-reactivity with Pseudomonas antibodies were investigated. METHODS: A research enzyme-linked immunosorbent assay (ELISA), and three commercial serologic assays (PyloriStat; BioWhittaker, Walkersville, MD, U.S.A.; Flexsure; SmithKline Diagnostics, Inc., San Jose, CA, U.S.A.; and HM-CAP; EPI, Stony Brook, NY, U.S.A.) at three independent laboratories determined the seroprevalence of anti-H. pylori IgG antibodies in 70 patients with CF. Cross-reactivity between solid-phase H. pylori antigens and Pseudomonas antibodies was ascertained by a competitive inhibition assay, preadsorbing sera of patients with CF with whole cell proteins from different Pseudomonas species, and serum reanalysis by each assay. Western blot analysis before and after adsorption was performed to identify potential cross-reactive antigens. RESULTS: The research ELISA, Flexsure, Pyloristat, and HM-CAP initially showed H. pylori seropositivity of 47%, 28%, 24%, and 37%, respectively. Postadsorption seropositivity declined to 8%, 0%, 0%, and 15%, respectively. All patients with research ELISA true-positive results were confirmed endoscopically to have H. pylori infection. Western blot analysis showed a 31-kDa H. pylori protein with antigenic epitopes common to both bacterial species. CONCLUSIONS: Cross-reactivity between solid-phase H. pylori antigens and anti-Pseudomonas antibodies occurs in patients with CF. A high index of suspicion should be assumed in evaluating results of serologic H. pylori tests in this population. Preadsorption of CF sera with Pseudomonas proteins should be used in serologic testing.

Adolescent↗
PubMed2000

High prevalence of Helicobacter pylori in the Alaska native population and association with low serum ferritin levels in young adults.

Iron deficiency anemia is a common public health problem in the Alaska Native population. Yet, a clear etiology has eluded researchers for decades. Previous studies suggested a link between Helicobacter pylori infection, gastrointestinal blood loss due to hemorrhagic gastritis, and generalized iron deficiency anemia in adult Alaska Natives. Therefore, we examined the association between the prevalence of H. pylori-specific immunoglobulin G (IgG) and serum ferritin levels, a marker of iron deficiency. A random sample of 2,080 serum samples from Alaska Native residents drawn between 1980 and 1986 from residents in 13 regions was selected, and the samples were stratified by age, sex, and region. Overall, 75% were positive for H. pylori-specific IgG. The rate of H. pylori seropositivity increased with age; by age 14 years, 78% of the residents were positive. There were no gender differences in H. pylori seropositivity. However, marked regional differences were observed. Serum ferritin levels of <12 ng/ml were found most commonly among persons <20 years of age and among women of childbearing age. A significant association between low serum ferritin levels and prevalence of H. pylori-specific IgG was found, particularly for people aged less than 20 years. H. pylori may be a factor contributing to the iron deficiency anemia in the Alaska Native population.

Adolescent↗
PubMed2000

The disease spectrum of Helicobacter pylori: the immunopathogenesis of gastroduodenal ulcer and gastric cancer.

Helicobacter pylori is a gram-negative bacterium that resides under microaerobic conditions in a neutral microenvironment between the mucus and the superficial epithelium of the stomach. From this site, it stimulates cytokine production by epithelial cells that recruit and activate immune and inflammatory cells in the underlying lamina propria, causing chronic, active gastritis. Although epidemiological evidence shows that infection generally occurs in children, the inflammatory changes progress throughout life. H. pylori has also been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer. These more severe manifestations of the infection usually occur later in life and in a minority of infected subjects. To intervene and protect those who might be at greatest risk of the more severe disease outcomes, it is of great interest to determine whether bacterial, host, or environmental factors can be used to predict these events. To date, several epidemiological studies have attempted to define the factors affecting the transmission of H. pylori and the expression of gastroduodenal disease caused by this infection. Many other laboratories have focused on identifying bacterial factors that explain the variable expression of clinical disease associated with this infection. An alternative hypothesis is that microorganisms that cause lifelong infections can ill afford to express virulence factors that directly cause disease, because the risk of losing the host is too great. Rather, we propose that gastroduodenal disease associated with H. pylori infection is predominantly a result of inappropriately regulated gastric immune responses to the infection. In this model, the interactions between the immune/inflammatory response, gastric physiology, and host repair mechanisms would dictate the disease outcome in response to infection.

Adenocarcinoma↗
PubMed1999

Gastritis and peptic ulcer disease in childhood.

UNLABELLED: Inflammation of the gastric and duodenal mucosa is the end result of an imbalance between mucosal defensive and aggressive factors. The degree of inflammation and imbalance between defensive and aggressive factors can then result in varying degrees of gastritis and/or frank mucosal ulceration. Gastritis and ulcers of the duodenum or stomach can be classified either as primary or secondary. The majority of children with chronic active or chronic gastritis and ulcers in the stomach or duodenum have secondary inflammation or mucosal ulceration. These ulcers generally occur due to a systemic condition like head trauma or overwhelming sepsis, or, as sequelae to drug ingestion (i.e., non-steroidal anti-inflammatory agents), but secondary gastroduodenal ulcers can also occur in specific disease conditions such as Zollinger-Ellison syndrome or Crohn's disease. The different causes of gastritis and peptic ulcer disease will be discussed in this paper. CONCLUSION: In almost all children presenting to their treating pediatric gastroenterologist with duodenal or gastric ulcers of these patients, mucosal inflammation and less frequently, ulceration is caused by a spiral shaped, gram-negative, microaerobic rod, properly named Helicobacter pylori. Recent epidemiological evidence has linked chronic H. pylori infection with the development of gastric carcinomas.

Adolescent↗
PubMed1999

Current therapy for Helicobacter pylori infection in children and adolescents.

Helicobacter pylori infects approximately 50% of the world's population and is a definitive cause of gastroduodenal disease (ie, gastritis, duodenal and gastric ulcers) in children and adults. Four consensus conferences held around the globe have brought together clinicians, scientists, epidemiologists and health care economists to discuss the role of the gastric pathogen H pylori in human gastroduodenal disease. At each of these conferences, the overriding objective was to reach a consensus on the development of practical guidelines for the diagnosis and treatment of H pylori-infected individuals. However, it was not until the Canadian H pylori Consensus Conference, held in November 1997, that the issues of H pylori infection in children were addressed. Therapies for H pylori infection in children, presented in part at the First Canadian Pediatric H pylori Consensus Conference, held in Victoria, British Columbia, November 1998, are reviewed in this paper.

Adolescent↗
PubMed1998

Inflammatory bowel disease in African-American children living in Georgia.

We describe the clinical characteristics of inflammatory bowel disease (IBD) African-American compared with non-African-American children. We identified 172 children with IBD; forty-nine (29%) were African-American. Median symptom duration before IBD diagnosis in African-American children (6 months) was shorter than that of non-African-American children (10 months). The most frequent presenting symptom was hematochezia (ulcerative colitis) and abdominal pain (Crohn's disease) in both racial groups. The estimated incidence of Crohn's disease in African-Americans ranged from 7 per 100,000 to 12 per 100,000, whereas the observed incidence in those with ulcerative colitis was between 5 and 7 per 100,000 during the 10 years of the study. Our pilot study suggests that IBD may be more common in African-American children than previously reported. Prospective population-based studies would be useful to determine whether inheritable factors linked with ethnicity are associated with IBD.

Adolescent↗
PubMed1998

Inhibition of Helicobacter pylori and Helicobacter mustelae binding to lipid receptors by bovine colostrum.

Helicobacter pylori, the etiologic agent of chronic-active gastritis and duodenal ulcers in humans, and Helicobacter mustelae, a gastric pathogen in ferrets, bind to phosphatidylethanolamine (PE), a constituent of host gastric mucosal cells, and to gangliotetraosylceramide (Gg4) and gangliotriaosylceramide (Gg3). The effect of a bovine colostrum concentrate (BCC) on the interaction of H. pylori and H. mustelae to their lipid receptors was examined. BCC blocked attachment of both species to Gg4, Gg3, and PE. Partial inhibition of binding was observed with native bovine and human colostra. BCC lacked detectable antibodies (by immunoblotting) to H. pylori surface proteins (adhesins). However, colostral lipid extracts contained PE and lyso-PE that bound H. pylori in vitro. These results indicate that colostrum can block the binding of Helicobacter species to select lipids and that binding inhibition is conferred, in part, by colostral PE or PE derivatives. Colostral lipids may modulate the interaction of H. pylori and other adhesin-expressing pathogens with their target tissues.

Adhesins, Bacterial↗