First evaluation of the serum level of anti-hepatitis B surface antigen after vaccination in Libya.

The hepatitis B virus (HBV) vaccination schedule in Libya follows international recommendations (1st dose at birth, 2nd after 1 month and 3rd after 6 months). This research aimed to evaluate the long-term protection of the HBV immunization programme in Tripoli and to determine the best age to administer booster doses. Serum levels of hepatitis B surface antigen were determined in 277 randomly selected children aged 1-12 years. The response to HBV vaccine in 1-3-year-olds was 93.2%, but this declined with age and at 7-9 years after initial vaccination only 53.1% of children had protective titres (> or = 10 mIU/mL). No significant differences between males and females in antibody persistence or response to vaccine were observed. We recommend continuing the HBV vaccination programme and that a booster dose be given to 6-year-old children to ensure maximum protection during the period of school entry and beyond.

Quantitative assessment of IgG antibodies to Helicobacter pylori and outcome of ischaemic heart disease.

Criticisms of serological studies on Helicobacter pylori and ischaemic heart disease (IHD) include: undiagnosed heart disease in live controls; no assessment of severity or outcome of IHD; and qualitative not quantitative measurements of IgG to the bacteria. The aim was to assess quantitatively IgG levels specific for H. pylori (ng ml(-1)) among patients who survived a myocardial infarction (MI) with those who died of IHD. Sera were from four groups: (1) men who survived one MI; (2) men matched for age and socioeconomic background to group 1; (3) individuals who died suddenly of IHD; (4) accidental deaths matched for age and sex to group 3. Levels of IgG to H. pylori increased with age (P<0.005) but were not associated with smoking or socioeconomic groups. There was a correlation between IgG to the bacteria and decreasing socioeconomic levels only among group 1 (P<0.01). IgG levels were higher for subjects who died of heart disease (median=151 ng ml(-1)) compared with survivors (median=88 ng ml(-1)) (P=0.034) and higher for survivors compared with their controls (median=58 ng ml(-1)) (P=0.039). Future serological studies of H. pylori in relation to IHD should be quantitative and severity of disease considered in analyses.

Increased inflammatory responses of persons of blood group O to Helicobacter pylori.

Persons of blood group O are at increased risk of peptic ulcers. Enhanced binding of Helicobacter pylori to epithelial cells of persons of blood group O has been demonstrated. Release of interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-alpha by human leukocytes from 40 donors (10 from each ABO blood group) was measured after incubation in vitro with outer membrane protein preparations of H. pylori. Isolates DU (from a patient with a duodenal ulcer), GC (from a patient with gastric cancer), NE (from a patient with normal endoscopic findings), and NCTC 11637 bound in significantly higher numbers to group O leukocytes. Bacterial binding correlated with release of IL-6 and TNF-alpha but not of IL-10. Group O cells released significantly more IL-6 in response to DU, NE, and NCTC 11637, and the cells released more TNF-alpha in response to DU and NCTC 11637. Increased density of colonization of epithelial cells and higher inflammatory responses to H. pylori of persons of blood group O might contribute to increased susceptibility to peptic ulceration.

Isolation of a cell surface component of Helicobacter pylori that binds H type 2, Lewis(a), and Lewis(b) antigens.

BACKGROUND & AIMS: Individuals of blood group O and nonsecretors of ABO blood group antigens are more susceptible to peptic ulcers. The aim of this study was to determine if blood group antigens associated with group O or secretor status are epithelial cell receptors for Helicobacter pylori. METHODS: Bacterial binding and binding of monoclonal antibodies to H type 2, Lewis(a), and Lewis(b) to Kato III, buccal epithelial, and gastric mucosal cells were shown by flow cytometry. Bacterial outer membrane proteins eluted from H type 2, Lewis(a), or Lewis(b) were shown by polyacrylamide gel electrophoresis. RESULTS: Kato III and human epithelial cells bound each monoclonal antibody; O cells bound more anti-H type 2 (P < 0.05). Binding indices for H. pylori correlated with those for anti-H type 2 (P < 0.005) and anti-Lewis(b) (P < 0.001) but not anti-Lewis(a). A 61-kilodalton protein was eluted from H type 2, Lewis(a), or Lewis(b). CONCLUSIONS: Our results indicate that H type 2 is an important receptor for the 61-kilodalton bacterial adhesin, partly explaining increased susceptibility of individuals of blood group O to ulcers. Lewis(b) binds H. pylori more efficiently than Lewis(a). If these interactions occur in vivo, lack of Lewis(b) in mucosal fluids of nonsecretors may contribute to colonization by H. pylori.

Helicobacter pylori in the mouth--negative isolation from dental plaque and saliva.

OBJECTIVE: To determine the colonization of Helicobacter pylori in dental plaque and saliva of individuals with H. pylori-associated gastritis. PATIENTS AND METHODS: One hundred and twenty adult dyspeptic patients attending for outpatient endoscopy were randomly selected. Saliva, dental plaques and antral biopsies were collected and cultured in Dent's medium. Antral biopsies were also taken for histological confirmation of colonization. RESULTS: Eleven patients were withdrawn owing to poor tolerance of endoscopy. Fifty-two patients (47%) were found to be H. pylori positive on culture from antral biopsies and on antral histology. H. pylori was not isolated from saliva and dental plaques in any of the patients irrespective of their infective status. The H. pylori seropositivity rate was higher in the Japanese (72%) than in the Dutch (33%). CONCLUSION: We failed to isolate H. pylori from saliva and dental plaque in a group of dyspeptic patients with H. pylori-associated gastritis. We believe that our finding strongly suggests that oral to oral route is not an important mode of transmission in the adult population.