Antimicrobial resistance and Helicobacter pylori: impacts on current and future therapies.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Hazell.
Explore the source record for details and available documents.
OBJECTIVE: The relationship between H. pylori and functional dyspepsia remains controversial. The aim of this study was to identify a potential link between the antibody response to specific H. pylori antigens and functional dyspepsia. METHODS: A total of 50 consecutive patients with functional dyspepsia, 50 patients with duodenal ulcer (DU), and 150 healthy blood donor control subjects with no history of peptic ulceration were studied. H. pylori status was determined by IgG antibodies using a validated ELISA. In H. pylori-positive subjects, antibodies against specific H. pylori antigens were identified by Western blot. RESULTS: All DU patients (100%; 95%; CI, 93-100), 30 of 50 patients with functional dyspepsia (60%; 95% CI, 45-74) and 65 of 150 (43.3%; 95% CI, 34.3-51) blood donor controls tested positive for H. pylori. Forty-six of 50 (92%; 95% CI, 81-98) DU patients tested positive for the 91 kDa antigen (vacA) compared with 46 of 65 (69%; 95% CI, 58-81) control subjects and 22 of 30 (73%; 95% CI, 54-88) functional dyspepsia patients (p < 0.01 DU versus controls). Similarly, the 120 kDa antigen (cagA) tended (p < 0.15) to be more prevalent in DU patients (82%; 95% CI, 69-91) compared with controls (69%; 95% CI, 57-80) but not functional dyspepsia (77%; 95% CI, 57-90). No specific H. pylori antigens were associated with dyspepsia subgroups. CONCLUSION: No specific H. pylori antigens are linked to functional dyspepsia.
Explore the source record for details and available documents.
Gastric atrophy is a precursor lesion in the development of gastric cancer. It has been proposed that atrophy is part of a natural progression of inflammatory changes that result from long term infection with the bacterium Helicobacter pylori. The aim of this study was to test this hypothesis using an animal model of human Helicobacter infection. Conventional mice were infected with either a cat isolate of Helicobacter felis or a human isolate of "Gastrospirillum hominis". All infected mice showed a slowly progressive chronic gastritis with increasing numbers of infiltrating mononuclear cells and polymorphonuclear leucocytes. After a year and a half, the inflammatory reaction was so severe that atrophic changes were seen in both the antral and fundic mucosa. Control animals initially showed no inflammatory changes however as the animals aged, the gastric mucosa of some animals became infected with a bacterium Helicobacter muridarum that normally inhabits the small and large bowel of the rodent. The presence of this bacterium was also associated with gastritis and atrophic changes. This is the first report of experimentally induced atrophic changes induced by a gastric bacterium and opens the way for important experiments that will help better understand the induction of gastric cancer.
The discovery of the gastric bacterium, Helicobacter pylori and the demonstration of its role in the pathogenesis of gastroduodenal disease, has been one of the major microbiological advances in the last decade. Recent demonstration of long term infection with this bacterium as a risk factor in gastric carcinoma suggests that intervention in a disease of major morbidity and mortality is possible. Using a model of Helicobacter infection in mice it has been shown that oral immunisation with a sonicate of Helicobacter felis plus the adjuvant cholera toxin results in protection against an oral challenge with large numbers of viable bacteria. The success of the immunising regimen has been shown to correlate with the development of local immunity. Formulation of equivalent safe vaccines of H. pylori will make possible the immunisation of children in countries such as China, Japan and Columbia and so prevent the establishment of long term inflammation and thus significantly reduce the incidence of gastric cancer in those societies. This animal model is proposed as a major tool in the development of effective oral immunisation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Parents of babies in neonatal units often feel distanced from their baby, saying there is nothing they can do to help. Staff in NNUs must help involve parents in the care of their baby, to soothe qualms about discharge.
Multiple pinch biopsies were taken from the duodenum and antrum of 137 subjects (46 active duodenal ulceration; 44 healed ulcers; 47 'normal'), and examined for the presence and grade of gastritis, gastric metaplasia, and Campylobacter pylori. These factors, as well as age, sex, cigarette, and anti-inflammatory agent intake were evaluated as possible risk factors for duodenal ulceration. Pentagastrin induced Congo Red staining of the duodenal bulb was performed in an additional 43 cases, to determine the presence of functioning parietal cells in the duodenum. Ninety eight per cent of patients with duodenal infection with C pylori had active or healed duodenal ulcers. Bacteria were confined to areas of gastric metaplasia which was always infiltrated with inflammatory cells. The metaplastic tissue was usually superficial in type, although patients had C pylori associated with heterotopic tissue: this has not been previously described. Congo Red staining of the duodenal bulb showed that functioning endogenous acid producing tissue could be found most often at the edges of duodenal ulcers, but also in non-ulcer subjects. Cigarette smoking, age, sex, and ingestion of non-steroidal anti-inflammatory agents were not to be found to be significant risk factors for duodenal ulceration. In contrast, the presence of duodenal infection with C pylori proved to be a strong risk factor for duodenal ulceration (RR = 51), together with gastric metaplasia (RR = 6.2), and antral C pylori infection (RR = 7.6). These data identify duodenal infection with C pylori as the strongest risk factor for development of duodenal ulceration. Our finding of endogenous acid production around the edges of duodenal ulcers suggests an active role for parietal cells in the duodenum. We postulate a synergistic role for duodenal C pylori and endogenous acid production in the development of duodenal ulceration.
Explore the source record for details and available documents.
Although parathyroid cyst has been infrequently reported until the past decade, its presumed rarity is attributed to nonrecognition. First reported in 1905, only 58 cases of parathyroid cyst had been documented in the world literature by 1967. Since then, however, substantial literature about this entity has been accumulating. The three cases we are reporting bring the cumulative total to 149. All three have been examined histologically and treated by aspiration or surgical excision. There is confusion clinically with thyroid cysts, and assay of fluid aspirate for parathormone and thyroxine may not accurately distinguish the origin of the cyst. Tissue diagnosis is confirmatory. Parathyroid cysts may be developmental, arising from vestigial remnants of the third and fourth branchial clefts; or coalescence of microcysts with associated hypersecretion may enlarge into macrocysts; or an adenoma may degenerate into a pseudocyst. Hyperparathyroidism, if present, is associated with only the last two.
A case of left ventricular outflow tract obstruction caused by a parachute accessory anterior mitral valve leaflet is presented. The abnormality was detected in an asymptomatic patient by systolic murmur and thrill and was demonstrated by echocardiography, as well as by cardiac catheterization and surgery. These findings are presented. Several previously reported cases of a similar nature are reviewed. An identical case was not found in the English literature.