Biomedical subjects
Publications and source records attributed to J H Baron.
Seventy-two per cent of all hospital doctors and medical students wear white coats and most wear them greater than 75% of the time. White coats are worn chiefly for easy recognition by colleagues and patients, to put items in the pockets and to keep clothes clean. Psychiatrists and paediatricians try to maximize rapport with patients by deliberately not wearing white coats.
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Ammonia, released in the gastric mucosa by the action of Helicobacter pylori urease on transuded plasma urea, curtails the biosynthesis of mucus and/or causes the mucus to be disassembled at the mucosal surface. These changes facilitate colonisation by H pylori and may promote gastric ulcer formation.
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Vagotomy and omeprazole effectively inhibited 2-deoxy-D-glucose (-91%) and pentagastrin (-72%) stimulated acid production in mice, respectively. Both vagotomy and omeprazole treatment were accompanied by massive increases in histamine secretion (8-fold or more, during both basal and stimulated states). Mucosal stores of histamine, however, were not depleted. Similar rises in luminal histamine have been observed in patients treated in these ways. The mouse model may thus be suitable to elucidate the kinetics of histamine release in patients.
The effect of tripotassium dicitrato bismuthate (De-Nol) on the breakdown of the gastric mucus barrier was investigated by measuring the output of mucus glycoprotein in pentagastrin-stimulated secretion from 13 patients before and after treatment for peptic ulcer, and by examining the accumulation of dialysable peptides and amino acids (DPAA) in stimulated secretion from ten of these patients. The accumulation of DPAA was significantly reduced after De-Nol (by 54%) and to a greater extent than was the output of mucus glycoprotein (by 27%). These observations are consistent with a decrease in the rate of breakdown of the mucus barrier as a result of De-Nol treatment. De-Nol significantly reduced pepsin output (by 32%) in the same group of patients. Comparison of the change in pepsin output with the change in accumulation of DPAA in stimulated juice indicated that De-Nol increases the resistance of the mucus barrier to acid-pepsin proteolysis and/or inhibits the secretion of amino acids and peptides from gastric mucosa.
Chronic cryptosporidial infection in man usually occurs in those who are immunocompromised. We report a patient with a one year history of bowel symptoms resulting from persistent cryptosporidial infection of the colon. Investigations showed underlying selective IgA and saccharomyces opsonin deficiencies but no evidence of cell mediated immune dysfunction. Both selective immunoglobulin A and opsonin deficiencies are relatively common in the general population and may be a cause of susceptibility to persistent cryptosporidial infection.
Fifty one patients with human immuno-deficiency virus (HIV-1) infection who had been consecutively endoscoped for upper gastrointestinal symptoms were biopsied (stomach or duodenum, or both) and compared with 59 age and sex matched controls for the presence of Campylobacter pylori. In 28 (47%) of the control group but in only seven (14%) of the HIV seropositive patients were C pylori seen on histological examination (p less than 0.001, odds ratio 5.6, 95% confidence interval 2.2-14.5). Sixteen patients who were HIV antibody positive had other index diseases for the diagnosis of AIDS in the biopsy material and, when these were excluded, comparison with the control group still showed a significant difference; p less than 0.01, odds ratio 3.6, 95%, confidence interval 1.4-9.6. In this series, therefore, C pylori were far less common in HIV antibody positive patients than in controls. Among the HIV positive patients, a higher proportion of C pylori negative cases had AIDS but this trend was not significant. The findings of this study indicate that whatever abnormalities of cell mediated mucosal immunoregulation are caused by HIV infection, they do not seem to be important in the response to infection by C pylori.
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Mice were exposed to a single dose of 9 or 15 Gy of X rays directed to the stomach. Histamine and histamine formation capacity (HFC) in the oxyntic region of the stomach were assayed at regular intervals for 7 weeks. After 9 Gy, mean gastric mural histamine fell to 61% of the control value (p less than 0.01) 7 days after irradiation while HFC rose to 172% (p less than 0.05). Both histamine and HFC returned to control values within 2 weeks after irradiation. With 15 Gy, on Day 7, histamine fell to 46% (p less than 0.01) and HFC rose to 260% (p less than 0.05). Histamine concentration remained low (less than half of the control value) while HFC returned to normal. These dose-dependent changes in histamine were observed neither elsewhere in the gut nor in the circulating blood. Further groups of mice were exposed to 3, 6, 9 or 15 Gy to the stomach, with gastric histamine and HFC assayed on Day 7. Histamine concentration was inversely related to dose (r = -0.59, p less than 0.001) and HFC was directly dose dependent (r = 0.52, p less than 0.001). These results suggest that irradiation of the stomach may reduce gastric histamine without inducing a general histamine release. The depletion of the gastric histamine store may explain the inhibitory effect of irradiation of the stomach on gastric acid secretion.
The polymerase chain reaction (PCR) was used to detect malignant lymphoma cells with the bcl-2 gene rearrangement in the peritoneal washings and bone marrow of a patient with an apparently localised gastric lymphoma. After four courses of cytotoxic drug treatment the cells could no longer be detected in either site. PCR is a useful addition to the staging investigations of non-Hodgkin lymphoma and can also be used to monitor response to treatment.
Two hundred forty-six patients with a wide range of upper gastrointestinal tract disorders were investigated for the presence of Campylobacter pylori infection in esophagus, gastric antrum, and duodenum. C. pylori was identified in 52% of patients in at least one site, and microbiological and histological techniques were used to exclude the presence of the organism. Esophageal infection was not significant and is probably due to reflux. Antral C. pylori was significantly associated with active gastritis and active duodenitis and is possibly pathogenic.