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Biomedical subjects

A D Beattie

Publications and source records attributed to A D Beattie.

At least 19 recordsLinked to original sources
PubMed1998

Reduced gastric mucosal vascularity in patients with chronic gastritis.

OBJECTIVES/DESIGN: Chronic inflammation is increasingly being linked to ischaemia, but the mechanism is poorly understood, and little is known about its effect on local gastric endothelial microvessels. We aimed at studying the number and surface area of gastric mucosal endothelial microstructures in the presence or absence of chronic gastritis. METHODS: Immunohistochemical assessments were carried out on gastric antral and body biopsies taken from patients with chronic gastritis and others with normal histology. The primary antibody (QB-END/10) was raised against CD34 antigen within the endothelial cell membranes. A computer attached to a microscope was used to count the number and measure the surface area of mucosal endothelial entities. RESULTS: In patients with Helicobacter pylori gastritis (n = 19), the median number of endothelial microstructures per section was 43 in the antrum and 86 in the gastric body, compared with 205 (P = 0.00004) and 165 (P = 0.002), respectively, in subjects with normal gastric histology (n = 11). The median surface area of the endothelial microstructures was also reduced in patients with gastritis. The normal gastric antrum had more endothelial entities than the normal body (median of 205 vs 165; P = 0.007). CONCLUSIONS: Within the normal stomach, the antrum is more richly vascularized than the gastric body. However, active chronic gastritis is associated with reduction in both the number and surface area of mucosal endothelial microstructures, with the reduction being more marked in the antrum. This is different from acute inflammation, and is relevant to our understanding of the natural history of mucosal defence, particularly the greater susceptibility of the gastric antrum to ulceration, compared with the gastric body.

Adult↗
PubMed1997

Randomised double blind controlled study of recurrence of gastric ulcer after treatment for eradication of Helicobacter pylori infection.

OBJECTIVE: To determine whether eradication of Helicobacter pylori infection reduces recurrence of benign gastric ulceration. DESIGN: Randomised, double blind, controlled study. Patients were randomised in a 1:2 ratio to either omeprazole 40 mg once daily for eight weeks or the same treatment plus amoxycillin 750 mg twice daily for weeks 7 and 8. A 12 month untreated follow up ensued. SETTING: Teaching and district general hospitals between 1991 and 1994. SUBJECTS: 107 patients with benign gastric ulcer associated with H pylori. MAIN OUTCOME MEASURES: Endoscopically confirmed relapse with gastric ulcer (analysed with life table methods), H pylori eradication, and healing of gastric ulcers (Mantel-Haenszel test). RESULTS: 172 patients were enrolled. Malignancy was diagnosed in 19; 24 were not infected with H pylori; four withdrew because of adverse events; and 18 failed to attend for start of treatment, leaving 107 patients eligible for analysis (35 omeprazole alone; 72 omeprazole plus amoxycillin). In the omeprazole/amoxycillin group 93% (67/72; 95% confidence interval 84% to 98%) of gastric ulcers healed and 83% (29/35; 66% to 94%) in the omeprazole group (P = 0.103). Eradication of H pylori was 58% (42/72; 46% to 70%) and 6% (2/35; 1% to 19%) (P < 0.001) and relapse after treatment was 22% (16/72) and 49% (17/35) (life table analysis, P < 0.001), in the two groups, respectively. The recurrence rates were 7% (3/44) after successful H pylori eradication and 48% (30/63) in those who continued to be infected (P < 0.001). CONCLUSIONS: Eradication of H pylori reduces relapse with gastric ulcer over one year. Eradication rates achieved with this regimen, however, are too low for it to be recommended for routine use.

Amoxicillin↗
PubMed1996

Sucralfate suppresses Helicobacter pylori infection and reduces gastric acid secretion by 50% in patients with duodenal ulcer.

BACKGROUND & AIMS: The mechanism(s) by which sucralfate heals duodenal ulcers remains unclear. The aim of this study was to determine the effect of sucralfate on Helicobacter pylori infection and on the accompanying hypersecretion of gastric acid the infection induces in patients with duodenal ulcer. METHODS: Basal and gastrin-releasing peptide (GRP) stimulated gastrin release and acid secretion. H. pylori density, gastric urease activity, and severity of gastritis were studied in patients with duodenal ulcer who were positive for H. pylori before, during, and after 4 weeks' treatment with sucralfate (2 g twice daily). RESULTS: The density of H. pylori decreased by 70% during sucralfate treatment and returned to the pretreatment level after discontinuation of therapy. This suppression of H. pylori infection was accompanied by an 80% decrease in gastric urease activity. GRP-stimulated plasma gastrin concentrations, GRP-stimulated acid output, and basal acid output all decreased by approximately 50% during sucralfate therapy and returned to pretreatment levels after treatment was discontinued. CONCLUSIONS: These findings indicate that sucralfate markedly suppresses H. pylori infection and the accompanying hypersecretion of acid the infection induces in patients with duodenal ulcer. These effects are likely to be important mechanisms by which the drug promotes duodenal ulcer healing.

Adult↗
PubMed1996

The European Diploma of Gastroenterology: progress towards harmonization of standards.

The European Diploma of Gastroenterology has now been established by the European Board of Gastroenterology (EBG) and has been awarded to several individual doctors and to training centres. The EBG is a working party of the Gastroenterology Section of the European Union of Medical Specialists. The Diploma can be awarded to individual doctors who have been recognized as specialists in their own countries; trained in approved centres; and satisfied the training criteria of the EBG. The Diploma can also be awarded as a recognition of training competence to hospitals that meet the requirements of the EBG. Hospitals seeking recognition will be visited by members of the EBG and must show evidence that they can provide adequate clinical and technical experience to trainee gastroenterologists.

Certification↗
PubMed1996

Insulin-like growth factor-I in Helicobacter pylori gastritis and response to eradication using bismuth based triple therapy.

AIMS: To measure insulin-like growth factor-I (IGF-I) concentrations in the presence and absence of Helicobacter pylori infection and in response to eradication of the organism. METHODS: An enzyme linked immunosorbent assay was used to measure gastric and fasting serum concentrations of IGF-I in 17 patients with and 11 without H pylori infection. Repeat assessments were performed in the infected patients six weeks after they received a two week course of bismuth chelate, metronidazole, and amoxycillin. RESULTS: IGF-I was detected at very low concentrations in gastric juice and in mucosal incubates. The median serum IGF-I concentration was 88 micrograms/l in the patients infected with H pylori compared with 90 micrograms/l in the non-infected controls; IGF-I concentrations dropped to 77 micrograms/l following eradication therapy (p = 0.014). CONCLUSION: The similarity in baseline IGF-I concentrations in the presence and absence of H pylori suggests that their subsequent drop after treatment is more likely to be due to the treatment.

Adult↗
PubMed1996

Gastric mucosal hepatocyte growth factor in Helicobacter pylori gastritis and peptic ulcer disease.

OBJECTIVES: Hepatocyte growth factor (HGF) is increasingly recognized for its role in a variety of hepatic and systemic diseases. Its relationship to gastritis has not been studied. We aimed at measuring gastric mucosal HGF levels in the presence or absence of Helicobacter pylori gastritis, in peptic ulcers, and in response to H. pylori eradication. METHODS: Fifty one patients were studied. Patients were not entered if they had liver disease, malignancy, or any systemic illness. HGF was measured in gastric antral incubates using an enzyme-linked immunosorbent assay. Assessments were repeated 6 wk after a 2-wk course of anti-H. pylori triple therapy in 12 patients. Code numbers were used for blinding. RESULTS: The median gastric mucosal HGF level was 36 ng/gm/tissue in patients with H. pylori gastritis (n = 33) compared with 19 ng/gm in 18 negative controls (p = 0.0024), 18 ng/gm after the eradication of H. pylori (p = 0.021), 23 ng/gm in all patients with ulcers (n = 10), and 26 ng/gm/tissue in H. pylori-positive ulcers (n = 7). CONCLUSIONS: Gastric mucosal HGF levels were elevated in H. pylori gastritis and reduced by its eradication. These results are relevant to our understanding of the increased gastric cell proliferation in patients with H. pylori-related gastritis.

Adult↗
PubMed1996

Pathogenesis of primary hepatocellular carcinoma.

Primary hepatocellular carcinoma (HCC) is a major cause of mortality world-wide, with a poorly understood pathogenesis. We review known aetiological factors and the mechanisms whereby they are associated with the development of hepatocellular carcinoma. The increasing knowledge of the dysregulation of cellular growth control that occurs during HCC development is discussed in detail.

Aflatoxins↗
PubMed1996

Altered urinary interleukin-8/creatinine ratio in peptic ulcer disease: pathological and diagnostic implications.

OBJECTIVES AND METHODS: To assess its clinicopathological and diagnostic significance, interleukin-8 (IL-8) was measured by radioimmunoassay in fasting urine specimens and in gastric mucosal incubates taken from 54 patients with dyspepsia. The presence of Helicobacter pylori, the activity of gastritis, and urine creatinine levels were also assessed. RESULTS: The median urinary IL-8/creatinine ratio was 0.1 x 10(-6) in patients with current peptic ulcers (n = 13) and 0.2 x 10(-6) in patients with a history of ulcers (n = 8), compared with 0.4 x 10(-6) (p < 0.0001) in patients without ulcers who were infected with H. pylori (n = 20) or not infected (n = 13). The activity of gastritis had a positive correlation with gastric IL-8 (r = 0.5870, p < 0.01) and a negative correlation with urinary IL-8/creatinine ratio (r = -0.6447, p < 0.005). The improvement in the activity of gastritis in 20 patients given anti-H. pylori triple therapy was associated with a significant fall in gastric mucosal IL-8 and a rise in urinary IL-8/creatinine ratio. CONCLUSIONS: An inverse relationship seems to exist between urinary IL-8 and the activity of gastritis and gastric IL-8. This may represent another concept in the pathogenesis of peptic ulcers and can assist in the noninvasive diagnosis of peptic ulcer disease.

Adult↗
PubMed1995

Use of a stable copper isotope (65Cu) in the differential diagnosis of Wilson's disease.

1. 65Cu/63Cu stable-isotope ratios have been measured in blood serum after oral administration of the stable isotope 65Cu. The incorporation of the isotope into the plasma protein pool was followed at various times for up to 3 days. The resulting patterns of enrichment in healthy control subjects, in Wilson's disease patients and in heterozygotes for the Wilson's disease gene, were similar in appearance to those found by others using copper radioactive isotopes. After an initially high enrichment at 2 h after dosage, the Wilson's disease cases, in contrast to the control subjects, did not show a secondary rise in isotope enrichment of the plasma pool after 72 h, demonstrating a failure to incorporate copper into caeruloplasmin. The Wilson's disease heterozygotes had variable degrees of impairment of isotope incorporation, not always distinguished from those of control subjects. 2. The stability of the isotope also permits the copper tracer to be followed for a longer period. Ten healthy subjects were studied for over 40 days, allowing the biological half-time of an oral dose of copper to be determined (median 18.5 days, 95% confidence interval 14-26 days). Known heterozygotes for the Wilson's disease gene were found to have a significantly increased biological half-time for removal of copper from the plasma pool (median 43 days, 95% confidence interval 32-77 days). 3. The incorporation of 65 Cu in patients with diseases of the liver (other than Wilson's disease) was found to be similar to that in control subjects, aiding differential diagnosis.

Adolescent↗
PubMed1995

Effect of omeprazole and feeding on plasma gastrin in patients with achlorhydria.

BACKGROUND: The mechanism of hypergastrinaemia during omeprazole therapy is unclear, but is generally assumed to be entirely a consequence of acid suppression. However, direct stimulation of G cells by omeprazole could also be a factor. In order to further investigate the mechanism of omeprazole-induced hypergastrinaemia, we have studied the effects of the drug on plasma gastrin in patients with achlorhydria, in whom altered acid secretion cannot play a role. METHODS: We estimated fasting and peptone meal stimulated plasma gastrin in nine patients (seven female) with pernicious anaemia and achlorhydria, before and on the final day of 4 weeks' dosing with omeprazole 40 mg daily. RESULTS: Despite the high fasting gastrin concentrations, the peptone meal produced a further elevation in plasma gastrin concentrations, median gastrin concentrations rising from 1500 ng/L (range 225-10,875 ng/L) to 3750 ng/L (range 585-15,600 ng/L) post-prandially (P = 0.004). The median post-prandial rise in plasma gastrin at this initial visit was 44% (3-260%), and the median time interval until plasma gastrin concentrations returned to fasting levels was 120 min (range 10- > 150 min). There was a significant negative correlation between fasting plasma gastrin concentrations and the percentage increase in plasma gastrin levels in response to meal stimulation (Spearman correlation coefficient -0.79, P = 0.01). Fasting plasma gastrin concentrations were similar pre-omeprazole (median 1950 ng/L, range 240-16,500 ng/L) and post-omeprazole (median 1500 ng/L, range 315-7650 ng/L). Likewise, peak plasma gastrin concentrations were also similar pre-omeprazole (median 2700 ng/L, range 585-16,500 ng/L) and post omeprazole (median 3420 ng/L, range 720-11,250 ng/L). CONCLUSIONS: (i) The hyperplastic G cell mass in patients with pernicious anaemia can be further stimulated by a peptone meal, which causes a prolonged rise in plasma gastrin concentrations. (ii) There is a negative correlation between fasting plasma gastrin concentrations and the percentage increase in plasma gastrin levels in response to meal stimulation. (iii) Omeprazole has no effect on plasma gastrin in achlorhydric patients, which is consistent with its hypergastrinaemic effect being entirely secondary to acid inhibition.

Achlorhydria↗
PubMed1994

A database on dyspepsia.

A prospective study of dyspepsia was carried out in a primary referral hospital between 1974-1987 including 1540 patients of whom 1433 were seen as outpatients. The study protocol was agreed in advance and a structured questionnaire was used to elicit relevant clinical information: up to three diagnoses were permitted for each patient. The commonest principal diagnoses were duodenal ulcer (26%), functional dyspepsia (22%), and irritable bowel syndrome (IBS) (15%); alcohol related dyspepsia (4%) was as common as gastric carcinoma or symptomatic gall stones. Multiple diagnoses were common (31% given two diagnoses, and 6% given three) so that in all 2111 diagnoses were given to 1540 patients; the functional disorders (IBS and functional dyspepsia) considered together accounted for 39% of all diagnoses made. Whereas organic conditions were diagnosed by clinicians with confidence (63-98% considered 'certain'), even when given as the principal or first diagnosis IBS was considered 'certain' in only 61% and functional dyspepsia 48%. The demographic symptom data, together with information on tobacco and alcohol use, and work lost are described in detail.

Adult↗
PubMed1994

Effect of Helicobacter pylori and its eradication on gastric juice ascorbic acid.

The presence of ascorbic acid in gastric juice may protect against gastric carcinoma and peptic ulceration. This study examined the effect of Helicobacter pylori (H pylori) on the secretion of ascorbic acid into gastric juice by measuring fasting plasma and gastric juice ascorbic acid concentrations in patients with and without the infection and also before and after its eradication. Gastric juice ascorbic acid concentrations in 19 H pylori positive patients were significantly lower (median 2.8, range 0-28.8 micrograms/ml) than those in 10 H pylori negative controls (median 17.8, range 5.6-155.4 micrograms/ml) (p < 0.0005) despite similar plasma ascorbic acid concentrations in both groups. The median gastric juice:plasma ascorbic acid ratio in the H pylori positive patients was only 1.16 (range 0.02-6.67), compared with a median ratio of 4.87 (range 0.76-21.33) in H pylori negative controls (p < 0.01). In the patients with H pylori infection there was a significant negative correlation between the severity of the antral polymorphonuclear infiltrate and gastric juice ascorbic acid concentrations (correlation coefficient -0.52, p = 0.02). After eradication of H pylori in 11 patients, gastric juice ascorbic acid concentrations rose from 2.4 (0-12.8 micrograms/ml) to 11.2 (0-50 micrograms/ml) (p = 0.01). The median gastric juice: plasma ascorbic acid ratio also increased from 1.33 (0.05-6.67) to 2.89 (0.01-166) (p = 0.01). In conclusion, the high gastric juice:plasma ascorbic acid ratio in H pylori negative subjects shows active secretion of ascorbic acid into gastric juice. Secondly, H pylori infection causes a reversible lowering of gastric juice ascorbic acid concentrations, which may predispose to gastric carcinoma and peptic ulceration.

Ascorbic Acid↗
PubMed1990

Heck's disease.

The clinical and histological findings in two adult caucasians with focal epithelial hyperplasia (Heck's disease) are described. The literature concerning this rare condition is reviewed.

Adult↗
PubMed1985

Temocillin in the treatment of serious gram-negative infections.

Temocillin was used to treat 32 patients with proven or suspected infection caused by aerobic Gram-negative bacteria. 25 of these patients were assessable on clinical and bacteriological grounds. All 25 were either cured or improved, although in 5 patients with urinary tract infection there was relapse of infection or reinfection following the cessation of therapy. Clinical improvement was usually rapid and no serious side effect was noted. Temocillin would thus appear to be an effective and safe agent for the treatment of bacterial infection caused by aerobic Gram-negative organisms.

Adult↗
PubMed1984

The effect of acute alcohol withdrawal on the serum potassium and total body potassium in heavy drinkers.

In a group of 20 patients with heavy alcohol intake a relation was found between withdrawal symptoms and fall in serum potassium. Total body potassium (TBK) was measured in all subjects and was lower in the group of subjects who displayed symptoms than in the group who did not. The subgroup of the four most severe reactors had a mean TBK value significantly less than the 'non-reactor' group. The minimum serum potassium levels observed for all subjects in the four day period following alcohol withdrawal correlated with their TBK values. We suggest that the mechanism for the serum potassium fall might be overactivity of the Na-K pump caused by ethanol consumption. There was also an association between withdrawal reaction and abnormal liver function and a transient rise in serum phosphate in the more severely reacting subjects.

Adenosine Triphosphatases↗