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Biomedical subjects

K E McColl

Publications and source records attributed to K E McColl.

At least 37 records · Page 2Linked to original sources
PubMed2000

Helicobacter pylori gastritis and gastric physiology.

It is now recognized that Helicobacter pylori infection exerts profound and diverse effects on gastric acid secretory function and that the alterations in acid secretion depend on the pattern of gastritis caused by the infection. In patients with an antral predominant nonatrophic gastritis, there is acid hypersecretion leading to duodenal ulcer disease. In patients with an atrophic pangastritis, there is markedly reduced acid secretion and increased risk for gastric cancer. It is now recognized that acid secretion also modifies H. pylori gastritis and a person's premorbid acid secretory status may be an important factor in determining the pattern of gastritis that an individual develops. This two-way interaction between H. pylori gastritis and gastric acid secretion is important in understanding the role of H. pylori infection in the response to proton-pump inhibitor therapy: It explains the more profound control of gastric acid secretion in H. pylori-positive patients and why rebound acid hypersecretion is confined to H. pylori-negative subjects.

Anti-Ulcer Agents↗
PubMed2000

The role of gastrin in ulcer pathogenesis.

Duodenal ulcer patients are characterized by an antrum-predominant, body-sparing, nonatrophic Helicobacter pylori (H. pylori) gastritis, which results in increased gastrin release and increased acid secretion. The increased gastrin release is caused by the infection impairing the acid-mediated inhibitory control of gastrin release. The elevated levels of the gastrin stimulate the healthy uninflamed, non-atrophic acid-secreting region of the stomach to secrete excess amounts of acid. The increased gastrin also exerts trophic effects on the oxyntic mucosa, causing hyperplasia of both the enterochromaffin-like cells and the parietal cells. These trophic changes in the mucosa further enhance its ability to secrete acid. The increased acid secretion results in an increased duodenal acid load, causing gastric metaplasia of the duodenal bulb and eventually the development of ulceration. In H. pylori-infected subjects without duodenal ulceration, a different pattern of gastritis is seen. This includes atrophy of the antrum, which reduces the number of G-cells and thus the degree of hypergastrinaemia induced by the antral infection. There are usually also varying degrees of inflammation and atrophy of the acid-secreting mucosa, which impair its ability to secrete acid in response to gastrin stimulation. The combined effects of the atrophy of the antrum and the inflammation of the antrum of the body mucosa therefore prevent H. pylori-induced acid hypersecretion and may result in varying degrees of hypochlorhydria. The particular pattern of gastritis that a subject develops in response to H. pylori infection and their likelihood of developing a duodenal ulcer is likely to be determinded by host genetic factors plus dietary factors.

Duodenal Ulcer↗
PubMed2000

Omeprazole, Helicobacter pylori status, and alterations in the intragastric milieu facilitating bacterial N-nitrosation.

BACKGROUND & AIMS: Omeprazole produces greater acid inhibition in Helicobacter pylori-positive than -negative subjects. We investigated whether this is accompanied by more profound changes in the intragastric milieu that facilitates bacterial synthesis of N-nitroso compounds. METHODS: Gastric juice pH; nitrite, ascorbic acid, and total vitamin C concentrations; and colonization by other bacteria were examined before and during omeprazole treatment in subjects with and without H. pylori infection. Studies were performed in the fasting state and after consumption of 2 mmol nitrate (equivalent to a salad meal). RESULTS: Before omeprazole, H. pylori-positive and -negative subjects were similar for all parameters. During omeprazole, H. pylori-positive subjects had a higher intragastric pH (7.8 vs. 3.0; P < 0.00001) and greater colonization with non-H. pylori species (5 x 10(7) vs. 5 x 10(5) CFU/mL; P < 0.05). These bacteria included nitrosating species. During omeprazole treatment, H. pylori-positive subjects had higher intragastric nitrite levels after the nitrate meal (median area under the concentration/time curve, 12,450 vs. 4708 micromol/L. min; P = 0.04). Omeprazole lowered intragastric vitamin C levels in H. pylori-positive but not -negative subjects (1.8 vs. 3.4 microg/mL, respectively; P = 0.02). CONCLUSIONS: In H. pylori-positive subjects, omeprazole produces disturbances in intragastric nitrite, vitamin C, and bacterial colonization that facilitate bacterial N-nitrosation. This may place them at increased risk of mutagenesis and carcinogenesis.

Adult↗
PubMed2000

Symptomatic benefit 1-3 years after H. pylori eradication in ulcer patients: impact of gastroesophageal reflux disease.

OBJECTIVES: Eradication of Helicobacter pylori (H. pylori) infection markedly reduces the recurrence of duodenal and gastric ulcers. However, there is little information regarding its efficacy in resolving dyspeptic symptoms in ulcer patients. The primary aim of this study was to assess the effect of eradicating H. pylori infection on dyspeptic symptoms in ulcer patients. The secondary aim was to identify predictors of symptomatic response to H. pylori eradication. METHODS: A total of 97 dyspeptic patients with active duodenal and/or gastric ulceration associated with H. pylori infection and unrelated to NSAID use had the severity and character of their dyspeptic symptoms measured before and again 1-3 yr after H. pylori eradication therapy. RESULTS: Pretreatment, the median dyspepsia score was 12 (4-16). Posttreatment, 55% of those eradicated of H. pylori had resolution of dyspepsia (score <2) compared with 18% of those not eradicated of the infection (95% CI for difference, 11-62%). Of the ulcer patients 31% had symptoms and/or endoscopic evidence of coexisting gastroesophageal reflux disease (GERD) at initial presentation and this influenced the symptomatic response to eradication of H. pylori. Of the 22 patients with heartburn or acid reflux as the predominant presenting symptom, but no endoscopic esophagitis, only 27% experienced resolution of dyspepsia after H. pylori eradication, compared with 68% of the 59 without those as predominant symptoms (95% CI for difference, 18-63%). Only one of the five patients with coexisting endoscopic esophagitis at initial presentation experienced resolution of dyspepsia after H. pylori eradication. Symptomatic benefit was unrelated to time lapsed since the infection was eradicated. Only three of 50 subjects developed de novo GERD symptoms after eradication of H. pylori, whereas 21 of 36 subjects experienced resolution of GERD symptoms after eradication of the infection. CONCLUSIONS: A substantial proportion of ulcer patients have symptoms and/or signs of coexisting GERD at initial presentation and this reduces the symptomatic benefit from H. pylori eradication. However, we have found no evidence that eradicating H. pylori induces de novo GERD symptoms in ulcer patients.

Adult↗
PubMed2000

Comparison of an enzyme immunoassay for the detection of Helicobacter pylori antigens in the faeces with the urea breath test.

BACKGROUND: Current diagnostic tests for Helicobacter pylori are invasive (endoscopy) or indirect (urea breath test, serology). AIMS: To evaluate a new enzyme immunoassay (EIA) which detects H pylori antigens in faeces, by comparing its sensitivity and specificity in children with the (13)C urea breath test (UBT). METHODS: A total of 119 children underwent a UBT and provided a faecal sample for antigen testing within seven days. After an overnight fast each child provided a pretest breath sample, and samples at 30 and 40 minutes after ingestion of 100 mg (13)C labelled urea. (13)C enrichment of breath was measured by isotope ratio mass spectrometry. Faeces were stored at -70 degrees C until antigen testing, using the EIA. Samples were read spectrophotometrically at 450 nm and results were interpreted using recommended cut offs of optical density <0.14 as negative, >/=0.16 as positive, with >/=0.14 and <0. 16 representing equivocal results. Sensitivity and specificity were calculated using the manufacturer's cut off compared with UBT. RESULTS: Sensitivity and specificity were 88% and 82%, respectively. Negative and positive predictive values were 97% and 58%. CONCLUSIONS: The EIA is an alternative, non-invasive, and easy to use method for the detection of H pylori in children. Its high negative predictive value suggests a role in screening out uninfected children.

Adolescent↗
PubMed2000

Helicobacter pylori-negative ulcer disease.

The proportion of ulcer patients without evidence of Helicobacter pylori infection varies considerably in different parts of the world, which may be explained by the different prevalence of H. pylori infection in the background population. In any ulcer patient with an H. pylori-negative test, it is important to consider that the test may be falsely negative due to treatment with antibiotics, bismuth preparations, or potent acid inhibitory therapy. The commonest cause of true H. pylori-negative ulcers is usage of nonsteroidal anti-inflammatory drugs, so patients should be carefully questioned about such therapy. Rarer causes of H. pylori-negative duodenal ulcers include gastroduodenal Crohn's disease and Zollinger-Ellison syndrome. About 50% of H. pylori-negative duodenal ulcer patients have no apparent explanation for the ulcer disease. A proportion of these patients have increased gastric acid secretion and increased duodenal acid load, which is likely to be of pathogenic significance. H. pylori-negative ulcers are more difficult to control with antisecretory drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

Omeprazole and dietary nitrate independently affect levels of vitamin C and nitrite in gastric juice.

BACKGROUND & AIMS: Hypochlorhydria is associated with an increased risk of gastric cancer. We have studied the effect of pharmacologically induced hypochlorhydria on the gastric juice ascorbate/nitrite ratio, which regulates the synthesis of potentially carcinogenic N-nitroso compounds. METHODS: Saliva, gastric juice, and serum from 20 healthy volunteers (9 positive for Helicobacter pylori), with a mean age of 30 years (range, 20-47 years), were analyzed for nitrite, ascorbic acid, and total vitamin C before and for 2 hours after ingestion of 2 mmol [corrected] nitrate (nitrate content of a standard salad meal). This was repeated after 4 weeks of treatment with omeprazole, 40 mg daily. RESULTS: Before omeprazole treatment, the nitrate meal lowered gastric ascorbic acid levels from 3.8 to 0.9 microg/mL (P < 0.05) and increased median salivary nitrite levels from 44 to 262 micromol/L (P < 0.001); gastric nitrite concentration remained undetected in 10 subjects. Omeprazole increased median fasting gastric nitrite levels from 0 to 13 micromol/L (P = 0.001) and decreased fasting gastric ascorbic acid levels from 3.8 to 0.7 microg/mL (P < 0.001). With omeprazole treatment, gastric nitrite levels after the nitrate meal were markedly increased at 154 micromol/L (range, 49-384 micromol/L; P < 0.001). In H. pylori-infected subjects, omeprazole also decreased total vitamin C levels in both gastric juice and serum. CONCLUSIONS: Omeprazole and dietary nitrate independently decrease the ascorbate/nitrite ratio. This may lead to an increased risk of gastric cancer.

Adult↗
PubMed1999

Rebound hypersecretion after omeprazole and its relation to on-treatment acid suppression and Helicobacter pylori status.

BACKGROUND & AIMS: There have been conflicting reports regarding acid secretion after treatment with omeprazole. This study examined acid secretion after treatment with omeprazole and its relation to Helicobacter pylori status and on-treatment gastric function. METHODS: Twelve H. pylori-negative and 9 H. pylori-positive subjects were examined before, on, and at day 15 after an 8-week course of 40 mg/day omeprazole. On each occasion, plasma gastrin, intragastric pH, and acid output were measured basally and in response to increasing doses of gastrin 17. RESULTS: In the H. pylori-negative subjects at day 15 after omeprazole treatment, basal acid output was 82% higher (P < 0.007) and maximal acid output 28% higher (P < 0.003) than before omeprazole. The degree of increase in maximal acid output was related to both on-treatment pH and on-treatment fasting gastrin levels, being 48.0% in subjects with an on-treatment pH of >4 vs. 21. 0% in those with a pH of <4 (P < 0.02) and 49.2% in subjects with an on-treatment gastrin of >25 ng. L-1 vs. 19.8% in those with a fasting gastrin of <25 ng. L-1 (P < 0.006). At day 15 after omeprazole treatment, the H. pylori-positive subjects showed a heterogeneous response with some having increased acid output and others persisting suppression. CONCLUSIONS: Rebound acid hypersecretion occurs in H. pylori-negative subjects after omeprazole treatment. Its severity is related to the degree of elevation of pH on treatment. Persisting suppression of acid secretion masks the phenomenon in H. pylori-positive subjects.

Adult↗
PubMed1999

The prevalence of dyspepsia and use of antisecretory medication in North Glasgow: role of Helicobacter pylori vs. lifestyle factors.

AIMS: To determine the prevalence of dyspepsia and associated antisecretory medication usage, and their associations with H. pylori infection in the general population. In addition, to compare the importance of H. pylori infection relative to other potential causes of dyspepsia: alcohol, smoking and obesity. METHODS: The study examined a random population sample of 784 men and 827 women from Glasgow. They completed a validated dyspepsia questionnaire and had their H. pylori status determined by serology. RESULTS: The overall prevalence of dyspepsia was 12%; prescribed antisecretory medication had been used over the last 6 months by 7%. The odds ratio (95% CI) for dyspepsia, comparing H. pylori-positives to negatives was 1.79 (1.03, 3.09) for men and 1.11 (0.70, 1.78) for women. Ever-smoking (both sexes) and obesity (women) had higher odds ratios for dyspepsia than did H. pylori. Adjustment for age, social class, ever-smoking, ever-drinking and obesity reduced the H. pylori odds ratios for dyspepsia to 1.38 (0.73, 2.60) for men and 0.99 (0. 57, 1.73) for women. The association between H. pylori and antisecretory medication usage was similar to that for dyspepsia. CONCLUSION: Obesity and smoking are more important risk factors, for dyspepsia and antisecretory medication usage, than is H. pylori. Reducing the burden and cost of dyspepsia will require lifestyle modification and not merely H. pylori eradication.

Adult↗