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T C Northfield

Publications and source records attributed to T C Northfield.

At least 19 recordsLinked to original sources
PubMed1996

Selection of patients for early discharge or outpatient care after acute upper gastrointestinal haemorrhage. National Audit of Acute Upper Gastrointestinal Haemorrhage.

BACKGROUND: Acute upper gastrointestinal haemorrhage is a common medical emergency and hospital admission has usually been regarded as obligatory until the risk of further haemorrhage has receded. This policy means that some patients at low risk stay in hospital for longer than is necessary especially when diagnostic endoscopy is delayed. We attempted to identify patients who had negligible risk of further bleeding or death and for whom early discharge or even outpatient management would be possible with no adverse effect on standards of care. METHODS: We used a validated risk scoring system based on age (score 0-2), presence of shock (0-2), comorbidity (0-3), diagnosis (0-2), and endoscopic stigmata of recent haemorrhage (0-2); the maximum possible score was 11. We studied patients identified through the UK national Audit of acute upper gastrointestinal haemorrhage; they had been admitted with upper gastrointestinal haemorrhage to hospitals in the UK during 4 months of 1993. This analysis was based on the 2531 patients from the national audit who underwent endoscopy after an acute admission. FINDINGS: 744 (29.4%) of the 2531 patients scored 2 or less on the risk score. Of these patients only 32 (4.3% [95% Cl 3.0-6.0] rebled and only one (0.1% [0.006-0.75] died). Thus, the risk score identifies patients at low risk of rebleeding or death. The median hospital stay increased with risk score. Within risk score categories of 5 or less, there was a trend of increasing hospital stay as the time between admission and endoscopy increased. INTERPRETATION: Our risk score identifies a large proportion of patients with acute upper gastrointestinal haemorrhage who are at low risk of further bleeding or death. Early endoscopy and discharge of such patients could allow substantial resource savings.

Acute Disease↗
PubMed1996

C reactive protein and its relation to cardiovascular risk factors: a population based cross sectional study.

OBJECTIVE: To test the hypothesis that minor chronic insults such as smoking, chronic bronchitis, and two persistent bacterial infections may be associated with increases in C reactive protein concentration within the normal range and that variations in the C reactive protein concentration in turn may be associated with levels of cardiovascular risk factors and chronic coronary heart disease. DESIGN: Population based cross sectional study. SETTING: General practices in Merton, Sutton, and Wandsworth. SUBJECTS: A random sample of 388 men aged 50-69 years from general practice registers. 612 men were invited to attend and 413 attended, of whom 25 non-white men were excluded. The first 303 of the remaining 388 men had full risk factor profiles determined. INTERVENTIONS: Measurements of serum C reactive protein concentrations by in house enzyme linked immunosorbent assay (ELISA); other determinations by standard methods. Coronary heart disease was sought by the Rose angina questionnaire and Minnesota coded electrocardiograms. MAIN OUTCOME MEASURES: Serum C reactive protein concentrations, cardiovascular risk factor levels, and the presence of coronary heart disease. RESULTS: Increasing age, smoking, symptoms of chronic bronchitis, Helicobacter pylori and Chlamydia pneumoniae infections, and body mass index were all associated with raised concentrations of C reactive protein. C Reactive protein concentration was associated with raised serum fibrinogen, sialic acid, total cholesterol, triglyceride, glucose, and apolipoprotein B values. C Reactive protein concentration was negatively associated with high density lipoprotein cholesterol concentration. There was a weaker positive relation with low density lipoprotein cholesterol concentration and no relation with apolipoprotein A I value. C Reactive protein concentration was also strongly associated with coronary heart disease. CONCLUSION: The body's response to inflammation may play an important part in influencing the progression of atherosclerosis. The association of C reactive protein concentration with coronary heart disease needs testing in prospective studies.

Aged↗
PubMed1996

Gastric DNA content in postgastrectomy patients. Relationship to mucosal dysplasia.

BACKGROUND: Gastric mucosal cellular DNA content was assessed in patients who had undergone gastric surgery for peptic ulcer disease more than 20 years previously, with the aim of examining the relationship between abnormal DNA content and gastric mucosal dysplasia, as well as determining the effect of different types of surgery on DNA content. METHODS: Sixty-five subjects underwent upper gastrointestinal endoscopy. In each, six biopsies were taken from the stoma or antrum and graded for severity of dysplasia. Cellular DNA was quantified using a microprocessor-controlled image analysis system with a fast densitometer card on Feulgen-stained slides. DNA histograms were evaluated using the 2c deviation index (2cDI) for proliferative activity and the 4c exceeding rate (4cER) and the 5c exceeding rate (5cER) as indices of malignant potential. RESULTS: In subjects with Billroth II operations, all the above DNA criteria were higher than in Billroth I (P < 0.05), vagotomy and pyloroplasty (P < 0.001), and controls (P < 0.0001). DNA values increased as dysplasia progressed in severity (2cDI, Rs = 0.67; 4cER, Rs = 0.61; 5cER, Rs = 0.72; respectively, P < 0.0001). Among subjects with no dysplasia, more aneuploid cells were found in the Billroth II group, (p < 0.005) compared with the other types of operation. CONCLUSIONS: Cellular DNA content is abnormal at an early stage in dysplasia and may even predate it. Increasing values of abnormal DNA content are related to the severity of dysplasia. DNA analysis may be a useful additional tool in surveillance programs to select high-risk patients for screening.

Aged↗
PubMed1996

Pathogenesis of gastric metaplasia of the human duodenum: role of Helicobacter pylori, gastric acid, and ulceration.

BACKGROUND & AIMS: The pathogenesis of gastric metaplasia (GM) in the duodenum is unclear. The aim of this investigation was to study the effect on the extent of GM of ulcer healing, Helicobacter pylori eradication, and acid suppression singly and in combination. The relationship between GM and gastroduodenal inflammation and H. pylori infection density was also studied. METHODS: Duodenal and gastric antral biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer and from H. pylori-positive nonulcer subjects. Biopsy procedures from patients with duodenal ulcer were repeated after 6 months of treatment. Nonulcer subjects were treated symptomatically and did not undergo re-endoscopy. RESULTS: Ulcer healing alone produced no change in GM or in gastroduodenal inflammation. H. pylori eradication produced a 42% reduction in GM and improvement in inflammation. Acid suppression produced a 43% reduction in GM but without a significant change in inflammation. A combination of H. pylori eradication and acid suppression produced an additive effect with a 66% reduction in GM. A positive relationship was detected between the extent of GM and antral H. pylori density, duodenitis score, and antral gastritis score. CONCLUSIONS: This study shows that the extent of duodenal GM is unrelated to the presence or absence of ulceration but is partly due to H. pylori and partly due to acid.

Adult↗
PubMed1996

Risk assessment after acute upper gastrointestinal haemorrhage.

The aim of this study was to establish the relative importance of risk factors for mortality after acute upper gastrointestinal haemorrhage, and to formulate a simple numerical scoring system that categorizes patients by risk. A prospective, unselected, multicentre, population based study was undertaken using standardised questionnaires in two phases one year apart. A total of 4185 cases of acute upper gastrointestinal haemorrhage over the age of 16 identified over a four month period in 1993 and 1625 cases identified subsequently over a three month period in 1994 were included in the study. It was found that age, shock, comorbidity, diagnosis, major stigmata of recent haemorrhage, and rebleeding are all independent predictors of mortality when assessed using multiple logistic regression. A numerical score using these parameters has been developed that closely follows the predictions generated by logistical regression equations. Haemoglobin, sex, presentation (other than shock), and drug therapy (non-steroidal anti-inflammatory drugs and anticoagulants) are not represented in the final model. When tested for general applicability in a second population, the scoring system was found to reproducibly predict mortality in each risk category. In conclusion, a simple numerical score can be used to categorize patients presenting with acute upper gastrointestinal haemorrhage by risk of death. This score can be used to determine case mix when comparing outcomes in audit and research and to calculate risk standardised mortality. In addition, this risk score can identify 15% of all cases with acute upper gastrointestinal haemorrhage at the time of presentation and 26% of cases after endoscopy who are at low risk of rebleeding and negligible risk of death and who might therefore be considered for early discharge or outpatient treatment with consequent resource savings.

Acute Disease↗
PubMed1995

Prospective screening of dyspeptic patients by Helicobacter pylori serology.

Helicobacter pylori infection is associated with 95% of duodenal ulcers and more than 80% of gastric ulcers. Several reports have indicated that screening for H pylori may avoid subsequent endoscopic examination. We screened 183 dyspeptic patients, aged under 45, by taking a history of sinister symptoms and regular use of non-steroidal anti-inflammatory drugs (NSAIDs), together with serological testing for H pylori. Endoscopy was performed on 113 patients, of whom 90 (49%) were seropositive, 14 (8%) had sinister symptoms, and 9 (5%) had used NSAIDs regularly. In 34 (19%) patients we detected peptic ulceration. The remaining 70 (38%) patients who were H pylori seronegative, had no sinister symptoms, and had not taken NSAIDs (screen-negative), did not undergo endoscopy but were returned to their primary care physician for treatment of symptoms. At subsequent reassessment (of the non-endoscoped group), symptom severity (p = 0.002), interference with life events (p = 0.01), and medication (p = 0.0002) were all significantly lower in the 6 months after screening than in the 6 month period before screening. Only three screen-negative patients were re-referred after screening but their endoscopic findings were normal. Thus, 67 (36%) endoscopies were avoided. When the non-endoscoped screen-negative patients were compared with a cohort of endoscoped screen-negative patients, the groups did not differ in terms of symptom severity (odds ratio 1.12, 95% CI 0.53-2.35, p = 0.77) or interference with life events (0.82, 0.38-1.76, p-0.61). However, medication use was significantly less (0.37, 0.17-0.80, p = 0.01) in those who did not have an endoscopy. Our study indicates that colonisation screening based on H pylori serology, a history of sinister symptoms, or a history of NSAID use was worthwhile in dyspeptic patients. We avoided 37% of endoscopies and reduced drug usage without disadvantaging those not endoscoped.

Adult↗
PubMed1995

Variation in outcome after acute upper gastrointestinal haemorrhage. The National Audit of Acute Upper Gastrointestinal Haemorrhage.

Hospital mortality after acute upper gastrointestinal haemorrhage varies widely. In a population-based, multi-centre, prospective survey of the management and outcome of unselected cases of acute upper gastrointestinal haemorrhage, we have assessed the effect of risk standardisation on this variation. We collected data from 74 acute hospitals in four health regions in the UK on patients aged 16 years and over who presented with acute upper gastrointestinal haemorrhage during 4 months in 1993 (3981 cases) and 3 months in 1994 (1584 cases). The overall mortality was 14.3% (798/5565). Crude mortality in individual hospitals ranged from 0% to 29%, and differed significantly from the overall rate in eight. Risk-standardised mortality ratios were calculated with a risk score derived from well-established risk factors. Only two hospitals had standardised mortality ratios significantly different from the reference value. When hospitals were ranked in order of increasing mortality, risk standardisation for age, shock, and comorbidity resulted in 21 of the 74 hospitals changing ranks by ten or more places. After further standardisation for diagnosis, endoscopic stigmata of recent haemorrhage, and rebleeding, 32 hospitals moved ten or more places from their original rank; one hospital moved 45 places. Risk standardisation to correct for variation in case mix results in apparently significant differences in mortality rates becoming non-significant. The current state of routine data collection does not allow for anything but the most basic case-mix adjustment to be made. Simple league tables of crude mortality are misleading in this disorder and cannot be regarded as a reflection of the quality of health care.

Acute Disease↗
PubMed1995

Incidence of and mortality from acute upper gastrointestinal haemorrhage in the United Kingdom. Steering Committee and members of the National Audit of Acute Upper Gastrointestinal Haemorrhage.

OBJECTIVE: To describe the current epidemiology of acute upper gastrointestinal haemorrhage. DESIGN: Population based, unselected, multicentre, prospective survey. SETTING: 74 hospitals receiving emergency admissions in four health regions in the United Kingdom. SUBJECTS: 4185 cases of acute upper gastrointestinal haemorrhage in which patients were aged over 16 years identified over four months. OUTCOME MEASURES: Incidence and mortality. RESULTS: The overall incidence of acute upper gastrointestinal haemorrhage in the United Kingdom is 103/100,000 adults per year. The incidence rises from 23 in those aged under 30 to 485 in those aged over 75. At all ages incidence in men was more than double that in women except in elderly patients. 14% of the haemorrhages occurred in inpatients already in hospital for some other reason. In 27% of cases (37% female, 19% male) patients were aged over 80. Overall mortality was 14% (11% in emergency admissions and 33% in haemorrhage in inpatients). In the emergency admissions, 65% of deaths in those aged under 80 were associated with malignancy or organ failure at presentation. Mortality for patients under 60 in the absence of malignancy or organ failure at presentation was 0.8%. CONCLUSIONS: The incidence of acute upper gastrointestinal haemorrhage is twice that previously reported in England and similar to that reported in Scotland. The incidence increases appreciably with age. Although the proportion of elderly patients continues to rise and mortality increases steeply with age, age standardised mortality is lower than in earlier studies. Deaths occurred almost exclusively in very old patients or those with severe comorbidity.

Acute Disease↗
PubMed1995

Prospective, multicenter study on value of computerized tomography (CT) in gallstone disease in predicting response to bile acid therapy.

The aim of the study was to assess the value of quantitative attenuation values (Hounsfield units) and of gallstone pattern by computerized tomography in predicting response to bile acid therapy. We carried out a prospective study in a multicenter setting on 90 consecutive outpatients with radiolucent gallstones. All received bile acid therapy (UDCA 10 mg/kg/day or UDCA + CDCA 5 mg/kg/day of each) up to two years. Hounsfield units for gallstones were recorded using standardized criteria and six categories of patterns were defined: hypodense, isodense, homogenously dense, laminated, rimmed and speckled. We assessed gallstone dissolution rate (percent reduction in volume), response to therapy (> 25% reduction in volume), and final outcome of therapy. Eighty-one percent of patients with hypodense/isodense and all four patients with speckled stone pattern responded to therapy, whereas none of the 10 patients with laminated/rimmed and only 45% of patients with homogenously dense stone pattern did. Complete dissolution was achieved by 68%, 50%, 35%, 0% of the hypodense/isodense, speckled, homogenously dense, rimmed/laminated gallstones, respectively. The use of Hounsfield units did not show an advantage over gallstone pattern for predicting either response or final outcome to bile acid therapy. We conclude that computerized tomography analysis of gallstones is of value in predicting response to bile acid therapy and that gallstone pattern alone predicts response in most cases without the need for quantitative assessment.

Chenodeoxycholic Acid↗
PubMed1995

Effects of acid suppression on microbial flora of upper gut.

Decreased acid secretion, due to therapy or disease, predisposes to increased bacterial counts in gastric juice. As bacterial numbers increase, the number of nitrate-reducing strains and the concentration of luminal nitrite usually also increase. However, there is controversy (mainly because of assay problems) about whether decreased acid increases generation of N-nitroso compounds: these may be produced by acid or by bacterial catalysis, and the relative contributions of each are still uncertain. Other potentially important factors include ascorbate secretion (can prevent nitrite conversion to nitroso compounds) and the particular spectrum of nitroso compounds produced. Nitrosation of several histamine H2-receptor antagonists has been demonstrated experimentally, but under conditions that are very unlikely to be encountered clinically. Some acid suppressant therapies have been claimed to aid eradication of Helicobacter pylori, but more work is needed to evaluate this. If ulcer treatment regimens do not also address eradication of H. pylori (when present), gastritis will progress, and the recently documented association between H. pylori and gastric carcinoma needs to be considered. Enteric flora probably also increase if acid secretion is markedly reduced: this does not appear to have nutritional consequences but probably reduces the resistance to occasional infections, of which cholera is the best documented.

Antacids↗
PubMed1995

Sensitization to painful distention and abnormal sensory perception in the esophagus.

BACKGROUND/AIMS: The mechanism of abnormal esophageal sensory perception in patients with unexplained chest pain is unknown. The aim of this study was to test the following two hypotheses: (1) similar to cutaneous nociceptors, esophageal stretch receptors can be sensitized by a noxious chemical stimulus, and (2) patients with esophageal chest pain have sensitized receptors. METHODS: Twenty-five patients with noncardiac chest pain underwent esophageal manometry, provocation tests, and 24-hour pH monitoring. Eleven patients had positive and 14 had negative results of esophageal provocation tests. Esophageal perception and pain thresholds for balloon stretch (in milliliters) and electrical stimulation (in milliamperes) were determined in patients and 7 healthy controls performed before and after randomized, double-blind esophageal perfusion with normal saline or 0.1N HCl. RESULTS: The basal balloon pain threshold was lower in patients with positive results of esophageal tests than in either those patients with negative results of esophageal tests or controls (P < 0.05). After acid perfusion, balloon perception and pain thresholds decreased in patients with negative results of esophageal tests (P < 0.05) and in controls (P < 0.05) but not in patients with positive results of esophageal tests. No change occurred after saline perfusion nor in electrical pain thresholds in any group after the perfusion of either fluid. CONCLUSIONS: In patients with negative results of esophageal tests and in controls, the pain threshold to balloon distention is lowered by acid. The lack of such effect in patients with positive results of esophageal tests implies that pain receptors may already be sensitized.

Acids↗
PubMed1995

Postprandial gallbladder motor function: refilling and turnover of bile in health and in cholelithiasis.

BACKGROUND & AIMS: Impaired gallbladder emptying is implicated in gallstone disease. Ultrasonography and scintigraphy have shown conflicting results because the former is influenced by postprandial refilling, whereas the latter is not influenced by refilling. The aim of this study was to measure postprandial refilling and turnover of bile by combining the two techniques. METHODS: Simultaneous scintigraphy and ultrasonography were used in 14 patients with gallstones and 11 healthy controls. Measurements were performed while the patients were fasting and at 10-minute intervals after a standard meal for 90 minutes, and the measurements were used to calculate postprandial refilling, turnover of bile (in milliliters), and turnover index. RESULTS: Ultrasonography and scintigraphy provided different gallbladder emptying patterns. Compared with controls, patients with gallstones had impaired emptying by both scintigraphy (P < 0.0001) and ultrasonography (P < 0.01). Postprandial refilling and turnover were both reduced between 60 and 90 minutes (P < 0.05), and the turnover index was markedly reduced (1.8 vs. 3.5; P < 0.001). CONCLUSIONS: Simultaneous scintigraphy and ultrasonography provide a new model of gallbladder motor function showing that refilling begins immediately postprandially. In healthy controls, the gallbladder postprandially handles up to six times its basal volume within a period of 90 minutes, but this turnover of bile is markedly reduced in cholelithiasis causing a reduced washout effect of the gallbladder contents, including cholesterol crystals.

Analysis of Variance↗
PubMed1995

Soluble E-selectin and vascular cell adhesion molecule-1 (VCAM-1) in primary biliary cirrhosis.

BACKGROUND/AIMS: E-selectin and vascular cell adhesion molecule-1, important in leucocyte adhesion, have recently been detected in soluble form in the circulation. However, their clinical significance remains unclear. Our aims were to determine whether the levels of these molecules are increased in primary biliary cirrhosis, and to relate these to histological disease stage, biochemical measures of liver damage and to lymphocyte activation. METHODS: We studied 42 patients with primary biliary cirrhosis, nine with primary sclerosing cholangitis, 14 with alcoholic liver disease and 17 healthy subjects. Circulating E-selectin and vascular cell adhesion molecule-1 levels were measured by enzyme-linked immunosorbent assay. In subgroups of patients with primary biliary cirrhosis, hepatic bile acid uptake and excretory rates and T-cell activation were also determined. RESULTS: Soluble E-selectin and vascular cell adhesion molecule-1 levels were significantly elevated in primary biliary cirrhosis compared to healthy controls. However, there was no difference between primary biliary cirrhosis and other liver disease groups. In primary biliary cirrhosis, both adhesion molecules correlated with disease stage, but differed in their relationships with specific liver function tests. They did not correlate with either hepatic bile acid uptake or excretion, or lymphocyte activation. CONCLUSIONS: We conclude that soluble E-selectin and vascular cell adhesion molecule-1 are elevated in chronic liver diseases. In primary biliary cirrhosis, they reflect the stage of disease and may reflect the degree of leucocyte adhesion and migration.

Adult↗
PubMed1995

Chlamydia pneumoniae: risk factors for seropositivity and association with coronary heart disease.

BACKGROUND: Two studies have suggested that seropositivity for Chlamydia pneumoniae (C. pneumoniae) is a risk factor for coronary heart disease (CHD) but the association remains tenuous. Further data is required in other populations to consolidate this observation. AIMS: Initially to determine descriptive risk factors for C. pneumoniae seropositivity in a general population sample and subsequently to examine the relation of seropositivity for this organism to CHD for the first time in a British population. SETTING: A single general practice health screening clinic and a cardiology clinic involving patients predominantly residing in south London and Surrey. SUBJECTS: 210 consecutive caucasian men (62%) and women (38%) aged 18-79 including 67 men aged 45-65. This latter group acting as controls were then also compared with 103 consecutive males aged 45-65 with angiographically confirmed coronary heart disease. METHODS: A questionnaire was administered by a research nurse and serum was analysed for IgG and IgA against C. pneumoniae and other Chlamydiae by a microimmunofluorescence test. Serum was said to be low positive at a specific IgG antibody titre of 16-32, and high positive if 64 or greater. RESULTS: Amongst the general practice health screening clinic population 14 subjects (7%) were excluded due to possible cross-reactivity with other Chlamydia species (predominantly C. trachomatis). Of the remaining 196 subjects, 13 (6%) had high positive C. pneumoniae IgG titres, 68 (35%) had low titres and 125 had no detectable antibody. After adjustment for sex, age, smoking history, social class and family size only one risk factor for high positive titres in this group was identified, which was the number of children currently living in the home (OR 2.29 (1.09-4.80), P = 0.03). No factors were significantly related to low titres. 22/100 (22%) cases with coronary heart disease and 3/64 (4.7%) of controls had high positive IgG titres for C. pneumoniae. Similarly 21% of cases and 9.4% of controls had positive C. pneumoniae specific IgA serology. 45% of cases and 44% of controls had low C. pneumoniae IgG titres. The association of CHD with a C. pneumoniae IgG titre of 64 or above was independent of all risk factors (OR 7.4 (1.7-33.1), P < 0.01). CONCLUSION: Serological evidence of C. pneumoniae infection is common amongst healthy British subjects. Smoking and social class are not important confounding variables in this study. Reinfection from contact with infected children in the home may be important in inducing higher titres in some subjects. These higher titres are more prevalent in subjects with coronary heart disease in the U.K. as reported in Finland and the U.S.A., and provide further evidence that C. pneumoniae may be important in the pathogenesis of this condition in these populations.

Adolescent↗
PubMed1995

Direct assessment of the mechanism for a raised serum bile acid level in chronic liver disease.

BACKGROUND: Impaired hepatic uptake is the major cause of raised serum bile acid levels in liver disease, but confirmation in humans by direct measurement is lacking. The synthetic gamma-labelled bile acid 75Se-homocholic acid taurine (75SeHCAT) provides a tool for the direct measurement of hepatic bile acid handling. OBJECTIVE: To determine the interrelationships among hepatic handling of 75SeHCAT, the kinetics of its disappearance from plasma and serum bile acid levels in patients with chronic liver disease. DESIGN: We studied 12 patients with primary biliary cirrhosis and 14 with cirrhosis arising from other causes. Fasting serum bile acid levels were measured enzymatically. After intravenous administration of 75SeHCAT, we determined plasma disappearance rates (initial K1, late K2) from serial blood samples and hepatic uptake and excretory rates directly from dynamic abdominal gamma-camera scanning. Both scanning and sampling were carried out over a period of 90 min. RESULTS: Serum bile acid concentrations correlated with K1 and with hepatic uptake (Rs = -0.53, P < 0.01; Rs = -0.47, P < 0.02, respectively) but neither with K2 nor with the excretory rate. K1 and uptake were reduced (P < 0.05) in patients with high serum bile acid levels and in those with varices. Serum bile acid levels were higher in patients with varices (P < 0.05), which might suggest that portosystemic shunting occurred. However, this is unlikely because the varices were not independent of liver function. CONCLUSION: Hepatic bile acid uptake and excretion are independent processes. Hepatic uptake is related to initial, whereas hepatic excretion is related to late, plasma disappearance. Impaired hepatic uptake is a major determinant of the rise in serum bile acid levels in chronic liver disease.

Adult↗
PubMed1995

The effects of unsaturated fatty acids on Helicobacter pylori in vitro.

The effects of three unsaturated free fatty acids on Helicobacter pylori growth in vitro was determined. Growth of H. pylori in Brucella broth was inhibited in a dose-dependent manner by arachidonic, linoleic and oleic acids. The degree of inhibition at any one concentration was related to the degree of fatty acid unsaturation. Triolein, a triacylglycerol ester of oleic acid did not inhibit growth. Inhibition of H. pylori growth was associated with disruption of cell membranes. Incubation with 14C linoleic acid and 14C oleic acid showed incorporation of these fatty acids into H. pylori cell mass and phospholipids leading to alteration of the phospholipid composition of the organism. Incorporation was greater with linoleic than oleic acid and this was associated with a greater inhibition of growth. These findings indicate that H. pylori is sensitive to unsaturated free fatty acids through their incorporation into phospholipids and membrane destruction. This may have therapeutic implications.

Arachidonic Acids↗
PubMed1995

Effect of Helicobacter pylori eradication on gastric metaplasia of the duodenum.

Helicobacter pylori associated duodenal ulcers occur in patches of gastric metaplasia. The pathogenesis of gastric metaplasia is unclear, but it has been produced in experimental animals by acute injury and has been shown to be present to a greater extent of H pylori positive subjects. This study aimed to discover if gastric metaplasia regressed with eradication of H pylori or healing of duodenal ulcers, or both. Thirty two duodenal ulcer patients with H pylori infection confirmed by biopsy urease test and by antral histological examination were studied. Patients were treated with triple therapy (deNol 240 mg twice daily, amoxycillin 500 mg three times daily, and metronidazole 400 mg three times daily) for two weeks after the first endoscopy and were subsequently re-endoscoped. Three duodenal bulb biopsy specimens were obtained per patient at each endoscopy. Biopsy sections were stained with haematoxylin and eosin to determine the severity of duodenitis, and with diastase periodic acid-Schiff/alcian blue to assess the extent of gastric metaplasia. Slides were assessed by two histopathologists unaware of treatment status. H pylori was eradicated in 63% of subjects and all ulcers were healed at follow up. The median extent of gastric metaplasia at the start of treatment and 6-18 months (median 10) after treatment was compared in the two groups. Gastric metaplasia declined in eradicators from 16% to 8% (p < 0.05) while in non-eradicators there was no significant change (25% initially and at follow up). A positive relation between extent of gastric metaplasia and duodenal inflammation score was present before treatment (r(s) = 0.74, p < 0.001) and was unchanged after treatment in the non-eradicator group (r(s) = 0.89, p < 0.001). In the eradicator group, however, the inflammation score had significantly declined (p < 0.02) and the close relation with gastric metaplasia was no longer present. These results suggest that H pylori itself is at least in part responsible for producing gastric metaplasia of the duodenum.

Adult↗