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Biomedical subjects

N Hudson

Publications and source records attributed to N Hudson.

At least 55 records · Page 3Linked to original sources
PubMed1994

Amoxycillin capsules with omeprazole for the eradication of Helicobacter pylori. Assessment of the importance of antibiotic dose timing in relation to meals.

BACKGROUND: Giving antibiotics after meals prolongs their gastric residence time and improves their intragastric distribution. We aimed to see whether this would result in improved eradication of Helicobacter pylori. METHODS: Eighty patients with H. pylori infection were treated with 40 mg omeprazole in the morning for 28 days and amoxycillin 500 mg q.d.s. for days 15-28. Amoxycillin dosing was randomised to either 1 h before or 10 min after food. Good compliance was pre-defined as missing less than four doses of amoxycillin or two of omeprazole. RESULTS: Amoxycillin dosing after meals was shown not to affect H. pylori eradication rate either when results were analysed on an intention-to-treat basis [amoxycillin before meals successful in 63% (25/40), after in 65% 26/40)] or for good compliers only [before meals 81% (17/21), after 71% (20/28)]. This excludes, with 95% confidence, a benefit of greater than 18% from dosing before, or 23% from dosing after meals. Good compliance, however, was shown to be important, with H. pylori eradication in 76% (37/49) of good compliers compared with 48% (11/23) of others completing the protocol (P < 0.05). CONCLUSIONS: The timing of antibiotic administration in relation to meals is not important in the treatment of H. pylori infection with this regimen of amoxycillin capsules and omeprazole. Good compliance, is however, an important determinant of treatment success.

Adolescent↗
PubMed1994

Distal biliary stricture as a complication of sclerosant injection for bleeding duodenal ulcer.

A patient undergoing repeated endoscopic injection therapy for important bleeding from a duodenal ulcer developed intestinal perforation followed by extrahepatic obstructive jaundice resulting from benign biliary stricture. It is proposed that these complications were a consequence of the use of ethanolamine oleate as part of the injection regimen and caution against the use of this material is needed, particularly as current clinical trials suggest that sclerosants offer no advantage over injection therapy with dilute adrenaline alone.

Aged↗
PubMed1994

Interobserver variation in assessment of gastroduodenal lesions associated with non-steroidal anti-inflammatory drugs.

Video endoscopic images were used to investigate whether gastroenterologists could agree on the definition of lesions within the stomach seen at endoscopy, with particular reference to those seen in patients taking non-steroidal anti-inflammatory drugs. Seven experienced endoscopists, unaware of the patients' clinical history or drug consumption, recorded their classification for 93 randomised video images of gastric lesions. There was complete agreement in the diagnosis of ulceration for nine images from patients who were not taking non-steroidal anti-inflammatory drugs; eight of nine were classified as deep ulcers, with 86% agreement for this subclassification. By contrast, the overall agreement for lesions in patients taking non-steroidal anti-inflammatory drugs was only 55%. Only nine of 44 ulcers were subclassified as deep, and there was considerable cross classification of non-haemorrhagic erosions and ulcers. In conclusion, ulcers that occur in patients taking non-steroidal anti-inflammatory drugs differ from those in patients who are not taking these drugs in that they are often more superficial and difficult to distinguish from erosions. The prognostic importance of these lesions is, therefore, uncertain.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1994

Localization of ovine follistatin and alpha and beta A inhibin mRNA in the sheep ovary during the oestrous cycle.

The sites of follistatin and alpha and beta A inhibin gene expression were examined by in situ hybridization in sheep ovaries during the early and mid-luteal phases (days 3 and 10) of the oestrous cycle and a prostaglandin F2 alpha (PGF 2 alpha)-induced follicular phase. Follistatin mRNA was detected in the granulosa cells of preantral, antral and early atretic follicles at all stages of the oestrous cycle, and in the corpora lutea at the early and mid-luteal stages of the cycle. However, only low levels of expression of follistatin were observed in the presumptive preovulatory follicle at 56 h after treatment with PGF 2 alpha. Both alpha and beta A inhibin were shown to be expressed in ovaries at all stages of the oestrous cycle. In situ hybridization localized alpha subunit mRNA to the granulosa cells of most, but not all, healthy antral follicles, and to no other ovarian cell type. In contrast, expression of the beta A subunit was confined to a few medium-to-large healthy antral follicles. In antral follicles expressing beta A inhibin, mRNAs for alpha inhibin and follistatin were always detected, but the converse was not true. Unlike follistatin, no alpha and beta A inhibin expression was seen in preantral follicles, developing corpora lutea, or follicles undergoing atresia. These results show that, in the adult sheep ovary, follistatin gene expression is a constitutive event in all growing follicles from the early preantral stage, and also provide indirect evidence of the involvement of follistatin, but not inhibin or activin, in the early stages of ovarian follicle development in sheep.

Animals↗
PubMed1993

Ileo-caecal ulceration associated with the use of diclofenac slow release.

A 38-year-old man with seropositive arthropathy on long-standing treatment with diclofenac slow release presented with abdominal pain, diarrhoea and anaemia. Upper gastrointestinal endoscopy and barium series were unremarkable. Five months later he presented with a right iliac fossa mass. Investigations revealed discrete ulceration in the terminal ileum and caecum confirmed at laparotomy. Other possible causes of intestinal ulceration were excluded suggesting a diagnosis of non-steroidal anti-inflammatory drug associated intestinal ulceration.

Adult↗
PubMed1993

Ranitidine bismuth citrate and aspirin-induced gastric mucosal injury.

The aim of this study was to investigate the protective action of a new compound, ranitidine bismuth citrate, in the prevention of aspirin-induced acute mucosal injury to the upper gastrointestinal tract of healthy human volunteers. In a double-blind randomized three-way cross-over study 24 male volunteers received placebo, 900 mg aspirin or 900 mg aspirin and 800 mg ranitidine bismuth citrate at 12-h intervals for nine doses with a 2-week wash-out period between each treatment. The median (interquartile range) number of erosions seen at endoscopy when ranitidine bismuth citrate was given with aspirin (1 [0-4]) was significantly lower than aspirin alone (24 [16-32]) (P < 0.001) and not significantly different from either baseline or placebo (0 [0-2]). These findings were similarly reflected in the effects on microbleeding following the ninth dose: 12.1 (7.1-21.0) microL/10 min following aspirin alone compared to levels with placebo of 1.2 (0.4-2.9), and with aspirin and ranitidine bismuth citrate of 1.6 (0.8-2.6) (P < 0.005). Ranitidine bismuth citrate conferred substantial protection from aspirin-induced injury to the gastric and duodenal mucosa as determined by both endoscopic assessment and microbleeding rates, reducing injury to placebo levels.

Adult↗
PubMed1993

Enhanced gastric mucosal leukotriene B4 synthesis in patients taking non-steroidal anti-inflammatory drugs.

The effects of longstanding non-steroidal anti-inflammatory drug (NSAID) treatment on gastric mucosal synthesis of leukotriene B4 (LTB4), leukotriene C4 (LTC4), and prostaglandin E2 (PGE2) was studied. Gastric antral biopsies in 65 patients with arthritis taking NSAIDs and 23 control patients were taken and eicosanoid concentrations, stimulated by vortex mixing or calcium ionophore, were measured by radioimmunoassay. Median gastric mucosal synthesis of LTB4 was increased in patients taking NSAIDs compared with non-users: (0.9(0.2-2.5) pg/mg v 0 (0-0.6) pg/mg (p < 0.001)). These differences persisted when subgroups of patients were analysed according to Helicobacter pylori colonisation or degree of mucosal injury. Synthesis of LTB4 was strongly associated with the presence of type C (chemical) gastritis. Increased synthesis of LTC4 was associated with Helicobacter pylori colonisation but not NSAID use. Synthesis of PGE2 was decreased in patients taking NSAIDs compared with control patients (p < 0.001). Enhanced gastric mucosal synthesis of LTB4 in patients taking NSAIDs may represent a primary effect of these drugs and could be implicated in the pathogenesis of gastritis and ulceration associated with NSAIDs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Effect of Helicobacter pylori colonisation on gastric mucosal eicosanoid synthesis in patients taking non-steroidal anti-inflammatory drugs.

Colonisation with Helicobacter pylori may influence susceptibility to gastroduodenal injury and ulceration in patients taking non-steroidal anti-inflammatory drugs (NSAIDs). The aim of this study was to determine if Helicobacter pylori colonisation altered eicosanoid synthesis by gastric mucosa in these patients. Sixty five patients with long-standing NSAID intake and 23 control subjects underwent endoscopy. In vitro gastric antral biopsies were stimulated by vortex mixing and eicosanoid measurements determined by radioimmunoassay. Helicobacter pylori colonisation was determined by a CLO test (a gel based rapid urease test) and histological assessment. Median prostaglandin E2 synthesis by gastric mucosa was 61.0 (interquartile range: 19.2-73.1) pg/mg in control subjects colonised with Helicobacter pylori compared with 46.5 (23.3-65.5) pg/mg in Helicobacter pylori negative subjects. This was not significantly different. Treatment with NSAIDs was associated with a significant difference (p < 0.001) in prostaglandin E2 (PGE2) synthesis between those colonised with Helicobacter pylori (37.5(22.0-77.3) pg/mg) compared with patients not infected (12.6(7.0-19.3) pg/mg). Values in patients taking NSAIDs who were colonised were not different from control subjects. Synthesis of PGE2 was strongly associated with type B (chronic active), but not type C (chemical) gastritis. Dyspeptic symptoms were more common in subject colonised with Helicobacter pylori (p < 0.002) and were associated with higher PGE2 synthesis. In patients taking NSAIDs Helicobacter pylori colonisation removes rather then enhances depression of PGE2 synthesis associated with NSAIDs and may promote dyspepsia associated with ulcers and prevent superficial mucosal injury.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Evaluation of changes in myocardial perfusion and function on exercise in patients with coronary artery disease by gated MIBI scintigraphy.

OBJECTIVE: To investigate the ability of gated methoxy-isobutylisonitrile (MIBI) scintigraphy to measure changes in myocardial function as well as perfusion with exercise. SETTING: Regional cardiothoracic centre. PATIENTS: 43 presenting with chest pain, 28 with coronary artery disease on angiography, and 15 with normal coronary arteriograms. RESULTS: Gated perfusion images showed an improvement in detecting regions with stenosed arteries compared with non-gated images (38/55 v 31/55, p < or = 0.01)). Functional analysis showed an increase in fractional shortening of 4.11% in subjects with normal coronary arteries, whereas in those with coronary disease a fall of 0.57% was found (p < or = 0.01). Both perfusion and function imaging showed an improved sensitivity compared with standard exercise testing (p < or = 0.01). When both function and perfusion imaging were analysed all patients with coronary disease were detected. There was agreement in abnormal regions in 33/55 territories supplied by a stenosed artery. Combined perfusion and function detected 49/55 (89%) of abnormal regions, thus improving the overall sensitivity from 38/55 (69%) by perfusion imaging alone (p < or = 0.01). CONCLUSIONS: Gated methoxy-isobutylisonitrile scintigraphy can successfully evaluate perfusion and function on exercise, so improving the diagnostic usefulness of this agent.

Adult↗
PubMed1992

Ranitidine: differential effects on gastric bleeding and mucosal damage induced by aspirin.

This study investigated the influence of ranitidine on mucosal injury and gastric bleeding in 20 normal volunteers taking 600 mg aspirin q.d.s. This study was a double-blind placebo controlled crossover study comparing ranitidine, as 150 mg b.d., 300 mg q.d.s. and 600 mg b.d. with placebo. Gastric mucosal injury was assessed at unsedated endoscopy by counting haemorrhagic and non-haemorrhagic erosions; bleeding was measured in gastric washings. Aspirin alone increased mucosal injury from 0 to 11.4 erosions (mean, P < 0.01) and bleeding from 1.77 to 9.11 microliters blood/10 min (mean P < 0.001). Ranitidine prophylaxis reduced bleeding to 5.34, 3.18 and 3.47 microliters/10 min with 150 mg b.d., 300 mg q.d.s. and 600 mg b.d. respectively (overall effect of ranitidine P < 0.001) and also reduced haemorrhagic erosions though it had no effect on the total number of erosions. Ranitidine is effective at reducing aspirin-induced gastric bleeding and whilst not reducing aspirin-induced gastric erosions, it does reduce the number that appear haemorrhagic. Ranitidine may have a role in the prophylaxis of aspirin-induced gastric bleeding.

Adult↗
PubMed1992

Mechanisms of gastric and duodenal damage and protection.

By binding to the cyclooxygenase enzyme, non-steroidal, anti-inflammatory drugs (NSAIDs) inhibit synthesis of prostanoids characteristic of the cell under consideration. For the gastric mucosa, the main products are prostaglandin (PG) E2 or PGI2; for platelets the main product is thromboxane. Aspirin irreversibly acetylates the cyclooxygenase enzyme. Consequently, it has more prolonged effects, particularly in cells like platelets, which are not rapidly turned over. Prostaglandin-dependent protective actions in the stomach and duodenum which are inhibited by NSAIDs include mucous and bicarbonate secretion, surface epithelial cell hydrophobicity and mucosal blood flow. Prostaglandins are also protective of the microvasculature and can increase the flux of water from serosa to mucosa, with possible dilution of injurious substances. Abrogation of these properties renders the mucosa more vulnerable to injury. In addition, salicylates have topical irritant properties. A number of repair mechanisms, including epithelial cell division and possibly angiogenesis, are prostaglandin dependent. As a consequence of these actions, acute damage and ulcers develop more easily and ulcers heal more slowly when individuals take NSAIDs. In some cases the anti-hemostatic effects of NSAIDs may be partly instrumental, and data in model systems have shown that aspirin and possibly piroxicam can enhance intragastric bleeding separately from their effects of mucosal injury. Smoking, which predisposes to peptic ulceration, also appears to reduce mucosal prostaglandin synthesis. Other predisposing factors such as age, sex and the ulcer diathesis have little effect. Some have found Helicobacter pylori to enhance leukotriene synthesis. We have shown that NSAIDs are also associated with increased leukotriene B4 as well as reduced prostaglandin synthesis in patients taking NSAIDs long term.

Animals↗
PubMed1991

Separation of the impairment of haemostasis by aspirin from mucosal injury in the human stomach.

1. An increasing body of data suggests that the antihaemostatic as well as the ulcerogenic actions of aspirin and other non-steroidal anti-inflammatory drugs may be operative when patients present with haematemesis and melaena. 2. We therefore developed methods to allow separate evaluation of the erosive and anti-haemostatic actions of aspirin in the human gastric mucosa. Volunteer subjects took 300 mg of aspirin daily in the morning or 600 mg of aspirin four times a day for 5 days under blinded randomized conditions. Changes in spontaneous gastric microbleeding, endoscopic signs of injury, spontaneous bleeding per gastric erosion, biopsy-induced bleeding and eicosanoids were studied. 3. Both doses of aspirin significantly inhibited gastric mucosal synthesis of prostaglandin E2 and reduced the serum thromboxane concentration. Erosions developed and regressed rapidly; compared with baseline 300 mg of aspirin daily in the morning caused substantial numbers of gastric erosions to develop (mean 5.3, 95% confidence limits 2.7-10.2) but this was significantly less than that caused by 600 mg of aspirin four times a day (10.9, 7.2-16.5, P less than 0.05). The presence of erosions was associated with enhanced spontaneous bleeding, but only during aspirin administration. 4. Aspirin significantly increased bleeding induced by mucosal biopsy and was associated with significant enhancements in the rate of bleeding per gastric erosion. Bleeding rate per erosion but not biopsy-induced bleeding showed a significant dose-related increase with 600 mg of aspirin four times a day. Enteric coating reduced endoscopic signs of injury, but did not affect the impaired haemostasis caused by aspirin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

The areas ratio of normal arterial junctions and its implications in pulse wave reflections.

STUDY OBJECTIVE: The aim of the study was to establish measurements for the area ratios of normal arterial junctions at various anatomical sites in order to estimate the significance of pulse wave reflections in the healthy arterial system. DESIGN: Coronary cineangiograms were used for the coronary junctions measurements and routine arteriograms for the rest of the junctions studied. A pair of digital calipers served to take measurements at a distance of one vessel diameter from the junction centre. MEASUREMENTS AND MAIN RESULTS: A bell shaped distribution of arterial area ratios was found with mean value for coronary bifurcations of 1.179 (95% confidence limits, 1.138-1.220). Slightly higher values were found for the higher order coronary junctions. Other junctions had similar area ratio values with the exception of the aortoiliac junctions where the area ratio was found 0.848 (0.775-0.920). Overall area ratio was 1.14 (1.113-1.167). Asymmetrical coronary bifurcations had higher area ratio than symmetrical ones (p less than 0.05). CONCLUSIONS: In the majority of cases the area ratios are in close agreement with the theoretically predicted values for forward matched junctions. Minimal pulse wave reflections are therefore expected to arise from the junctions of a healthy arterial system. We therefore consider that, contrary to the established view, the presence of reflected waves in the central arterial system is a potential pathological phenomenon and not a characteristic of the healthy system. This may have important theoretical implications for the way hemodynamic findings are interpreted. Finally we suggest that arterial area ratio can be considered as another criterion of normality of arterial junctions in the interpretation of angiograms.

Anthropometry↗
PubMed1990

Effect of long-term hypophysectomy on ovarian follicle populations and gonadotrophin-induced adenosine cyclic 3',5'-monophosphate output by follicles from Booroola ewes with or without the F gene.

Long-term (i.e. approximately 70 days) hypophysectomy led to a significant (P less than 0.05) reduction in ovarian weight but no reduction in the total number of antral follicles (greater than 0.1 mm in diameter). In hypophysectomized ++ Booroola ewes (N = 8) follicles were always less than or equal to 3 mm and in hypophysectomized FF Booroola ewes (N = 6) follicles were always less than or equal to 2 mm in diameter; in ewes of both genotypes follicles reached diameters which were approximately 40% of their predicted final size at ovulation. Under in-vitro conditions, follicles from the FF and ++ hypophysectomized ewes produced significant increases in cAMP within 1 h of exposure to gonadotrophins (P less than 0.05) although no genotypic differences in cAMP production were noted. We conclude that ovarian follicles in FF and ++ ewes have absolute requirements for pituitary hormone on reaching diameters of 2 mm and 3 mm respectively and that appreciable numbers of antral follicles in ewes of both genotypes remain responsive to pituitary gonadotrophins despite prolonged deprivation of these hormones.

Animals↗