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Biomedical subjects

I N Marks

Publications and source records attributed to I N Marks.

At least 19 recordsLinked to original sources
PubMed1992

Helicobacter pylori lipopolysaccharide stimulates gastric mucosal pepsinogen secretion.

The effect of Helicobacter pylori lipopolysaccharide on guinea pig gastric mucosal pepsinogen secretion has been examined using an Ussing chamber technique. Luminal addition of H. pylori lipopolysaccharide resulted in a fifty-fold stimulation of pepsinogen secretion compared to a twelve-fold increase with E. coli lipopolysaccharide. Electron microscopy showed marked degranulation of zymogen granules but no evidence of chief cell disruption.

Animals↗
PubMed1992

Changes in nocturnal and peak acid outputs after duodenal ulcer healing with sucralfate or ranitidine.

Changes in basal and stimulated acid secretion after duodenal ulcer healing have been previously shown to be influenced by the nature of the treatment. This study aimed to determine possible changes in nocturnal acid secretion on duodenal ulcer healing in patients treated with sucralfate or ranitidine. Nocturnal acid output and peak acid output in response to pentagastrin stimulation were studied in 20 patients before and after duodenal ulcer healing with sucralfate (n = 9) or ranitidine (n = 11). Details regarding cigarette smoking were obtained from each subject. Median 10 hour nocturnal acid output fell significantly (p less than 0.05) from 82.4 (29.1-188.3) mmol (median range) to 45.2 (14.7-144.4) mmol after healing with sucralfate, and rose significantly (p less than 0.05) from 54.7 (16.8-74.3) mmol to 86.2 (11.7-118.1) mmol after ulcer healing with ranitidine. Peak acid output fell from 39.6 (22.0-52.8) mmol/hour to 27.8 (13.8-38.2) mmol/hour (p less than 0.01) after healing with sucralfate and was unchanged after healing with ranitidine. There was no correlation between smoking and nocturnal acid output. These results provide further evidence that acid secretion decreases with sucralfate healing and remains the same or may even increase after ranitidine healing.

Adult↗
PubMed1992

Triple therapy with sucralfate is as effective as triple therapy containing bismuth in eradicating Helicobacter pylori and reducing duodenal ulcer relapse rates.

Duodenal ulcer relapse rates after therapy with sucralfate or bismuth are lower than those after H2-receptor antagonist therapy. This may be mediated by an antibacterial effect of these drugs on Helicobacter pylori. Bismuth has become an integral part of 'triple therapy' because of its documented anti-H. pylori effect. In vitro and clinical data suggest that sucralfate may also have an anti-H. pylori effect. The aim of this randomized, prospective therapeutic trial was to compare the efficacy of triple therapy containing bismuth with that containing sucralfate and to determine the effect of therapy with these combinations on duodenal ulcer relapse. Forty H. pylori-positive duodenal ulcer patients were healed with omeprazole and randomized to receive either 1 g sucralfate four times daily or 120 mg bismuth compound four times daily. All patients received 400 mg metronidazole three times daily and either 250 or 500 mg tetracycline four times daily for 7-14 days. Thirty-five patients could be analysed. Overall eradication rates did not differ in the treatment groups (10 of 17 eradicated with sucralfate and 11 of 18 with bismuth). Relapse rates were significantly lower in the eradicated group (1 of 21 compared with 8 of 14 in the non-eradicated group) and did not differ between treatment groups in those patients not eradicated. A triple therapy regimen utilizing sucralfate appears to be as effective as the bismuth-containing regimen.

Bismuth↗
PubMed1992

Acid secretion, 1932-92: advances, adaptations, and paradoxes.

This paper reviews the evolution of our understanding of various aspects of gastric acid secretion over the past 60 years. Embryologic aspects and neonatal acid secretion are considered, and the relationship between parietal cell mass and acid secretion and the changing concepts of parietal cell activation are discussed. The effect of aging on acid secretion and the relevance of acid secretion in health and disease are reviewed, and current views on adaptation to therapeutic inhibition of acid secretion presented. The aetiologic link between acid secretion and ulcer disease is re-examined, and the role of pepsin, growth factors, and Helicobacter pylori briefly considered.

Adaptation, Physiological↗
PubMed1991

Acid secretory responses and parietal cell sensitivity following duodenal ulcer healing with omeprazole, sucralfate, and Maalox.

Acid secretory responses and parietal cell sensitivity (PCS) have been studied in 21 duodenal ulcer patients before and after successful treatment with omeprazole (n = 7), sucralfate (n = 7), or Maalox (n = 7). The second study was carried out 3 days after documented healing and withdrawal of treatment in the sucralfate- and Maalox-treated groups and 14 days after documented healing and withdrawal of treatment in the omeprazole-treated patients. Acid output (mmol/hour) was measured as basal secretion, and in response to 0.1 microgram/kg/hour pentagastrin (low-dose) and 6.0 micrograms/kg/hour pentagastrin (high-dose) stimulation. PCS was calculated as the ratio of low dose:high dose acid output (expressed as a percentage). Ulcer healing with sucralfate resulted in significant (p less than 0.05) decreases in low-dose acid output from 36.4% (13.2-51.0) (median [range]) to 8.4% (3.2-45.4) mmol/hour and PCS from 69.1% (44.9-91.4) to 22.0% (16.0-85.6), whereas no significant decreases in any of the measured parameters were noted following ulcer healing with Maalox. Ulcer healing with omeprazole resulted in significant (p less than 0.05) decreases in basal acid output from 6.3 (1.5-22.9) (median [range]) to 2.2 (0-6.9) mmol/hour, and low-dose acid output from 31.0 (6.0-58.0) to 23.0 (1.4-44.8) mmol/hour. These findings suggest that acid secretory responses following ulcer healing vary according to the therapeutic agent used.

Adult↗
PubMed1991

Acid secretory changes and early relapse following duodenal ulcer healing with ranitidine or sucralfate.

Controversial aspects relating to acid secretory changes following duodenal ulcer healing, and the effect of histamine-2 (H2)-receptor blockers on such changes are discussed. Recent studies comparing the effects of ranitidine or sucralfate on changes in the acid secretory responses in the healing of duodenal ulcers are described, and the relevance of these changes to early relapse considered. The duration of therapy and timing of acid-secretory studies and endoscopies are standardized in all studies, but the acid-secretory parameters vary. These comprised acid secretory responses to graded doses of an intravenous infusion of pentagastrin or histamine, sham-feeding responses, and basal and nocturnal acid secretion. In all studies, healing with sucralfate was associated with a significant decrease in the various parameters of acid secretion. In the ranitidine-healed groups, no appreciable decrease was noted and there was, indeed, a significant increase in nocturnal acid secretion. Routine endoscopies performed 4-6 weeks after documented ulcer healing showed a recurrence of 3 of the 32 (9%) sucralfate-healed and in 14 of the 35 (40%) ranitidine-healed ulcers. Increased acid secretory responsiveness following duodenal ulcer healing was strongly correlated with subsequent early relapse.

Clinical Trials as Topic↗
PubMed1991

Reflux esophagitis therapy: sucralfate versus ranitidine in a double blind multicenter trial.

Sucralfate (Sc) suspension 6 g/day and ranitidine (Rn) tablets, 150 mg, were compared in 125 patients in a double-blind, multicenter, endoscopically controlled trial in the treatment of reflux esophagitis. Inclusion criteria were symptomatic reflux (number and severity of attacks) and endoscopic evidence of esophagitis (grades 1 to 4). Clinical assessments were performed on entry, and at 4 and at 8 weeks, and endoscopy was repeated at 8 weeks. Sc suspension and Rn placebo or Sc placebo and Rn tablets were taken on waking and immediately before retiring at night. Of the 125 patients, 27 were withdrawn because of default (Rn = 4; Sc = 14), noncompliance (Rn = 1; Sc = 2), or the development of congestive cardiac failure (Rn = 1), diarrhea (Rn = 1; Sc = 1), nausea (Sc = 1), constipation (Sc = 1), and hematemesis (Sc = 1). Analysis was performed on the remaining 98 patients, 43 of whom had been treated with Sc and 55 with Rn. Heartburn, acid regurgitation, epigastric pain, dysphagia, and chest pain were relieved in 34% vs 40%, 67% vs 72%, 71% vs 57%, and 86% vs 63% for Sc and Rn, respectively. There was no significant difference between the two groups. Endoscopic healing occurred in 47% of the Sc- and in 31% of the Rn-treated patients (chi 2 = 2.50), and healing or improvement was noted in 81% of the Sc- and 64% of the Rn-treated patients. This difference approached statistical significance (chi 2 = 3.73). There was no obvious endoscopic benefit in 8 of the 43 and 20 of the 55 patients in the groups treated with Sc and Rn, respectively. Although the findings with sucralfate and ranitidine in patients with reflux esophagitis completing the trial suggest a benefit of these agents, the absence of a placebo control group and the high default rates, particularly for those receiving sucralfate, preclude any firm conclusions as to relative or specific efficacy of these agents in this condition.

Administration, Oral↗
PubMed1991

A comparison of omeprazole and ranitidine for duodenal ulcer in South African patients. A multiracial study.

The study was a multicenter double-blind parallel-group comparison of omeprazole, a proton-pump inhibitor, with the H2-receptor antagonist, ranitidine, in 206 patients with duodenal ulcer. There were 145 men and 62 women of mixed racial origin with an average age of 40 years (range 19-76); 63 of them were white, 7 black, 135 coloured and 1 Asian. Each drug was given for four weeks and ulcer healing rate, symptom relief, and adverse events were recorded and compared between treatment groups. Patients received either 20 mg omeprazole once daily in the morning (N = 104) or ranitidine 300 mg once daily at night (N = 106). Healing rates were significantly higher in the omeprazole group than in the ranitidine group at both two weeks (80% vs 52%, P less than 0.001) and four weeks (95% vs 85%, P less than 0.05), using the "per protocol" approach, and these results were confirmed using the "intention to treat" approach. Omeprazole-treated patients reported significantly less daytime epigastric pain (P = 0.02) and heartburn (P = 0.04) after two weeks than ranitidine-treated patients. By four weeks, there were no significant differences in symptom reporting between groups. Both treatments were well tolerated, and there were no serious adverse events.

Adult↗
PubMed1991

Basal and maximum acid output after continuous overnight gastric aspiration.

Basal and maximum acid outputs were measured on two occasions in a group of 15 duodenal ulcer (DU) patients in remission. The initial study was carried out after a nocturnal acid collection, whereas the second was carried out in the conventional manner without preceding nocturnal aspiration. No difference in the basal acid output, concentration, or volume of secretion was found between the two study days. Maximum acid output on the other hand, was significantly (p less than 0.02) reduced from 30.9 (14.2-41.2) mmol/h, median (+range), to 23.7 (8.1-33.7) mmol/h after overnight aspiration. The reduction in maximum acid output was attributable to a fall in the volume of gastric secretion from 280 (170-371) ml to 230 (142-280) ml. No fall in acid concentration was seen. We conclude that overnight gastric aspiration does not affect basal gastric secretion, but reduces the maximum acid output as a result of a reduced secretory volume.

Adult↗
PubMed1991

Sucralfate--safety and side effects.

The safety of sucralfate in terms of aluminium absorption, excretion, tissue accumulation, and toxicity is discussed, with special reference to the small amount of aluminium absorbed, its ready excretion by the normal kidney, and the hazard of toxicity in patients with advanced renal failure. The various manifestations of aluminium toxicity are described, and the notion that Alzheimer's disease should be included in this category is refuted. The clinical relevance of possible intraluminal binding and drug-drug interactions in patients receiving sucralfate therapy is also considered. Evidence is presented to show that sucralfate reduces the hyperphosphataemia in chronic uraemia, albeit at the risk of raised blood aluminium levels, but has no measurable effect on normal phosphate levels in patients with good renal function. The bioavailability of phenytoin, fluoroquinolone antibiotics, and H2-receptor blockers may be impaired by concomitant dosing with sucralfate, but normal kinetics are restored by administering the drug 2 h before sucralfate.

Biological Availability↗
PubMed1990

Simple closure of perforated duodenal ulcer: a prospective evaluation of a conservative management policy.

One hundred and thirteen consecutive patients admitted with a perforated duodenal ulcer over a 5-year period (1978-82) and treated by simple closure have been followed prospectively over a median period of 43 months. Patients were divided into two categories according to their previous history of dyspepsia; group 1 (66 patients) with a chronic history of more than 3 months and group 2 (47 patients) where there was no history of dyspepsia or a history of less than 3 months duration. The follow-up periods were similar (group 1, 44 months; group 2, 43 months). The overall recurrence rate was 42 per cent and to date only 14 per cent of the total group of 113 patients have required a definitive operation. The incidence of ulcer recurrence was higher in group 1 than in group 2 in terms of total recurrence (group 1, 50 per cent; group 2, 32 per cent) and patients requiring further surgery (group 1, n = 14, 21 per cent; group 2, n = 7, 15 per cent). Five of these 21 patients required an emergency procedure for haemorrhage or reperforation (group 1, n = 2; group 2, n = 3). There were no significant differences between the 5-year predictive recurrence rate or the requirement for definitive surgery between the groups. Five of the 27 patients currently on medical treatment have required maintenance treatment while the remaining patients receive active treatment for a mean of 20 per cent of the time since they developed recurrent ulceration. These results support continuation of our 'wait and see' policy following simple closure of perforated duodenal ulcer, even in patients with a history of chronic dyspepsia.

Adult↗
PubMed1990

Common variable hypogammaglobulinemia. A case report.

We describe a patient with severe common variable hypogammaglobulinemia (CVH) whose clinical course was dominated by resistant giardiasis requiring prolonged hospitalization. The giardiasis was eventually controlled by initial metronidazole and subsequent mepacrine therapy, but side effects necessitated the withdrawal of both of these drugs. Replacement immunoglobulin treatment failed to restore normal serum immunoglobulin levels, but despite this, they appeared to be of value in reducing the liability to recurrent giardiasis. We discuss the use of immunoglobulin supplementation in this condition and the frequent association between CVH and pentagastrinfast achlorhydria.

Agammaglobulinemia↗
PubMed1990

Duodenal ulcer healing and acid secretory responses to modified sham feeding and pentagastrin stimulation.

The effect of duodenal ulcer healing on the acid secretory responses to modified sham feeding and maximal pentagastrin stimulation has been studied in 17 patients treated successfully with ranitidine (n = 9) and sucralfate (n = 8). Parietal cell sensitivity was calculated as the ratio of the modified sham feeding response to the peak pentagastrin response, expressed as a percentage. Ulcer healing after sucralfate therapy resulted in significant falls in modified sham feeding stimulated acid output (P less than 0.02), from 9.4 (1.8-17.0) (median + range) to 3.7 (0.2-9.4) mmol/h; in peak acid output (P less than 0.05) from 42.8 (23.0-61.4) to 27.7 (7.2-51.0) mmol/h; and in the parietal cell sensitivity (P less than 0.05) from 19.2 (4.4-42.6) to 14.3 (2.8-19.7)%. No significant falls in any of these parameters were noted following ulcer healing with ranitidine. Duodenal ulcer healing with sucralfate results in decreased acid secretory responses to vagal and pentagastrin stimulation.

Adult↗