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Biomedical subjects

I N Marks

Publications and source records attributed to I N Marks.

At least 37 records · Page 2Linked to original sources
PubMed1995

Effect of sucralfate on Helicobacter pylori and severity of gastritis in patients with duodenal ulcer.

BACKGROUND: Duodenal ulcer relapse rates have been reported to be lower following healing with sucralfate. The question arises whether this is related to an effect on Helicobacter pylori. METHODS: In order to investigate this possibility, 43 patients with active duodenal ulcer were entered into a study. Endoscopy was performed at entry, following 6 weeks' treatment with sucralfate 1 g q.i.d., and at 4 and 12 weeks of post-documented healing. Antral and gastric corpus biopsies were taken for assessment of H. pylori status (CLOtest), density of infection, and severity of gastritis. In addition, 14C urea breath tests (UBT) were performed. RESULTS: Sucralfate therapy induced a significant decrease in the density of H. pylori infection, with a trend to improvement of the gastritis in the antrum, but not in the corpus. However, all patients remained CLOtest positive, and the overall gastric urease activity was unchanged following therapy. These effects did not appear to influence either initial duodenal ulcer healing or subsequent relapse rates. CONCLUSION: Sucralfate has a suppressive effect on H. pylori infection in the gastric antrum but the clinical relevance of this is uncertain.

Adolescent↗
PubMed1994

Fat-soluble vitamin concentration in chronic alcohol-induced pancreatitis. Relationship with steatorrhea.

In order to study the fat-soluble vitamin concentration of patients with chronic alcohol-induced pancreatitis (CAIP) we measured vitamins A and E, total lipids, and retinol-binding protein (RBP) in the plasma of 44 patients with CAIP and 83 controls (44 healthy controls; 39 Crohn's disease patients). Mean plasma vitamin E and vitamin E/total lipid ratio were significantly lower in CAIP when compared with either control or Crohn's disease groups. A low vitamin E/total lipid ratio was found in 75% of CAIP patients (91% with steatorrhea) and a ratio less than 1.0 was virtually 100% predictive of steatorrhea. The mean plasma vitamin A level for the CAIP group was significantly lower (overall 16%, 38% with steatorrhea) than in controls. Patients with CAIP show subnormal plasma levels vitamin E more often as compared to vitamin A. Further, the plasma vitamin E/total lipids ratio may be a sensitive and practical means in the detection and follow-up of steatorrhea in these patients.

Adolescent↗
PubMed1994

Effect of buprenorphine on pancreatic enzyme synthesis and secretion in normal rats and rats with acute edematous pancreatitis.

Pancreatic enzyme secretion is inhibited during acute pancreatitis, resulting in an increase in acinar zymogen content. Since the premature activation of zymogens has been assigned a central role in the pathogenesis of acute pancreatitis, minimizing the amount of stored zymogens might lead to less severe acute pancreatitis. Inhibition of enzyme synthesis or stimulation of enzyme secretion would result in reduction of zymogen stores. Opiates have a varying effect on pancreatic secretion, depending on the dosage, site of administration, and presence of pancreatic stimulants. The effect of opiates and acute pancreatitis on individual pancreatic enzyme synthesis is unknown. The following study was undertaken in order to examine the effects of an opiate on pancreatic enzyme secretion and synthesis during experimental acute pancreatitis. Four groups of rats were studied. Group I received cerulein (25 micrograms/kg); group II received an opiate, buprenorphine (BPN, 0.5 mg/kg); and group III received cerulein and BPN. Drugs were dissolved in gelatin/saline and injected subcutaneously. A control group (group IV) received only gelatin/saline. Rats were sacrificed 4 hr after injection, and pancreatic mass was measured. Pancreatic acini were prepared and assayed for amylase and DNA content. Amylase, trypsinogen, chymotrypsinogen and lipase synthesis, and amylase secretion were measured for 2 hr. Results showed that, compared to controls, acini of rats with AP had increased amylase content, a finding consistent with decreased in vivo amylase secretion. Total protein and individual enzyme synthesis rates were significantly lower in the acini of the rats with AP than in those of the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

Obesity: an important prognostic factor in acute pancreatitis.

Ninety-nine patients with acute pancreatitis in whom body mass index (BMI = weight (kg)/height2 (m2)) was measured were studied prospectively to determine the importance of obesity as a prognostic factor in this disease. Of 19 obese patients (BMI > or = 30 kg/m2), 12 developed severe pancreatitis; seven had abscesses, of whom five died, and two further patients died. In 80 non-obese patients, the incidence of severe pancreatitis (n = 5), abscess formation (n = 4) and death (n = 4) was significantly less (P = 0.0007). The mean(s.d.) BMI of 17 patients with severe acute pancreatitis was significantly higher than that in 82 patients with mild acute disease (31.2(5.6) versus 23.3(5.6) kg/m2, P < 0.001). As a single prognostic factor, obesity had a sensitivity of 63 per cent and a specificity of 95 per cent for predicting disease severity. When five obese women with gallstone pancreatitis were excluded, the sensitivity of obesity increased to 86 per cent. Severe pancreatitis occurred in all eight obese patients with disease of an alcoholic aetiology. These data suggest that increased fat deposits in the peripancreatic and retroperitoneal spaces in obese patients may increase the risk of peripancreatic fat necrosis, abscess and death. Consideration should be given to including obesity as a prognostic factor in acute pancreatitis.

Acute Disease↗
PubMed1993

Local cellular and immune response by antral mucosa in patients undergoing treatment for eradication of Helicobacter pylori.

Thirty-six patients with nonhealing or recurrent duodenal ulcers (DU) were treated with omeprazole; 20 mg/day for one month followed by triple therapies (metronidazole, 400 mg three times a day, tetracycline, 500 mg four times a day with either colloidal bismuth, 120 mg four times a day or sucralfate 1 g four times a day. At least two gastric mucosal samples were collected from the antral portion of the stomach and from the duodenum before and immediately after omeprazole therapy and four weeks after completion of triple therapies. Samples were fixed in buffered formaldehyde and glutaraldehyde and examined histologically and histochemically for inflammation, density of H. pylori colonization, and immunohistochemically for the density of gastrin-secreting cells, immunoglobulins (IgA, IgG, IgM), kappa and lambda light chains and T-lymphocyte population. H. pylori colonization of the antral mucosa before treatment was noted in 100% and active gastritis in 86% of patients. The histologically assessed clearance rate after omeprazole treatment was 47.3%, and after triple therapies, 69.5%. The prevalence of gastritis was observed in 63.9% and 33.3% respectively. All therapies were associated with an accumulation of serous fluid, increased population of lymphocytes and plasma cells, and secretion of immunoglobulins, particularly IgG and IgM in the upper part of the lamina propria. These changes, together with increased numbers of T lymphocytes within the crypt epithelium and the lamina propria, were associated with the presence of H. pylori organisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Duodenal juice total protein and pancreatic enzyme synthesis, turnover, and secretion in patients after acute pancreatitis.

It is controversial whether acute pancreatitis has longterm effects on pancreatic function. Pancreatic enzyme synthesis, turnover, and secretion were measured in 10 patients in clinical remission who had had one or more (one to six) attacks of acute alcoholic pancreatitis. The studies were done between two and 29 months after the most recent attack. A control group included five patients with no evidence of pancreatic disease. A four hour primed/continuous intravenous infusion of [14C]L-leucine tracer was given with secretin (2 U/kg/h) and cholecystokinin (0.5 U/kg/h) and secreted duodenal juice aspirated. Amylase and trypsin were extracted from duodenal juice by affinity chromatography, permitting measurement of the rate of isotope incorporation into total protein, amylase, and trypsin. The results showed non-parallel changes in enzyme synthesis and turnover with decreases in total enzyme protein and amylase synthesis and turnover but preservation of trypsin synthesis and turnover. The low turnover rates may be ascribed to continuing pancreatic cell malfunction after recovery from acute alcoholic pancreatitis and suggest that the decreased amylase secretion rates are partly a consequence of impaired amylase synthesis and not simply because of loss of pancreatic tissue.

Acute Disease↗
PubMed1993

Distribution of Helicobacter pylori colonisation and associated gastric inflammatory changes: difference between patients with duodenal and gastric ulcers.

AIMS: To determine the gastric distribution of Helicobacter pylori in patients with duodenal and gastric ulcers; and to examine the mucosal inflammatory response. METHODS: Patients with newly diagnosed, uncomplicated duodenal and gastric ulcers were endoscoped and two biopsy specimens each taken from the antrum and the body. Specimens were evaluated blind by one pathologist to determine H pylori activity (scored 0-3) and inflammatory changes (according to the Sydney classification). RESULTS: Adequate biopsy material was obtained from 40 and 44 patients with gastric and duodenal ulcers, respectively. Although antral colonisation with H pylori was more common in the antrum of the latter, the organism was equally likely to be found in the body of both sets of patients; the density of colonisation was higher in those with gastric ulcers. Active gastritis and mucosal atrophy were more common in the body of those with gastric ulcers; intestinal metaplasia was also more common in the antrum of these patients. CONCLUSIONS: Gastritis in patients with duodenal ulcers is mainly antral, but the incidence of gastric body colonisation with H pylori seems to be the same in patients with either type of ulcer. There is, however, a significant difference in colonisation density. The cause and importance of this are not obvious and may be related to either host or organism factors.

Adult↗
PubMed1993

Endoscopic laser therapy in a case of gastric antral vascular ectasia (watermelon stomach).

We report the case history of a 75-year-old female patient suffering from extensive gastric antral vascular ectasia (watermelon stomach) with portal hypertension in alcoholic liver cirrhosis. Iron deficiency anaemia, due to chronic blood loss from the antral lesions, required repeated transfusions. Conservative treatment failed, but a surgical intervention (antrectomy) was discarded in view of concomitant diseases. Endoscopic laser photocoagulation therapy with a Nd:YAG-laser eradicated the characteristic antral lesions, which was accompanied by a significant reduction of transfusion requirements. No relapse has been observed since then. Endoscopic laser photocoagulation appears to be an efficacious and safe alternative in the treatment of gastric antral vascular ectasia.

Aged↗
PubMed1993

Abdominal tuberculosis: still a potentially lethal disease.

The findings in a 4-yr survey of 82 patients with abdominal tuberculosis are described and compared with those encountered in previous surveys. Fourteen cases of intestinal, 11 of mesenteric-lymphnodal, and 57 of peritoneal tuberculosis were identified. The disease occurred essentially in patients living under worsening socioeconomic conditions, and 51 of them had associated pulmonary tuberculosis. Symptoms and clinical findings were again nonspecific, but newer imaging, endoscopic, and other invasive procedures were helpful in establishing a definite diagnosis. In addition, adenosine deaminase determination showed great promise as a noninvasive diagnostic procedure in patients with tuberculous ascites. The six hospital deaths in the series highlight the hazard of potentially lethal delays in early diagnosis and treatment, even in centers with a high awareness of the disease.

AIDS Serodiagnosis↗
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↗