[Acid reducing drugs in prevention of stress ulcer: cause for development of nosocomial pneumonia? Arguments contra].
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Anti-Ulcer Agents↗
Biomedical subjects
B Simon
Publications and source records attributed to B Simon.
Quantum Hall effect and the relative index for projections.
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Journal Article↗
[Gastrointestinal tolerance of 30 mg versus 300 mg acetylsalicylic acid daily. An endoscopically controlled double-blind study of healthy subjects].
Acetylsalicylic acid (ASS) is increasingly used in the prevention of cardiovascular diseases. In recent years daily ASS-doses (100 to 300 mg) have been given for this indication. Studies with still lower ASS-doses (f. i. 30 mg daily) are the focus of ongoing clinical trials. In a randomized double-blind study we have evaluated the gastroduodenal tolerability of 30 mg ASS and 300 mg ASS daily in 20 healthy volunteers using upper GI-endoscopy. Both ASS-dosages have been taken for a period of four weeks. Endoscopic controls were performed at entry and repeated after seven, 14 and 28 days of treatment. 30 mg ASS daily did not induce significant gastroduodenal damages during the whole treatment period in contrast to 300 mg ASS daily (p less than 0.05). The lesions score under 300 mg ASS on day 7 and 28 was almost identical. Our data suggest that extremely low doses of ASS are almost harmless to the human gastroduodenal mucosa. No adaptive phenomena occur during a 28 days treatment with 300 mg ASS daily.
Adult↗
[Treatment of hyperlipoproteinemia in patients with diabetes mellitus].
In a large percentage of cases, diabetes mellitus leads to hyperlipidemia. In addition to the diabetes-related secondary hyperlipidemias, all types of primary disturbances of lipid metabolism can also be observed in diabetics. Depending upon the degree of severity and type of metabolic disorder presenting, not only suitable dietetic treatment, but also the various lipid-lowering drugs, fibrates, nicotinic acid, probucol, cholestyramine and the HMG-CoA reductase inhibitors should be introduced into therapy. As in all groups with an elevated coronary risk, strict management of the lipid levels is mandatory in diabetics, too.
Combined Modality Therapy↗
Epithelial glycoprotein is a member of a family of epithelial cell surface antigens homologous to nidogen, a matrix adhesion protein.
The cell surface antigen, epithelial glycoprotein, defined by the monoclonal antibody HEA 125, is expressed on virtually all epithelial cell membranes but not on mesodermal or neural cell membranes. The cDNA encoding epithelial glycoprotein was isolated by HEA 125 antibody enrichment of colon tumor cDNA expressed transiently in COS cells. The sequence of the epithelial glycoprotein antigen is identical to the cell membrane protein recognized by the monoclonal antibody KS 1/4 and is homologous to the tumor-associated antigen GA733. These proteins share sequence homology to nidogen, an extracellular matrix component that appears to participate in cell-matrix adhesion. These proteins also share a homologous domain found in the B1 chain of laminin, a matrix adhesion protein, and placental protein 12, an insulin-like growth factor I binding protein secreted during pregnancy that has been implicated in regulation of fetal growth. This common domain is also repeated multiple times within the thyroglobulin precursor. These findings suggest epithelial glycoprotein is a cell surface molecule involved in cell-cell or cell-matrix interaction.
Amino Acid Sequence↗
Single intravenous administration of the H+, K(+)-ATPase inhibitor BY 1023/SK&F 96022--inhibition of pentagastrin-stimulated gastric acid secretion and pharmacokinetics in man.
The effects of H+, K(+)-ATPase inhibitor BY 1023/SK&F 96022 on pentagastrin-stimulated acid secretion have been studied in healthy male volunteers (n = 12). The gastric acid response to submaximal pentagastrin-stimulation (0.6 micrograms/h/kg b.w.) was dose-dependently inhibited. A single dose of 5 mg decreased acid output by 22% while after 60 mg and 80 mg secretion was almost completely abolished. A good dose linearity was observed for AUC (0, infinity) and Cmax over the dose range from 5 to 80 mg. Elimination half-life, total clearance and volume of distribution of the parent compound were independent of the dose. The drug was well tolerated up to the highest dose of 80 mg. No clinically relevant influence was found on either laboratory screen or cardiovascular parameters.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Effect of repeated oral administration of BY 1023/SK&F 96022--a new substituted benzimidazole derivative--on pentagastrin-stimulated gastric acid secretion and pharmacokinetics in man.
Pentagastrin stimulated gastric secretion was measured in 12 healthy male subjects after repeated once daily oral administration of 20 and 40 mg BY 1023/SK&F 96022--a new substituted benzimidazole derivative. Twenty milligrams inhibited acid output compared with placebo by 24% (2.5-3.5 h) and 26% (24.5-25.5 h) after the first oral intake. Inhibition increased to 56% and 50%, respectively, after the seventh oral dose. Forty milligrams inhibited acid output by a mean of 51% (2.5 to 3.5 h) and 52% (24.5-25.5) after the first oral intake. After the seventh dose mean inhibition rose to 85% and 66%, respectively. The drug was well tolerated, no drug-related changes in clinical laboratory, ECG, heart rate and blood pressure were observed. Fasting gastrin serum concentrations tended to increase with both doses, the mean values being within the normal range. AUC, Cmax and t1/2 of the drug after repeated oral intake were not significantly different when compared with a single dose at either 20 mg or 40 mg.
2-Pyridinylmethylsulfinylbenzimidazoles↗
[Effective prevention of piroxicam-induced lesions of the gastric mucosa with nizatidine].
12 healthy volunteers participated in this single-blind, randomized, cross-over study. All subjects were given Piroxicam 20 mg mane on three different 14 days treatment periods in the presense of Nizatidine 150 or 300 mg bid and placebo respectively. Only subjects without endoscopically revealed gastroduodenal lesions were enrolled into the study. Endoscopy was repeated at day 14 of therapy. Between treatment periods a 2 weeks wash out phase was interposed. The gastroduodenal lesion score was the following: score 0 = no injury, score 1 = erythema, score 2 = less than or equal to 9 lesions, score 3 = greater than or equal to 10 lesions (petechiae/erosions), score 4 = ulcer. The mean lesion score with Piroxicam averaged 1.5 +/- 0.35 (+/- SEM) when placebo was coadministered. The mucosal lesion scores were reduced to 0.17 +/- 0.08 and 0.42 +/- 0.19 (+/- SEM) when Nizatidine 150 or 300 mg bid was given concurrently. This protection afforded by Nizatidine was significant when compared with placebo (p less than 0.01). The difference between the two Nizatidine doses, however, did not reach statistical significance. Our data suggest that Nizatidine markedly improves the gastroduodenal tolerability of Piroxicam.
Adult↗
[Pharmacokinetics and tolerability of telenzepine in patients with compensated liver cirrhosis].
Pharmacokinetics and Tolerability of Telenzepine in Patients with Chronic Liver Diseases. The pharmacokinetics and tolerability of the new selective muscarinic M1-antagonist telenzepine (BY 803; CAS 80880-90-6) were studied in 10 patients with compensated liver cirrhosis who were treated over 4 weeks with 3 mg at night. 3 mg telenzepine was well tolerated. There was no deterioration of laboratory parameters during the 4 weeks treatment course. Following a single oral dose of 3 mg telenzepine the mean maximal plasma level (cmax) averaged 5.7 (1.9-10.1) ng/ml. After repeated dosing 3 patients displayed different kinetic behaviour resulting in higher values of AUC on day 14/15 in comparison to day 1/2. tmax and cmax remained unchanged. It can be concluded that even in patients with compensated liver cirrhosis no significant accumulation of the compound will occur.
Adolescent↗
Pentagastrin-stimulated gastric acid secretion and pharmacokinetics following single and repeated intravenous administration of the gastric H+, K(+)-ATPase-inhibitor pantoprazole (BY1023/SK&F96022) in healthy volunteers.
The objective of the study was to investigate the pharmacodynamics and pharmacokinetics of the gastric H+, K(+)-ATPase inhibitor pantoprazole in man following repeated i.v. dosing. 8 healthy male volunteers aged from 25 to 31 years (median: 29 years), body weight between 72 and 95 kg (median: 82 kg) entered this single-blind two-period cross-over study. Each subject underwent two treatment periods of 5 days each with daily infusion of 15 mg or 30 mg pantoprazole, respectively. A placebo day preceeded the trial. On the placebo day as well as on days 1, 4 and 5 of each treatment period, gastric secretion was stimulated submaximally by a pentagastrin infusion of 0.6 micrograms/h/kg over a period of 4 h, starting one hour before administration of drug or placebo. Repeated once-daily infusion (15 min) of pantoprazole resulted in a rapidly increasing pharmacodynamic effect: as compared to placebo the mean percent inhibition of acid output measured from 1 to 3 h after start of infusion was 22%, 63% and 78% for the 15 mg dose, and 56%, 97% and 99% for the 30 mg dose on days 1, 4 and 5, respectively. The pH also increased in relation to the dose and the duration of treatment. Mean fasting gastrin serum concentrations increased by about 50%, yet remained within the normal range. Only in one subject, one of the individual values was above the upper limit of the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
2-Pyridinylmethylsulfinylbenzimidazoles↗
[3 mg telenzepine nocte in the treatment of benign stomach ulcer disease: a double-blind comparative study with 300 mg ranitidine nocte].
163 patients with endoscopically proven benign gastric ulcers were randomly allocated to treatment with either telenzepine 3 mg nocte or ranitidine 300 mg nocte for up to 8 weeks in a prospective double-blind study. The two groups were similar with regard to age, sex, number of patients with ulcer recurrence, smoking habits etc. After 4 weeks treatment 51/80 patients (64%) healed on telenzepine 3 mg nocte and 49/83 patients (59%) on ranitidine 300 mg nocte. The corresponding healing rates after 8 weeks were 85% (68/80) on telenzepine and 89% (74/83) on ranitidine. At each time there was no statistical difference between the two groups. After 8 weeks of treatment 58 patients (73%) on telenzepine and 72 patients (87%) on ranitidine were totally free from stomach pain (n.s.). Other ulcer related symptoms such as fullness etc. were more rapidly relieved with ranitidine. Anticholinergic side effects occurred significantly more frequent in patients on telenzepine than in patients on ranitidine. Dry mouth was the most frequent side effect in the telenzepine group. Telenzepine 3 mg at night appears to be as good as ranitidine 300 mg at night in the healing of benign gastric ulcer disease.
Adolescent↗
[Stomach tolerance of buffered and unbuffered low-dose acetylsalicylic acid: an endoscopy controlled double-blind study in volunteers].
In this randomised double-blind cross-over study the gastroduodenal tolerability of buffered acetylsalicylic acid (ASS) (Aspalox = 325 mg ASS plus 300 mg magnesium aluminium hydroxide) daily has been compared with unbuffered ASS (325 mg) daily in 12 healthy volunteers using upper Gl-endoscopy. The treatment period lasted 14 days: endoscopic controls were performed at entry and repeated at day 14. At day 0 the mean endoscopic score averaged 0.8 +/- 0.1 in both groups (MW +/- SEM). One tablet Aspalox daily induced marked gastroduodenal damage at day 14 (6.5 +/- 1.5). The median lesion score rose from 1.0 (day 0) to 7.0 at day 14. Unbuffered ASS evoked almost identical gastroduodenal injuries at day 14 (7.5 +/- 1.8). The corresponding median values were 1.0 (day 0) and 7.0 at day 14. Our data suggest, that the amount of buffering in the Aspalox preparation is not sufficient enough to protect human gastroduodenal mucosa against low dose acetylsalicylic acid.
Adult↗
[Gastroprokinetics in the treatment of stomach ulcer: a direct comparative study of cisapride versus ranitidine].
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Adult↗
Regulation of femoral vascular resistance by adenine nucleotides via endothelial and smooth muscle receptors.
It is well established that adenosine (ADO) and adenine nucleotides are potent vasodilators, but their role in local blood flow control is still under debate. Recent findings on contribution of vascular endothelium to the vasomotor regulation pointed out this problem. In the present study the effects of adenine nucleotides were investigated in vivo on the femoral arterial flow (FAF) and femoral vascular resistance (FVR). Selective suppression of the endothelium mediated dilation was achieved by gossypol (35 mumol/l). On intact hindlimbs ADO (4 mmol/l) and ATP (0.5 mmol/l) elicited 3.5-fold increase of FAF, in average. Resistance decreased by 6.24 +/- 0.58 and 7.23 +/- 1.12 peripheral resistance units (PRU100), respectively. After gossypol, ATP-induced dilation was either significantly suppressed (resistance-decrease was 3.70 +/- 0.58 PRU100; p less than 0.02 vs control) or turned to strong constriction (FAF decreased by 50%). ADO-induced dilation remained unchanged. These results, in agreement with in vitro data, suggest that adenosine directly relaxes the vascular smooth muscle of resistance vessels via P1-purinoceptors, while ATP-induced vasomotion is composed of a dilator effect mediated by endothelial P2y-receptors, and a direct constrictor effect on the vascular smooth muscle via P2x-purinoceptors.
Adenosine↗
[Endoscopic studies on the gastric tolerance of paracetamol and acetylsalicylic acid. A placebo-controlled, double-blind study in healthy volunteers].
Endoscopic Studies on the Gastric Tolerance Following 6 Days Treatment of Paracetamol and Acetylsalicylic Acid/A placebo-controlled double-blind-study in healthy volunteers. In placebo-controlled randomized double-blind cross-over-fashion the gastric and duodenal tolerance of a 6 day treatment with 3000 mg acetylsalicylic acid (ASA; as a commercially available preparation) and 3000 mg paracetamol (Tylenol) were directly compared in 12 healthy volunteers. An endoscopic evaluation of the gastric and duodenal mucosa was performed. 3000 mg ASA daily evoked significant more gastro-duodenal lesions than 3000 mg paracetamol daily and placebo. Difference between Paracetamol and placebo did not reach statistical significance. Based on the comparable analgetic potency of both compounds and the apparently better gastro-duodenal tolerability paracetamol is the drug of choice when a non-inflammatory problem requires an analgesic.
Acetaminophen↗
[Lowering of the plasma lipid concentration with lovastatin. A clinical study in patients with primary hypercholesterolemia].
A study of 27 patients (18 males and 9 females; median age 57 [35-70] years) with hypercholesterolaemia examined the lipid-reducing effect, clinical reliability and tolerance of lovastatin, an HMG-CoA-reductase inhibitor, given in a single evening dose. After a four-week period on placebo and a lipid-reducing diet the patients received 20 mg lovastatin for four weeks. If, at the end of this period, total cholesterol levels were still above 200 mg/dl, the dose was increased to 40 mg, after a further four weeks to 80 mg. After a three-month treatment period total cholesterol concentration in lovastatin-treated patients was 28% lower than in the placebo group (289.4 +/- 42.2 vs 208.0 +/- 39.9 mg/dl; P less than 0.0001). LDL-cholesterol concentration had fallen by 40% (215.1 +/- 44.4 vs 130.1 +/- 24.7 mg/dl; P less than 0.0001), while plasma triglyceride concentrations had fallen by 15% (166.3 +/- 71.8 vs 141.8 +/- 69.8 mg/dl; P less than 0.01). At the same time, HDL-cholesterol levels had risen by 12% (42.9 +/- 12.4 vs 47.9 +/- 18.2 mg/dl; P less than 0.01). These results confirm the marked lipid-reducing effect of lovastatin.
Adult↗
[Treatment of non-steroidal anti-inflammatory drug-induced damage to gastric mucosa using ranitidine. Comparison of the effectiveness of 2 dosages].
339 patients with rheumatic diseases suffering from dyspepsia and endoscopically proven gastroduodenal lesion entered an open multicenter study with ranitidine 150 mg bid or ranitidine 300 mg administered at night in a single dose over 4 weeks. For entry the patients had to have been treated for at least 3 months with the non-steroidal anti-inflammatory drugs diclofenac, indomethacin and piroxicam. During the trial all patients were continued on NSAID. The data of 248 patients were evaluable. At entry, patients in both treatment groups had a total gastric damage score of 2.0. The duodenal lesion score was on average 1.43 in the ranitidine 150 mg bid group, and 1.8 in the 300 mg single dose ranitidine at night group. After 4 weeks of treatment the mean lesion score was significantly reduced in the stomach as well as in the duodenum with both ranitidine regimens, no differences being seen between the groups. In addition, rapid symptomatic relief was observed in both groups. After 4 weeks of treatment more than 80% of the patients were symptom-free or markedly improved.
Anti-Inflammatory Agents, Non-Steroidal↗
[Inhibition of 24-hour acidity by nizatidine].
In a randomized, double-blind, placebo-controlled, comparative cross-over study, we studied the effect of four H2-receptor antagonists on intragastric 24-hour acidity, nocturnal volume and acid output. Ten healthy male volunteers were administered 300 mg or 150 mg nizatidine, 800 mg cimetidine, 300 mg ranitidine, 40 mg famotidine, or placebo on several days, in each case at 9:000 PM. Nocturnal intragastric H+ concentration (mmol/l) (11:00 PM to 7:00 AM) was significantly reduced by all H2 blockers compared with placebo. We obtained the following inhibition rates: Cimetidine 67%; ranitidine 95%; famotidine 89%; nizatidine 80% (300 mg) and 69% (150 mg). Nocturnal acid (mmol/l) and volume output (ml/h) were also significantly (compared with placebo) inhibited by all four H2-receptor antagonists. Inhibition of nocturnal acid secretion was almost identical on nizatidine 300 mg nocte, ranitidine 300 mg nocte, famotidine 40 mg nocte, and cimetidine 800 mg nocte. Nizatidine 300 mg nocte and 150 mg nocte exclusively reduced acid secretion at night, without an aftereffect into the following day (8:00 AM to 6:00 PM). These results suggest that the clinical efficacy of these H2-receptor antagonists is identical with respect to healing peptic ulcer disease and providing freedom from pain. It is generally accepted today that gastric acid inhibitors used in the treatment of peptic ulcer disease should interfere with daytime gastric acid secretion as little as possible, particularly since the acid protects the stomach from bacteria ingested with the food during the day.
Cimetidine↗