[Comparison of the protective effects of roxatidine and misoprostol on diclofenac gastroduodenal pathology. An endoscopic, controlled study of volunteers]. / Vergleich der Schutzwirkung von Roxatidin und Misoprostol bei Diclofenac-Gastroduodenopathie. Endoskopisch kontrollierte Studien an freiwilligen Probanden.

For prophylaxis of gastroduodenal lesions induced by non-steroidal antirheumatic drugs (NSAID) acid-lowering as well as mucosa protective substances are used. Direct comparison of both therapeutic regimens are lacking. In randomized parallel studies the gastroduodenal tolerability of 100 mg diclofenac daily in slow-release form was evaluated in the presence and absence of 150 mg roxatidine (CAS 78273-80-0) daily as well as in the presence of 75 mg bid roxatidine or 200 micrograms bid misoprostol (CAS 59122-46-2). The drugs were taken over a period of 14 days. Endoscopic controls were performed at entry, as well as after 14 days of treatment. A quantitative damaging score was used. Study A: Both treatment groups (n = 20) had at entry comparable mucosal damages: placebo/diclofenac: 0.9 +/- 0.1 (+/- SEM), roxatidine/diclofenac: 0.9 +/- 0.1; after 14 days of treatment the score increased in the diclofenac/placebo group to 7.6 +/- 1.9 and, in the corresponding diclofenac/roxatidine group, only to 2.1 +/- 0.9. The difference between the two treatment groups after 14 days was significant (p < 0.05). Study B: Both treatment groups (n = 24) had comparable mucosal damages at entry: diclofenac/roxatidine: 0.9 +/- 0.1, diclofenac/misoprostol: 0.8 +/- 0.1. Following 14 days treatment with 100 mg diclofenac daily the damaging score in both group rose to comparable levels: roxatidine group 2.1 +/- 0.7 and misoprostol group 2.0 +/- 0.4 (n.s.). The data suggest that for prophylaxis of NSAID-induced gastroduodenal lesions substances with different mechanism of action can be used. The findings underline the complex way by which NSAID can damage the mucosa of the upper gastrointestinal tract.

[Circadian aspects of acetylsalicylic acid induced injury and protective effect of ranitidine on the the upper gastrointestinal tract]. / Zirkadiane Aspekte einer Schädigung durch Acetylsalicylsäure und Schutzwirkung durch Ranitidin am oberen Gastrointestinaltrakt.

Circadian Aspects of Acetylsalicylic Acid Induced Injury and Protective Effect of Ranitidine on the Upper Gastrointestinal Tract. In a randomised parallel double-blind study the gastric and duodenal effects of 300 mg acetylsalicylic acid (ASA, CAS 50-78-2) daily in the presence and absence of 150 mg ranitidine (Zantic, CAS 66357-35-5) daily was evaluated in 32 healthy volunteers undergoing upper gastrointestinal endoscopy. Drugs were taken over a period of 7 days either at 8 a.m. (n = 16) or at 8 p.m. (n = 16). Endoscopic controls were performed at entry and repeated after 7 days of treatment. At entry both groups showed comparable mucosal damages: 8 a.m. group: ASA/placebo 0.8 +/- 0.1 (stomach) and 0.1 +/- 0.1 (duodenum): ASA/ranitidine 1.0 +/- 0.0 (stomach) and 0.07 +/- 0.06 (duodenum). 8 p.m. group: ASA/placebo 0.9 +/- 0.06 (stomach) and 0.1 +/- 0.09 (duodenum). ASA/ranitidine 0.8 +/- 0.08 (stomach) and 0.07 +/- 0.06 (duodenum). After 7 days of treatment the lesions score increased in the ASA/Placebo group in the 8 a.m. group to 9.1 +/- 1.1 (stomach) and 2.7 +/- 1.0 (duodenum), and in the 8 p.m. group to 10.9 +/- 1.1 (stomach) and to 3.9 +/- 0.9 duodenum). The corresponding values in the ASA/ranitidine group were 2.6 +/- 0.8 (stomach) and 0.2 +/- 0.08 (duodenum) (8 a.m.) and 4.8 +/- 0.8 (stomach) and 0.3 +/- 0.1 (duodenum) (8 p.m.). There was no statistical difference between the morning- and the evening dose of ASA. In addition, ranitidine protection was also time-independent.(ABSTRACT TRUNCATED AT 250 WORDS)

[Circadian dependency of ibuprofen gastropathy and the protective effect of ranitidine. An endoscopic, controlled double-blind pilot study]. / Tageszeitliche Abhängigkeit der Ibuprofen-Gastropathie und der Schutzwirkung von Ranitidin. Eine endoskopische, kontrollierte Doppelblind-Pilotstudie.

Circadian Dependency of Ibuprofen Gastropathy and Protective Effect of Ranitidine/An endoscopic, controlled double-blind pilot study. In a randomized parallel double-blind study, the gastric and duodenal effects of 600 mg S(+)-ibuprofen (CAS 15687-27-1) daily in the presence and absence of 300 mg ranitidine (CAS 66357-35-5) was evaluated in 20 healthy volunteers undergoing upper GI-endoscopy. Drugs were taken over a period of 7 days either at 8 a.m. (n = 10) or at 8 p.m. (n = 10). Endoscopic controls were performed at entry and repeated after 7 days of treatment. A damage score according to Lanza et al. was used. At entry both groups showed comparable mucosal damages. 8 a.m.-group: ibuprofen/placebo (stomach) 0.9 +/- 0.1 and 0.0 +/- 0.0 (duodenum); ibuprofen/ranitidine 0.8 +/- 0.1 (stomach) and 0.1 +/- 0.1 (duodenum). 8 p.m.-group: ibuprofen/placebo 0.9 +/- 0.1 (stomach) and 0.2 +/- 0.1 (duodenum); ibuprofen/ranitidine 0.9 +/- 0.1 (stomach) and 0.1 +/- 0.1 (duodenum). After 7 days of treatment the lesion score increased in the ibuprofen/placebo-group in the 8 a.m.-group to 3.2 +/- 1.2 (stomach) and to 0.7 +/- 0.5 (duodenum), and in the 8 p.m.-group to 8.4 +/- 1.9 (stomach) and to 2.9 +/- 1.2 (duodenum). The corresponding values in the ibuprofen/ranitidine-group were 1.8 +/- 0.8 (stomach) and 0.1 +/- 0.1 (duodenum) (8 a.m.-group) as well as 5.1 +/- 1.4 (stomach) and 0.1 +/- 0.1 (duodenum) (8 p.m.-group). The difference between the morning and the evening dose of ibuprofen as well as ranitidine protection reached statistical significance when the corresponding data were pooled (p < 0.05). Our data suggest that the gastrolesive effects of S(+)-ibuprofen are dependent of the time of drug ingestion; protection by ranitidine, however, was time-independent.

[Circadian aspects of diclofenac gastroduodenopathy and the protective effect of roxatidine]. / Zirkadiane Aspekte der Diclofenac-Gastroduodenopathie und der Schutzwirkung von Roxatidin.

The gastrointestinal side-effect profile of non-steroidal anti-inflammatory drugs should follow a circadian rhythm. In a randomized, parallel, double-blind study the gastric duodenal effects of 100 mg diclofenac retard daily in the presence and absence of 150 mg roxatidine was evaluated in 20 healthy volunteers undergoing upper GI-endoscopy. Drugs were taken over a period of 14 days either at 8 a.m. (n = 10) or at 8 p.m. (n = 10). Endoscopic controls were performed at entry and repeated after 14 days of treatment. A damaging score according to Lanza et al. was used. At entry both groups showed comparable mucosal damages: 8 a.m.-group: placebo 0.9 +/- 0.1 (+SEM), roxatidine 0.9 +/- 0.1; 8 p.m.-group: placebo 1.0 +/- 0.0, roxatidine 0.9 +/- 0.1. After 14 days of treatment the lesion score increased in the diclofenac retard/placebo-group in the 8 a.m.-group to 7.6 +/- 1.9 and in the 8 p.m.-group to 7.2 +/- 1.1. The corresponding values in the diclofenac/roxatidine-group were 2.1 +/- 0.9 (8 a.m.-group) and 1.4 +/- 0.4 (8 p.m.-group). This protection afforded by roxatidine was significant when compared with placebo (p < 0.05). Our data suggest that the gastrolesive effects of diclofenac retard are independent of the time of drug ingestion; in addition protection by roxatidine was also time-independent.

Detection of carotid thrombi with indium-111 platelet scintigraphy.

In order to prove that platelet scintigraphy (PSC) is able to detect carotid thrombi formations, we performed PSC in 15 patients directly before or immediately after a percutaneous carotid angiography. PSC was successful in demonstrating iatrogenic fresh carotid thrombi in 13 out of 15 cases. Out of 53 patients with cerebrovascular disease and carotid stenosis a pathologic platelet accumulation was seen in 39 carotid arteries, 31 on the symptomatic side; more often in slight- and middle-sized stenoses than in high degree stenoses. We assume that in these cases PSC detected carotid thrombi which caused arterio-arterial emboli.