[Drug information: newer anti-inflammatory and weaker-acking painkilling agents. Acetylsalicylic acid (Acetard). 2].
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The authors report two cases of benign intracranial hypertension associated to Aspirin therapy promptly regressed after withdrawal of the drug. This side effect did never described and its pathogenetic mechanism is unknown.
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The possible antithrombotic potential of acetyl salicylic acid (ASA) has been established in recent years and the preparation has been employed extensively in ischaemic cardiac disease and cerebrovascular conditions. The inhibiting effect of ASA on platelet function by means of blocking of cyclo-oxygenase is mentioned and, similarly, the presumed role in thrombosis development and atherogenesis is mentioned. ASA's pharmacokinetics are illustrated with emphasis on optimal anti-thrombotic ASA dosage, in particular, in relation to the effects of the preparation on the thromboxan A2 (TxA2)/prostacyclin (PGI2)-ratio. This is probably best achieved by means of low oral dosage in the form of sustained-release ASA formulation where the inhibition of platelet function probably occurs mainly in the presystemic circulation. It is concluded that a daily dosage of 80-100 mg ASA ensures effective and rapid inhibition of TxA2 production. Administration of 30-50 mg ASA daily results in a corresponding blockage of TxA2 production but not until after treatment for three to four days.
18 male volunteers (age 24 +/- 4 years; Broca index 0.94 +/- 0.08; mean +/- SD) underwent six upper endoscopies (three control and three test investigations) in a single blind two treatments-crossover designed study which evaluated the effect of buffering on aspirin-induced (one single oral dose of 0.5 g aspirin to fasted subjects) gastroduodenal mucosal injury. All subjects had a normal endoscopy prior to applications of 0.5 g plain aspirin (group A; swallowed) or 0.5 g aspirin + 0.3 g calcium carbonate (group B; chewed before swallowing). The sequence groups were A-B-B (n = 9) or B-A-A (n = 9). In advance fo the performed tests a washout period of six days was chosen. Endoscopies were performed two hours after ingestion of the respective tablets. The appearance of corpus, antrum, and duodenum was scored. Biopsies were taken for histological examinations. 15 volunteers experienced no gastrointestinal side effects. Three complained short-lasting gastric burning (two of group A, one of group B). In both treatment groups no significant lesions of the duodenum were found. Buffering significantly (p less than 0.0005) reduced mucosal injuries which occurred mainly as submucosal hemorrhage but without histological alterations of the mucosal architecture after aspirin ingestion. These findings suggest that oral administration of calcium carbonate buffered, chewable aspirin tablets is less harmful to the gastric mucosa than plain aspirin.
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Five white rabbits are given by rectal route a single dose of 100 mg of Aspirin at regular hours: 7 a.m.; 10 a.m. and 2 p.m. the 7 a.m. administration results in lowest CMAX and AUC and the slowest elimination, whereas 10 a.m. and 2 p.m. administration results in the highest CMAX and AUC and shortest elimination time.
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In a multicentric study by the European Study Group of Drug Allergy, 69 patients suffering from immediate type reaction after the intake of non-steroidal antiphlogistica were examined with regard to allergy or pseudo-allergy. Apart from the scratch test on the original substance, we performed cutaneous tests with salicyloyl and pyrazol conjugates, and determined IgE and IgG by means of a modified RAST method. There were 3 groups to be distinguished: (1) "intolerance" reaction of the aspirin type as a pseudo-allergic reaction (15 cases); (2) true IgE-mediated allergy (16 cases); (3) pyrazol "idiosyncrasy" (33 cases). 5 patients showed a combination of the three pathomechanisms.