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Results for “Aspirin”

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At least 19 recordsLinked to original sources

PubMed1977

A comparison of a new slow release aspirin ("slow aspirin") with plain aspirin in the treatment of rheumatoid disease.

In a single centre double-blind crossover study in eighteen patients with established rheumatoid disease, a new slow release aspirin ("slow aspirin") was compared with plain aspirin with respect to patient tolerability and gastric mucosal damage as observed at gastroscopy. "Slow aspirin" was significantly better than plain aspirin with regard to gastroscopic findings. With "slow aspirin", the gastric mucosal appearances were definitely better in eight patients, worse in two, and eight showed no difference. There was a high incidence of gastric ulceration or erosions in the groups as a whole (39%) but few patients complained of dyspepsia. There was little difference in the ability of both plain and "slow aspirin" in controlling the patients' joint symptoms. Evidence has been provided to suggest that "slow aspirin" is less injurious to the gastric mucosa. In an attempt to reduce gastric mucosal damage due to prolonged aspirin treatment it is therefore concluded that "slow aspirin" merits consideration in the management of chronic rheumatoid disease.

Adult↗

PubMed1979

Modified USP assay for simultaneous determination of aspirin and nonaspirin salicylates in aspirin and buffered aspirin tablets.

Modified USP procedures are described for the simultaneous determination of nonaspirin salicylates and aspirin in aspirin and buffered aspirin tablets. The existing USP procedures are not stability indicating for intact aspirin when significant levels of nonaspirin salicylates are present, as is often the case in short-term, high temperature stability programs. The modified procedures yeld considerably shorter analysis times and stability-indicating assays for intact aspirin without the need for sophisticated equipment other than that presently required by USP XIX.

Aspirin↗

PubMed1976

Immunological mechanisms in aspirin hypersensitivity. Studies on the immunogenicity of free aspirin.

Anti-aspiryl antibodies were produced in rabbits and guinea pigs by inoculation of aspirin incorporated in complete or incomplete Freund's adjuvant. These antibodies were readily detected by passive haemagglutination using rabbit erythrocytes incubated with aspirin at alkaline pH. Aspiryl conjugates with ovalbumin, human gamma-globulin, bovine gamma-globulin and rabbit serum were also prepared by incubating the proteins with aspirin at alkaline pH. Aspiryl conjugates prepared by this technique behaved, immunologically, identically with the conjugates prepared from aspirin chloride. By contrast, the molar absorbance at 305 nm of the conjugates prepared from aspirin was about 25 times lower than the molar absorbance of the conjugates prepared from aspirin chloride. Since the absorbance of salicylic acid is about eight times greater than that of aspirin, the conclusion is drawn that the aspiryl/salicylyl ratio is significantly higher in the conjugates prepared by incubating proteins with aspirin at alkaline pH than in the conjugates prepared from aspirin chloride. In parallel experiments, salicylic acid did not induce formation of specific antibodies capable of reacting with aspirin- or salicylic acid-treated red cells. Sera giving positive passive haemagglutination with aspirin-treated erythrocytes did not react with erythrocytes treated with salicylic acid or acetic anhydride.

Anhydrides↗

PubMed1978

Aspirin and aspirin-caffeine in postpartum pain relief.

In two double-blind randomized, balanced, single oral dose studies with 140 women, a combination of 800 mg aspirin and 64 mg caffeine (aspirin-caffeine) was compared to 650 mg aspirin and to placebo. In patients with moderate to severe uterine or episiotomy pain, there was greater analgesic response with active drugs when the initial pain intensity was more severe. In patients with severe episiotomy pain, aspirin-caffeine was more effective than 650 mg aspirin (p less than 0.05) at the second and third hours. There was no difference between analgesic effects of aspirin and aspirin-caffeine in women with severe uterine pain.

Adolescent↗

PubMed1976

Refractory period to aspirin in a patient with aspirin-induced asthma.

Oral aspirin challenge was used to detect unrecognized aspirin intolerance in a select group of 50 asthmatic patients who denied aspirin intolerance. A double-blind protocol was used to further study those patients who reacted to initial graded aspirin challenge. In one patient the use of a double-blind protocol led to the serendipitous discovery of a 72-hr refractory period to the adverse effects of aspirin, after initial ingestion of aspirin resulted in respiratory and systemic symptoms.

Adult↗

PubMed1978

The role of aspirin in gastric ulceration . Some factors involved in the development of gastric mucosal damage induced by aspirin in rats exposed to various stress conditions.

The gastric irritant effects of aspirin were studied in rats treated with a variety of physical and "disease" (inflammatory) stress conditions (which may mimic responses to some stress states encountered clinically) with the object of establishing whether these stress states increase the susceptibility of the gastric mucosa to the potentially ulcerogenic actions of aspirin. While exposure to physical (eg, cold) stress conditions markedly increased the sensitivity of the gastric mucosa to aspirin, exposure to various disease stressors (eg, adjuvant arthritis, acute pain, or paw inflammation) did not appreciably affect the mucosal sensitivity to this drug. Attempts were made to determine the mechanisms of the physical stress plus aspirin interaction by use of pharmacological agents. The results suggest a major involvement of the parasympathetic-vagal, sympathetic, and histamine-producing systems, but not the adrenocortical axis, in this model of gastric ulcerogenesis. No differences were observed in the mucosal uptake of [14C]aspirin, showing that accelerated uptake of the drug is not a factor in the development of gastric ulceration.

Animals↗

PubMed1978

Aspirin intolerance: unaltered susceptibility of platelet cyclo-oxygenase to inhibition by aspirin in vitro.

Inhibition of prostaglandin (PG) biosynthesis has been proposed as a mechanism of aspirin-induced asthma. In order to verify the existence of a generalized abnormal sensitivity of the PG cyclo-oxygenase in intolerant patients, we have compared the inhibitory effects of aspirin on platelet PGE2 and PGF2alpha spontaneous formation in vitro, in 10 healthy subjects, 10 aspirin-sensitive asthmatics, and 10 nonasthmatic aspirin-sensitive patients. No statistically significant differences were found in the pattern nor in the absolute concentrations of both PGs in the control platelet superfusates. Moreover, the synthesis and release of both PGs were inhibited by aspirin with the same potency in the three groups studied.

Adult↗

PubMed1977

Aspirin and gastric ulceration: light and electron microscopic observations in a model of aspirin plus stress-induced ulcerogenesis.

The gastric mucosa of rats given aspirin orally and concomitantly exposed to mild (cold) stress conditions has been examined under the electron microscope. In this model of gastric ulceration greater involvement is seen of the parietal and zymogen cells than is evident after aspirin treatment alone (which leads to mucosal erosions but not ulceration per se). Evidence of considerable autolytic and proteolytic activity is seen in aspirin-plus-stress-treated animals developing in ulceration. Little damage was observed in animals exposed to these mild stress conditions. The synergistic interaction between aspirin and stress could have its basis in greater sensitizing of parietal and zymogen cells to damage not seen in aspirin-treated animals.

Animals↗

PubMed1978

Selective cytotoxic actions of aspirin on parietal cells: a principal factor in the early stages of aspirin-induced gastric damage.

Electronmicroscopic observations are reported on the effects of orally administered aspirin on the rat gastric mucosa to establish the cytotoxic events that occur during the early stages of the development of gastric damage induced by this drug. The results show that aspirin, apart from damaging superficial mucous cells, causes selective damage to the acid-secreting parietal cells located deep in the fundic mucosa. It is suggested that the selective accumulation of salicylates in the parietal cells may account for the specific cytotoxic actions of aspirin on these cells.

Animals↗

PubMed1979

Effect of other drugs and chemicals on the degradation of aspirin in vitro: possible extrapolation to in vivo metabolism of aspirin.

To assess the possible influence of other drugs and chemicals on the metabolic degradation of aspirin in man, their effect on the serum aspirin esterase activity was determined in vitro. The activation or inhibition of the enzyme as observed with these compounds suggest the possibility that simultaneous ingestion of these drugs with aspirin may influence the pharmacology and toxicity of the analgesic.

Anticoagulants↗

PubMed1977

Serum aspirin esterase activity in women with habitual aspirin intake.

A method for the determination of aspirin esterase activity in serum is described. Sera from 59 pregnant women who were habitual aspirin users were found to have a mean enzyme activity value statistically lower than those of 68 non-pregnant women controls or of 12 pregnant women controls who were either occasional users of the drug or were non-users. The distribution of enzyme activity in the experimental group was also significantly different from that of the control group. It is postulated that the low enzyme activity may further aggravate the injurious effects of high intake of aspirin.

Adult↗

PubMed1976

Prolonged bleeding times after aspirin ingestion in patients with aspirin idiosyncrasy.

Measurements of the bleeding time after the ingestion of small doses of aspirin in patients with aspirin idiosyncrasy demonstrate a marked prolongation compared with control patients. Confirmation of this finding offers a clue to the pathogenesis of this condition. Despite the prolonged bleeding time, gastrointestinal haemorrhage is an uncommon event in patients with aspirin idiosyncrasy.

Adult↗

PubMed1976

Application of gas-liquid chromatography and high-performance liquid chromatography to the analysis of trace amounts of salicylic acid, acetylsalicylic anhydride and acetylsalicylsalicylic acid in aspirin samples and aspirin formulations.

The gas-liquid chromatographic (GLC) determination of salicylic acid (SA) in 12 commercial acetylsalicylic acid (aspirin, ASA) samples and 12 ASA formulations is reported. The GLC determination of SA as an impurity in ASA, utilising methylation with methyl iodide in the presence of potassium carbonate, requires a column chromatographic separation of SA prior to derivatization. Trace amounts of SA in ASA have also been determined by high-performance liquid chromatography (HPLC) on a Sil-X-I adsorption column using light petroleum-ethyl acetate-acetic acid as the mobile phase. Acetylsalicylic anhydride (ASN) and acetylsalicylsalicylic acid (ASSA) were determined by HPLC on a reversed-phase C18 column with water-methanol mixtures as the mobile phase. GLC was also applied to the determination of ASN as an impurity in ASA formulations.

Anhydrides↗

PubMed1977