Acetylsalicylic acid

ASA has analgesic, antipyretic, antiphlogistic effects and inhibits platelet aggregation. Prostaglandin synthesis is inhibited by irreversible inhibition of cyclooxygenase.

ASA has an exceptional position within the COX inhibitors. The acetylation of salicylic acid (a development of the chemist Felix Hofmann) improved the tolerability and expanded the active profile of salicylic acid. This is because the acetyl group, which is rapidly cleaved in the portal circulation (HWZ of ASS only 15 -20 min!), has clinical effects that go beyond COX inhibition. ASA has still been shown to inhibit the proinflammatory ubiquitous transcription factor NFκB, iNOS, and COX-2 expression. These effects are probably independent of enzymatic COX inhibition.

Pharmacokinetic data show that ASA is rapidly (HWZ: 15min) and presystemically (in the mucosa of stomach and dodenum) converted to the active metabolite salicylic acid (SS) by cleavage of the acyl moiety. COX inhibition by ASA is irreversible. PG synthesis is inhibited by SS inhibiting transcription of the inducible COX-2 gene and thus inhibiting COX-2 synthesis. SS is excreted directly or in the form of inactive (after conjugation with glucuronic acid or glycine in the liver) metabolites) in a pH-dependent manner via the kidneys.

Acute pain

Acute treatment of the various forms of coronary heart disease, cerebrovascular diseases, PAD.

secondary prevention of myocardial and cerebral infarction

Follow-up treatment of crown interventions (balloon dilatation, stent implantation) and aortocronary bypass surgery (100mgASS+75mg clopedigrel)

Aftercare of venous thromboembolism

Polcythaemia vera (100mg/day)

Depending on the indication, the standard dosage varies greatly. Usual single doses for adults are:

• 100 mg for blood thinning (1 x daily as a permanent treatment)
• 300 - 1000 mg as analgesic (several times a day at intervals of 4-8 hours)
• 1000 mg for migraine
• The maximum daily dose is usually 3000 mg. For the treatment of acute and chronic inflammatory diseases such as rheumatoid arthritis, daily doses of 4-8 g may be used.

Common: Mild gastrointestinal discomfort. Occasional: hyperhidrosis, nausea, vomiting, diarrhea. Rarely (especially after long-term therapy) gastric bleeding or gastric ulceration. Transaminases increase with high-dose therapy.

Notice. ASA can be reactive in about 20-30% of patients with chronic urticaria but can also cause angioedema or anaphylactic shock (see intolerance reaction below).

Rare: serious bleeding such as cerebral hemorrhage, hemolysis, and hemolytic anemia (in patients with severe glucose-6-phosphate dehydrogenase deficiency), hemorrhage such as Nasal bleeding, gingival bleeding, skin bleeding, or urogenital tract bleeding with possible prolongation of bleeding time, hypersensitivity reactions of the respiratory tract, gastrointestinal tract, and cardiovascular system, especially in asthmatics (possible symptoms include: Blood pressure drop, attacks of shortness of breath, rhinitis, nasal congestion, anaphylactic shock or Quincke's edema), headache, dizziness, impaired hearing, ringing in the ears (tinnitus) (may be signs of overdose), mental confusion (may be signs of overdose), visual disturbances (may be signs of overdose), somnolence (may be signs of overdose), Gastrointestinal ulcers, which very rarely may lead to perforation, Gastrointestinal bleeding, which very rarely may lead to iron deficiency anemia, Gastrointestinal inflammation, Thrombocytopenia, Granulocytosis, Hemorrhagic vasculitis, Hypersensitivity reactions such as severe skin reactions (up to erythema multiforme), Menorrhagia, Reye's syndrome.

A syndromal combination with aspirin intolerance, asthma and polyposis nasi has been described as Widal 's disease and plays a role in ENT medicine.

Notice. Dizziness and tinnitus can be symptoms of an overdose (especially in children and elderly patients).

The biography of ASS already shows many elements of the modern pharmaceutical business at the end of the 19th century. First of all, the question of patenting: the Imperial Patent Office had rejected the application to patent the acetylation of salicylic acid. The question of the trade name had to be based on the biological origin of salicylaldehyde from flowers of meadowsweet (Spiraea syn. Filipendula ulmaria). The trade name "Euspirin" was also available. In the end, the vowel "A" (from acetyl) won the race. During World War I, Bayer lost company assets and protection for patents and trademarks, including that of Aspirin®, in the United States in 1917. It was not until 1994 that Bayer was able to reacquire the rights to its own name and to Aspirin® in the United States through the acquisition of Sterling-Winthrop.

Major drug interactions of acetylsalicylic acid