Non-steroidal anti-inflammatory drug

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A nonsteroidal anti-inflammatory ( NSAIDs ) - including non-steroidal anti ( NSAP ) or NSAIDs ( non-steroidal anti-inflammatory drug ) - is a painkiller that because of its anti-inflammatory ( anti-inflammatory ) effect symptomatically and for rheumatism therapy is used. In contrast, glucocorticoids are known as steroidal anti- inflammatory drugs . The category was introduced in the late 1950s to emphasize the difference to 'steroidal anti-inflammatory drugs' with their sometimes severe side effects.

Classification

Nonsteroidal anti-inflammatory drugs belong to the group of non-opioid analgesics because they do not act on the opioid receptors , but essentially intervene in the prostaglandin metabolism by inhibiting cyclooxygenases .

Depending on the point of attack, one differentiates:

Non-selective COX-1/2 inhibitors

Substances from this group work by inhibiting both cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) (COX-1 and 2 inhibitors). Which includes:

Selective COX-2 inhibitors

Since 1999, active substances have been available that specifically block cyclooxygenase-2 ( COX-2 inhibitors , coxibs), such as:

Compared to the above-mentioned non-selective NSAIDs, COX-2 inhibitors show better gastrointestinal tolerance, but have a more damaging effect on the cardiovascular system.

effect

  • The NSAIDs inhibit symptoms of inflammatory processes such as pain and swelling, reduce fever to varying degrees ( antipyretics ) and inhibit the cross-linking of blood platelets ( thrombocyte aggregation ) due to the reduced synthesis of thromboxanes .
  • They work by inhibiting cyclooxygenases . This reduces the synthesis of prostaglandins . At the same time, a higher proportion of arachidonic acid is available for the lipoxygenase pathway, which means that more leukotrienes are formed. Unlike steroidal anti-inflammatory drugs ( glucocorticoids ), NSAIDs do not inhibit all phases of inflammation . The steroidal anti-inflammatory drugs, on the other hand, also block arachidonic acid formation and thus prevent the synthesis of leukotrienes.
  • In the presence of acetylsalicylic acid, the COX-1-mediated thromboxane synthesis of the platelets is permanently and irreversibly switched off, so that the blood's ability to clot is restricted. Low doses of acetylsalicylic acid are prescribed long-term to protect against heart attack or cerebral infarction . The thrombocytes are not able to synthesize new COX enzymes because, as nucleus-free cell fragments, they have no possibility of protein synthesis. The length of the anticoagulant effect corresponds to the life of the platelets of about one week.

Side effects

  • The most frequently observed side effects of NSAIDs are gastric mucosal damage with ulcer formation due to the reduced synthesis of prostaglandin E2 (PGE 2) and further the kidney-damaging effects in long-term therapy.
  • In 2007, statutory health insurers spent almost 125 million euros annually on the treatment of gastrointestinal side effects of NSAIDs. 1100 to 2200 people die in Germany every year from gastrointestinal complications (estimates). The number of unreported cases is likely to be significantly higher.
  • In predisposed patients, the increased supply of leukotrienes can trigger an analgesic asthma. That is why bronchial asthma is a contraindication.
  • In a Medwatch warning from July 9, 2015, the FDA warns again of possible heart attacks and strokes when using nonsteroidal anti-inflammatory drugs.
  • While the coxib rofecoxib was withdrawn from the market in 2004 due to an increased risk of heart attack, ibuprofen and diclofenac are still available and widely used, although a new study suggests a similarly high risk. In contrast to rofecoxib, however, there is an increased risk only with long-term use. According to a report from the Medicines Adverse Reactions Committee (MARC) from New Zealand, warnings are issued against all NSAIDs regarding an increased risk of cardiovascular insecurity.
  • There is evidence that NSAIDs (and in particular the selective COX-2 inhibitors) have a negative influence on bone healing. Their use in the case of bone injuries and injuries to tendon attachments must therefore be viewed critically and should only be carried out on medical advice.
  • Hypersensitivity reactions including anaphylactic shock , which is life-threatening, have occurred very rarely .

Combination preparations

To increase gastrointestinal tolerance, combination preparations have been developed which, in addition to NSAIDs, also contain an active ingredient to reduce gastric acid production. Examples are Arthotec (diclofenac with the prostaglandin E 1 derivative misoprostol ) and Vimovo (naproxen with the proton pump inhibitor esomeprazole ).

Individual evidence

  1. ^ Jonas Kure Buer: Origins and impact of the term 'NSAID'. In: Inflammopharmacology , 22, 2014, p. 263, doi: 10.1007 / s10787-014-0211-2 . PMID 25064056 .
  2. ^ B. Wedi: Current diagnostics in NSAID hypersensitivity. In: AllergoJ int. , 26, 2017, pp. 204–211.
  3. ↑ Quoted after Reduces the pain, protects the organs. In: The general practitioner , 9/2007, p. 39.
  4. ↑ Quoted from tNSAR versus Coxibe: What is certain? - Around 2,200 deaths annually due to complications in the GI tract. In: Ärztliche Praxis , 22, 29 May 2007, p. 8.
  5. ↑ FDA warning about possible heart attacks and strokes
  6. ↑ Small increase in heart risk from common painkillers. ( Memento from August 12, 2014 in the Internet Archive )
  7. ^ Risk of cardiovascular events with NSAIDs
  8. ↑ JA Paoloni, C. Milne, J. Orchard, B. Hamilton: Non-steroidal anti-inflammatory drugs in sports medicine: guidelines for practical but sensitive use. In: British Journal of Sports Medicine. 43, October 2009, pp. 863-865.
  9. ^ B. Su, JP O'Connor: NSAID therapy effects on healing of bone, tendon, and the enthesis. In: Journal of Applied Physiology , 115, September 2013, pp. 892-899, doi: 10.1152 / japplphysiol.00053.2013 .
  10. ↑ Do painkillers (NSAIDs) harm the healing process? sportsandmedicine.com, March 26, 2017.