Anti-inflammatory

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Anti-inflammatory or antiphlogistic is the property of a substance or treatment that reduces inflammation or swelling. Anti-inflammatory drugs, also called anti-inflammatories, make up about half of analgesics. These drugs remedy pain by reducing inflammation as opposed to opioids, which affect the central nervous system to block pain signaling to the brain.

Nonsteroidal anti-inflammatory drugs[edit]

Nonsteroidal anti-inflammatory drugs (NSAIDs) alleviate pain by counteracting the cyclooxygenase (COX) enzyme.[1] On its own, COX enzyme synthesizes prostaglandins, creating inflammation. In whole, the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the inflammation and resulting pain.[citation needed]

Some common examples of NSAIDs are aspirin, ibuprofen, and naproxen. The newer specific COX-inhibitors are not classified together with the traditional NSAIDs, even though they presumably share the same mode of action.

On the other hand, there are analgesics that are commonly associated with anti-inflammatory drugs but that have no anti-inflammatory effects. An example is paracetamol (known as acetaminophen in the U.S). Contrary to NSAIDs, which reduce pain and inflammation by inhibiting COX enzymes, paracetamol has—as early as 2006—been shown to block the reuptake of endocannabinoids,[2][3] which only reduces pain, likely explaining why it has minimal effect on inflammation; paracetamol is sometimes combined with an NSAID (in place of an opioid) in clinical practice to enhance the pain relief of the NSAID, while still receiving the injury/disease modulating effect of NSAID-induced inflammation reduction (which is not received from opioid/paracetamol combinations).[4]

Side effects[edit]

Long-term use of NSAIDs can cause gastric erosions, which can become stomach ulcers and in extreme cases can cause severe haemorrhage, resulting in death. The risk of death as a result of GI bleeding caused by the use of NSAIDs is 1 in 12,000 for adults aged 16–45.[5] The risk increases almost twentyfold for those over 75.[5] Other dangers of NSAIDs are exacerbating asthma and causing kidney damage.[5] Apart from aspirin, prescription and over-the-counter NSAIDs also increase the risk of heart attack and stroke.[6]

Antileukotrienes[edit]

Antileukotrienes are anti-inflammatory agents which function as leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists (cysteinyl leukotriene receptors), and consequently oppose the function of these inflammatory mediators. Although they are not used for analgesic benefits, they are widely utilized in the treatment of diseases related to inflammation of the lungs, such as asthma and COPD, as well as sinus inflammation in allergic rhinitis.[7][8] They are also being investigated for use in diseases and injuries involving inflammation of the brain (e.g., Parkinson's disease).[9][10]

See also[edit]

References[edit]

  1. ^ Knights KM, Mangoni AA, Miners JO (November 2010). "Defining the COX inhibitor selectivity of NSAIDs: implications for understanding toxicity". Expert Rev Clin Pharmacol. 3 (6): 769–76. doi:10.1586/ecp.10.120. PMID 22111779. S2CID 207209534.
  2. ^ Ottani, Alessandra; Leone, Sheila; Sandrini, Maurizio; Ferrari, Anna; Bertolini, Alfio (February 15, 2006). "The analgesic activity of paracetamol is prevented by the blockade of cannabinoid CB1 receptors". European Journal of Pharmacology. 531 (1–3): 280–281. doi:10.1016/j.ejphar.2005.12.015. hdl:11380/613413. PMID 16438952.
  3. ^ Dani, Mélina; Guindon, Josée; Lambert, Chantal; Beaulieu, Pierre (November 14, 2007). "The local antinociceptive effects of paracetamol in neuropathic pain are mediated by cannabinoid receptors". European Journal of Pharmacology. 573 (1–3): 214–215. doi:10.1016/j.ejphar.2007.07.012. PMID 17651722.
  4. ^ Merry AF, Gibbs RD, Edwards J, Ting GS, Frampton C, Davies E, Anderson BJ (January 2010). "Combined acetaminophen and ibuprofen for pain relief after oral surgery in adults: a randomized controlled trial". British Journal of Anaesthesia. 104 (1): 80–8. doi:10.1093/bja/aep338. PMC 2791549. PMID 20007794.
  5. ^ a b c "Table 7". NSAIDs and adverse effects. Bandolier. Archived from the original on February 18, 2012. Retrieved December 20, 2012.
  6. ^ Trelle, Sven; Reichenbach, Stephan; Wandel, Simon; Hildebrand, Pius; Tschannen, Beatrice; Villiger, Peter M.; Egger, Matthias; Jüni, Peter (11 January 2011). "Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis". British Medical Journal (Clinical Research Ed.). 342: c7086. doi:10.1136/bmj.c7086. PMC 3019238. PMID 21224324.
  7. ^ Dvorak J, Feddermann N, Grimm K (July 2006). "Glucocorticosteroids in football: use and misuse". British Journal of Sports Medicine. 40 (Suppl 1): i48–54. doi:10.1136/bjsm.2006.027599. PMC 2657490. PMID 16799104.
  8. ^ Scott JP, Peters-Golden M (September 2013). "Antileukotriene agents for the treatment of lung disease". Am. J. Respir. Crit. Care Med. 188 (5): 538–544. doi:10.1164/rccm.201301-0023PP. PMID 23822826.
  9. ^ Hamzelou, Jessica (23 October 2015). "Old rat brains rejuvenated and new neurons grown by asthma drug". New Scientist. Retrieved 28 October 2015.
  10. ^ Yirka, Bob. "Asthma drug found to rejuvenate older rat brains". medicalxpress.com. Retrieved 3 November 2015.