NSAIDs in the Management of Rheumatoid Arthritis: Difference between revisions

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=== Overview ===
<div class="editorbox"> '''Original Editor '''- Kristie Nguyen '''Top Contributors''' - {{Special:Contributors/{{FULLPAGENAME}}}}</div>
 
== Overview ==
NSAIDS are commonly used for antipyretic, anti-inflammatory and analgesic purposes. The main indications are pain, inflammation and infection.<ref>Sohail R, Mathew M, Patel KK, Reddy SA, Haider Z, Naria M, Habib A, Abdin ZU, Chaudhry WR, Akbar A, Patel KK. Effects of non-steroidal anti-inflammatory drugs (NSAIDs) and gastroprotective NSAIDs on the gastrointestinal tract: a narrative review. Cureus. 2023 Apr 3;15(4).</ref>
 
Non-steroidal anti-inflammatory drugs ([[NSAIDs]]) are the first drugs used to symptomatically treat RA.<ref>O'Dell JR. Therapeutic strategies for rheumatoid arthritis. N Engl J Med. 2004;350(25):2591-2602.</ref> While they are not as potent anti-inflammatory drugs as glucocorticoids, they tend to have fewer side effects and offer pain relief.<ref>Gotzche PC, Johansen HK. Short-term low-dose corticosteroids vs placebo and nonsteroidal antiinflammatory drugs in rheumatoid arthritis. Cochrane Databse Syst Rev. 2004;(3):CD000189. doi:10.1002/14651858.CD000189.pub2</ref><ref>Adebajo A. Non-steroidal anti-inflammatory drugs for the treatment of pain and immobility-associated osteoarthritis: consensus guidance for primary care. BMC Fam Pract. 2012;13:23. doi:10.1186/1471-2296-13-23.</ref> In addition, they may later be combined with [[DMARDs in the Management of Rheumatoid Arthritis|DMARD]]<nowiki/>s to control the disease process.<ref>Blumenauer B, Cranney A, Clinch J, Tugwell P. Quality of life in patients with rheumatoid arthritis: which drugs might make a difference. Pharmacoeconomics. 2003;21(13):927-940.</ref> The NSAIDs focused on below are ibuprofen, diclofenac, and celecoxib.
Non-steroidal anti-inflammatory drugs ([[NSAIDs]]) are the first drugs used to symptomatically treat RA.<ref>O'Dell JR. Therapeutic strategies for rheumatoid arthritis. N Engl J Med. 2004;350(25):2591-2602.</ref> While they are not as potent anti-inflammatory drugs as glucocorticoids, they tend to have fewer side effects and offer pain relief.<ref>Gotzche PC, Johansen HK. Short-term low-dose corticosteroids vs placebo and nonsteroidal antiinflammatory drugs in rheumatoid arthritis. Cochrane Databse Syst Rev. 2004;(3):CD000189. doi:10.1002/14651858.CD000189.pub2</ref><ref>Adebajo A. Non-steroidal anti-inflammatory drugs for the treatment of pain and immobility-associated osteoarthritis: consensus guidance for primary care. BMC Fam Pract. 2012;13:23. doi:10.1186/1471-2296-13-23.</ref> In addition, they may later be combined with [[DMARDs in the Management of Rheumatoid Arthritis|DMARD]]<nowiki/>s to control the disease process.<ref>Blumenauer B, Cranney A, Clinch J, Tugwell P. Quality of life in patients with rheumatoid arthritis: which drugs might make a difference. Pharmacoeconomics. 2003;21(13):927-940.</ref> The NSAIDs focused on below are ibuprofen, diclofenac, and celecoxib.


=== Pharmacokinetics ===
== Pharmacokinetics ==
NSAIDS exert their effects by inhibiting the COX-1 and COX-2 forms of enzymes that synthesize prostaglandins.<ref name=":0">Vane JR, Botting RM. The mechanism of action of aspirin. Thromb Res. 2003;110(5-6):255-258.</ref> Inhibition of COX-1 blocks the production of beneficial and protective prostaglandins, whereas inhibition of COX-2 blocks the synthesis of prostaglandins in inflamed tissues. Ibuprofen and diclofenac block both forms of the enzyme (Roberts & Morrow, 2001).<ref>Roberts LJ, Morrow JD. Analgesic-antipyretic and antiinflammatory agents and drugs employed in the treatment of gout. In: Hardman JG et al, ed. The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw Hill;2001.</ref> Celecoxib, on the other hand, selectively inhibits only COX-2.<ref name=":0" />
NSAIDS exert their effects by inhibiting the COX-1 and COX-2 forms of enzymes that synthesize prostaglandins.<ref name=":0">Vane JR, Botting RM. The mechanism of action of aspirin. Thromb Res. 2003;110(5-6):255-258.</ref> Inhibition of COX-1 blocks the production of beneficial and protective prostaglandins, whereas inhibition of COX-2 blocks the synthesis of prostaglandins in inflamed tissues. Ibuprofen and diclofenac block both forms of the enzyme (Roberts & Morrow, 2001).<ref>Roberts LJ, Morrow JD. Analgesic-antipyretic and antiinflammatory agents and drugs employed in the treatment of gout. In: Hardman JG et al, ed. The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw Hill;2001.</ref> Celecoxib, on the other hand, selectively inhibits only COX-2.<ref name=":0" /><ref>Machado GC, Abdel-Shaheed C, Underwood M, Day RO. Non-steroidal anti-inflammatory drugs (NSAIDs) for musculoskeletal pain. Bmj. 2021 Jan 29;372.</ref>
 
To determine which NSAID should be prescribed, the pharmacokinetics of the drugs should be considered. The half-lives of NSAIDs vary, ranging from a couple of hours (ibuprofen and diclofenac) to eleven hours (celecoxib). Absorption methods also differ. Ibuprofen is primarily absorbed by the GI tract and diclofenac undergoes first-pass metabolism via the liver, resulting in 50% bioavailability. The exact absorption mechanism for celecoxib is still unknown. All three undergo metabolism via the liver and are typically excreted in urine.<ref name=":1">U.S. Food and Drug Administration. Motrin® Ibuprofen Tablets, USP. https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/017463s105lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.</ref><ref name=":2">U.S. Food and Drug Administration. Voltaren®  (diclofenac sodium enteric-coated tablets). https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019201s046lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.</ref>
 
== Therapeutic Effects Of NSAIDS ==
* NSAIDs are the first line of treatment for rheumatoid arthritis which helps in symptomatic relief.
* It mainly reduces pain and stiffness of the affected joints. the mechanism behind this is inhibition of prostaglandin production in peripheral tissues. Prostaglandin also plays an important role in neuronal sensitization.
* It also has an anti inflammatory effect on juvenile rheumatoid arthritis.<ref>Crofford LJ. Use of NSAIDs in treating patients with arthritis. Arthritis research & therapy. 2013 Jul;15:1-0.</ref>
 
== Adverse Effects ==
There are various toxicities linked with NSAIDS. The effect of it varies based on the compound and dosage.
 
* Gastrointestinal- ulcer, colitis, Esophagitis
* Cardiovascular- Myocardial infarction, stroke
* Neuro- dizziness, confusion, seizures
* Renal- water retention, hypertension, weight gain<ref name=":2" /><ref name=":3">U.S. Food and Drug Administration. Celebrex® celecoxib capsules. https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020998s026lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.</ref>


To determine which NSAID should be prescribed, the pharmacokinetics of the drugs should be considered. The half-lives of NSAIDs vary, ranging from a couple of hours (ibuprofen and diclofenac) to eleven hours (celecoxib). Absorption methods also differ. Ibuprofen is primarily absorbed by the GI tract and diclofenac undergoes first-pass metabolism via the liver, resulting in 50% bioavailability. The exact absorption mechanism for celecoxib is still unknown. All three undergo metabolism via the liver and are typically excreted in urine.<ref name=":1">U.S. Food and Drug Administration. Motrin® Ibuprofen Tablets, USP. https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/017463s105lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.</ref><ref name=":2">U.S. Food and Drug Administration. Voltaren®  (diclofenac sodium enteric-coated tablets). https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019201s046lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.</ref><ref name=":3">U.S. Food and Drug Administration. Celebrex® celecoxib capsules. https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020998s026lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.</ref>
== Clinical Implications ==
[[File:NSAIDS .jpg|center|thumb|376x376px|Mechanism of action Of NSAIDS                        ]]<ref>Bindu S, Mazumder S, Bandyopadhyay U. Non-steroidal anti-inflammatory drugs (NSAIDs) and organ damage: A current perspective. Biochemical pharmacology. 2020 Oct 1;180:114147. </ref>


=== Clinical Implications ===
* NSAIDS are the most common medications used in treating arthritis, CV disease  and pain.
NSAIDs have relatively low side effects, but potential adverse effects should still be considered. Because most NSAIDs are non-selective for COX-1 and COX-2, ibuprofen and diclofenac can cause GI bleeding. Conversely, the selectivity of celecoxib may lead to cardiovascular problems. In either case, edema, exfoliative dermatitis, Stevens-Johnson Syndrome, and renal failure may occur. Physical therapists and other clinicians treating patients with RA should be cognizant of these side effects and monitor for appearance of related symptoms. Dizziness, heart rate, and weakness can affect gait and functional activities. Expecting mothers and those with a history of cardiovascular disease or diabetes should consult their physician prior to use of these medications.<ref name=":1" /><ref name=":2" /><ref name=":3" />
* It has been proven that NSAIDS causes delay in ulcer healing and produce gastrointestinal ulcer.<ref>Tarnawski AS, Jones MK. Inhibition of angiogenesis by NSAIDs: molecular mechanisms and clinical implications. Journal of molecular medicine. 2003 Oct;81:627-36.</ref>
* It can even lead to intestinal obstruction , GI erosion and GI bleeding.


=== References ===
== References ==
<references />
<references />


====== [[Pharmacological Management of Rheumatoid Arthritis|<<Back to Pharmacological Management of Rheumatoid Arthritis]] ======
====== [[Pharmacological Management of Rheumatoid Arthritis|<<Back to Pharmacological Management of Rheumatoid Arthritis]] ======

Latest revision as of 11:41, 26 June 2024

Original Editor - Kristie Nguyen Top Contributors - Nupur Smit Shah, Kristie Nguyen, Kim Jackson and Lucinda hampton

Overview[edit | edit source]

NSAIDS are commonly used for antipyretic, anti-inflammatory and analgesic purposes. The main indications are pain, inflammation and infection.[1]

Non-steroidal anti-inflammatory drugs (NSAIDs) are the first drugs used to symptomatically treat RA.[2] While they are not as potent anti-inflammatory drugs as glucocorticoids, they tend to have fewer side effects and offer pain relief.[3][4] In addition, they may later be combined with DMARDs to control the disease process.[5] The NSAIDs focused on below are ibuprofen, diclofenac, and celecoxib.

Pharmacokinetics[edit | edit source]

NSAIDS exert their effects by inhibiting the COX-1 and COX-2 forms of enzymes that synthesize prostaglandins.[6] Inhibition of COX-1 blocks the production of beneficial and protective prostaglandins, whereas inhibition of COX-2 blocks the synthesis of prostaglandins in inflamed tissues. Ibuprofen and diclofenac block both forms of the enzyme (Roberts & Morrow, 2001).[7] Celecoxib, on the other hand, selectively inhibits only COX-2.[6][8]

To determine which NSAID should be prescribed, the pharmacokinetics of the drugs should be considered. The half-lives of NSAIDs vary, ranging from a couple of hours (ibuprofen and diclofenac) to eleven hours (celecoxib). Absorption methods also differ. Ibuprofen is primarily absorbed by the GI tract and diclofenac undergoes first-pass metabolism via the liver, resulting in 50% bioavailability. The exact absorption mechanism for celecoxib is still unknown. All three undergo metabolism via the liver and are typically excreted in urine.[9][10]

Therapeutic Effects Of NSAIDS[edit | edit source]

  • NSAIDs are the first line of treatment for rheumatoid arthritis which helps in symptomatic relief.
  • It mainly reduces pain and stiffness of the affected joints. the mechanism behind this is inhibition of prostaglandin production in peripheral tissues. Prostaglandin also plays an important role in neuronal sensitization.
  • It also has an anti inflammatory effect on juvenile rheumatoid arthritis.[11]

Adverse Effects[edit | edit source]

There are various toxicities linked with NSAIDS. The effect of it varies based on the compound and dosage.

  • Gastrointestinal- ulcer, colitis, Esophagitis
  • Cardiovascular- Myocardial infarction, stroke
  • Neuro- dizziness, confusion, seizures
  • Renal- water retention, hypertension, weight gain[10][12]

Clinical Implications[edit | edit source]

  • NSAIDS are the most common medications used in treating arthritis, CV disease and pain.
  • It has been proven that NSAIDS causes delay in ulcer healing and produce gastrointestinal ulcer.[13]
  • It can even lead to intestinal obstruction , GI erosion and GI bleeding.

References[edit | edit source]

  1. ↑ Sohail R, Mathew M, Patel KK, Reddy SA, Haider Z, Naria M, Habib A, Abdin ZU, Chaudhry WR, Akbar A, Patel KK. Effects of non-steroidal anti-inflammatory drugs (NSAIDs) and gastroprotective NSAIDs on the gastrointestinal tract: a narrative review. Cureus. 2023 Apr 3;15(4).
  2. ↑ O'Dell JR. Therapeutic strategies for rheumatoid arthritis. N Engl J Med. 2004;350(25):2591-2602.
  3. ↑ Gotzche PC, Johansen HK. Short-term low-dose corticosteroids vs placebo and nonsteroidal antiinflammatory drugs in rheumatoid arthritis. Cochrane Databse Syst Rev. 2004;(3):CD000189. doi:10.1002/14651858.CD000189.pub2
  4. ↑ Adebajo A. Non-steroidal anti-inflammatory drugs for the treatment of pain and immobility-associated osteoarthritis: consensus guidance for primary care. BMC Fam Pract. 2012;13:23. doi:10.1186/1471-2296-13-23.
  5. ↑ Blumenauer B, Cranney A, Clinch J, Tugwell P. Quality of life in patients with rheumatoid arthritis: which drugs might make a difference. Pharmacoeconomics. 2003;21(13):927-940.
  6. ↑ 6.0 6.1 Vane JR, Botting RM. The mechanism of action of aspirin. Thromb Res. 2003;110(5-6):255-258.
  7. ↑ Roberts LJ, Morrow JD. Analgesic-antipyretic and antiinflammatory agents and drugs employed in the treatment of gout. In: Hardman JG et al, ed. The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw Hill;2001.
  8. ↑ Machado GC, Abdel-Shaheed C, Underwood M, Day RO. Non-steroidal anti-inflammatory drugs (NSAIDs) for musculoskeletal pain. Bmj. 2021 Jan 29;372.
  9. ↑ U.S. Food and Drug Administration. Motrin® Ibuprofen Tablets, USP. https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/017463s105lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.
  10. ↑ 10.0 10.1 U.S. Food and Drug Administration. Voltaren® (diclofenac sodium enteric-coated tablets). https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019201s046lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.
  11. ↑ Crofford LJ. Use of NSAIDs in treating patients with arthritis. Arthritis research & therapy. 2013 Jul;15:1-0.
  12. ↑ U.S. Food and Drug Administration. Celebrex® celecoxib capsules. https://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020998s026lbl.pdf. Last Modified January 20, 2007. Accessed November 21, 2018.
  13. ↑ Tarnawski AS, Jones MK. Inhibition of angiogenesis by NSAIDs: molecular mechanisms and clinical implications. Journal of molecular medicine. 2003 Oct;81:627-36.
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