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Antirheumatics: NSAIDs, Glucocorticoids, DMARDs, and Biologic Treatments

Learn about the different types of antirheumatic drugs used for the treatment of rheumatoid arthritis (RA) and osteoarthritis (OA), including NSAIDs, glucocorticoids, DMARDs, and biologic treatments.

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Antirheumatics: NSAIDs, Glucocorticoids, DMARDs, and Biologic Treatments

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  1. Antirheumatics

  2. Treatment of RA 1. Non-steroidal anti-inflammatorydrugs (NSAIDs) 2. Glucocorticoids 3. Diseasemodifying anti-rheumaticdrugs - DMARDs - imunosupressiveeffect - slowlyonsetofthetherapeutic effect - newest - biologictreatment (monoclonalantibodies and solubilereceptors ) forexample inhibitorsof TNF (infliximab, adalimumab; etanercept)

  3. Non-steroidalanti-inflammatorydrugs (NSAIDs)

  4. Non-steroidalanti-inflammatorydrugs Division according to COX selectivity:

  5. Effects of NSAIDs • Analgesic effect • Antipyretic effect • Antiflogistic effect (mainly higher doses) • Antiaggregatory effect (not every NSAID, most important is ASA because of irreversible blocade of COX-1- be careful with combination of ASA for anti-aggregation and other NSAIDs- mostly ibuprofen) • Other effects- for example reduced incidence of some tumors (for example colorectal carcinoma), uricosuric effekt ...

  6. NSAIDs– oneofthe most widelyuseddruggroups→ theirADRsrepresent a seriousmedical / publichealth / economicalproblemthere are big differencesbetweenvariousNSAIDsin thelevel risk ofparticularpossibleADRs

  7. AdverseeffectsofNSAIDs • GIT-erosions and ulcersofthegastricmucosa (also in otherlocalisationsinthe GIT), nausea, vomitus, meteorism, diarrhoea, constipation... (mainlyinhibitionof COX-1) • kidney-reductionofglomerularfiltration, retentionof Na and fluids, edema, hyperkaliemia, kidneyfailure, interstitialnephrits...(inhibitionof COX-1 and 2) • CVS-thromboticevents, increaseofbloodpressure, heartfailure...(mainly COX-2 (mostly in thromboticevents)) • CNS- cephalea, weakness, sleapdisorders, dizziness, epilepticseizures... • other- hepatotoxicity, bleeding, provocationofasthmaticattack, Ray´ssyndrom, prolongedchildbirth, urticaria, decreasednumberofwhitebloodcells...

  8. Gastrointestinal ADRs • most serious – ↓ production of prostaglandins in the gastric mucosa → peptic ulcer (most often in the stomach and duodenum; the mucosa can get damaged by NSAIDs also in other places in the GIT) • roughly 25 % of chronic NSAID users might develop erosions and ulcers, in 2-4 % perforation or bleeding can occure

  9. Kidney ADRs • Decreased production of prostanoids → negative effect on the perfusion of the kidneys, glomerular filtration, excretion of sodium and water and on production of renin →circulation overload, oedemas, hypertension ; hyperkalemia ; in severe cases symptoms of acute kidney failure • serious complication– interstitial nephritis (immunological reasons) • Incidence of kidney ADRs is poughly 18%, severe cases- roughly 1%

  10. CardiovascularADRs • Increased blood pressure- mostly in hypertensive patients treated with antihypertensives (mainly ACEIs, ARBs, beta blockers), there are big differences between various NSAIDs • Development/worsening of heart failure-the risk is highest during the first weeks of treatment, mainly in patients with preexisting congestive heart failure; possibly 19% of all cases of congestive heart failure could be caused (at least partially) by NSAID therapy • Thrombotic events- acute myocardial infarction, stroke, thromboembolic disease

  11. NSAIDs • Symptomatic treatment • Analgetic effect: in several minutes • Antiinflammatory effect: in 7-14 days • Interindividual variability in response to different drugs • Different types of NSAIDs are not combined together

  12. GLUCOCORTICOIDS • The most effective symptomatic treatment • Their are applied only till DMARDs start to be effective • Given is the lowest effective dose and for the shortest time needed • Rebound effect!!! (prolonged administration cannot be stopped abruptly

  13. DMARDs = disease-modifying antirheumatic drugs Used nowadays are especially: methotrexate (antagonist of folic acid) – drug of choice sulfasalazine hydroxychloroquine leflunomid If methotrexate not effective, use another DMARDs or combination therapy

  14. DMARDs Biologic treatment Anti TNF: infliximab, adalimumab, certolizumab, golimumab (monoclonal antibodies) etanercept (solubile receptor) Against IL-6 receptor: tocilizumab Against protein CD20 (on B lymphocytes): rituximab Against protein B7 (decrease the activity of T lymphocytes through inhibition of their interaction with antigen presenting cells): abatacept

  15. Treatment of OA • Rapid actingdrugs 1. Analgeticdrugs • Paracetamol, metamizol • Nonsteroidalantiinflammatorydrugs • Weakopioids – tramadol 2. Topicaltransdermaltreatment • NSAID (diclofenac, ketoprofen) • Irritants (capsaicin, menthol) 3. Steroidantiflogisticdrugs (corticoids) intra-articularadministration • triamcinolone, betametazone • avoidfrequentadministration • Slowlyactingdrugs chondroprotectives 1. Diseasemodifyingdrugs (DMOAD)? • Glucosaminsulphate • Chondroitinsulphate • Hyaluronicacid No provenagentsthatreverseosteoarthritis (alternative to pharmacotherapy in advancedstages of thediseaseissurgery).

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