Medical treatment regimens range from nonsteroidal anti-inflammatory drugs (NSAIDs) to disease-modifying antirheumatic drugs (DMARDs) to newer biologic therapies, such as the anti–tumor necrosis factor (TNF)-alpha medications. Although traditional therapy has consisted of NSAIDs and local corticosteroid injections, with DMARDs being reserved for NSAID-resistant cases, the finding that 40% of patients may develop erosive and deforming arthritis suggests that early, more aggressive treatment with DMARDs may be warranted.
Symptomatic treatment. NSAIDs are considered a first-line therapy for very mild joint disease, but early consideration should be given to DMARDs. NSAIDs may be used in combination with topical therapy for skin involvement. In some cases, NSAIDs may cause worsening of skin involvement, in which case, a different family of NSAIDs should be used (although a randomized controlled trial showed no worsening of psoriasis in patients treated with the NSAID nimesulide). In addition, more aggressive therapy with methotrexate (MTX) or TNF-alpha inhibitors may be used as an initial therapy in order to allow for control of both psoriasis and psoriatic arthritis. TNF inhibitors also prevent the development of joint destruction in psoriatic patients with joint symptoms.
The most widely used DMARDs are MTX, sulfasalazine, cyclosporine, and leflunomide. These are safe and effective in treating active peripheral arthritis but are not effective in treating axial disease. In addition, no controlled studies have evaluated their efficacy in preventing radiologic joint damage. Combining MTX with cyclosporine or sulfasalazine, as is seen in the treatment of rheumatoid arthritis, may be more effective in some patients
Antimalarials are generally avoided in patients with psoriatic arthritis for fear of exacerbating psoriatic skin lesions. However, 2 case series describing 50 and 31 patients treated with hydroxychloroquine (Plaquenil) found that no patients had exacerbations of their skin lesions. Given the lack of controlled trials, use of this therapy is not encouraged. Systemic corticosteroids are generally avoided because of possible withdrawal-induced rebound of skin disease.
Although indomethacin is the strongest of the available traditional NSAIDs, it is best used for short-term treatment of acute flare-ups because of its GI and CNS adverse effects and its potential to increase blood pressure. Cyclo-oxygenase-2 (COX-2) selective inhibitors may be the optimal agents in patients at risk for GI toxicity with NSAIDs as with traditional NSAIDs, caution should be exercised in the elderly and those with impaired renal function.
Nonsteroidal anti-inflammatory drugs
These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action may be inhibition of COX activity and prostaglandin synthesis. Other mechanisms, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions, may also exist.
Ibuprofen (Motrin, Ibuprin, Advil, Excedrin IB) drug of choice for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. The adult dose is 400 mg orally (PO )every 4-6 hour (h), 600 mg orally every(q) 6hour, or 800 mg orally every8hour while symptoms persist; not to exceed 3.2 g per day .The Pediatric 20-70 mg/kg/day orally divided three times daily (tid)/four times daily (qid) ; start at lower end of dosing range and titrate; not to exceed 2.4 g/day .Should be avoided in pregnancy, Caution should be taken in case of congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy.
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase prothrombin time (PT) when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently.
Diclofenac (Voltaren, Cataflam) Inhibits prostaglandin synthesis by decreasing activity of COX, which, in turn, decreases formation of prostaglandin precursors.The adult dose (more than 12 years) Persistent night pain or morning stiffness: Up to 100 mg orally at bed time (qhs) may help to relieve pain; not to exceed total daily dose of 200 mg .Should be avoided in pregnancy, Caution should be taken in case of Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low WBC counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if leukopenia, granulocytopenia, or thrombocytopenia persists . the same interactions as Ibuprofen .
Naproxen (Anaprox, Naprelan, Naprosyn, Aleve) For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of COX, which is responsible for prostaglandin synthesis.The adult dose 250-500 mg orally two times daily (bid); may increase to 1.5 g/day for limited periods . Should be avoided in pregnancy, the same precautions as diclofenac . the same interactions as Ibuprofen .
Indomethacin (Indocin) Inhibits prostaglandin synthesis. Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. The adult dose 25-50 mg orally twice daily(bid) /three times daily (tid) and 75 mg sustained release (SR)twice daily; not to exceed 200 mg/day. the pediatric dose is 1-2 mg/kg/day orally divided twice daily(bid) /four times daily (qid); not to exceed 4 mg/kg/d or 150-200 mg/d.
Sulindac (Clinoril) Decreases activity of COX and, in turn, inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators. The adult dose 150-200 mg orally twice dailly or 300-400 every day; not to exceed 400 mg/d.Not established for pediatrics .
Meloxicam (Mobic) Decreases activity of COX, which, in turn, inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators. 7.5 mg orally every day; may increase to 15 mg orally every day .
Celecoxib (Celebrex) For those at risk of GI toxicity with NSAIDs. Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek lowest dose for each patient.the adult dose is 200 mg/d orally every day ; alternatively, 100 mg two times daily and not established for pediatrics . Coadministration with fluconazole may cause increase in plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease plasma concentrations , so spacing between two drugs should be done at least for two hours. May cause hypersensitivity . Avoided in pregnancy . May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; caution in severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate therapy when symptoms or laboratory results suggest liver dysfunction .
0 التعليقات:
إرسال تعليق