It has been a long time, non-steroidal anti-inflammatory drugs have been the primary choice for acute gouty arthritis treatment. But now, corticosteroids are considered the first choice substitute because they have milder side effects and the same approximate effectiveness.

Corticosteroid Vs NSIDs In Acute Gouty Arthritis
Acute Gouty Arthritis
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Gouty arthritis is an inflammation of the joints caused by monosodium urate crystals deposition in synovial fluid and other tissues. The American College of Rheumatology (ACR) guidelines recommend giving pharmacological treatment for acute gouty arthritis in the first 24 hours. The treatment options recommended by the ACR and European League Against Rheumatism (EULAR) are oral corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), and colchicine.

Since colchicine often causes side effects such as diarrhea and kidney disorders, NSAIDs are the main choice to replace colchicine. The side effects of using NSAIDs, such as gastrointestinal bleeding and cardiovascular diseases, must be noted, especially for NSAIDs, which are not classified as selective cyclo-oxygenase-2 (COX-2) inhibitors (COXIBs). This should be pointed out because the average gout arthritis sufferers are old and often have comorbidities. According to AAFP, First-line therapy is indometacin 3 x 500 mg.

Recommended ACR dosages for the treatment of  acute gouty arthritis attacks are as follows:

1. Colchicine: 1.2 mg (first dose) followed by 0.6 mg the next 1 hour,
2. NSAID in full dose
3. Prednisolone: ​​0.5 mg/kg per day for 5-10 days or 2-5 days full dose and tapering off for 7-10 days.

Monotherapy with one of the three options above can be given mild to moderate pain in one or several small joints or 1-2 large joints. Combination therapy is recommended for severe pain and large joints. The Combinations are colchicine with NSAIDs, colchicine with oral steroids, or intra-articular steroids with oral medications.

Steroids for treating acute gouty arthritis can be given in oral, intra-articular, and intramuscular preparations. The intra-articular dosage depends on the joint's size and can be provided with or without oral steroids. Intra-articular steroid administration is recommended in acute attacks in 1-2 large joints. If this is not possible, oral steroids are the first choice. The dose for intramuscular is 60 mg triamcinolone acetone with the addition of oral steroids.

Rainer et al. (2016) compared treatment with prednisolone versus indomethacin in 376 patients with acute gouty arthritis. The parameter used is the pain scale. Oral prednisolone was found to have the same effectiveness as indometacin (p = 0.69). Minor side effects arose, more in the prednisolone group than indomethacin (10% vs. 6%, p = 0.001). More research was needed because patients with a history of gastrointestinal bleeding had been excluded from the study.

Janssens et al. (2008), in a randomized, double-blind study, compared oral prednisolone with naproxen in reducing pain in gouty arthritis. Gouty arthritis was diagnosed through synovial fluid analysis. This method was not commonly used and increases the risk of septic arthritis. The reduction in pain scale within 90 hours was not significantly different in the two groups, and only a few minor side effects were found. As with previous studies, a history of gastrointestinal bleeding and peptic ulcers was excluded. In both groups, the pain was resolved in 3 weeks.

The first study comparing steroids and NSAIDs in gouty arthritis was conducted by Man et al. (2007) with a randomized trial comparing prednisolone with indometacin (also given a 75 mg intramuscular injection of diclofenac) and in each group combined with 1 gram of paracetamol. Pain reduction measured by the pain scale was more in the oral steroid group than NSAIDs, where this difference is statistically significant (-2.9 mm vs. -1.7 mm, p - 0.0026). The indomethacin group's side effects were more experienced (P <0.05), and the most frequently encountered were nausea, dyspepsia, heartburn, headaches, and gastrointestinal bleeding. In this study, no gastrointestinal bleeding was found in the steroid group. The recurrence rates in the two groups were not much different.

Furthermore, in Man et al. 's study, Which combined paracetamol as adjunctive therapy for pain relief, paracetamol was more needed in the steroid group. Within 14 days, an average of 10.3 grams and 6.4 grams were required in the steroid and NSAID groups. Pain reduction may be affected by paracetamol administration, but it may not be due to the difference of only 4 grams in 14 days.

ACR recommends oral steroids as second-line prophylactic therapy. The first line is giving uric acid-lowering drugs combined with low-dose colchicine (1-2 x 0.5 mg) or low-dose NSAIDs with or without proton pumping. The prophylactic dose of steroids (prednisolone) is <10 mg/day. There is no further research on the benefits and risks of pharmacological drugs for this prophylaxis.

Using steroids in gouty arthritis is still rare. In the United States, only 9% are found. 3 studies that have been described found that oral steroids have the same effect as NSAIDs. So that steroid administration needs to be considered in patients with contraindications to NSAIDs such as kidney disorders.

Long-term steroids have a better anti-inflammatory effect compared to NSAIDs but have greater side effects. Giving steroids in the short term (1 week) tends to be safe. However, in patients with certain conditions such as uncontrolled diabetes mellitus, immunocompromised, active peptic ulcers, osteoporosis, and herpes infections, they need to consider the benefits and risks, even if given for a short time.

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