Gout
In medicine, gout is a "hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi."[1]
Treatment
A randomized controlled trial found that patients who used ice packs had better relief of pain with no negative side effects.[2]
| Patients | Interventions | Results | ||
|---|---|---|---|---|
| Steroid | NSAID | |||
| Janssens et al 2008[3] | 120 total patients with uric acid crystals on arthrocentesis | Prednisolone 35 mg once daily for 5 days | Naproxen 500 mg twice daily for 5 days | NSAID tended to be better |
| Man et al 2007[4] | 90 total patients with clinical diagnosis of gout† | Initially prednisolone 30 mg Followed by prednisolone 30 mg daily for 5 days and as needed acetaminophen |
Initially diclofenac 75 mg with indomethacin 50 mg Followed by indomethacin 50 mg every 8 hrs for 2 days then 25 mg every 8 hrs for 3 days and as needed acetaminophen. |
Steroids faster reduction in pain. Steroids used more acetaminophen. More adverse effects from indomethacin. |
| Notes: † Clinical diagnosis of gout was "pain and warmth in a joint, and presented within 3 days of the onset of pain and also had 1 or more of the following: metatarsal-phalangeal joint involvement; knee or ankle joint involvement and aspirate containing crystals; or typical gouty arthritis, with either gouty tophi present or previous joint aspiration confirming the diagnosis of gout." Seven patients allowed arthrocentesis and all were positive for gout. | ||||
Randomized controlled trials find similar benefit from non-steroidal anti-inflammatory agents and oral glucocorticoids. In the first trial[4] , less adverse drug reactions occurred in the glucocorticoids group; however, the NSAID group received a high dose[5].
In the second randomized controlled trial statistically equal effect resulted from prednisolone 35 mg orally per day or naproxen 500 mg orally per day; however there was an insigificant 8% improvement in the NSAID group.[3]
Colchicine
Colchicine is better than placebo according to a systematic review by the Cochrane Collaboration[6] that found a single randomized controlled trial[7].
Prognosis
Acute flares
Without treatment, one third of flares improve within 2 days.[7]
Prevention
Diet
Avoiding products with high fructose such as sugary soft drinks (sweetened with high fructose corn syrup), and other high-fructose products, such as fruit juice, apples, and oranges may help.[8]
Medications
Xanthine oxidase inhibitors
Allopurinol can reduce frequency of attacks. However, when allopurinol is started, colchicine 0.6 mg twice daily should also be used. In a randomized controlled trial, co-treatment with colchicine 0.6 mg twice daily while allopurinol was tapered up from 100 mg/day until 3 months after the serum urate concentration < 6.5 mg/dl, reduced flares of gout from 77% in the placebo broup to 33% with colchicine prophylaxis. Most of these patients had tophi.[9]
Allopurinol should be increased as possible to achieve a goal serum urate of <6 mg/dl (360 micromoles/liter).[10]
Febuxostat, a non-purine inhibitor, is equally effective as allopurinol when compared in a randomized controlled trial.[11]
Uricosuric agents
References
- ↑ Anonymous (2024), Gout (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Schlesinger N, Detry MA, Holland BK, et al (2002). "Local ice therapy during bouts of acute gouty arthritis". J. Rheumatol. 29 (2): 331–4. PMID 11838852. [e]
- ↑ 3.0 3.1 Janssens HJ, Janssen M, van de Lisdonk EH, van Riel PL, van Weel C (May 2008). "Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial". Lancet 371 (9627): 1854–60. DOI:10.1016/S0140-6736(08)60799-0. PMID 18514729. Research Blogging.
- ↑ 4.0 4.1 Man CY, Cheung IT, Cameron PA, Rainer TH (2007). "Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute goutlike arthritis: a double-blind, randomized, controlled trial". Annals of emergency medicine 49 (5): 670–7. DOI:10.1016/j.annemergmed.2006.11.014. PMID 17276548. Research Blogging.
- ↑ Henry D, Lim LL, Garcia Rodriguez LA, et al (June 1996). "Variability in risk of gastrointestinal complications with individual non-steroidal anti-inflammatory drugs: results of a collaborative meta-analysis". BMJ 312 (7046): 1563–6. PMID 8664664. PMC 2351326. [e]
- ↑ Schlesinger N, Schumacher R, Catton M, Maxwell L (2006). "Colchicine for acute gout". Cochrane Database Syst Rev (4): CD006190. DOI:10.1002/14651858.CD006190. PMID 17054279. Research Blogging.
- ↑ 7.0 7.1 Ahern MJ, Reid C, Gordon TP, McCredie M, Brooks PM, Jones M (June 1987). "Does colchicine work? The results of the first controlled study in acute gout". Aust N Z J Med 17 (3): 301–4. DOI:10.1111/j.1445-5994.1987.tb01232.x. PMID 3314832. Research Blogging.
- ↑ Hyon K Choi and Gary Curhan, “Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study,” BMJ (January 31, 2008): bmj.39449.819271.BE.
- ↑ Borstad GC, Bryant LR, Abel MP, Scroggie DA, Harris MD, Alloway JA (2004). "Colchicine for prophylaxis of acute flares when initiating allopurinol for chronic gouty arthritis". J. Rheumatol. 31 (12): 2429–32. PMID 15570646. [e]
- ↑ Perez-Ruiz F, Lioté F (2007). "Lowering serum uric acid levels: What is the optimal target for improving clinical outcomes in gout?". Arthritis Rheum. 57 (7): 1324–8. DOI:10.1002/art.23007. PMID 17907217. Research Blogging.
- ↑ Becker MA, Schumacher HR Jr, Wortmann RL, MacDonald PA, Eustace D, Palo WA, Streit J, Joseph-Ridge N.Febuxostat compared with allopurinol in patients with hyperuricemia and gout.N Engl J Med. 2005 Dec 8;353(23):2450-61. PMID 16339094