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==[[Diagnosis]]==
==[[Diagnosis]]==
=== Diagnosis of acute gout ===
=== Diagnosis of intercritical and tophaceous gout ===
* In patients where a diagnosis of gout wasn’t ascertained during an acute flare, a synovial fluid analysis identifying urate crystals from the previously affected joints would allow a late establishment of the disease.
* Urate crystals are present in synovial fluid of all untreated gouty patients and in approximately 70 percent of those under urate-lowering therapy. 8624633 10577299 444319
* For tophaceous gout, demonstration of urate crystals in aspirates of tophi provides an easy way to confirm the diagnosis 10834006
=== Clinical diagnosis “rule” for acute gout ===
* In patients with acute gout where a diagnosis couldn’t be confirmed due to a negative synovial fluid analysis for MSU crystals, a clinical diagnostic approach can be implemented. 20625017
* This approach utilizes a set of clinical parameters with a scoring value. The parameters are derived from history, clinical presentation, and the laboratory findings. 25231179
* This approach has been shown to improve the accuracy of diagnosis without joint fluid analysis of a gout flare in primary care practice settings 20625017
* The model uses seven variables to calculate a total score to distinguish three levels of risk for gout. These are:
*# Male sex (2 points)
*# Previous patient-reported arthritis flare (2 points)
*# Onset within one day (0.5 points)
*# Joint redness (1 point)
*# First metatarsal phalangeal joint involvement (2.5 points)
*# Hypertension or at least one cardiovascular disease (1.5 points)
*# Serum urate level greater than 5.88 mg/dL (3.5 points)
* Based upon the total score, patients can be identified as having low (≤4 points), intermediate (>4 to <8 points), or high (≥8 points) probability of having acute gout.
* In patients with an intermediate score (>4 but <8 points), a preliminary diagnosis of gout may be made for the purpose of clinical management based upon a prevalent clinical features favoring gout.
* This diagnostic approach is not recommended for patients presenting with oligoarticular and polyarticular arthritis, as it was developed studying patients with monoarthritis seen by family physicians.  


==[[Treatment]]==
==[[Treatment]]==

Revision as of 19:45, 28 May 2020

Figure 1:Tophaceous gout affecting the right great toe and finger interphalangeal joints. Note the asymmetrical swelling and yellow-white discolouration.[1]


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Synonyms and keywords: Urate crystal arthropathy; uric acid crystal deposition in joint; gouty arthritis; podagra

Overview

Historical Perspective

Pathophysiology

Differentiating Gout from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Treatment

Clinical practice guidelines address treatment.[2][3][4] However, trials comparing glucocorticoids (steroids) and non-steroidal anti-inflammatory agents (NSAIDs) were not published till after the guidelines.

A nurse-led protocol with treatment goal of 6 mg/dL was beneficial[5].

Regarding medications, if there are no mitigating factors in choosing a drug, glucocorticoids, non-steroidal anti-inflammatory agents (NSAIDs), and colchicine all work; however, colchicine consistently causes drug toxicity.

A combination treatment is ice four times a day with oral prednisone 30 mg orally tapered over 6 days (30 mg for two days, 20 mg for two days, 10 mg for two days) and colchicine 0.6 mg/day.[6] An advantage of this regimen is the reduced toxicity from the low dose of colchicine and that the colchicine helps prevent flares if allopurinol is later started. Colchicine has been combined with NSAIDs[7] that are not metabolized by the CYP3A4 isoenzyme of cytochrome P-450 (naproxen is not metabolized by CYP3A4). Combining glucocorticoids with NSAIDs increased the risk for gastrointestinal drug toxicity[8]

Local ice

Ice packs, applied for 30 minutes 4 times per day, can help according to a randomized controlled trial without allocation concealment.[6] In this trial, ice reduced the visual pain analog score by an additional 33 mm beyond the reduction provided by a combination of glucocorticoids and colchicine.

Non-steroidal anti-inflammatory agents

Non-steroidal anti-inflammatory agents (NSAIDs) are better than placebo according to a randomized controlled trial of 30 total patients.[9] According to a summary of this trial, "the knee was affected in 14 cases and the great toe in only two cases. After 24 h, 67% of tenoxicam group had ≥50% reduction in pain compared with 26% of placebo group (P<0.05). However, at the end of the treatment (4 days), there was no significant difference between the groups."[10]

Glucocorticoids

Comparison of NSAID and steroids for acute gout
  Patients Interventions Results
Steroid NSAID
Janssens et al 2008[11] 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 trended better (88% versus 80% response; p=0.3)
No differences in rates of drug toxicity.
Man et al 2007[12] 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.

Indomethacin trended to more relapses at 2 weeks (11% vs 17%).

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 the reduction in visual analog scale after 5 days was 44.7 with prednisolone and 46.0 with naproxen.[12] Less adverse drug reactions occurred in the glucocorticoids group; however, the NSAID group received a high dose (50 mg every 8 hours for 2 days, followed by 25 mg every 8 hours for 3 days)[13].

In the second randomized controlled trial statistically equal effect resulted from prednisolone 35 mg orally per day or naproxen 500 mg orally twice per day; however there was an insignificant 8% improvement in the NSAID group.[11] There were no significant differences in drug toxicity.

Colchicine

Colchicine is better than placebo according to a systematic review by the Cochrane Collaboration[14] that found a single randomized controlled trial of 43 patients[15]. In this study, colchicine 1 mg orally, followed by 0.5 mg every two hours led to a 50% reduction in pain in about 70% of patients compared to about 35% of patients who received placebo. However, all patients had drug toxicity from colchicine and in 90% of the patients toxicity occurred before 50% reduction in pain.

Regarding the best dose, 1.2 mg followed by 0.6 mg in 1 hour may be as effective as higher dose.[16]

To avoid drug toxicity, lower doses of colchicine (0.6 per day) have been used in combination with glucocorticoids.[6] The UK National Library for Health recommends 0.5 mg two to four times a day.[17]

Anti-cytokines

The monoclonal antibody against interleukin-1 beta, canakinumab, may help according to a randomized controlled trial.[18]

Prognosis

Acute flares

Without treatment, one third of flares improve within 2 days.[15]

Case Studies

Case #1

Related Chapter

External Links

  • "Answers and Questions on Gout". U.S. National Institutes of HealthNational Institute of Arthritis and Musculoskeletal and Skin Diseases. September 28th, 2007. Retrieved 2007-08-28. Check date values in: |date= (help)
  • "Coffee Consumption and Reduced Gout Risk". Drinking coffee reduces risk of gout in middle age men. U.S. National Institutes of Health. Retrieved 2007-05-25.

References

  1. Roddy, Edward (2011). "Revisiting the pathogenesis of podagra: why does gout target the foot?". Journal of Foot and Ankle Research. 4 (1). doi:10.1186/1757-1146-4-13. ISSN 1757-1146.
  2. Khanna D, Khanna PP, Fitzgerald JD, Singh MK, Bae S, Neogi T; et al. (2012). "2012 American College of Rheumatology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis". Arthritis Care Res (Hoboken). 64 (10): 1447–61. doi:10.1002/acr.21773. PMID 23024029.
  3. Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T; et al. (2012). "2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia". Arthritis Care Res (Hoboken). 64 (10): 1431–46. doi:10.1002/acr.21772. PMID 23024028.
  4. Zhang W, Doherty M, Bardin T; et al. (2006). "EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT)". Ann. Rheum. Dis. 65 (10): 1312–24. doi:10.1136/ard.2006.055269. PMID 16707532. Unknown parameter |month= ignored (help)
  5. Doherty M, Jenkins W, Richardson H, Sarmanova A, Abhishek A, Ashton D; et al. (2018). "Efficacy and cost-effectiveness of nurse-led care involving education and engagement of patients and a treat-to-target urate-lowering strategy versus usual care for gout: a randomised controlled trial". Lancet. 392 (10156): 1403–1412. doi:10.1016/S0140-6736(18)32158-5. PMC 6196879. PMID 30343856.
  6. 6.0 6.1 6.2 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.
  7. 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. Unknown parameter |month= ignored (help)
  8. Fries JF, Williams CA, Bloch DA, Michel BA (1991). "Nonsteroidal anti-inflammatory drug-associated gastropathy: incidence and risk factor models". Am. J. Med. 91 (3): 213–22. PMID 1892140. Unknown parameter |month= ignored (help)
  9. García de la Torre, Ignacio. (1987) Estudio doble-ciego paralelo, comparativo con tenoxicam vs placebo en artritis gotosa aguda (A comparative, double-blind, parallel study with tenoxicam vs placebo in acute gouty arthritis). Invet Med Int '14:'92–7 [Abstract in Spanish]
  10. Sutaria S, Katbamna R, Underwood M (2006). "Effectiveness of interventions for the treatment of acute and prevention of recurrent gout--a systematic review". Rheumatology (Oxford). 45 (11): 1422–31. doi:10.1093/rheumatology/kel071. PMID 16632483. Unknown parameter |month= ignored (help)
  11. 11.0 11.1 Janssens HJ, Janssen M, van de Lisdonk EH, van Riel PL, van Weel C (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. Unknown parameter |month= ignored (help)
  12. 12.0 12.1 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.
  13. Henry D, Lim LL, Garcia Rodriguez LA; et al. (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. PMC 2351326. PMID 8664664. Unknown parameter |month= ignored (help)
  14. 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.
  15. 15.0 15.1 Ahern MJ, Reid C, Gordon TP, McCredie M, Brooks PM, Jones M (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. Unknown parameter |month= ignored (help) Summary at Bandolier
  16. Terkeltaub RA, Furst DE, Bennett K, Kook KA, Crockett RS, Davis MW (2010). "High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study". Arthritis Rheum. 62 (4): 1060–8. doi:10.1002/art.27327. PMID 20131255.
  17. CKS (2007) Gout - Management (Topic Review). Clinical Knowledge Summaries. http://cks.library.nhs.uk/gout/management [Accessed: Date]
  18. So A, De Meulemeester M, Pikhlak A, Yücel AE, Richard D, Murphy V; et al. (2010). "Canakinumab for the treatment of acute flares in difficult-to-treat gouty arthritis: Results of a multicenter, phase II, dose-ranging study". Arthritis Rheum. 62 (10): 3064–76. doi:10.1002/art.27600. PMID 20533546.

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