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Management of gout

9 December 2024

Anna Pettit looks at the causes, symptoms and management of this painful form of chronic inflammatory arthritis.

Gout is the most common form of chronic inflammatory arthritis, characterised by sudden, severe attacks of pain, swelling, redness and tenderness in one or more joints, most often the big toe.

Gout occurs due to a build-up of monosodium urate crystals (a salt made of sodium and uric acid) in the joints.1 These crystals can form when you have high levels of uric acid in your blood. Uric acid (UA) is the end product of purine breakdown in the human body.2 In normal conditions, uric acid can be excreted in your urine. Evidence suggests that the main reason for UA build-up is due to insufficient excretion of UA via the kidneys and the gut.1,2,3,4

Persistent hyperuricemia is a risk factor for gout development, which is defined by a serum uric acid (SUA) above 7 mg/dL.5 However, many people with high levels of serum UA levels will never develop gout, which makes gout aetiology more complex than previously thought.2,6

The prevalence of gout tends to be higher in men, 3–4%, versus 1-2% in women in developed countries.9,10 In women, the risk of gout increases dramatically during menopause. A large US study involving more than 60,000 women revealed that menopausal women had a 26% higher risk of gout, particularly pronounced in women who had surgical menopause or experienced natural menopause before 45 years of age.27 One suggested biological mechanism behind this relationship is the influence of oestrogen and progesterone on the efficient removal of UA through the kidneys.

Gout foot pain

Gout diagnosis

The gold standard for gout diagnosis is confirmation of monosodium urate crystals by polarising light microscopy of synovial fluid or tophaceous material – chalky, gritty accumulations of UA crystals in the soft tissue of a gouty joint.11

Risk factors for gout development (adapted from Dalbeth et al.11)

Age and sex

  • Male

  • Increasing age

  • Menopause for women

Genetics

  • Genetic variants of renal urate transporters

Medical conditions

  • Chronic kidney disease

  • Heart disease

  • Obstructive sleep apnoea

  • Anaemia

Medications

  • Some diuretics

  • Immunosuppressants

  • Blood pressure-lowering drugs

  • Heart medication such as beta blockers

Diet

  • Red meat

  • Seafood

  • Beer, spirits

  • Sugar-sweetened beverages

Other

  • Overweight and obesity

  • Lead exposure

Gout management

Gout symptoms come and go. However, it is important to manage symptoms and to prevent flares. Management of gout includes both medical management and dietary management. Medical management involves taking nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine or corticosteroids and allopurinol to prevent flare-ups.10,12

Dietary modifications can be safely used alongside medications and include the following:2,12

Manage weight

Weight optimisation should be a priority where excess weight is identified.12,16 Cardiometabolic factors such as obesity, raised blood pressure, insulin resistance and abnormal lipids all affect renal function and can lower the clearance of UA causing an accumulation of UA

Reduce purine intake

Purine-rich foods include meat (particularly organ meat), fish and shellfish.2,3,9 There is a lack of well conducted research on the purine-restricted diet effectiveness.18 One study on people with hyperuricemia reported a modest 0.57 mg/dL drop in uric acid after two weeks on a low purine diet. However, this study lacked a control group.18

Dietary purine restriction alone does not always lead to complete resolution or improvement of hyperuricemia symptoms but can be effectively used as an adjacent therapy.5 Exactly how much purine restriction can lower uric acid levels may depend on baseline purine intake and degree of restriction, so should be assessed individually.18 Alcohol and fructose from sugary beverages should also be limited2,15,16

Follow an anti-inflammatory diet

The Mediterranean diet is often described as an anti-inflammatory eating pattern. Research suggests that diet interventions such as a low-calorie diet, purine-restricted diet, and the Mediterranean diet are all able to decrease UA in patients with asymptomatic hyperuricemia or gout.5

However, the overall evidence is low-to-moderate quality with high risk of bias and lack of control groups.5 A recent systematic review concluded more scientifically robust studies are required to support the use of lifestyle and dietary modifications for improving outcomes in people with chronic gout16

Consider supplements

Vitamin C and skimmed milk supplements have been researched and recommended in gout20,21 but the most recent systematic review did not find any solid evidence behind any of the supplements.22 There have been some studies suggesting that probiotic strains Lactobacillus brevis DM9218 and Lactobacillus salivarius CECT 30632 can be useful as an adjacent therapy in gout to reduce UA level, but more robust research is required to make any firm recommendations23,24,25

Individualised care that includes regular review

An individualised approach in patient management is vital.2,17 In addition, the British Society of Rheumatology recommends all gout patients be reviewed after an initial urate-lowering medication trial at four-to-six weeks for patient education and to modify lifestyle and diet to encourage a well-balanced diet, low in fat and added sugars and high in vegetables and fibre12

Conclusion

Gout is a complex chronic condition that requires ongoing medical treatment.

Dietary and lifestyle modifications can be used to lower UA levels and to reduce or prevent metabolic complications in gout, but more robust research is required to identify the best dietary pattern. Purine-restricted diet is often recommended. The Mediterranean diet with low meat intake, high fibre and low alcohol can be a good option to manage gout patients holistically. Probiotics in gout is an emerging area of research with no firm recommendations yet.

References

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  2. Zhang Y, Chen S, Yuan M, Xu Y, Xu H. Gout and Diet: A Comprehensive Review of Mechanisms and Management. Nutrients. [Online] Nutrients; 2022;14(17): 3525. Available from: doi:10.3390/nu14173525
  3. Li R, Yu K, Li C. Dietary factors and risk of gout and hyperuricemia: a meta-analysis and systematic review. Asia Pac J Clin Nutr. 2018;27(6):1344-1356. doi:10.6133/apjcn.201811_27(6).0022. PMID: 30485934.
  4. Loeb JN. The influence of temperature on the solubility of monosodium urate. Arthritis Rheum 1972; 15: 189–92.
  5. Vedder D, Walrabenstein W, Heslinga M, De Vries R, Nurmohamed M, Van Schaardenburg D, et al.. Dietary Interventions for Gout and Effect on Cardiovascular Risk Factors: A Systematic Review. Nutrients. [Online] Nutrients; 2019;11(12): 2955. Available from: doi:10.3390/nu11122955
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  8. Lin KC, Lin HY, Chou P. The interaction between uric acid level and other risk factors on the development of gout among asymptomatic hyperuricemic men in a prospective study. J Rheumatol. 2000 Jun;27(6):1501-5. PMID: 10852278.
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  11. Dalbeth N, Merriman TR, Stamp LK.Lancet. 2016 Oct 22;388(10055):2039-2052. doi: 10.1016/S0140-6736(16)00346-9. Epub 2016 Apr 21.PMID: 27112094
  12. Hui M, Carr A, Cameron S et al. British Society for Rheumatology and British Health Professionals in Rheumatology guideline for management of gout. Rheumatology 2017;56:e1-e20 doi:10.1093/rheumatology/kex156
  13. Brul. D, Sarwar G, Savoie L. Changes in serum and urinary uric acid levels in normal human subjects fed purine-rich foods containing different amounts of adenine and hypoxanthine. J Am Coll Nutr. 1992 Jun;11(3):353-8. doi: 10.1080/07315724.1992.10718238.PMID: 1619189.
  14. Coelho MOC, Monteyne AJ, Kamalanathan ID, Najdanovic- Visak V, Finnigan TJA Stephens FB, Wall BT. Short-Communication: Ingestion of a Nucleotide-Rich Mixed Meal Increases Serum Uric Acid Concentrations but Does Not Affect Postprandial Blood Glucose or Serum Insulin Responses in Young Adults. Nutrients. 2020 Apr 17;12(4):1115. Doi: 10.3390/nu12041115
  15. Schwingshackl L, Neuenschwander M, Hoffmann G, Buyken AE, Schlesinger S. Dietary sugars and cardiometabolic risk factors: a network meta-analysis on isocaloric substitution interventions. Am J Clin Nutr. 2020 Jan 1;111(1):187-196. doi: 10.1093/ajcn/nqz273. PMID:31711109.
  16. Moi JH, Sriranganathan MK, Edwards CJ, Buchbinder R. Lifestyle interventions for chronic gout. Cochrane Database of Systematic Reviews. [Online] Cochrane Database of Systematic Reviews; 2013;2019(9). Available from: doi:10.1002/14651858.cd010039.pub2
  17. Juraschek S., Gelber A.C., Choi H.K., Appel L.J., Miller E.R. Effects of the Dietary Approaches to Stop Hypertension (DASH) Diet and Sodium Intake on Serum Uric Acid. Arthritis Rheumatol. 2016;68:3002–3009. doi: 10.1002/art.39813.
  18. Cardona F, Tinahones FJ, Collantes E, Garcia-Fuentes E, Escudero A, Soriguer F. Response to a urate-lowering diet according to polymorphisms in the apolipoprotein AI-CIII-AIV cluster. J Rheumatol. 2005 May;32(5):903- 5. PMID: 15868628.
  19. Yokose C., McCormick N., Lu N., Joshi A.D., Curhan G., Choi H.K. Adherence to 2020 to 2025 Dietary Guidelines for Americans and the Risk of New-Onset Female Gout. JAMA Intern. Med. 2022;182:254–264. doi: 10.1001/ jamainternmed.2021.7419.
  20. Juraschek SP, Gaziano JM, Glynn RJ, Gomelskaya N, Bubes VY, Buring JE, Shmerling RH, Sesso HD. Effects of vitamin C supplementation on gout risk: results from the Physicians’ Health Study II trial. Am J Clin Nutr. 2022 Sep 2;116(3):812-819. doi: 10.1093/ajcn/nqac140. PMID:35575611; PMCID: PMC9437983.
  21. Choi HK, Gao X, Curhan G. Vitamin C intake and the risk of gout in men: a prospective study. Arch Intern Med. 2009 Mar 9;169(5):502-7. doi: 10.1001/ archinternmed.2008.606. PMID: 19273781; PMCID: PMC2767211.
  22. Andr.s M, Sivera F, Buchbinder R, Pardo Pardo J, Carmona L. Dietary supplements for chronic gout. Cochrane Database Syst Rev. 2021 Nov 12;11(11):CD010156. doi: 10.1002/14651858.CD010156. pub3. PMID: 34767649; PMCID:PMC8589461.
  23. JWang H, Mei L, Deng Y, Liu Y, Wei X, Liu M, Zhou J, Ma H, Zheng P, Yuan J, Li M. Lactobacillus brevis DM9218 ameliorates fructose-induced hyperuricemia through inosine degradation and manipulation of intestinal dysbiosis. Nutrition. 2019 Jun;62:63-73. doi: 10.1016/j.nut.2018.11.018. Epub 2018 Nov 26. PMID: 30852460.
  24. Li M, Yang D, Mei L, Yuan L, Xie A, Yuan J. Screening and Characterization of Purine Nucleoside Degrading Lactic Acid Bacteria Isolated from Chinese Sauerkraut and Evaluation of the Serum Uric Acid Lowering Effect in Hyperuricemic Rats. PLOS ONE. [Online] PLOS ONE; 2014;9(9): e105577. Available from: doi:10.1371/journal.pone.0105577
  25. Rodr.guez JM, Garranzo M, Segura J, Orgaz B, Arroyo R, Alba C, Beltr.n D, Fern.ndez L. A randomized pilot trial assessing the reduction of gout episodes in hyperuricemic patients by oral administration of Ligilactobacillus salivarius CECT 30632, a strain with the ability to degrade purines. Front Microbiol. 2023 Feb 14;14:1111652. doi: 10.3389/fmicb.2023.1111652. PMID: 36865781; PMCID: PMC9971985.
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  27. Hak AE, Curhan GC, Grodstein F, Choi HK. Menopause, post menopausal hormone use and risk of incident gout. Annals of the Rheumatic Diseases. [Online] Annals of the Rheumatic Diseases; 2010;69(7): 1305–1309. Available from: doi:10.1136/ard.2009.10988
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