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Gout: Understanding gout and treatment recommendations

Men's Health, Pain, General | February 13, 2015 | Author: The Super Pharmacist

men, Pain

Gout: Understanding gout and treatment recommendations

Gout, also known as hyperuricaemia, is a condition associated with increased concentrations of uric acid in the blood1. This may result in the accumulation of uric acid crystals (or monosodium urate) in many types of soft tissue and in joints2.

Symptoms of gout

Gout may affect a number of joints in the body, resulting in a range of symptoms that resemble those of arthritis1. This is due to the accumulation of uric acid crystals in the protective synovial fluid within joints3. Gout is also associated with inflammation, or the release of inflammatory molecules into joints and other tissues, which may be associated with chronic pain3. Therefore, gout is often regarded as a rheumatological condition. The symptoms of gout may include:

  • Rapid-onset pain
  • A sensation of warmth in affected joints or tissues
  • Redness and swelling in these joints, which may be visible to the point of being very noticeable under the skin

Risk Factors

Pre-existing Conditions

Certain disorders and conditions may affect the probability of increased circulating uric acid in the body. These may include4,5:

  • High blood pressure
  • Obesity and/or the metabolic syndrome
  • Type II diabetes
  • Chronic kidney disorders

Conversely, the presence of gout may increase the risk of other conditions. A study of approximately 54,000 patients found that the risk of developing diabetes was increased, and that this risk was greater in women with gout than in men with this condition6. Increased blood levels of uric acid are also associated with the increased risk of coronary artery disease and heart attack7. Gout is also associated with increased risks of kidney damage, and of death related to kidney failure3.

Genetics

Gout may be hereditary, or passed on from generation to generation. An analysis of data on over one million patients found that the risk of the condition was significantly higher for those with first-order relatives who had gout8. The risk of gout may be associated with mutations in various genes. 12 of these variations have been found to be associated with the risk of gout in studies involving European participants9. Some mutations are related to the control of uric acid in the blood7. These include variants of the genes ABCG2 and SLC2A97. A mutation in NPT1, a gene expressing a urate-transporting protein, was found to be associated with gout that affects the kidneys10. Mutations in the genes CLNK and ZNF518B were found to be significantly associated with risk in a Chinese study including 145 patients and over 300 matched healthy control subjects9.

Diet

The risk of gout may also be associated with a range of dietary factors and deficiencies. These are in some cases related to foods rich in the 'building blocks' (e.g. purines) the body may use to produce uric acid. A study of over 47,000 men with no history of gout at the outset found that those who consumed the most meat and seafood were at a significantly higher risk of gout than those who ate the least of these foods11. Those who had an increased intake of low-fat dairy products had a significantly reduced risk of developing the condition11. The theory of purine-rich foods does not hold up in all cases, however; this study found no association between the consumption of high-purine vegetables and the risk of gout11. However, the theory that fructose increases uric acid concentrations may have some weight. A study including over 46,000 adult participants found that increased fructose (a common sugar used extensively in commercial food production, e.g. high-fructose corn syrup) intake from soft drinks, fruit juices or fruits was associated with an increased risk of gout12. Decreases in vitamin C levels may also be associated with the increased probability of this condition13. Coffee (but not necessarily caffeine) consumption was associated with a significantly reduced risk in another study of over 45,000 adult men14.

Treatment Strategies

There are a number of options available to manage gout. This condition has become relatively easy to treat and manage. However, some factors may affect the efficacy of treatment in gout. These are mainly the difficulty in diagnosing the condition, and adherence to a treatment regimen once a diagnosis is made3. However, diagnosis of gout has improved recently, mainly through the use of non-invasive imaging techniques. Diagnostic methods that may aid detection of gout include3:

  • Microscopy (this is the classic method, in which gout is diagnosed through the observation of crystals in samples taken from relevant areas, such as synovial fluid)
  • Computed tomography (CT)
  • Magnetic resonance imaging (MRI)
  • Nuclear imaging
  • Radiography
  • Ultrasound

Treatment strategies may include15:

Urate-lowering therapy

These are interventions that are directed at reducing the uric acid concentrations in the body. These are often in the form of drugs called xanthine oxidase inhibitors. These urate-lowering drugs include:

  • Allopurinol: This is often used in cases of gout presenting with kidney disorder15.
  • Febuxostat: This is a relatively new xanthine oxidase inhibitor, indicated for use in cases for which allopurinol cannot be prescribed2. A review of the studies on this drug indicated that this drug may be associated with improvements in symptoms and in uric acid concentrations2.
  • Pegloticase: This is used to reduce uric acid in cases of gout in which the conventional options as above have failed. Unlike the drugs as above, this is an enzyme, or a protein that converts uric acid into a less harmful form16. However, pegloticase is linked to a relatively high rate of discontinuation due to adverse effects17.
  • Benzbromarone: This is a drug that acts on a part of the kidney to remove more uric acid from the body (i.e. incorporate more of it into urine), thus reducing its concentrations in the blood18. A review of five clinical trials concluded that this may be as effective as allupurinol in treating hyperuricaemia18.

Treatment of acute gout

During flare-ups or attacks of gout, patients may require pain relief. The following chart shows appropriate management of attacks as directed by physicians.

Patient education

This involves an ideally comprehensive programme of advice, educational material and information on the condition in question provided to the patient. The goal of patient education is that the individual in question fully understands their condition, treatment options and other information such as risk factors and how best to avoid them if possible. Patient education may reduce depressive symptoms and/or treatment apathy, if these are associated with the disorder, and improve management through lifestyle changes. This may also result in improvements in life quality. Some evidence indicates that patient education is a viable component of treatment in cases of gout4. This may improve the ability of patients with gout to manage, improve and live with their condition.

References:

  1. Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. 1987;82(3):421-426.
  2. Bridgeman MB, Chavez B. Febuxostat for the treatment of gout. Expert Opin Pharmacother. 2015;16(3):395-398.
  3. Chowalloor PV, Siew TK, Keen HI. Imaging in gout: A review of the recent developments. Ther Adv Musculoskelet Dis. 2014;6(4):131-143.
  4. Khanna D, Fitzgerald JD, Khanna PP, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res (Hoboken). 2012;64(10):1431-1446.
  5. Roddy E, Doherty M. Epidemiology of gout. Arthritis Res Ther. 2010;12(6):223.
  6. Kim SC, Liu J, Solomon DH. Risk of incident diabetes in patients with gout: a cohort study. Arthritis Rheumatol. 2015;67(1):273-280.
  7. Stark K, Reinhard W, Grassl M, et al. Common polymorphisms influencing serum uric acid levels contribute to susceptibility to gout, but not to coronary artery disease. PLoS One. 2009;4(11):e7729.
  8. Kuo C-F, Grainge MJ, See L-C, et al. Familial aggregation of gout and relative genetic and environmental contributions: a nationwide population study in Taiwan. Ann Rheum Dis. 2015;74(2):369-374.
  9. Jin T-B, Ren Y, Shi X, et al. Genetic variations in the CLNK gene and ZNF518B gene are associated with gout in case-control sample sets. Rheumatol Int. 2015.
  10. Chiba T, Matsuo H, Kawamura Y, et al. NPT1/SLC17A1 Is a Renal Urate Exporter in Humans and Its Common Gain-of-Function Variant Decreases the Risk of Renal Underexcretion Gout. Arthritis Rheumatol. 2015;67(1):281-287.
  11. Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. The New England journal of medicine. 2004;350(11):1093-1103.
  12. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. 2008;336(7639):309-312.
  13. Choi HK, Gao X, Curhan G. Vitamin C intake and the risk of gout in men: a prospective study. Arch Intern Med. 2009;169(5):502-507.
  14. Choi HK, Willett W, Curhan G. Coffee consumption and risk of incident gout in men: a prospective study. Arthritis Rheum. 2007;56(6):2049-2055.
  15. Jeyaruban A, Larkins S, Soden M. Management of gout in general practice-a systematic review. Clin Rheumatol. 2015;34(1):9-16.
  16. Baraf HSB, Yood RA, Ottery FD, Sundy JS, Becker MA. Infusion-related reactions with pegloticase, a recombinant uricase for the treatment of chronic gout refractory to conventional therapy. J Clin Rheumatol. 2014;20(8):427-432.
  17. Kydd AS, Seth R, Buchbinder R, et al. Urate-lowering therapy for the management of gout: a summary of 2 Cochrane reviews. J Rheumatol Suppl. 2014;92:33-41.
  18. Kydd ASR, Seth R, Buchbinder R, Edwards CJ, Bombardier C. Uricosuric medications for chronic gout. Cochrane Database Syst Rev. 2014;11:CD010457.

 

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