Medical Perspectives | Others

May 11, 2021

Wilmark N. Gular, MD

            Once known as the disease of kings, gout has now become the king of diseases. The high consumption of alcohol and meat by the noble class during the renaissance period has earned gout its former reputation.1 At present, the same type of diet and alcoholic drinking has predisposed a significant number of individuals to gout, hence its latest moniker.2

            Globally, gout has maintained 0.08% prevalence.3 In the Philippines it was found to have a 1.6% prevalence.4 This roughly translates to 1.6 million Filipinos with gout, with more men affected.5 Gout may be encountered frequently in primary care clinics, prompting a comprehensive understanding of its diagnosis and management at the primary level.

            Despite efforts to curb the prevalence of gout, it continues to persist, posing a great burden on patients. Estimates from the Global Burden of Disease 2010 Study showed a 49% increase in the Disability-Adjusted Life Years (DALYs) for gout over a ten-year period.3 DALYs correspond to the years of healthy life lost from premature death or disability.

Gout Explained

            Gout literally means a drop or a bead since it was once thought to come from a drop of viscous humor of the blood going into the joints.6 The current understanding is that it results from impaired metabolism or under excretion of uric acid. Excess uric acid can crystallize and can get deposited in a joint, making gout a crystal-associated arthropathy.7

Gout is also an immune-mediated, autoinflammatory disease. Uric acid can activate an inflammasome, a part of the innate immune system, cascading an inflammatory reaction.7 Gout also has a genetic component demonstrated by a loss or reduction-in-function mutation in renal secretory urate transporter genes. This causes high blood uric acid levels.8

Hyperuricemia or levels of blood uric acid >7mg/dL in men and postmenopausal women and >6mg/dL in premenopausal women is a risk factor for the development of gouty arthritis. Excess uric acid crystals can also deposit into renal tubules causing uric acid or gouty nephropathy, tubulointerstitial disease, and nephrolithiasis.7         

Males are more prone to develop of gout. Premenopausal women have lower incidence of gout due to the enhanced urate excretion in the presence of estrogen.9 Dietary risk factors for gout include consumption of excess alcoholic beverages, high fructose or sugar-sweetened beverages, meats, organ meats, and seafood.9 These can precipitate an attack.7

Gout is associated with obesity and noncommunicable diseases such as hypertension and diabetes mellitus are associated with gout.9 Other conditions that increase risk of gout include myeloproliferative disease and psoriasis. Medications such as thiazide diuretics and cytotoxic chemotherapeutics can induce gout.7


Pains and Nodules

            Acute gouty attack usually presents with nocturnal joint pain, swelling, redness, and warmth of the big toe (podagra). The ankles and the knees may later be involved.  Heberden’s nodes at the distal interphalangeal (DIP) joints and Bouchard’s nodes of the proximal interphalangeal (PIP) joints may be the first manifestations, particularly among the elderly.7

The attacks may last from 3 to 10 days and may subside spontaneously.7 These may recur in the presence of precipitating factors or in the absence of medications for control. The quiescent period in between acute attacks is called intercritical phase.10

            Left untreated, gouty arthritis can result to chronic tophaceous gout.10 This is heralded by the presence of tophi, a chalk-like subcutaneous nodule over the skin of an affected joint which, at certain times, can drain into the surface of the skin. Tophi are frequently located at the helix of the earlobe, the elbow, and the joints of the fingers.11

            Chronic tophaceous gout presents with prolonged periods of low grade inflammation interspersed by flares of acute gouty attack. The presence of tophi can result to joint deformity and this can be debilitating, limiting full range of motion of the affected joints.10

Gout or Not?

            Gout is considered in patients presenting with abrupt onset monoarticular arthritis. However, it is not the only disease presenting as such. Septic arthritis must be considered and ruled out. Furthermore, gout is only one of the crystal-associated arthropathies. Pseudogout, which results from deposition of calcium pyrophosphate (CPP), is another differential.

            In 2015, the American College of Rheumatology (ACR) along with the European League Against Rheumatism (EULAR) developed a classification criteria for gout. The criteria is based on the composite score of clinical, laboratory, and imaging parameters.11

            Clinically, gout has recurrent symptomatic episodes of pain, swelling, or tenderness of the peripheral joint or bursa, specifically the metatarsophalangeal joint of the first toe, the ankle, or the midfoot. Tophi is also a component of the clinical parameter which is individually scored.11

            Laboratory parameters include observation of monosodium urate (MSU) crystals in the synovial fluid aspirate. MSU appear as needle-shaped, negatively elongated, birefringent crystals under polarized light microscopy.7 Serum uric acid levels must also be identified ideally at a time when urate-lowering drugs have not been started and prior to an attack.11

Serum uric acid does not always correlate with disease activity; however, its determination may help in the diagnosis and in monitoring the response to therapy with urate-lowering agents and uricosurics.7

Imaging parameters proposed by the ACR/EULAR were evidence of urate deposition on dual-energy computed tomography (DECT) or on ultrasound, where gout presents with double contour sign. Another imaging parameter involves evidence of joint damage on radiography.11

Gout is mainly diagnosed clinically but definitive diagnosis relies on the demonstration of MSU crystals under polarized microscopy.7 The ACR/EULAR criteria can be used to score and determine the probability of gout using the three parameters mentioned above.

Prevent Gout the Natural Way

            With the metabolic nature of gout and its association to purine-rich food and alcohol, dietary prescription for the management of gout cannot be overemphasized. The ACR in 2012 released a guideline highlighting nonpharmacologic and pharmacologic approaches to the management of gout.12

            Patient education is vital to the prevention of gout.12-14 The British Society for Rheumatology and British Health Professionals in Rheumatology (BSR/BHPR) released an updated guideline in 2017 which directs primary caregivers to provide information to patients with gout particularly the benefits of urate-lowering therapy.13

                Dietary recommendations for gout from the ACR include avoidance of the following: organ meats high in purine, high-fructose corn syrup-sweetened beverages, alcoholic beverages more than the daily allowable number (>2 drinks for men/day and >1 drink for women/day), and alcohol intake during acute attack. Meats (pork, lamb, and beef), seafood, and sweetened beverages should be limited. Consumption of low-fat or non-dairy products and vegetables are encouraged.12

            The ACR also recommends patients with gout to maintain a healthy lifestyle through exercise. Obese patients are advised to lose weight and maintain a normal body mass index (BMI). Smoking cessation and adequate hydration complete the lifestyle recommendations.12 Drugs inducing gout must also be identified and discontinued if necessary.

Stop the Attacks

Nonpharmacologic and preventive therapy would be sufficient with adequate compliance. However, they are not enough to thwart an already ongoing acute attack of gout. In such case, a nonsteroidal inflammatory drug (NSAID), colchicine, or steroid can be given to ablate the pain.

The ACR recommends initiation of the abovementioned agents within 24 hours of an acute attack of gout.12 NSAIDs with short half-life and cyclooxygenase-2 inhibitors (COX-2) as well as colchicine at 1.2 mg initially, are appropriate first-line therapies. A steroid such as prednisone, either oral or intraarticular, is reserved for those who have allergy or contraindication to NSAID or those intolerant to colchicine.7

Urate-lowering therapy (ULT) with the xanthine oxidase inhibitor (XOI) allopurinol, remains a cornerstone in the treatment of gout. 12 It is started at a low dose (50-100mg) and up-titrated to target a serum uric acid level of less than 6mg/dL.14 Febuxostat, also a XOI, is used as an alternative in patients with allergy to allopurinol. Allopurinol along with urine alkalinization can also help prevent formation of uric acid stones.7 

Previously, urate-lowering therapy (ULT) with allopurinol was withheld during acute attacks of gout since it was believed to prolong or worsen the attack. The ACR in 2012 recommends to continue allopurinol if it has been in use prior to the attack.  Recently, two clinical trials have found that allopurinol does not cause or prolong an attack and can be safely started in acute gouty arthritis.15,16

Colchicine must be given as anti-inflammatory prophylaxis for acute gouty arthritis along with a hypouricemic agent such as allopurinol for 6 months or longer until target serum uric acid have been achieved.7,14 Other hypouricemic agents include uricosuric drugs such as probenecid, benzbromarone, and lenisurad,  which can be used in patients with chronic gouty arthritis or chronic tophaceous gout.7

The understanding of gout has evolved from a purely metabolic standpoint to an immune-mediated, autoinflammatory pathology with a genetic component. With these updates and the current guidelines available, primary care providers are equipped with the armamentarium to prevent an attack of the gout.


  1. A Protein's Well-Known Cousin Sheds Light on Its Gout-Linked Relative. Retrieved from: Accessed September 20, 2019.
  2. Hamburger, M. et al. Gout: The King of Diseases. Collier’s Magazine. June 2012. Retrieved from: Accessed: September 20, 2019.
  3. Smith, E. et The global burden of gout: estimates from the Global Burden of Disease 2010 Study. BMJ Publishing Group Ltd. March 2014.
  4. Dans LS, Salido EO, Penserga EG, Navarra SV for the 2003 NNHeS Group. National, Nutrition and Health Survey (NNHeS) : Prevalence of rheumatic diseases among adult, Filipinos. Philippine Journal of Internal Medicine 2006.
  5. Philippine Rheumatology Association. PRA Launches Its Gout Awareness Campaign. March 1, 2015. Retrieved from: Accessed: September 20, 2019.
  6. Retrieved from: Accessed: September 20, 2019.
  7. Jameson et al. Harrison’s Principles of Internal Medicine 20th McGraw Hill Education. 2018.
  8. Reginato, A. et al. The genetics of hyperuricemia and gout. Nat Rev Rheumatol. October 8, 2012.
  9. MacFarlane, L. and Kim, S. Gout: a review of non-modifiable and modifiable risk factors. Rheum Dis Clin North Am. November 2014.
  10. Li-Yu, J. et al. Philippine Clinical Practice Guidelines for the Management of Gout. Philippine Rheumatology Association.2007.
  11. Neogi, T. et al. 2015 Gout Classification Criteria. An American College of Rheumatology/European League Against Rheumatism Collaborative Initiative. Arthritis and Rheumatology. 2015.
  12. Khanna, D. 2012 American College of Rheumatology Guidelines for Management of Gout. Arthritis Care and Research. 2012.
  13. Mallen, C. Improving management of gout in primary care: a new UK management guideline. Clinical Intelligence. 2017.
  14. Robinson, P. and Stamp, L. The management of gout: Much has changed. The Royal Australian College of General Practitioners. 2016.
  15. Hill E. et al.Does starting allopurinol prolong acute treated gout? A randomized clinical trial. J Clin Rheumatol. 2015.
  16. Taylor T. et al.Initiation of allopurinol at first medical contact for acute attacks of gout: A randomized clinical trial. Am J Med. 2012.

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