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Gout

Who Gets Gout?

Robert Terkeltaub, MD; N. Lawrence Edwards, MD, MACP, MACR; Puja Khanna, MD, MPH 
Reviewed on July 16, 2024
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Epidemiology of Gout and Hyperuricemia

Gout epidemiology studies date back to the age of Hippocrates (Table 2-1), who recognized that gout is predominantly a disease of adult men and rarely occurs in men before adolescence or in women before menopause. A key aspect of gout epidemiology is that the disease is common, although assessing epidemiology of gout is challenging, in part due to episodic symptoms and inaccuracies in self-reported and medical diagnoses. It was previously estimated that gout affects 5 to 6 million individuals in the United States, with at least 3 million subjects having active disease. In 2007-2008, Choi and colleagues estimated a history of self-reported gout in ~8.3 million Americans. The 2007–2016 National Health and Nutrition Examination Survey (NHANES) estimated the self-reported prevalence of gout in the United States to be 3.9%, which corresponds to ~9.2 million people. Furthermore, the 2007–2016 NHANES data suggested that gout prevalence in…

Epidemiology of Gout and Hyperuricemia

Gout epidemiology studies date back to the age of Hippocrates (Table 2-1), who recognized that gout is predominantly a disease of adult men and rarely occurs in men before adolescence or in women before menopause. A key aspect of gout epidemiology is that the disease is common, although assessing epidemiology of gout is challenging, in part due to episodic symptoms and inaccuracies in self-reported and medical diagnoses. It was previously estimated that gout affects 5 to 6 million individuals in the United States, with at least 3 million subjects having active disease. In 2007-2008, Choi and colleagues estimated a history of self-reported gout in ~8.3 million Americans. The 2007–2016 National Health and Nutrition Examination Survey (NHANES) estimated the self-reported prevalence of gout in the United States to be 3.9%, which corresponds to ~9.2 million people. Furthermore, the 2007–2016 NHANES data suggested that gout prevalence in African American, Caucasian and Hispanic individuals in the United States stood at 4.8%, 4% and 2%, respectively. It is important to note that the gout incidence and prevalence across indigenous populations is different from the incidence and prevalence in the United States as a whole. The global burden of gout is likewise substantial, with 41 million affected individuals in 2017, compared to 19 million for rheumatoid arthritis. According to the Global Burden of Disease data, the prevalence of gout in 1990-2019 was highest in Australasia and high-income North America. The global prevalence of gout is shown in Figure 2-1.

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Enlarge  Figure 2-1: The Global Prevalence of Gout. The figure shows the prevalence in different parts of the world, as indicated in the key. Prevalence is highest in developed countries, whereas data are lacking for some parts of the developing world, particularly Africa and South America. Source: Adapted from Dehlin M, et al. Nat Rev Rheumatol. 2020;16(7):380-390.
Figure 2-1: The Global Prevalence of Gout. The figure shows the prevalence in different parts of the world, as indicated in the key. Prevalence is highest in developed countries, whereas data are lacking for some parts of the developing world, particularly Africa and South America. Source: Adapted from Dehlin M, et al. Nat Rev Rheumatol. 2020;16(7):380-390.

Heritability of Gout

A family history of gout is seen in at least 20% of gout patients, and its heritability has been estimated at 30%. Inborn errors of purine metabolism do not have a significant footprint in the overall epidemiology of gout. In contrast, the substantial heritable component of gout is now well known to be commonly attributable to hyperuricemia mediated by alterations in renal proximal tubule epithelial cell urate transporters (including URAT1 and SLC2A9) and the intestinal urate transporter ABCG2 (see Disease Definition and Overview). For example, gout prevalence among persons of certain Asian subgroups (including Pacific Islanders and Maori) is substantially higher than among Whites, and ABCG2 genetic variants (particularly in Japanese subjects) and SLC2A9 genetic variants have been implicated in some of these population effects. A twin study in White male United States veteran identical and fraternal twins confirmed hyperuricemia as a significant shared genetic trait, with development of the gout phenotype influenced significantly by shared environmental factors (e.g., diet and alcohol consumption) rather than genetic factors. Gender-specific effects are statistically significant at the most prominent loci, with SLC2A9 exhibiting a stronger influence in women, while ABCG2 shows a greater influence in men. However, the issue of heritability of gout has not yet been adequately addressed in women, and may vary among different racial and ethnic populations.

Increasing Gout Prevalence and Complexity

The gout patient caricature as an overweight, overindulgent, affluent, middle-aged man fond of alcohol has lost relevance, as gout has been “democratized” as a disease of the population at large. In the last 3 decades in the United States, there has been a substantial increase in gout incidence (Figure 2-2) and a surge in prevalence (Figure 2-3). In addition, significant growth has been observed in many other countries, including New Zealand and Taiwan, although apparently not in Britain. Earlier age at onset, increased tophi and proportionally more women have been documented in many nations. The increase in gout incidence and prevalence in the United States has been most marked in older individuals and highest above the age of 75. The sex ratio of gout narrows after menopause, and there has been a steady increase in gout incidence and prevalence in elderly women. Gout prevalence may now be ~5% in elderly women in the United States and at least 7% in elderly men.

Asymptomatic hyperuricemia (defined by a single reading >7 mg/dL) was documented in ~13.2% of adults in the United States in 2007-2008 by Zhu and colleagues; the mean serum urate in US adults was 5.48 mg/dL in this analysis. The duration and level of hyperuricemia directly correlate with the risk of development of gout, which starts to accelerate when serum urate rises above 8 mg/dL and rises explosively when serum urate is above 9 mg/dL (Figure 2-4). Nevertheless, a minority of individuals (20% to 25%) with sustained hyperuricemia go on to develop clinical gout. This is partly because increases in serum urate levels are relatively mild (ie, serum urate <8 mg/dL) in most individuals or occur temporarily after changes in diet and drug therapies (e.g., in management of hypertension). However, even with serum urate >9 mg/dL, the incidence of new gout in men is estimated to be ~20% after 5 years from past study. Hence, asymptomatic hyperuricemia without gout is not a disease state, although attention to the cause of the hyperuricemia is clinically warranted.

A “perfect storm” of factors (Table 2-2) have led to the increased gout prevalence and clinical complexity in the United States, including increasing longevity via markedly declining cardiovascular (CV) death rates, increased hypertension, chronic kidney disease (CKD), and metabolic syndrome, and the broad use of thiazide and loop diuretics. The uricosuric effect of estrogen is well appreciated, and this largely explains the observation of Hippocrates on the rarity of premenopausal gout (we now know gout is more than nine times more common in young men than in premenopausal women). Dietary megatrends and lifestyle risk factors for development of gout (reviewed in Approach to Diet, Alcohol, and Other Lifestyle Factors) have contributed to high rates of obesity and metabolic syndrome in the United States. Obesity (Table 2-3) and insulin resistance are at the core of metabolic syndrome; both promote hyperuricemia principally by impairing renal uric acid excretion. Suboptimal treatment of gout and lack of options for refractory cases also have contributed to increased gout clinical complexity, but this will hopefully change, with new medications having been approved and more in the pipeline.

Obesity increases the risk of developing gout, and weight loss of >10 lb significantly decreases the risk of gout flares (Table 2-3). Hyperuricemia is one of the components of metabolic syndrome (Table 2-4). The prevalence of metabolic syndrome has been exponential in the United States over the last few decades; NHANES data for the periods 1988-1994, 1999-2006 and 2007-2012 are shown in Figure 2-5. In 2007-2012, metabolic syndrome was present in >25% of adults (30% of women) and >50% of individuals over age 70 (>60% of women in this age category). By 2017-2018, the overall prevalence of metabolic syndrome rose to 42%. Approximately 60% of men with gout have metabolic syndrome. In metabolic syndrome (and type 2 diabetes), insulin resistance not only increases renal urate reabsorption but also causes a urine alkalinization defect that promotes uric acid urolithiasis in acid urine (Figure 2-6).

Enlarge  Figure 2-2: The Incidence of Gout Increased From the Late 1980s to 2010, Particularly in Late Middle-Aged and Elderly Subjects. Incidence of gout among adult (age ≥18 yrs) Olmsted County, Minnesota, USA residents in 1989–1992 and 2009–2010, based on the earliest date of fulfillment of the 1977 American Rheumatism Association, Rome, or New York criteria, according to age and sex. Source: Adapted from Elfishawi MM, et al. J Rheumatol. 2018;45(4):574-579.
Figure 2-2: The Incidence of Gout Increased From the Late 1980s to 2010, Particularly in Late Middle-Aged and Elderly Subjects. Incidence of gout among adult (age ≥18 yrs) Olmsted County, Minnesota, USA residents in 1989–1992 and 2009–2010, based on the earliest date of fulfillment of the 1977 American Rheumatism Association, Rome, or New York criteria, according to age and sex. Source: Adapted from Elfishawi MM, et al. J Rheumatol. 2018;45(4):574-579.
Enlarge  Figure 2-3: Markedly Increased Prevalence of Gout in the 1990s in US Managed-Care Population of ~8 Million. 1) Number of cases increased from 2.9/1000 in 1990 to 5.2/1000 in 1999. Major findings of Wallace et al. [graph]: ~70% increase in overall prevalence of gout, >33% increase in 65 to 74 year olds, and ~100% increase in >75 year olds. 2) By comparison, US National Health Interview Survey of 1996 Self-Reported Gout Prevalence: men 4.6% and women 2%. Source: Wallace KL, et al. J Rheumatol. 2004;31(8):582-1587. Source: Lawrence RC, et al. Arthritis Rheum. 998;41(5):778-799.
Figure 2-3: Markedly Increased Prevalence of Gout in the 1990s in US Managed-Care Population of ~8 Million. 1) Number of cases increased from 2.9/1000 in 1990 to 5.2/1000 in 1999. Major findings of Wallace et al. [graph]: ~70% increase in overall prevalence of gout, >33% increase in 65 to 74 year olds, and ~100% increase in >75 year olds. 2) By comparison, US National Health Interview Survey of 1996 Self-Reported Gout Prevalence: men 4.6% and women 2%. Source: Wallace KL, et al. J Rheumatol. 2004;31(8):582-1587. Source: Lawrence RC, et al. Arthritis Rheum. 998;41(5):778-799.
Enlarge  Figure 2-4: Elevated Serum Urate (>9 mg/dL) Is a Particular Risk Factor for Developing Gout. a) Cumulative evidence of acute flares reached 22% after 5 years from enrollment. Source: Campion EW, et al. Am J Med. 1987;82(3):421-426; Saag KG, et al. Arthritis Res Ther. 2006;8(suppl 1):S2.
Figure 2-4: Elevated Serum Urate (>9 mg/dL) Is a Particular Risk Factor for Developing Gout. a) Cumulative evidence of acute flares reached 22% after 5 years from enrollment. Source: Campion EW, et al. Am J Med. 1987;82(3):421-426; Saag KG, et al. Arthritis Res Ther. 2006;8(suppl 1):S2.
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Enlarge  Figure 2-5: The Metabolic Syndrome Is Increasing in the United States. Prevalence of metabolic syndrome among US adult men (A) and women (B), National Health and Nutrition Examination Survey (NHANES), 1988–2012. Metabolic syndrome was defined by using the criteria agreed to jointly by the International Diabetes Federation; the National Heart, Lung, and Blood Institute in the United States; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Source: Adapted from Moore JX, et al. Prev Chronic Dis. 2017;14:160287.
Figure 2-5: The Metabolic Syndrome Is Increasing in the United States. Prevalence of metabolic syndrome among US adult men (A) and women (B), National Health and Nutrition Examination Survey (NHANES), 1988–2012. Metabolic syndrome was defined by using the criteria agreed to jointly by the International Diabetes Federation; the National Heart, Lung, and Blood Institute in the United States; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Source: Adapted from Moore JX, et al. Prev Chronic Dis. 2017;14:160287.

Comorbidity and Medication-List Worksheet for Gout and Hyperuricemia

A comprehensive worksheet for clinical practice to guide recognition and assessment of the comorbidities and medications that promote hyperuricemia is presented in Table 2-5. Comorbidity-related risk factors for gout include excess alcohol consumption, dietary excess, CKD, metabolic syndrome and use of thiazide and loop diuretics. An important aspect of primary care is to recognize asymptomatic hyperuricemia since serum urate is not part of the metabolic panel. Detecting hyperuricemia and thereafter considering the elimination of nonessential diuretic or niacin use, encouraging moderation in diet and alcohol consumption, and placing the patient on appropriate weight-loss and fitness programs can intervene at the preventive level for gout. Conversely, hyperuricemia should be recognized as a marker for metabolic syndrome and other comorbidities, many of which cause major morbidity and increase mortality. Since most patients with hypertension require multiple drugs, including thiazides, for optimal control, the clinician should weigh the impact of changes in hypertension management in a particularly thoughtful way in gout patients.

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Antihypertensive Medications and Gout

A close link exists between hypertension and both hyperuricemia and gout. The prevalence of hyperuricemia in subjects with hypertension is 20% to 40%. A large epidemiologic study has shown that 74% of gout subjects have hypertension. Hypertension by itself is independently associated with the risk of incident gout. Conversely, even asymptomatic hyperuricemia is associated with increased incidence of hypertension. Certain antihypertensive drugs, however, may either increase or decrease the incidence of gout depending on their effects on serum urate levels (Table 2-6). In patients 65 years of age and older, amlodipine (a calcium channel blocker) is associated with a lower risk of gout compared to lisinopril (an ACE inhibitor) and chlorthalidone (a diuretic).

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Hyperuricemia and Comorbidities

There is substantial experimental biology and epidemiology to suggest that asymptomatic hyperuricemia may contribute directly to the pathogenesis of hypertension, cardiovascular disease, chronic kidney disease, insulin resistance and the metabolic syndrome. At the very least, hyperuricemia is a marker and adverse prognostic factor in vascular disease, myocardial infarction, insulin resistance, chronic kidney disease and end-stage renal disease, as well as all-cause mortality. Increased pro-inflammatory effects and promotion of arterial endothelium oxidative stress by xanthine oxidase also may play a role in hyperuricemia-associated CV disease (Figure 2-7). Conversely, the inhibition of xanthine oxidase has been demonstrated to improve markers of endothelial function (flow-mediated dilatation of brachial artery and forearm blood flow response to acetylcholine) and lessen markers of oxidative stress (Figure 2-7). Data from a 2022 case-control suggest that gout flares are associated with higher CV event risk in the period following the flare.

A risk model for myocardial infarction (MI) that incorporates gout and hyperuricemia with other factors (Figure 2-8) argues that patients with gout, hyperuricemia and other cardiac risk factors merit particular attention to preventive strategies for coronary disease, such as attention to hyperlipidemia and to smoking cessation. Hyperuricemia is a marker for hypertension and diabetes as well. However, the age when the hyperuricemia is present appears to have a large influence on these associations. Hyperuricemia in adolescents and teenagers is purported to be a predictor for the development of primary hypertension in the twenties. Similarly, hyperuricemia in the mid-twenties is an independent marker for predicting diabetes and pre-diabetes among young adults in the subsequent 15 years (Figure 2-9).

Enlarge  Figure 2-7: Xanthine Oxidase Inhibition (XOI) for the Treatment of Cardiovascular Disease. Source: Higgins P, et al. Cardiovasc Ther. 2012;30:217-226.
Figure 2-7: Xanthine Oxidase Inhibition (XOI) for the Treatment of Cardiovascular Disease. Source: Higgins P, et al. Cardiovasc Ther. 2012;30:217-226.
Enlarge  Figure 2-8: Risk Model for Hyperuricemia, Gouty Arthritis, and Acute MI
Figure 2-8: Risk Model for Hyperuricemia, Gouty Arthritis, and Acute MI
Enlarge  Figure 2-9: Risk of Developing Diabetes, Prediabetes, and Insulin Resistance by Quartile of Serum Urate: CARDIA Trial of Young Adults, 1986-2001. Source: Krishnan E, et al. Am J Epidem. 2012;176:108-116.
Figure 2-9: Risk of Developing Diabetes, Prediabetes, and Insulin Resistance by Quartile of Serum Urate: CARDIA Trial of Young Adults, 1986-2001. Source: Krishnan E, et al. Am J Epidem. 2012;176:108-116.

Health Care Utilization and Financial Impact of Gout

By far, the majority of patient visits for gout are to primary care health care professionals. Gout is clearly costly to patients and the health care system. Patients with acute gouty arthritis miss an average of 3 to 5 days of work annually. The estimated total annual cost of gout to employer per employee is more than 80% higher in those with gout compared with those without gout. Gout flares are expensive, and inadequate control of serum urate is associated with more frequent, costly flares. Furthermore, gout-related costs account for ~6% of total health care costs in elderly patients with gout; serum urate levels of ≥9 mg/dL and tophaceous disease are linked to increased health care utilization and costs in this patient population. Chronic refractory gout is particularly expensive to treat. There is evidence that rheumatology referral for assessment of gout care is cost-saving.

Take-Away Messages

  • Gout is self-reported in >9 million adults in the United States.
  • Gout is the most common inflammatory joint disorder in men >40 years of age.
  • Self-reported prevalence in adult men in the United States is ~5.2% and 2.7% in adult women.
  • Uricosuric effect of estrogen and lower serum urate contribute to gout being at least nine times more common in young men than in premenopausal women.
  • The sex ratio of the occurrence of gout narrows after menopause and is close to equal in the elderly.
  • The substantial heritable component of gout is far more commonly due to alterations in renal and intestinal urate transport than inborn errors of purine metabolism.
  • Best estimates: incidence and prevalence of gout have at least doubled over the last 3 decades in the United States.
  • A perfect storm of factors, including iatrogenic and dietary influences and rising comorbidities that promote hyperuricemia, are responsible for increased prevalence and severity of gout.
  • Recent increases in gout prevalence have been most marked in the elderly.
  • A surge of cases in elderly women is linked to diuretic use and CKD; gout prevalence may now be ~5% in elderly women.
  • Asymptomatic hyperuricemia is not necessarily benign and is a marker for increased CV disease.
  • Primary health care professionals see and treat the majority of gout in the United States.
  • Gout flares and uncontrolled hyperuricemia and disease chronicity in gout increase health care costs.

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