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PubMed2006

Serum urate levels and gout flares: analysis from managed care data.

BACKGROUND: The desired serum urate level (SUA) for prevention of gout attacks is widely recommended to be in the subsaturating range, <6.0 mg/dL. OBJECTIVES: The objectives of this study were to evaluate attainment of this target SUA among gout patients on allopurinol in a naturalistic setting and to assess its impact on gout flare risk. METHODS: : This was a retrospective, observational study in a southeastern U.S. managed care organization of approximately 2.2 million members. The first gout claim/prescription within the intake period (January 1, 2000-December 31, 2002) was the index date. Included patients had > or =2 visits with gout International Classification of Diseases, 9th Revision code (274.xx) or > or =1 pharmacy script(s) for allopurinol, colchicine, probenecid, or sulfinpyrazone. Excluded patients were <18 years and/or did not have a 1-year continuous eligibility pre-/postindex date. Gout flares were defined by office/emergency room visit with gout or joint pain code(s) and > or =1 of the following within 7 days of the visit: intraarticular aspiration/injection, joint fluid microscopy, or pharmacy claim for nonsteroidal antiinflammatory drug, colchicine, corticosteroid, or ACTH. Multivariable regression analyses were conducted to evaluate gout flare risk/rate and association with target SUA. RESULTS: Approximately 40% of 5942 gout patients identified used allopurinol postindex. Among allopurinol users with pre-/postindex SUA data (n = 162), mean SUA was lowered from 8.7 mg/dL to 7.1 mg/dL; reduction was significant (P < 0.001). Among allopurinol users who did not have SUA <6.0 mg/dL preindex (n = 147), only 25% reached target levels during postindex. Despite pharmacotherapy, patients with nontarget levels were 59% more likely to flare than those at target. Allopurinol users who were not at target were 75% more likely to flare. CONCLUSION: The failure of allopurinol users to achieve target SUA levels of <6.0 mg/dL may be attributed to lack of awareness of optimal SUA, allopurinol dosing, compliance, and efficacy. Patients who did not achieve target SUA were at increased flare risk.

Adolescent↗

PubMed2026

Investigating the causal role of smoking in gout: A triangulation approach combining NHANES data, genetic correlation, and Mendelian randomization.

The relationship between smoking and the development of gout is not well understood. To address this, we adopted a triangulation framework that integrates observational analysis, genetic correlation estimation, and two-sample Mendelian randomization (MR) to examine whether smoking confers a causal risk for gout. We first performed a cross-sectional analysis using information for 13,626 participants from the National Health and Nutrition Examination Survey between 2013 and 2018. The association of smoking with gout was subsequently assessed through logistic regression models. We next investigated the extent of shared genetic factors between smoking phenotypes and gout. We were able to demonstrate this using the linkage disequilibrium score regression applied to genome-wide association study data of European ancestry. Finally, to verify the causality of our relationship, we carried out a two-sample MR analysis. We selected the inverse-variance weighted (IVW) method and confirmed the consistency of using the IVW method with other statistical methods, including weighted median, weighted mode, and simple mode, as well as MR-Egger regression. We performed sensitivity analyses to investigate the heterogeneity of the hypothesis and stability of the data. Our findings based on National Health and Nutrition Examination Survey data reveal that there is a strong positive association between smoking and the risk of gout (odds ratio [OR] = 1.94, 95% confidence interval [CI] = 1.48-2.55, P < .001). This association persisted after confounding adjustments (OR = 1.41, 95% CI = 1.04-1.91, P = .027). In the subgroup analyses, former smokers and current smokers of 10 to 20 cigarettes per day had a substantially increased risk. Post-linkage disequilibrium score regression analysis revealed that the significantly positive genetic correlations of smoking initiation and lifetime smoking index with gout risk were both significantly positive. Additional evidence for causality is presented by MR. Genetic prediction of smoking initiation statistically increases gout risk (IVW OR = 1.55, 95% CI = 1.26-1.90, P = 3.17 × 10-5). A much stronger association is evident for lifetime smoking index (IVW OR = 1.99, 95% CI = 1.44-2.76, P = 3.24 × 10-5). These findings are the same with or without heterogeneity by sensitivity analysis. In light of our integrated analysis, smoking is a causative factor for gout. This suggests that public health interventions like anti-smoking campaigns might reduce gout incidence.

Humans↗

PubMed2006

Pathophysiology, clinical presentation and treatment of gout.

Gout is a common form of inflammatory arthritis that has been managed primarily in general medical practices for centuries. It appears that there has been an increasing prevalence of gout over the past decades, implying a growing public health burden. Accurate diagnosis and recognition of the various stages and manifestations of gout enable realistic goal setting for management. Recent evidence suggests new risk factors and potentially refutes others. Management of gout requires characterising and modifying risk factors and associated disorders, and commonly initiating drug therapy. Pharmacotherapy of gout includes the management of acute flares with anti-inflammatory agents such as NSAIDs and glucocorticoids and long-term treatment with urate-lowering drugs. Although pharmacotherapy is generally safe and effective, there are caveats and limitations to all gout therapies. Patient non-adherence and errors with the use of drugs for gout treatment are important factors leading to medical failures. With early intervention, careful monitoring and patient education, gout is a condition that can be managed very effectively. The advent of new drugs (such as febuxostat and urate oxidase [uricase]) and enhanced understanding of the pathogenesis of gout continue to improve our therapeutic options, particularly in a subset of patients with refractory disease and those who are intolerant to currently available medications.

Acute Disease↗

PubMed1988

Gout and coronary heart disease: the Framingham Study.

The relationship between gout, not associated with the use of diuretics, and the development of coronary heart disease was examined in 5209 subjects originally enrolled in the Framingham Study. Based on 32 years of follow-up, the two year incidence of gout was six times greater in men (3.2/1000) as compared to women (0.5/1000). For both sexes, the incidence of gout showed no clear relationship with age. Among men who never received diuretics, those afflicted by gout, as compared to those without gout, experienced a 60% excess of coronary heart disease (95% confidence limits, 1.1-2.2), primarily attributed to a two fold excess of angina pectoris (95% confidence limits, 1.2-3.1). Although gout was usually associated with other atherogenic risk factors, control of systolic blood pressure, total cholesterol, alcohol intake, body mass index, and diabetes failed to alter the effect of gout on the preceding coronary events in men. For women, there were no significant associations between gout and coronary heart disease. We conclude that gout, unrelated to the intake of diuretics, imparts an additional risk of coronary heart disease in men, unexplained by clinically measured risk factors.

Adult↗

PubMed2003

A case-control study of the association of diet and obesity with gout in Taiwan.

BACKGROUND: Gout has been a significant metabolic disorder for Chinese men in Taiwan; however, there is insufficient information on diet and lifestyle risk factors in this population. OBJECTIVE: The purpose of this case-control study was to explore potential dietary and lifestyle risk factors associated with gout in Chinese men. DESIGN: Between 1998 and 1999, we recruited and conducted face-to-face interviews with patients from outpatient clinics in Taipei who had incident gout (n = 92) and with their healthy coworkers (controls; n = 92). RESULTS: Systolic blood pressure, diastolic blood pressure, waist-to-hip ratio, waist-to-height ratio, and body mass index were significantly higher in cases than in controls. Family histories of gout and diabetes mellitus were strong risk factors for gout. Frequencies of vegetable and fruit consumption were significantly lower in cases than in controls. Logistic regression analyses showed that high alcohol intake and low intakes of fiber, folate, and vitamin C increased the risk of gout, but no association was found with purine intake. After covariates were controlled for, the adjusted odds ratios for the middle and highest tertiles of waist-to-height ratio (0.50-0.54 and >/==" BORDER="0"> 0.55, respectively) were 3.89 (95% CI: 1.32, 11.46) and 4.37 (1.18, 16.22), respectively, but no linear association was found for waist-to-hip ratio and waist circumference. CONCLUSIONS: Consumption of alcohol, but not of purine, may be a significant dietary risk factor for gout. Food sources rich in dietary fiber, folate, and vitamin C, such as fruit and vegetables, protect against gout. Waist-to-height ratio, which indicates central obesity, has a significant linear effect on gout occurrence, independent of body mass index.

Adult↗

PubMed2006

New insights into gout epidemiology.

PURPOSE OF REVIEW: The systematic study of gout dates to antiquity, to Hippocrates' initial descriptions of disease risk factors including advancing age, female menopause, and male sex. Although urate crystal diagnosis remains the gold standard for diagnosis it is impractical at a population level. Beyond crystal diagnosis, progress in gout epidemiology has been hampered by the lack of a standardized approach in defining case status. RECENT FINDINGS: Substantial progress has been made in furthering our understanding of gout over the last few decades. Taken together, epidemiologic investigations suggest that gout frequency is on the rise worldwide. Our understanding of gout risk factors continues to expand with the recent availability of well designed prospective cohort studies from both the USA and abroad. Moreover, recent investigations have shed important insight on the complex relationships of hyperuricemia, gout, and comorbid conditions, particularly the association of serum urate levels with cardiovascular morbidity and mortality. SUMMARY: Despite our growing understanding of the many facets of this age-old condition, current evidence continues to underscore the frequency with which gout is characterized by suboptimal care. Below we review our current knowledge of gout epidemiology with an emphasis on the association of hyperuricemia with cardiovascular comorbidity and evidence and determinants of continued suboptimal care in gout.

Cardiovascular Diseases↗

PubMed2005

Gout epidemiology: results from the UK General Practice Research Database, 1990-1999.

OBJECTIVE: To examine the epidemiology of gout and gout treatment in the United Kingdom using a large national practice based population. METHODS: Data from the UK General Practice Research Database from 1990 to 1999 were examined. Physician diagnoses and drug codes were used, and trends in gout incidence and treatment examined. Additionally, disease prevalence for the year 1999 was assessed. To examine the association of gout with comorbid disease, the prevalence of select health conditions and drug use was compared with the corresponding prevalences seen in osteoarthritis, adjusting for both age and sex. RESULTS: From 1 January 1990 to 31 December 1999 overall gout incidence remained relatively stable, ranging from a low of 11.9 cases (95% confidence interval (CI) 11.5 to 12.3) in 1991 to a high of 18.0 cases (95% CI 17.6 to 18.4) per 10 000 patient-years in 1994. Gout prevalence in 1999 was 1.4% with rates approaching 7% in men over the age of 65. Drugs used for the treatment of gout remained constant in prevalent cases with the exception of a significant decline in non-steroidal anti-inflammatory drug use over the 10 year follow up. Compared with patients with osteoarthritis, patients with gout were significantly more likely to have cardiovascular disease, hypertension, diabetes, and chronic renal failure, and were more likely to have used diuretics or ciclosporin, or both. CONCLUSION: Although gout is common in the UK, particularly among older men, the incidence of the disease seems to have remained stable during the 1990s.

Adult↗

PubMed2005

Gout, not induced by diuretics? A case-control study from primary care.

BACKGROUND: It is taken for granted that diuretics may induce gout, but there is a general lack of evidence on this topic. OBJECTIVES: To determine the incidence of gout in patients who use diuretics, taking into account concurrent hypertension and cardiovascular diseases. METHODS: A case-control study was designed. From a primary care population all patients with a first gout registration (59 men, 11 women; mean (SD) age 55.1 (13.5)) were identified as cases. To relate the occurrence of gout to diuretic use a matched reference series of three controls for each case was compiled. Conditional logistic regression analyses were applied to estimate incidence rate ratios (IRRs) of gout, and 95% confidence intervals (CIs), in subjects with and without diuretic treatment, hypertension, and cardiovascular diseases. Additional stratification analyses were made, particularly in the subjects not using diuretics. RESULTS: The IRRs of gout in subjects with v those without diuretic treatment, hypertension, heart failure, and myocardial infarction were 2.8 (95% CI 1.2 to 6.6), 2.6 (95% CI 1.2 to 5.6), 20.9 (95% CI 2.5 to 173.8), and 1.9 (95% CI 0.7 to 4.7), respectively. After adjustment, the IRR of gout for diuretic use dropped to 0.6 (95% CI 0.2 to 2.0), while the IRRs of gout for hypertension, heart failure, and myocardial infarction were still >1. This was also the case for subjects with hypertension or myocardial infarction, who had not used diuretics. CONCLUSION: The results suggest that diuretics do not actually increase the risk of gout. Cardiovascular indications for treatment may have confounded previous inferences.

Adult↗

PubMed2006

EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT).

OBJECTIVE: To develop evidence based recommendations for the diagnosis of gout. METHODS: The multidisciplinary guideline development group comprised 19 rheumatologists and one evidence based medicine expert, representing 13 European countries. Ten key propositions regarding diagnosis were generated using a Delphi consensus approach. Research evidence was searched systematically for each proposition. Wherever possible the sensitivity, specificity, likelihood ratio (LR), and incremental cost-effectiveness ratio were calculated for diagnostic tests. Relative risk and odds ratios were estimated for risk factors and co-morbidities associated with gout. The quality of evidence was categorised according to the evidence hierarchy. The strength of recommendation (SOR) was assessed using the EULAR visual analogue and ordinal scales. RESULTS: 10 key propositions were generated though three Delphi rounds including diagnostic topics in clinical manifestations, urate crystal identification, biochemical tests, radiographs, and risk factors/co-morbidities. Urate crystal identification varies according to symptoms and observer skill but is very likely to be positive in symptomatic gout (LR = 567 (95% confidence interval (CI), 35.5 to 9053)). Classic podagra and presence of tophi have the highest clinical diagnostic value for gout (LR = 30.64 (95% CI, 20.51 to 45.77), and LR = 39.95 (21.06 to 75.79), respectively). Hyperuricaemia is a major risk factor for gout and may be a useful diagnostic marker when defined by the normal range of the local population (LR = 9.74 (7.45 to 12.72)), although some gouty patients may have normal serum uric acid concentrations at the time of investigation. Radiographs have little role in diagnosis, though in late or severe gout radiographic changes of asymmetrical swelling (LR = 4.13 (2.97 to 5.74)) and subcortical cysts without erosion (LR = 6.39 (3.00 to 13.57)) may be useful to differentiate chronic gout from other joint conditions. In addition, risk factors (sex, diuretics, purine-rich foods, alcohol, lead) and co-morbidities (cardiovascular diseases, hypertension, diabetes, obesity, and chronic renal failure) are associated with gout. SOR for each proposition varied according to both the research evidence and expert opinion. CONCLUSIONS: 10 key recommendations for diagnosis of gout were developed using a combination of research based evidence and expert consensus. The evidence for diagnostic tests, risk factors, and co-morbidities was evaluated and the strength of recommendation was provided.

Advisory Committees↗

PubMed2006

The economic burden of gout on an employed population.

OBJECTIVE: To examine the economic burden of illness of gout in an employed population, quantifying the impact on employers annual health benefit costs for medical and prescription claims, sick leave, short- and long-term disability, and workers' compensation. METHODS: Adjudicated claims data from 300000 employees from 2001 through 2004 were utilized. T-tests were used to compare demographic data and medical costs and services by Agency for Healthcare Research and Quality (AHRQ) diagnostic categories. Two-part models were used to determine average annual health benefit costs overall and medical costs by place of delivery. A risk stratification quintile analysis was also performed utilizing gout-specific medical and pharmaceutical costs. RESULTS: There were 1171 employees with gout identified (total n = 249 038). All demographic variables between the two groups were statistically different (p <or= 0.05). The total annual cost for the employee with gout versus without gout was $6870 versus $3705, respectively, with significantly higher costs for medical claims, prescription claims, sick leave, short-term disability, and workers' compensation benefits. Costs were significantly higher by location of service for office, outpatient hospital or clinic, inpatient hospital, and laboratory. For the gout cohort, the top major diagnostic category in average cost was 'circulatory system' and in average services was 'endocrine, nutritional, metabolic, and immunologic systems'. Only 0.9% of employees with gout generated 20% of the total gout-specific medical and prescription costs. CONCLUSION: Gout inflicts a substantial burden of illness upon employers in terms of medical and prescription costs, as well as other work-related benefits.

Costs and Cost Analysis↗

PubMed2006

Epidemiology, risk factors, and lifestyle modifications for gout.

Gout affects more than 1% of adults in the USA, and it is the most common form of inflammatory arthritis among men. Accumulating data support an increase in the prevalence of gout that is potentially attributable to recent shifts in diet and lifestyle, improved medical care, and increased longevity. There are both nonmodifiable and modifiable risk factors for hyperuricemia and gout. Nonmodifiable risk factors include age and sex. Gout prevalence increases in direct association with age; the increased longevity of populations in industrialized nations may contribute to a higher prevalence of gout through the disorder's association with aging-related diseases such as metabolic syndrome and hypertension, and treatments for these diseases such as thiazide diuretics for hypertension. Although gout is considered to be primarily a male disease, there is a more equal sex distribution among elderly patients. Modifiable risk factors for gout include obesity, the use of certain medications, high purine intake, and consumption of purine-rich alcoholic beverages. The increasing prevalence of gout worldwide indicates that there is an urgent need for improved efforts to identify patients with hyperuricemia early in the disease process, before the clinical manifestations of gout become apparent.

Aged↗

PubMed1976

[Needle biopsy in gout and pseudogout (author's transl)].

INTRODUCTION: Radiological and morphological findings in advanced arthritis urica and pyrophosphate arthropathy are well known. In contrast, the early changes of synovial membrane in these disturbances of metabolism pose diagnostic problems. With the assistance of various cytological techniques and polarizing microscopical as well as electron microscopical investigation it was examined to what extent needle biopsies can be helpful in the differential diagnosis of gout and pseudogout. MATERIAL AND METHODS: In 8 patients with gout and 11 patients with pseudogout synovial fluid and small tissue specimens could be obtained with the aid of the Parker-Pearson needle. Both fluid and tissue specimens were investigated light and electron microscopically. Cell counts were evaluated in a Rosenthal chamber. The differentiation of the cells in stained smears was done by counting 200-600 cells per case. Crystals were identified by polarizing microscopy in wet preparations of freshly aspirated synovial fluid. RESULTS: Polarizing microscopy of synovial fluid detected intra- as well as extracellular urate and pyrophosphate crystals. The wedge-shaped urate crystals and the larger partly polygonal pyrophosphate crystals showed different polarizing microscopical properties and a negative birefringence. The absolute cell counts in gout were higher than those in pseudogout. The relative cell counts of the different cell types in synovial fluid showed more variation in gout than in pseudogout. Cases with acute gout developed a relative leukocytosis in contrast to a relative lymphocytosis in chronic gout. A relative leukocytosis was constant in all patients with pseudogout. Sclerosed areas with scarce and plump villi as well as sometimes hyperplastic and polymorphous synovial cell layers could be demonstrated histologically in the tissue specimens of the needle biopsies in cases with gout. Urate crystals were less frequent in specimens fixed in formalin. The histological alterations in pseudogout were uniform, 2-4 rows of slightly pleomorphic synovial cells lined the inner surface of the joint capsule, sclerosing alterations were less frequent. Pyrophosphate crystals and calcified particles were seen within the synovial lining cells, the connective tissue and the enodthelial cells of the blood vessels in pseudogout specimens. Intra- as well as extracellular crystals could also be demonstrated with the aid of scanning electron microscopy in sediments of synovial fluid in gout and pseudogout. Transmission electron microscopical investigations of synovial tissue specimens detected proliferated and pleomorphic synovial lining cells in gout in contrast to a more monomorphic appearance of these cells in pseudogout. The crystals were washed out during the preparation techniques for transmission electron microscopy so that needle-like empty spaces resulted within cytoplasm of the phagocytic cells. These clefts were surrounded by phagosomal structures and densified cytoplasmic ground substance; sometimes they were also lined by membranes...

Aged↗

PubMed2005

Gout in solid organ transplantation: a challenging clinical problem.

Hyperuricaemia occurs in 5-84% and gout in 1.7-28% of recipients of solid organ transplants. Gout may be severe and crippling, and may hinder the improved quality of life gained through organ transplantation. Risk factors for gout in the general population include hyperuricaemia, obesity, weight gain, hypertension and diuretic use. In transplant recipients, therapy with ciclosporin (cyclosporin) is an additional risk factor. Hyperuricaemia is recognised as an independent risk factor for cardiovascular disease; however, whether anti-hyperuricaemic therapy reduces cardiovascular events remains to be determined. Dietary advice is important in the management of gout and patients should be educated to partake in a low-calorie diet with moderate carbohydrate restriction and increased proportional intake of protein and unsaturated fat. While gout is curable, its pharmacological management in transplant recipients is complicated by the risk of adverse effects and potentially severe interactions between immunosuppressive and hypouricaemic drugs. NSAIDs, colchicine and corticosteroids may be used to treat acute gouty attacks. NSAIDs have effects on renal haemodynamics, and must be used with caution and with close monitoring of renal function. Colchicine myotoxicty is of particular concern in transplant recipients with renal impairment or when used in combination with ciclosporin. Long-term urate-lowering therapy is required to promote dissolution of uric acid crystals, thereby preventing recurrent attacks of gout. Allopurinol should be used with caution because of its interaction with azathioprine, which results in bone marrow suppression. Substitution of mycophenylate mofetil for azathioprine avoids this interaction. Uricosuric agents, such as probenecid, are ineffective in patients with renal impairment. The exception is benzbromarone, which is effective in those with a creatinine clearance >25 mL/min. Benzbromarone is indicated in allopurinol-intolerant patients with renal failure, solid organ transplant or tophaceous/polyarticular gout. Monitoring for hepatotoxicty is essential for patients taking benzbromarone. Physicians should carefully consider therapeutic options for the management of hypertension and hyperlipidaemia, which are common in transplant recipients. While loop and thiazide diuretics increase serum urate, amlodipine and losartan have the same antihypertensive effect with the additional benefit of lowering serum urate. Atorvastatin, but not simvastatin, may lower uric acid, and while fenofibrate may reduce serum urate it has been associated with a decline in renal function. Gout in solid organ transplantation is an increasing and challenging clinical problem; it impacts adversely on patients' quality of life. Recognition and, if possible, alleviation of risk factors, prompt treatment of acute attacks and early introduction of hypouricaemic therapy with careful monitoring are the keys to successful management.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2002

[Summary of the Dutch College of General Practitioners' "Gout" Standard].

The typical form of acute gout can be clinically diagnosed. The term 'complicated gout' is used if there are more than three acute attacks of gout per year, tophi or urate stones in the urinary tracts. In the case of recurrent probable acute gout, a diagnostic fine needle aspirate from the joint during an attack is indicated. First choice treatment of acute gout consists of NSAIDs. Colchicine is the second choice treatment and the third choice treatment consists of corticosteroids. Excessive alcohol use should be limited. Treatment of chronic gout depends on the uric acid excretion in the 24-hour urine. If the level of excretion is too low, the first choice should be benzbromarone, and if the uric acid output is too high, allopurinol should be the treatment of first choice. Increased fluid intake is recommended; maintenance treatment with colchicine is not advised. Consultation with or referral to a rheumatologist is indicated in the case of doubt about the diagnosis of 'acute gout' or 'complicated gout', or (suspected) bacterial arthritis and insufficient treatment effect.

Acute Disease↗

PubMed1991

Female gout. Clinical spectrum and uric acid metabolism.

We reviewed the clinical features and uric acid metabolism in 37 female patients with gout. In 32 female patients (86%), gout was diagnosed after menopause. Among the five premenopausal patients, four had renal insufficiency and one had superactivity of phosphoribosylpyrophosphate synthetase. More than 50% of the female patients had osteoarthritis, hypertension, or renal insufficiency or were treated with diuretics. Comparison with 220 male patients with gout showed that female patients developed gout significantly later, more frequently had associated diseases, and more often were receiving diuretics, whereas significantly more male than female patients had alcoholism. The articular features of gout were similar in both groups. However, the prevalence of tophi was higher and its localization different in female than in male patients. Female patients with gout had a higher mean serum urate concentration and a lower mean urinary uric acid excretion than did male patients with gout. These differences were significant and independent of the effects of age, renal insufficiency, alcoholism, or previous diuretic intake. Renal underexcretion of uric acid appears to be more severe in female than in male patients with gout.

Adult↗

PubMed1995

Racial differences in the incidence of gout. The role of hypertension.

OBJECTIVE: To estimate the incidence of and examine risk factors for the development of gout in black and white male physicians. METHODS: Data from 2 cohorts of former medical students, 352 black men in the Meharry Cohort Study and 571 white men in the Johns Hopkins Precursors Study, were analyzed. Cases of gout were identified by self-report. Baseline variables and incident hypertension were examined as risk factors for the development of gout in both cohorts. RESULTS: The incidence of gout was 3.11 and 1.82 per 1,000 person-years in the black men and the white men, respectively (P < 0.05); the cumulative incidence was 10.9% and 5.8%, respectively (P = 0.04). The relative risk (RR) for gout among the black men was 1.69 (95% confidence interval [95% CI] 1.02-2.80). This excess risk persisted after adjustment for baseline systolic blood pressure (adjusted RR = 1.96 [95% CI 1.14-3.38]). Incident hypertension was independently associated with the development of gout in univariate analysis (RR = 3.78 [95% CI 2.18-6.58]); when this variable was included as a time-dependent covariate in a Cox model, the excess risk for gout in black men was reduced and no longer significant (adjusted RR = 1.30 [95% CI 0.77-2.19]). CONCLUSION: The approximately 2-fold excess risk for gout among black men is explained, in part, by a greater risk of incident hypertension.

Adult↗

PubMed1999

Lipid abnormalities in Taiwan aborigines with gout.

An epidemiologic study to determine lipids and biochemical traits was performed in central Taiwan aborigines with and without gout and in the local Han Chinese. The lipid profile included measurement of serum triglyceride, cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A-I (apoA-I), and apoB. The results showed no significant difference for body mass index (BMI) and cholesterol between the three groups. Greater alcohol consumption was found in aborigines with gout compared with the other two groups. With univariate analysis, serum triglyceride, uric acid, creatinine, LDL-C, and apoB were significantly higher in aborigines with gout versus aborigines without gout or Han people (P<.001). By contrast, HDL-C and apoA-I were significantly lower in aborigines with gout (P<.001 or .01). However, with multivariate analysis, only serum triglyceride, uric acid, and apoB-1 were significantly different between aborigines with versus without gout. In conclusion, the apparent lipid abnormalities, particularly triglyceride and apoB, in Taiwan aborigines with gout are unlikely secondary to obesity. Instead, excessive alcohol intake or genetic factors may play a role in inducing hyperlipidemia in gout.

Adult↗

PubMed1984

Chronic renal failure with gout: a marker of chronic lead poisoning.

EDTA (calcium disodium edetate) lead mobilization and x-ray fluorescence (XRF) finger bone lead tests were done in 42 patients with chronic renal failure and without persisting lead intoxication. Nineteen of 23 patients with gout and 8 of 19 without gout had positive EDTA lead mobilization tests. Those patients with gout excreted significantly more excess lead chelate than those without gout. In the gout group 17 patients denied any childhood or industrial exposure to lead. They had a greater number of positive tests and excreted significantly more excess lead chelate than 14 patients with neither gout nor lead exposure. These results confirm that gout in the presence of chronic renal failure is a useful marker of chronic lead poisoning. Of 27 patients with positive lead mobilization tests, only 13 had elevated XRF finger bone lead concentrations (sensitivity 48%). Three of 15 patients with negative lead mobilization tests had elevated XRF finger bone lead concentrations (specificity 80%). Although the XRF finger bone lead test is a convenient noninvasive addition to the diagnostic evaluation of patients with chronic renal failure and gout, its application is limited due to the lack of sensitivity of the method.

Aged↗