Risk factors for gout developed from hyperuricemia in China: a five-year prospective cohort study

The aim of the study was to investigate the factors that promote the development of gout in Chinese patients with hyperuricemia. Chinese cohort with 659 patients with hyperuricemia who had no history of gout at base line had been followed up for 5 years. The baseline data of the general states (gender, age, occupation and education level), lifestyle and behavior (smoking, drinking, and diet), the major chronic diseases (diabetes and hypertension), family history and gout attacks, physical examination (height, weight and blood pressure), and blood parameters (creatinine, urea nitrogen, triglycerides, total cholesterol and high-density lipoprotein cholesterol) were recorded before the follow-up. Over the five-year period, 75 hyperuricemia patients developed gout. In the logistic regression model, shrimp intake and shell intake were the risk factors (P = 0.038 and P < 0.001, respectively) and, combined with diabetes, also served as risk factor for gout developed from hyperuricemia, with relative risk (RR) of 2.571 (95 % confidence interval (95 % CI), 1.110–5.953), and females served as protective factors of gout, with RR of 0.113 (95 % CI, 0.041–0.312, referred to male). We identified that shrimp intake and shell intake, combined with diabetes, were the independent risk factors, and females served as protective factors of gout in those suffering from hyperuricemia in coast regions of Shandong province, China.     

Panniculitis: another clinical expression of gout

Gouty panniculitis is an unusual clinical manifestation of gout, characterized by the deposition of monosodium urate crystals in the lobular hypodermis. Its pathogenesis is poorly understood but is associated with hyperuricemia, and the clinical presence of indurate subcutaneous plaques, which may precede or appear subsequently to the articular clinical expression of tophaceous gout. The aim of this report is to describe the clinical characteristics and potential risk factors for the development of lobular panniculitis secondary to chronic tophaceous gout. This is a retrospective clinical review of 6 patients with gouty panniculitis seen at the rheumatology service at the National University of Colombia. All cases fulfill diagnostic criteria for gout. The presenting clinical characteristics of each case were analyzed. All 6 patients were men, with an average age of 26 years. Two patients initially presented with cutaneous manifestations, and in the remainder 4 joint involvements preceded the cutaneous manifestations. Articular involvement first developed in lower extremities, of intermittent nature, and subsequent occurrence of polyarthritis of upper and lower extremities. A positive family history of gout was observed in half of the patients. Smoking and high alcohol intake were relevant risk factors. On physical examination, all exhibited the presence of erythematous, irregular surface, deep indurate subcutaneous plaques. Biopsy of skin and deep dermis including panniculus revealed the presence of granulomatous inflammatory changes with deposition of amorphous eosinophilic material surrounded by palisading histocytes and lymphocytes. Characteristic negative birefringent monosodium urate crystals were observed in the synovial fluid of patients with arthritis. All patients exhibited high levels of serum uric acid and were non-complaint to treatment with allopurinol, NSAIDs, and colchicine. Gouty panniculitis should be considered in the differential diagnosis of panniculitis, especially in the presence of high levels of uric acid. It is usually observed in the third decade of life and may appear prior to the inflammatory articular manifestations of tophaceous gout.     

川东北地区原发性痛风的临床特点及发病危险因素分析

目的：探讨川东北地区原发性痛风的临床特点及发病危险因素。方法采用统一调查表,对583例原发性痛风患者及459例健康体检者进行临床调查及相关实验室指标检测,采用Logistic回归分析痛风的发病危险因素。结果①94．9％的患者首次发作时累及一个关节,其中累及第一跖趾关节者占68．6％。②痛风发作无诱因者占37．6％;有诱因者占62．4％,其中88．2％与饮食因素有关。③痛风并发痛风石者占12．2％,高血压者占35．7％,高脂血症者占66．9％。④并发痛风石者多发生于痛风后3～8年,其病程长于无痛风石患者,血尿酸（sUA）水平高于无痛风石患者（P均＜0．01）。⑤Logistic回归分析发现,高sUA、饮酒、BMI、高TG、高嘌呤饮食、高血压及吸烟均与痛风发病相关（P＜0．01或＜0．05）。结论原发性痛风发病受多因素影响,高sUA、饮酒、BMI、高TG、高嘌呤饮食、高血压及吸烟均可能增加其发病风险。     

Chronic tophaceous gouty arthritis mimicking rheumatoid arthritis.

OBJECTIVES: To analyze the factors which differentiate chronic tophaceous arthritis from rheumatoid arthritis. METHODS: We describe two cases of chronic gouty arthritis masquerading as rheumatoid arthritis. The characteristic features of each of these two conditions and the diagnostic approach are discussed in light of relevant literature. RESULTS: The correct diagnosis was reached by the combination of accurate history taking (family history of gout, alcoholism, previous diuretic therapy and renal stones), guiding clinical features (subcutaneous tophaceous deposits) and specific radiological (assymetrical erosions with sclerotic margins and overlying edges) and laboratory findings (hyperuricemia and hyperuricosuria). It was confirmed by the identification of monosodium urate (MSU) crystals in the synovial and subcutaneous tissues. CONCLUSIONS: Gout and rheumatoid arthritis rarely coexist. Chronic gouty arthritis may mimic rheumatoid arthritis, and vice-versa. Clinical suspicion supplemented by characteristic laboratory, radiological and histologic findings help at reaching an accurate diagnosis.     

Moonshine and lead Relationship to the Pathogenesis of Hyperuricemia in Gout

Thirty-three patients with gouty arthritis were evaluated for clinical features of gout as well as for causes of hyperuricemia. None of the gout patients overexcreted urate and all exhibited a decrease in urate clearance. Fifty-five percent of these patients had a history of significant illicit alcohol ingestion, while only 27% had evidence of excessive lead stores. There was no correlation between extent of depression in urate or creatinine clearance and amount of lead excreted following EDTA infusion. There was also no evidence of an increased prevalence of anemia, hypertension, or peripheral neuropathy in the gout patients with excessive versus those with normal lead stores. Nineteen patients with a comparable history of moonshine ingestion but no evidence of gouty arthritis were also studied. Eight patient volunteers with no history of moonshine ingestion or arthritis served as controls. None of the controls had evidence of excessive lead stores, while 42% of the non-arthritis moonshine drinkers excreted over 500 m̈g of lead after EDTA administration. There was no evidence of decreased urate or creatinine clearance or increased prevalence of anemia, hypertension, or peripheral neuropathy in those patients with excessive lead stores. We conclude that factors other than lead nephropathy, such as obesity, ethanol consumption, hypertension, and hereditary factors, are responsible for the decreased urate clearance observed in over 70% of our gout patients, many of whom give a history of moonshine ingestion. The results in non-gout patients indicate that increased lead excretion following EDTA administration cannot be equated with lead nephropathy or clinical lead toxicity. Thus it is uncertain whether gout patients with evidence of excessive lead stores necessarily have lead nephropathy as the reason for their reduction in urate clearance and consequent hyperuricemia.     

Severe tophaceous gout. Characterization of low socioeconomic level patients from México

OBJECTIVE: To describe a group of patients with frequent tophaceous gout, the variables associated with severe tophaceous gout and to compare them with other patients with gout described elsewhere. METHODS: We looked for 65 demographic clinical and paraclinical variables from patients with gout who attended our gout clinic from 1995-2000 and were evaluated by the same group of physicians. RESULTS: Three hundred and sixteen patients were included, 98% males, 82% live in México city, the mean age at onset, educational level and disease duration were 37.5 +/- 12.4, 6.3 +/- 3.9 and 12.6 +/- 10.3 years respectively. Tophaceous gout was present in 62% of the patients with a mean tophi number of 4.7 +/- 6.3 and mean HAQ score 0.13 +/- 0.37. Severe tophaceous gout (>or= 5 tophi) was found in 34% and these patients had significantly: earlier age at onset, longer duration of the disease, lesser frequency of obesity and higher frequency of: intradermal tophi, HAQ > 0.5, hospitalizations, radiographic score III/IV, uric acid under-excretion, renal function impairment and previous (oral and parenteral) auto-prescribed chronic glucocorticoid treatment compared with patients with non-severe tophaceous gout. In the multiple logistic regression the significant variables were renal function impairment (p = 0.000) and previous chronic parenteral glucocorticoid treatment (p = 0.011) . CONCLUSION: Our patients compared with those from other countries who have earlier age at onset, very low frequency of gout among females, frequent tophaceous gout and severe tophaceous gout. Severe tophaceous gout in this group is associated with renal function impairment and previous chronic parenteral glucocorticoid treatment.     

《2010年中国痛风临床诊治指南》解读

《2010年中国痛风临床诊治指南》指出,在诊断痛风时要特别注意痛风患者的病程阶段:即无症状高尿酸血症、急性痛风性关节炎或慢性痛风,强调关注患者是否为无症状高尿酸血症或痛风合并其它情况(糖尿病、高血压病,或心脑血管的危险因素)。除了合理应用非甾类抗炎药或糖皮质激素积极治疗急性关节炎急性发作外,痛风患者的综合管理尤为重要,包括对所有患者去除引起高尿酸血症的诱因及给予非药物干预(生活方式和饮食调整、减轻体重、适度饮酒,停用引起尿酸升高的药物等),有效控制合并症。对反复发作的、间歇期或慢性痛风患者给予降尿酸药物治疗以维持血尿酸水平低于327μmol/L,以及为严重的慢性痛风石患者寻找可能的手术治疗机会。     

Acute gouty arthritis during pyrazinamide treatment: a case report

Gout is a disease caused by an inflammatory response to an aggregation of monosodium urate crystals that develop secondary to hyperuricemia. Throughout its natural history it has four stages: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout, and chronic tophaceous gout. In this article, we report the case of a patient who had asymptomatic hyperuricemia secondary to pyrazinamide, which was prescribed for pulmonary tuberculosis, and had developed an acute gouty arthritis immediately after the “Feast of Sacrifice” due to a dietary excess of purine.     

Acute gouty arthritis during pyrazinamide treatment: a case report

Abstract

Gout is a disease caused by an inflammatory response to an aggregation of monosodium urate crystals that develop secondary to hyperuricemia. Throughout its natural history it has four stages: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout, and chronic tophaceous gout. In this article, we report the case of a patient who had asymptomatic hyperuricemia secondary to pyrazinamide, which was prescribed for pulmonary tuberculosis, and had developed an acute gouty arthritis immediately after the “Feast of Sacrifice” due to a dietary excess of purine.     

Community based epidemiological study on hyperuricemia and gout in Kin-Hu, Kinmen

OBJECTIVE: This is a population survey conducted in 1991-92 among residents aged > or =30 years in Kin-Hu, Kinmen, with a 77.7% response rate to study the prevalence of hyperuricemia and hyperuricemia associated gout. A stratified analysis based on sex and age was used to assess the interaction and analyze the associated risk factors for hyperuricemia and gout. METHODS: Hyperuricemia was defined as uric acid > or =7.0 mg/dl for men and > or =6.0 mg/dl for women. Gout was clinically diagnosed by a senior rheumatologist based on patient's history and examination according to the clinical criteria of Wallace. Basic demographic and lifestyle variables as well as biochemical data were collected. RESULTS: The prevalence of hyperuricemia was 25.8% (391/1515) in men and 15.0% (250/1670) in women. The prevalence of gout among hyperuricemic subjects was 11.5% for men and 3% for women. According to age spectrum, the risk factor for hyperuricemia was hyperlipidemia in young adults (30-39 yrs); lifestyle and some clinical syndromes played a significant role in middle aged persons (40-59 yrs). The different risk factors between the sexes in middle age were alcohol consumption effect in men and menopause effect in women. Impaired renal function and use of diuretics became the important factors in the elderly (> or =60 yrs). The risk factors for gout among either the general population or subjects with hyperuricemia were concentration of serum uric acid, alcohol consumption, and central obesity. CONCLUSION: Risk factors for hyperuricemia tended to be different with respect to sex and age. Alcohol consumption and central obesity were independent predictors of gout among hyperuricemic subjects irrespective of uric acid level.     

Gout and hyperuricemia

The prevalence of gout in the United States has been rising steadily for the past two decades. Hyperuricemia is considered a necessary but not sufficient precondition for gout. Known risk factors for gout include male sex, hypertension, renal insufficiency, obesity/weight gain, diuretic use, lead exposure, and family history. The association of gout and hyperuricemia with coronary artery disease is controversial. Current evidence from the Framingham Study suggests that gout is in fact an independent risk factor for CHD. These data suggest that patients with gout should be screened for modifiable risk factors for CHD, and that early intervention in such patients may be worthwhile. Finally, the effect of AHU as risk factor for CHD remains unclear but is probably a weak one.     

Hyperuricemia and associated diseases

After introduction of urate-lowering therapy, asympotomatic hyperuricemia was treated with allopurinol or uricosuric agents in the belief that hyperuricemia and/or gout caused chronic kidney disease. Epidemiologic studies in the 1970s, however, failed to confirm the view that hyperuricemia and gout were independent risk factors for chronic kidney disease. As a result, urate-lowering pharmacotherapy is generally not recommended at the present time in the management of asymptomatic hyperuricemia even though recent epidemiological, experimental, and clinical studies have prompted reexamination of a causal role for hyperuricemia (with or without gout) in chronic kidney disease as well as other important disorders including cardiovascular disease, hypertension, and metabolic syndrome. The issue of such a role remains unresolved and this article reviews the current status of the relationship between hyperuricemia and associated disorders.     

新疆汉、维吾尔、哈萨克族成年人高尿酸血症及痛风的流行病学调查

应用四阶段整群随机抽样法,在新疆地区调查了13 559名汉、维吾尔、哈萨克族成年人的高尿酸血症及痛风患病率.汉、维吾尔、哈萨克族高尿酸血症标化患病率分别为11.00%、3.27%和3.94%;痛风患病率分别为1.32%、0.65%和0.70%,差异均有统计学意义(均P＜0.05).非条件logistic回归分析显示,维吾尔族及哈萨克族患高尿酸血症的风险较汉族低;体重指数、肾功能及血脂为高尿酸血症的危险因素;女性及体力活动为保护因素.食海鲜及动物内脏是汉族患高尿酸血症的独立危险因素,食动物内脏及饮酒是哈萨克族的独立危险因素.

Abstract：

Four-stage selected random samples were used to analyze the prevalence and distributing feature of hyperuricemia and gout in 13 559 Han,Uighur,and Hazakh adults in Xinjiang. The prevalence of hyperuricemia was 11.00%,3.27%,and 3.94% respectively in Han,Uighur,and Hazakh populations,and 1.32%, 0.65%,and 0.70% for gout,with statistically significant difference among three groups(all P＜0.05). No-conditional logistic regression analysis showed that nationality,body mass index,renal function,and serum lipid were risk factors of hyperuricemia,while female and physical activity were protective factors. Eating seafood and animal visceral organs were independent risk factors of hyperuricemia in Han population. Eating animal visceral organs and drinking alcohol were independent risk factors of hyperuricemia in Hazakh population.     

膳食营养与高尿酸血症和痛风的关系

饮食治疗在高尿酸血症及痛风的作用已被研究证实,随着研究的不断深入,传统的低蛋白、低嘌呤治疗观念正逐步被更新.高尿酸血症及痛风患者常合并高血压、心血管疾病等,因此饮食治疗不仅应控制食物种类,还要进行饮食结构的调整,以便在高尿酸血症及痛风得到缓解的同时降低伴发疾病的风险.     

Gout in African Americans

Purpose

African Americans have a substantially higher prevalence of risk factors for gout than Caucasians. The aim of the present study was to compare the risk for incident gout among African Americans and Caucasians.

Methods

Incidence rates of physician-diagnosed gout among 11,559 Caucasian men and 931 African American men aged 35 to 57 years and at high cardiovascular risk, observed for 7 years as a part of the Multiple Risk Factor Intervention Trial, were analyzed. Cox regression models were used to account for potential confounding by age, body mass index, diuretic use, hypertension and diabetes status, aspirin and alcohol consumption, and kidney disease.

Results

At baseline, after accounting for risk factors, African Americans had a 14% lower prevalence of hyperuricemia than Caucasians. Incidence of gout increased with increasing prevalence of risk factors in both Caucasians and African Americans. Ethnic disparities in incidence rates were most apparent among those without other risk factors for gout. In separate Cox regression models, after accounting for risk factors, African American ethnicity was associated with a hazard ratio of 0.78 (95% confidence interval [CI], 0.66-0.93) for physician-diagnosed gout and 0.88 (95% CI, 0.85-0.90) for incident hyperuricemia. Significant interactions were observed; the association was the strongest (hazard ratio 0.47; 0.37-0.60). These associations were unaffected by addition of serum urate as a covariate or by using alternate case definitions for gout.

Conclusions

After accounting for the higher prevalence of risk factors, African American ethnicity is associated with a significantly lower risk for gout and hyperuricemia compared with Caucasian ethnicity.     

Asymptomatic hyperuricemia: the case for conservative management

The management of asymptomatic hyperuricemia is controversial. Reported benefits from treatment prevention of acute gouty arthritis, chronic tophaceous gout, urolithiasis, or gouty nephropathy. A review of experimental and clinical data suggests that the risks of asymptomatic hyperuricemia are small or unknown and the efficacy of long-term treatment in preventing gout or renal disease is unproved. The costs and risks of prolonged drug administration and practical considerations such as patient compliance mitigate against long-term therapy in asymptomatic persons. We offer some recommendations for an expectant approach to the management of asymptomatic hyperuricemia.     

非酒精性脂肪性肝病发病影响因素的病例对照研究

目的 调查非酒精性脂肪性肝病(NAFLD)发病的影响因素,为预防NAFLD的发生提供可靠的流行病学依据.方法 采用病例对照研究方法,对福建医科大学附属协和医院2007年1-8月体检确诊的NAFLD患者385例和同期的体检健康人群825人进行调查.自制调查表收集两组一般情况、生活方式、饮食习惯、疾病既往史及生物化学检查结果,并对过程进行质量控制.两组间均衡检验采用t检验和χ2检验;单因素分析采用χ2检验;采用非条件Logistic逐步回归分析筛选变量,找出NAFLD的影响因素.结果 两组在饮酒量(g/周)、是否喝茶、是否吸烟、运动指数、进餐速度、应酬频率、食用油种类、是否食用海产品、是否有脂肪肝家族史及是否有高血压,血糖增高、血脂异常、ALT增高、AST增高、高尿酸血症、肥胖、高密度脂蛋白降低、低密度脂蛋白增高18个方面的差异有统计学意义(P值均＜0.05).非条件Logistic逐步回归分析结果显示,以上18个因素中有12个因素进入模型,其中肥胖(OR=6.35)、高血压(OR=3.82)、血脂异常(OR=2.95)、高密度脂蛋白降低(OR=2.85)、高血糖(OR=2.82)、ALT增高(OR=2.80)、高尿酸血症(OR=2.35)、HBsAg阳性(OR=1.99)、脂肪肝家族史(OR=1.79)及常吃海产品(OR=1.58)是NAFLD的危险因素,而饮茶(OR=0.72)和经常运动(OR=0.90)则是NAFLD的保护因素. 结论 影响NAFLD发病的因素有多种,主要是生活方式,与遗传因素也有关.     

中国华东地区人群胃癌癌前病变发病相关危险因素分析

目的探讨各种危险因素与中国华东地区人群胃癌癌前病变发病风险的关系,为胃癌癌前病变的个体化预防提供科学依据。方法收集中国华东地区胃癌癌前病变501例,浅表性胃炎523例;对两组多种危险因素进行描述性对比分析。结果与浅表性胃炎组比较,胃癌癌前病变组中的H.pylori感染、食管癌家族史、胃癌家族史、慢性萎缩性胃炎家族史、家族性腺瘤性息肉病、慢性萎缩性胃炎个人史、胃溃疡个人史、阿司匹林等非甾体抗炎药的使用、胃食管反流病、饮酒、亚硝基化合物饮食、不吃早餐三餐不定时、经常食用烟熏炙烤肉类食品、经常食用煎炸食品、经常食用辛辣食品、焦虑及抑郁的构成比,差异有统计学意义(P0.05)。与胃癌癌前病变相关的危险因素分析依次是慢性萎缩性胃炎个人史、家族性腺瘤性息肉病、胃癌家族史、阿司匹林等非甾体抗炎药的使用、经常食用辛辣食品、H.pylori感染、家族食管癌史、饮酒、焦虑、胃溃疡个人史、胃食管反流病、慢性萎缩性胃炎家族史。结论对于中国华东地区来说,慢性萎缩性胃炎个人史是胃癌癌前病变最突出的危险因素,其次为家族性腺瘤性息肉病和胃癌家族史。     

The interaction between uric acid level and other risk factors on the development of gout among asymptomatic hyperuricemic men in a prospective study

OBJECTIVE: To investigate the incidence of gout and the interaction between uric acid level and other risk factors in the development of gout. METHODS: Two hundred twenty-three asymptomatic hyperuricemic men initially studied in 1991-92 were reassessed in 1996-97. Gout was clinically diagnosed by a senior rheumatologist based on history and physical according to the clinical criteria of Wallace. Basic demographic and lifestyle variables as well as biochemical data were collected in both baseline and followup periods. Both the stability analysis and the analysis of repeated relationships were applied. RESULTS: The 5-year cumulative incidence of gout was 18.83% (42/223). The risk factors for gout based on the analysis of repeated relationships were uric acid level, alcohol consumption, use of diuretics, and obesity. The only predictor of gout at baseline was uric acid level. After adjusting for baseline uric acid level, followup uric acid increase, persistent alcohol consumption, use of diuretics in the followup period, and body mass index increase were independent predictors for gout among asymptomatic hyperuricemic men. Excessive alcohol consumption, particularly if occasional, was the most important factor in the development of gout, even when the concentration of uric acid level was below 8 mg/dl. CONCLUSION: Uric acid level is the key factor for prevention of gout and needs constant monitoring. Other contributing or possible etiologic factors such as alcohol consumption, diuretics use, and excess weight gain carry an increased risk of gout attack among patients with hyperuricemia.     

原发性高尿酸血症患者发生痛风的前瞻性研究

目的 明确原发性高尿酸血症(HUA)患者发生痛风的危险因素.方法 对2004年山东沿海流行病学调查和本院健康体格检查高尿酸血症患者随访3年,主要观察指标为是否发生痛风,评估膳食因素对痛风发生的影响和患者血生化指标变化.结果 536例HUA患者,102例发生痛风,发生率为19%.年龄(OR=1.046,P＜0.05)、血尿酸(OR=1.021,P＜0.05)、空腹血糖(OR=1.021,P＜0.05)、甘油三酯(OR=1.008,P＜0.05)、蟹贝类摄入量(OR=5.992,P＜0.05)和啤酒摄入量(OR=1.012,P＜0.05)是HUA患者发生痛风的危险因素.结论 HUA患者蟹贝类、啤酒等过量摄入造成血尿酸波动是发生痛风的主要危险因素.调整糖脂代谢紊乱、减少高嘌呤食物摄入、控制血尿酸水平是减少痛风发作的重要措施.

Abstract：

Objective To determinate the risk factors of gout in patients with hyperuricemia.Methods Patients detected with hyperuricemia both in epidemiological survey of Shandong coastal areas in 2004 and in health examination of our hospital were followed up for three years to observe the incidence of gout, relationship of diet and gout, and changes of biochemical indicators.Results During 3 years, 102 patients (19%) out of 536 patients with hyperuricemia developed gout. Age(OR=1.046, P＜0.05), serum uric acid(OR=1.021, P＜0.05), fasting plasma glucose(OR=1.021, P＜0.05), triglyceride(OR=1.008, P＜0.05), tony crab intake ( OR=5.992, P＜0.05),and beer intake(OR=1.012, P＜0.05) were the risk factors of gout attack in patients with hyperuricemia.Conclusions Excess intake of tony crab and beer resulting in fluctuation of serum uric acid is the main risk factor of gout in patients with hyperuricemia. Correcting metabolic disorder of glucose and lipid, reducing the intake of high-purine food, and controlling the level of serum uric acid are the measures to reduce gout attack.