The misdiagnosis of gout and hyperuricemia

Of 9,108 consecutive new patients seen in an outpatient rheumatology clinic, 155 (1.7%) were diagnosed as having gout. But 164 (1.8%) had been incorrectly diagnosed as having gout in the community. Misdiagnosis was more likely in those with psoriatic arthritis (odds ratio 3.841, 1.944-7.590) and pseudogout (odds ratio 4.152, 2.422-7.119) and less common in patients with nonspecific arthralgias (odds ratio 0.536, 0.326-0.881). Seventy-six percent of incorrectly diagnosed patients received allopurinol while slightly more than 15% were treated with uricosuric agents.     

An approach to hyperuricemia and gout

Arthrocentesis and patient and family histories make gout relatively easy to diagnose. The next step is to distinguish between primary and secondary hyperuricemia. Hyperuricemia results from either impaired renal excretion or excessive production of uric acid--or both. Determining the cause guides the choice of therapy.     

高尿酸血症及痛风的遗传学背景和防治

高尿酸血症和痛风的发病率旱逐年上升趋势,其遗传学研究和防治工作也受到越来越多的关注.以下探讨了从人类尿酸形成的遗传学背景,总结了可能引起高尿酸血症形成的机制;从改变生活和药物治疗两个方面综述了防治高尿酸血症和痛风的研究进展.     

高尿酸血症及痛风的遗传学背景和防治

高尿酸血症和痛风的发病率旱逐年上升趋势,其遗传学研究和防治工作也受到越来越多的关注.以下探讨了从人类尿酸形成的遗传学背景,总结了可能引起高尿酸血症形成的机制;从改变生活和药物治疗两个方面综述了防治高尿酸血症和痛风的研究进展.     

高尿酸血症及痛风的遗传学背景和防治

高尿酸血症和痛风的发病率旱逐年上升趋势,其遗传学研究和防治工作也受到越来越多的关注.以下探讨了从人类尿酸形成的遗传学背景,总结了可能引起高尿酸血症形成的机制;从改变生活和药物治疗两个方面综述了防治高尿酸血症和痛风的研究进展.     

原发性高尿酸血症和痛风分子遗传学研究进展

近年来原发性高尿酸血症和痛风的发病率逐年上升,高尿酸血症为痛风的早期阶段,长期高尿酸血症除易诱发痛风外,尚易累及肾脏和心脑血管系统,导致严重的肾脏及心脑血管疾病,但其遗传模式和易感基因尚不清楚。近年来的研究发现,嘌呤代谢过程中关键酶的缺陷及4个尿酸盐转运蛋白基因变异与高尿酸血症和痛风相关。本文对高尿酸血症和痛风的遗传模式、相关的易感基因及其染色体定位进行综述。     

Renal outcomes of gout and hyperuricemia.

Azotemia and urolithiasis as outcomes of gout or hyperuricemia were examined in several ways. Azotemia occurred in two (1.8 per cent) of 113 patients with asymptomatic hyperuricemia followed for eight years and in four (2.1 per cent) of 193 normouricemic control subjects; it was mild in all instances. Azotemia was also mild when it occurred in 168 patients with gout followed for 10 years and was unrelated to the degree of control of serum uric acid levels in these patients. Projected degrees of azotemia after 40 years of sustained hyperuricemia were mild and probably of no clinical significance until levels of serum uric acid reached 10 mg/100 ml in women and 13 mg/100 ml in men. Among 1,356 men, aged 60 to 69 years when serum uric acid was measured, follow-up for 10 years showed no death from renal failure that was attributable to hyperuricemia.Risks of urolithiasis were small; approximately one stone per 295 patients per year in those with asymptomatic hyperuricemia compared with one stone per 852 patients per year in normouricemic control subjects, and one stone per 114 patients per year in those with established gout. Among the gouty patients, initial level of serum uric acid was not a predictor of stone; significantly more of those in whom urolithiasis developed were taking medication to lower serum uric acid levels than in those not taking such medicine, but the differences between those taking probenecid and those taking allopurinol were not significant. Also, among the gouty patients, the control of serum uric acid levels was similar in those in whom stones developed and in those in whom they did not.It is concluded that (1) azotemia attributable to hyperuricemia is generally mild and probably of no clinical importance until serum uric acid levels reach 13 mg/100 ml in men and 10 mg/100 ml in women; and (2) the risk of urolithiasis is sufficiently low to justify awaiting the occurrence of the first stone before commencing drug therapy to lower serum uric acid levels.     

Metabolic defects of primary hyperuricemia and gout

Gout is a syndrome of multiple pathogeneses rather than a single disease entity. Reviewed here are the metabolic defects of primary gout, with major emphasis upon two well characterized, although uncommon, variants due to specific enzyme abnormalities: (1) structural mutants of phosphoribosylpyrophosphate (PP-ribose-P) synthetase with increased activities, resulting in increased rates of synthesis of PP-ribose-P, a key substrate of purine biosynthesis, and (2) structural mutants of hypoxanthineguanine phosphoribosyltransferase (HGPRT) with reduced activities, resulting in reduced consumption of PP-ribose-P and therefore a surplus in the amount available for purine biosynthesis de novo. The present state of our limited knowledge of control of purine biosynthesis is also reviewed briefly, and the potential mechanisms of excessive uric acid production in idiopathic gout are discussed in terms of possible excesses of substrates (PP-ribose-P or L-glutamine) of the first specific reaction of purine biosynthesis, possible defects of control of the enzyme catalyzing this reaction, or defects in maintenance of optimal concentrations of nucleotide regulators of this reaction. It is likely that the rate of production of uric acid in man is influenced by availability of substrates, cofactors and regulatory compounds, and activities of enzymes at many reaction sites other than the first specific reaction of the purine sequence, but their influences upon the rate of purine production can be conveniently analyzed in terms of their indirect effects upon this reaction. Examples cited include glucose-6-phosphatase deficiency glycogen storage disease, in which marked hyperuricemia and purine overproduction are present, and elevated activities of hepatic xanthine oxidase in gouty patients with increased uricaciduria, perhaps occurring secondary to other factors but nevertheless contributing to the excessive purine production. The basic lesions of the more than 95 per cent of patients with primary gout who do not have abnormalities of either PP-ribose-P synthetase or HGPRT remain to be defined, but will almost certainly turn out to be multiple, complex and, in many cases, subtle deviations of metabolic control.     

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.     

原发性高尿酸血症和痛风的规范诊治

痛风(gout)意指血中尿酸盐沉积所致的关节炎症及/或痛风石病变,是最常见的晶体性关节炎。在高尿酸血症(hyperuricemia)的情况下,可表现为特征性急性关节炎、痛风石形成及慢性关节炎;部分患者可发生尿酸盐肾病、尿酸性尿路石等。上述表现可呈不同的组合,体现了本病的异质性(heterogeneous)。近年来高尿酸血症及痛风在我国的患病率明显上升,中老年及更年期后妇女患病率较高,且呈现年轻化的趋势。一、高尿酸血症与痛风尿酸(即氧化形成的嘌呤)为嘌呤代谢的终末产物,主要由肾脏清除。血中尿酸的平衡取决于嘌呤的吸收、生成与分解、排泄。体内的嘌…     

Recent advances in the management of gout and hyperuricemia

PURPOSE OF REVIEW: To review the recent advances in the management of gout and hyperuricemia. RECENT FINDINGS: The first quality indicators for gout management have been proposed. Selective COX II inhibitors, as well as traditional NSAIDs, are effective in acute gout. A new xanthine oxidase inhibitor, febuxostat, and pegylated uricases are in clinical trials. SUMMARY: The therapeutic aims in gout include termination of the acute attack as promptly and gently as possible, prevention of future attacks, prevention or reversal of complications of the, and prevention or reversal of associated features such as obesity, hypertriglyceridemia, hypertension, or alcoholism.     

高尿酸血症/痛风流行病学特点及危险因素

高尿酸血症/痛风的患病率逐年攀升,呈现高流行、年轻化、男性高于女性、沿海高于内地的流行趋势.肥胖、高血压、高血脂、高血糖等与高尿酸血症/痛风的发生、发展密切相关.小剂量阿司匹林、袢利尿剂和噻嗪类利尿剂等药物亦可促进血清尿酸水平的升高.高尿酸血症是2型糖尿病、高血压、动脉粥样硬化、心血管事件、脑卒中和慢性肾脏病等疾病的独立危险因素,是痛风发作的最主要生化基础和最直接病因.对于高尿酸血症/痛风患者,应强调早期发现和早期治疗.     

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.     

痛风与高尿酸血症的分子流行病学研究进展

高尿酸血症和痛风是遗传和环境因素共同作用的结果。近年来,随着分子生物学和流行病学研究的进展,有关高尿酸血症和痛风的分子流行病学研究亦不断深入,本文简要介绍这一领域的研究进展。1痛风和高尿酸血症的流行病学特征1.1发病率和患病率随着人们生活水平的不断提高和饮食结构的改变,痛风和高尿酸血症的患病率在全球范围呈逐年上升的趋势。据估计,痛风的发病率在男性中为600/10万,女性约为100/10万,高尿酸血症在人群中的患病率约为5%~30%[1]。美国的一项交叉组合研究显示,1990~1999年,≥75岁人群痛风与高尿酸血症发病率从2·1%增至4·1%,65…