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[高尿酸血症]

[Hyperuricemia].

作者信息

Slot O

机构信息

Reumatologisk afdeling, Hvidovre Hospital, København.

出版信息

Ugeskr Laeger. 1994 Apr 18;156(16):2396-401.

PMID:8009701
Abstract

Uric acid is formed by catabolism of purine nucleotides. Approximately 25% is excreted through the intestines and the rest through the kidneys. A little less than 5% of the population in western industrialised countries have hyperuricaemia, primarily men and postmenopausal women. Hyperuricaemia is in most cases caused by reduced renal excretion, which may be idiopathic with otherwise normal renal function. But the condition is often associated with hypertension, nephropathy and treatment with diuretics and certain other drugs. Hyperuricaemia due to increased purine metabolism is seen in malignant haematological diseases, other conditions with increased cellular turnover and during initiation of chemotherapy in malignant diseases. Moreover hyperuricaemia is associated with some metabolic disturbances and risk factors of atherosclerotic cardiovascular disease including hypertension, overweight, insulin resistance and hyperlipidaemia. Hyperuricaemia is rarely caused by constitutional enzymatic abnormalities influencing purine metabolism. In most cases hyperuricaemia is asymptomatic. It may though be complicated by gout, urolithiasis and possibly gouty nephropathy. The risk of complications is correlated to the degree and duration of hyperuricemia. Consequently, measures to affect predisposing and associated conditions should be taken including weight reduction, physical exercise and diet guidance, treatment of hypertension and possibly changes in medication. Urate lowering drug treatment is normally not indicated in asymptomatic hyperuricaemic individuals.

摘要

尿酸由嘌呤核苷酸的分解代谢形成。约25%通过肠道排泄,其余通过肾脏排泄。在西方工业化国家,略少于5%的人口患有高尿酸血症,主要是男性和绝经后女性。在大多数情况下,高尿酸血症是由肾脏排泄减少引起的,这可能是特发性的,肾功能在其他方面正常。但这种情况通常与高血压、肾病以及使用利尿剂和某些其他药物的治疗有关。在恶性血液疾病、其他细胞更新增加的情况以及恶性疾病化疗开始期间,可见由于嘌呤代谢增加导致的高尿酸血症。此外,高尿酸血症与一些代谢紊乱以及动脉粥样硬化性心血管疾病的危险因素有关,包括高血压、超重、胰岛素抵抗和高脂血症。高尿酸血症很少由影响嘌呤代谢的先天性酶异常引起。在大多数情况下,高尿酸血症是无症状的。不过,它可能会并发痛风、尿路结石,也可能并发痛风性肾病。并发症的风险与高尿酸血症的程度和持续时间相关。因此,应采取措施改善易感因素和相关状况,包括减轻体重、体育锻炼和饮食指导、治疗高血压以及可能的药物调整。对于无症状的高尿酸血症患者,通常不建议使用降尿酸药物治疗。

相似文献

1
[Hyperuricemia].[高尿酸血症]
Ugeskr Laeger. 1994 Apr 18;156(16):2396-401.
2
Hereditary nephropathy associated with hyperuricemia and gout.与高尿酸血症和痛风相关的遗传性肾病。
Arch Intern Med. 1993 Feb 8;153(3):357-65.
3
[Diagnostic value of renal urate excretion].[肾尿酸排泄的诊断价值]
Z Gesamte Inn Med. 1978 Mar 15;33(6):180-4.
4
Clinical aspects of monosodium urate monohydrate crystal deposition disease (gout).一水合尿酸钠晶体沉积病(痛风)的临床方面
Rheum Dis Clin North Am. 1988 Aug;14(2):377-94.
5
Pathogenesis, clinical findings and management of acute and chronic gout.急性和慢性痛风的发病机制、临床表现及治疗
Minerva Med. 2006 Dec;97(6):495-509.
6
Precocious familial gout with reduced fractional urate clearance and normal purine enzymes.伴有尿酸清除分数降低和嘌呤酶正常的早熟性家族性痛风。
Q J Med. 1990 May;75(277):441-50.
7
The effect of control and self-medication of chronic gout in a developing country. Outcome after 10 years.发展中国家慢性痛风的控制与自我药疗效果。10年后的结果。
J Rheumatol. 2003 Nov;30(11):2437-43.
8
[Prevention and therapy of disorders of purine metabolism].
Z Gesamte Inn Med. 1982 Jul 1;37(13):431-6.
9
Hyperuricaemia: more than just a cause of gout?高尿酸血症:不仅仅是痛风的病因?
J Cardiovasc Med (Hagerstown). 2013 Jun;14(6):397-402. doi: 10.2459/JCM.0b013e3283595adc.
10
[Pathogenesis, diagnostics and therapy of gout].[痛风的发病机制、诊断与治疗]
Vnitr Lek. 2006 Jul-Aug;52(7-8):736-41.

引用本文的文献

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Febuxostat in the management of hyperuricemia and chronic gout: a review.非布司他在高尿酸血症和慢性痛风治疗中的应用:综述。
Ther Clin Risk Manag. 2008 Dec;4(6):1209-20. doi: 10.2147/tcrm.s3310.
2
Identification of proteins binding to E-Box/Ku86 sites and function of the tumor suppressor SAFB1 in transcriptional regulation of the human xanthine oxidoreductase gene.鉴定与E-Box/Ku86位点结合的蛋白质以及肿瘤抑制因子SAFB1在人黄嘌呤氧化还原酶基因转录调控中的功能。
J Biol Chem. 2008 Oct 31;283(44):29681-9. doi: 10.1074/jbc.M802076200. Epub 2008 Sep 4.
3
The influence of dairy products on plasma uric acid in women.
乳制品对女性血浆尿酸的影响。
Eur J Epidemiol. 1995 Jun;11(3):275-81. doi: 10.1007/BF01719431.