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原发性无症状性痛风患者的继发性高甘油三酯血症和高脂蛋白血症。

Secondary hypertriglyceridemia and hyperlipoproteinemia in patients with primary asymptomatic gout.

作者信息

Naito H K, Mackenzie A H

出版信息

Clin Chem. 1979 Mar;25(3):371-5.

PMID:262176
Abstract

We carefully selected 30 men with primary gout, rendered asymptomatic by therapy, to examine the frequency and type of hyperlipidemia and hyperlipoproteinemia, with the objective of determining whether serum uric acid, alcohol intake, liver function, kidney function, and (or) drugs were participating in the secondary lipid disorder. Sixty-one age- and sex-matched men were used as controls. About 73% of the gout patients had hypertriglyceridemia, 1.6-fold the frequency found in the control group. Types IV and IIb lipoprotein electrophoretic patterns were most prevalent in the gout group. Neither alcohol intake nor hyperuricemia, per se, seems to be the cause of the lipid and lipoprotein disorder and cannot be related to liver or kidney dysfunctions. Obesity was the major underlying factor associated with the lipidemia. The study suggests that diet and, possibly, defective clearance of triglycerides may be etiologic factors associated with the abnormal serum triacylglycerol (triglyceride) and lipoprotein concentrations in these individuals.

摘要

我们精心挑选了30名经治疗后无症状的原发性痛风男性患者,以检查高脂血症和高脂蛋白血症的发生率及类型,目的是确定血清尿酸、酒精摄入量、肝功能、肾功能和(或)药物是否与继发性脂质紊乱有关。61名年龄和性别匹配的男性作为对照。约73%的痛风患者有高甘油三酯血症,其发生率是对照组的1.6倍。IV型和IIb型脂蛋白电泳图谱在痛风组最为常见。酒精摄入量和高尿酸血症本身似乎都不是脂质和脂蛋白紊乱的原因,也与肝肾功能障碍无关。肥胖是与血脂异常相关的主要潜在因素。该研究表明,饮食以及可能存在的甘油三酯清除缺陷可能是这些个体血清三酰甘油(甘油三酯)和脂蛋白浓度异常的病因。

相似文献

1
Secondary hypertriglyceridemia and hyperlipoproteinemia in patients with primary asymptomatic gout.原发性无症状性痛风患者的继发性高甘油三酯血症和高脂蛋白血症。
Clin Chem. 1979 Mar;25(3):371-5.
2
[Hyperlipoproteinemia in primary gout and asymptomatic hyperuricemia].
Wien Med Wochenschr. 1988 May 31;138(10):221-5.
3
Hyperlipoproteinaemia in primary gout: hyperlipoproteinaemic phenotype and influence of alcohol intake and obesity in Japan.原发性痛风中的高脂蛋白血症:日本的高脂蛋白血症表型以及酒精摄入和肥胖的影响
Ann Rheum Dis. 1986 Apr;45(4):308-13. doi: 10.1136/ard.45.4.308.
4
[Lipid disorders in gout and hyperuricemias].[痛风和高尿酸血症中的脂质紊乱]
Rev Rhum Mal Osteoartic. 1973 Feb;40(2):95-105.
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Relationship between hypertriglyceridemia and uric acid production in primary gout.原发性痛风中高甘油三酯血症与尿酸生成的关系。
Metabolism. 1989 Jul;38(7):698-701. doi: 10.1016/0026-0495(89)90110-8.
6
Hyperlipidemia in primary gout.
Semin Arthritis Rheum. 1978 May;7(4):233-44. doi: 10.1016/0049-0172(78)90024-0.
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[Lipid disorders in gout and in hyperuricemia with myalgia].痛风及伴有肌痛的高尿酸血症中的脂质紊乱
Mars Med. 1972;109(10):609-25.
8
[Frequency and distribution of hyperlipoproteinemias in arterial diseases, diabetes, and gout. Results of 20 examinations carried out in a hospital setting].[动脉疾病、糖尿病和痛风中高脂蛋白血症的频率与分布。在医院环境中进行的20项检查结果]
Ann Biol Clin (Paris). 1973;31(2):151-2.
9
Gout and hyperlipidaemia. Effect of overweight on the levels of circulating lipids.
Ann Clin Res. 1977 Aug;9(4):239-45.
10
Hyperlipidaemia in gout.痛风中的高脂血症
Clin Chim Acta. 1975 Jul 9;62(1):103-6. doi: 10.1016/0009-8981(75)90285-5.

引用本文的文献

1
Epidemiological association between uric acid concentration in plasma, lipoprotein(a), and the traditional lipid profile.血浆尿酸浓度、脂蛋白(a)与传统血脂谱的流行病学关联。
Clin Cardiol. 2010 Feb;33(2):E76-80. doi: 10.1002/clc.20511.
2
Apolipoprotein E phenotypes in patients with gout: relation with hypertriglyceridaemia.痛风患者的载脂蛋白E表型:与高甘油三酯血症的关系。
Ann Rheum Dis. 1995 May;54(5):351-4. doi: 10.1136/ard.54.5.351.
3
Hyperlipoproteinaemia in primary gout: hyperlipoproteinaemic phenotype and influence of alcohol intake and obesity in Japan.
原发性痛风中的高脂蛋白血症:日本的高脂蛋白血症表型以及酒精摄入和肥胖的影响
Ann Rheum Dis. 1986 Apr;45(4):308-13. doi: 10.1136/ard.45.4.308.
4
Effect of treatment on erythrocyte phosphoribosyl pyrophosphate synthetase and glutathione reductase activity in patients with primary gout.治疗对原发性痛风患者红细胞磷酸核糖焦磷酸合成酶和谷胱甘肽还原酶活性的影响。
Ann Rheum Dis. 1986 Nov;45(11):941-4. doi: 10.1136/ard.45.11.941.
5
A DNA polymorphism of an apoprotein gene associates with the hypertriglyceridaemia of primary gout.载脂蛋白基因的DNA多态性与原发性痛风的高甘油三酯血症相关。
Hum Genet. 1988 Jan;78(1):55-9. doi: 10.1007/BF00291235.