Hyperlipoproteinaemia in primary gout: hyperlipoproteinaemic phenotype and influence of alcohol intake and obesity in Japan.

Hyperlipoproteinaemia in primary gout: hyperlipoproteinaemic phenotype and influence of alcohol intake and obesity in Japan.
复制标题

原发性痛风的高脂蛋白血症:日本高脂蛋白血症表型以及酒精摄入和肥胖的影响。

DOI:
10.1136/ard.45.4.308
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发表时间:
1986
影响因子:
27.4
通讯作者:
Sheng Jiao
Sheng Jiao
中科院分区:
医学1区
文献类型:
--
作者:
Sheng Jiao;K. Kameda;Yuji Matsuzawa;Sheng Jiao

文献摘要

被引文献

相似文献

研究了108例男性原发性痛风患者治疗前的血清脂蛋白谱,以阐明共存的高脂蛋白血症的每种表型的患病率及其致病因素。痛风患者血清甘油三酯(TG)和总胆固醇(TC)的平均水平分别为2.10 +/- 0.14 mmol/l和5.26 +/- 0.10 mmol/l(平均+/- SEM),显著高于同龄对照组(1.30 +/- 0.07 mmol/l和4.77 +/- 0.08 mmol/l) (p < 0.01和p < 0.05)。与对照组相比,痛风患者血清高密度脂蛋白胆固醇(HDL-C)值略有下降(1.24 +/- 0.08 mmol/l vs 1.40 +/- 0.03 mmol/l, p < 0.05)。61例(56%)患者出现高脂蛋白血症,其中IIa型、IIb型和IV型高脂蛋白血症患者分别占13%、15%和69%。因此,与原发性高脂血症和原发性高脂血症相比,原发性痛风患者中IV型高脂血症的患病率较高(69% vs 43%, p < 0.01)。采用逐步多元回归分析评价患者临床资料对血脂浓度的独立影响和相对影响。血清TG水平的两个主要预测因子为酒精摄入量(p < 0.01)和血清尿酸水平(p < 0.05)。最显著的预测变量为酒精摄入量,但其影响较小(r2 = 0.067)。其他变量,包括肥胖指数,都没有显著的影响。这些变量与血清TC或HDL-C水平之间的关系均不显著。此外,对没有肥胖(定义为理想体重的120%或更多)和有酒精摄入史的患者的血脂水平进行了调查。血清TG和TC浓度均显著高于对照水平。因此,原发性痛风的高脂蛋白血症不太可能继发于过量饮酒或肥胖,或两者兼而有之。相反,它可能是由遗传因素引起的,如综合高脂血症特征。
Serum lipoprotein profiles were investigated in 108 male patients with primary gout before treatment to elucidate the prevalence of each individual phenotype of coexisting hyperlipoproteinaemia and pathogenic factors responsible for it. The mean serum triglyceride (TG) and total cholesterol (TC) levels in the patients with gout were 2.10 +/- 0.14 mmol/l and 5.26 +/- 0.10 mmol/l (mean +/- SEM) respectively, which were significantly higher (p less than 0.01 and p less than 0.05 respectively) than the levels in age matched controls without gout (1.30 +/- 0.07 mmol/l and 4.77 +/- 0.08 mmol/l respectively). Serum high density lipoprotein cholesterol (HDL-C) values were slightly decreased in patients with gout compared with controls (1.24 +/- 0.08 mmol/l v 1.40 +/- 0.03 mmol/l, p less than 0.05). Hyperlipoproteinaemia was seen in 61 patients (56%), of whom patients with type IIa, IIb, and IV hyperlipoproteinaemia formed 13, 15, and 69% respectively. Thus the prevalence of type IV hyperlipoproteinaemia was high in primary gout as compared with primary hyperlipoproteinaemia with primary hyperlipoproteinaemia (69% v 43%, p less than 0.01). The independent and relative influences of clinical data of the patients upon the concentrations of serum lipids were assessed by stepwise multiple regression analysis. Two major predictors of serum TG level were alcohol intake (p less than 0.01) and serum uric acid level (p less than 0.05). The most significant predictive variable was alcohol intake, but its influence was judged to be small (r2 = 0.067). None of the other variables, including obesity index, had any significant influence. The relationships between any of these variables and serum TC or HDL-C levels were not significant. In addition, serum lipid levels were investigated in patients with neither obesity (defined as 120% or more of ideal body weight) nor a history of alcohol intake. Their serum TG and TC concentrations were also significantly higher than the respective control levels. Thus hyperlipoproteinaemia in primary gout its unlikely to be secondary to excess alcohol intake or obesity, or both. Instead, it may result from genetic factors such as a combined hyperlipidaemic trait.