Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis.

Reduction in high density lipoproteins by anabolic steroid (stanozolol) therapy for postmenopausal osteoporosis.
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DOI:
10.1016/0026-0495(82)90166-4
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发表时间:
1982-11
期刊:
Metabolism: clinical and experimental
影响因子:
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通讯作者:
Hugh McA. Taggart;Hugh McA. Taggart;D. Applebaum-Bowden;D. Applebaum-Bowden;Steven M. Haffner;Steven M. Haffner;G. Warnick;G. Warnick;Marian C. Cheung;Marian C. Cheung;John J. Albers;John J. Albers;C. H. Chestnut;C. H. Chestnut;William R. Hazzard;William R. Hazzard
Hugh McA. Taggart;Hugh McA. Taggart;D. Applebaum-Bowden;D. Applebaum-Bowden;Steven M. Haffner;Steven M. Haffner;G. Warnick;G. Warnick;Marian C. Cheung;Marian C. Cheung;John J. Albers;John J. Albers;C. H. Chestnut;C. H. Chestnut;William R. Hazzard;William R. Hazzard
中科院分区:
其他
文献类型:
--
作者:
Hugh McA. Taggart;Hugh McA. Taggart;D. Applebaum-Bowden;D. Applebaum-Bowden;Steven M. Haffner;Steven M. Haffner;G. Warnick;G. Warnick;Marian C. Cheung;Marian C. Cheung;John J. Albers;John J. Albers;C. H. Chestnut;C. H. Chestnut;William R. Hazzard;William R. Hazzard

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在一项短期(6周)前瞻性研究中,对10名正常血脂、绝经后、骨质疏松的妇女评估了斯坦诺唑尔(17-甲基- 2h -5α-androst-2-eno [3,2 -c]吡唑尔-17β-醇)对脂蛋白水平的影响。虽然总胆固醇和甘油三酯水平保持不变,但低密度脂蛋白(LDL)胆固醇(+ 30.9±28.1 mg/dl [mean±SD], p< 0.01,增加21%)和高密度脂蛋白(HDL)胆固醇(- 32.5±11.9 mg/dl [mean±SD], p< 0.001,下降53%)的反应相同且相互抵消。因此,LDL - HDL比值从2.5±0.7急剧增加到6.8±2.5。在HDL中,stanozolol与HDL 2(从26.0±7.4 mg/dl降至3.8±1.9 mg/dl, p< 0.001,下降85%)相比,HDL 2(从35.7±3.2降至24.1±5.8 mg/dl, p< 0.001,下降35%)的下降幅度更大。主要HDL载脂蛋白也下降(AI平均下降41%,a - ii平均下降24%,均p< 0.001)。肝素后肝脏甘油三酯脂肪酶升高(治疗前74±42 nmol游离脂肪酸min−1 mol−1,治疗后242±110,n= 6, p= 0.06)。所有变化在停药后5周逆转。这些脂蛋白变化提示长期服用斯坦诺唑尔时要谨慎,特别是那些没有临床适应症的患者。
The effects of stanozolol, 17-methyl-2H-5α-androst-2-eno [3, 2-c] pyrazol-17β-ol, on lipoprotein levels were assessed in a short-term (6 wk) prospective study of 10 normolipidemic, postmenopausal, osteoporotic women. While total cholesterol and triglyceride levels remained constant, equal and offsetting responses were seen in low density lipoprotein (LDL) cholesterol (+ 30.9±28.1 mg/dl [mean±SD], p< 0.01, a 21% increase) and high density lipoprotein (HDL) cholesterol (− 32.5±11.9 mg/dl [mean±SD], p< 0.001, a 53% decline). Hence the LDL HDL ratio increased dramatically, from 2.5±0.7 to 6.8±2.5. Within HDL, stanozolol was associated with a greater decline in HDL 2 (from 26.0±7.4 mg/dl to 3.8±1.9 mg/dl, p< 0.001, an 85% decrease) than HDL 2 (which diminished from 35.7±3.2 to 24.1±5.8 mg/dl, p< 0.001, a 35% decrease). The major HDL apolipoproteins also declined (AI by a mean of 41% and A-II by 24%, both p< 0.001). Postheparin hepatic triglyceride lipase increased (off treatment 74±42 nmole free fatty acid min− 1 mole− 1, on treatment 242±110, n= 6, p= 0.06). All changes were reversed by 5 wk following termination of the drug. These lipoprotein changes suggest caution in the long term prescription of stanozolol, particularly in those without overriding clinical indications for its use.