Anagnostis Panagiotis, Karras Spyridon, Lambrinoudaki Irene, Stevenson John C, Goulis Dimitrios G
Unit of Reproductive Endocrinology, First Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Second Department of Obstetrics and Gynecology, National and Capodestrian University of Athens, Athens, Greece.
Int J Clin Pract. 2016 Dec;70(12):967-977. doi: 10.1111/ijcp.12903.
Lipoprotein(a) [Lp(a)], a low-density lipoprotein (LDL)-like particle, has been independently associated with increased cardiovascular disease (CVD) risk in various populations, such as postmenopausal women. The purpose of this narrative review is to present current data on the role of Lp(a) in augmenting CVD risk in postmenopausal women and focus on the available therapeutic strategies.
PubMed was searched for English language publications until November 2015 under the following terms: "therapy" OR "treatment" AND ["lipoprotein (a)" OR "Lp(a)"] AND ("postmenopausal women" OR "menopausal women" OR "menopause").
Only hormone replacement therapy (mainly oral estrogens) and tibolone have been specifically studied in postmenopausal women and can reduce Lp(a) concentrations by up to 44%, although evidence indicating a concomitant reduction in CVD risk associated with Lp(a) is lacking. As alternative treatments for women who cannot, or will not, take hormonal therapies, niacin and the upcoming proprotein convertase subtilisin / kexin type 9 (PCSK-9) inhibitors are effective in reducing Lp(a) concentrations by up to 30%. Statins have minimal or no effect on Lp(a). However, data for these and other promising Lp(a)-lowering therapies including mipomersen, lomitapide, cholesterol-ester-transfer protein inhibitors and eprotirome are derived from studies in the general, mainly high CVD risk, population, and include only subpopulations of postmenopausal women.
Past, present and emerging therapies can reduce Lp(a) concentrations to a varying extent. Overall, it remains to be proven whether the aforementioned reductions in Lp(a) by these therapeutic options are translated into CVD risk reduction in postmenopausal women.
脂蛋白(a)[Lp(a)]是一种低密度脂蛋白(LDL)样颗粒，在不同人群如绝经后女性中，其与心血管疾病(CVD)风险增加独立相关。本叙述性综述的目的是介绍关于Lp(a)在增加绝经后女性CVD风险中作用的当前数据，并关注可用的治疗策略。
在PubMed中检索截至2015年11月的英文出版物，检索词如下：“治疗”或“疗法”以及“脂蛋白(a)”或“Lp(a)”，和（“绝经后女性”或“更年期女性”或“绝经”）。
仅对绝经后女性专门研究了激素替代疗法（主要是口服雌激素）和替勃龙，它们可使Lp(a)浓度降低多达44%，尽管缺乏表明与Lp(a)相关的CVD风险随之降低的证据。对于不能或不愿接受激素疗法的女性，烟酸和即将上市的前蛋白转化酶枯草溶菌素/克新9型(PCSK-9)抑制剂作为替代治疗有效降低Lp(a)浓度多达30%。他汀类药物对Lp(a)影响极小或无影响。然而，这些以及其他有前景的降低Lp(a)疗法的数据，包括米泊美生、洛美他派、胆固醇酯转运蛋白抑制剂和依普罗酮，均来自一般人群（主要是CVD高风险人群）的研究，且仅包括绝经后女性亚组。
过去、现在和新兴疗法均可不同程度降低Lp(a)浓度。总体而言，上述治疗方案降低Lp(a)是否能转化为绝经后女性CVD风险降低仍有待证实。
