Abstract：
BACKGROUND: Recently, an inverse relationship between the blood concentration of lipoprotein(a) (Lp(a)) and triglycerides (TG) has been demonstrated. The larger the VLDL particle size, the greater the presence of VLDL rich in apoliprotein E and in subjects with the apoE2/E2 genotype, the lower Lp(a) concentration. The mechanism of this inverse association is unknown. The objective of this analysis was to evaluate the Lp(a)-TG association in patients treated at the lipid units included in the registry of the Spanish Society of Atherosclerosis (SEA) by comparing the different dyslipidemias.
METHODS: Five thousand two hundred and seventy-five subjects ≥18 years of age registered in the registry before March 31, 2023, with Lp(a) concentration data and complete lipid profile information without treatment were included.
RESULTS: The mean age was 53.0 ± 14.0 years, with 48% women. The 9.5% of subjects (n = 502) had diabetes and the 22.4% (n = 1184) were obese. The median TG level was 130 mg/dL (IQR 88.0-210) and Lp(a) 55.0 nmol/L (IQR 17.9-156). Lp(a) concentration showed a negative association with TG concentration when TG values exceeded 300 mg/dL. Subjects with TG > 1000 mg/dL showed the lowest level of Lp(a), 17.9 nmol/L, and subjects with TG < 300 mg/dL had a mean Lp(a) concentration of 60.1 nmol/L. In subjects without diabetes or obesity, the inverse association of Lp(a)-TG was especially important (p < 0.001). The median Lp(a) was 58.3 nmol/L in those with TG < 300 mg/dL and 22.0 nmol/L if TG > 1000 mg/dL. No association was found between TG and Lp(a) in subjects with diabetes and obesity, nor in subjects with familial hypercholesterolemia. In subjects with multifactorial combined hyperlipemia with TG < 300 mg/dL, Lp(a) was 64.6 nmol/L; in the range of 300-399 mg/dL of TG, Lp(a) decreased to 38. 8 nmol/L, and up to 22.3 nmol/L when TG > 1000 mg/dL.
CONCLUSIONS: Our results show an inverse Lp(a)-TG relationship in TG concentrations > 300 mg/dL in subjects without diabetes, obesity and without familial hypercholesterolemia. Our results suggest that, in those hypertriglyceridemias due to hepatic overproduction of VLDL, the formation of Lp(a) is reduced, unlike those in which the peripheral catabolism of TG-rich lipoproteins is reduced.
METHODS: Five thousand two hundred and seventy-five subjects ≥18 years of age registered in the registry before March 31, 2023, with Lp(a) concentration data and complete lipid profile information without treatment were included.
RESULTS: The mean age was 53.0 ± 14.0 years, with 48% women. The 9.5% of subjects (n = 502) had diabetes and the 22.4% (n = 1184) were obese. The median TG level was 130 mg/dL (IQR 88.0-210) and Lp(a) 55.0 nmol/L (IQR 17.9-156). Lp(a) concentration showed a negative association with TG concentration when TG values exceeded 300 mg/dL. Subjects with TG > 1000 mg/dL showed the lowest level of Lp(a), 17.9 nmol/L, and subjects with TG < 300 mg/dL had a mean Lp(a) concentration of 60.1 nmol/L. In subjects without diabetes or obesity, the inverse association of Lp(a)-TG was especially important (p < 0.001). The median Lp(a) was 58.3 nmol/L in those with TG < 300 mg/dL and 22.0 nmol/L if TG > 1000 mg/dL. No association was found between TG and Lp(a) in subjects with diabetes and obesity, nor in subjects with familial hypercholesterolemia. In subjects with multifactorial combined hyperlipemia with TG < 300 mg/dL, Lp(a) was 64.6 nmol/L; in the range of 300-399 mg/dL of TG, Lp(a) decreased to 38. 8 nmol/L, and up to 22.3 nmol/L when TG > 1000 mg/dL.
CONCLUSIONS: Our results show an inverse Lp(a)-TG relationship in TG concentrations > 300 mg/dL in subjects without diabetes, obesity and without familial hypercholesterolemia. Our results suggest that, in those hypertriglyceridemias due to hepatic overproduction of VLDL, the formation of Lp(a) is reduced, unlike those in which the peripheral catabolism of TG-rich lipoproteins is reduced.
摘要：
背景：最近，已证明脂蛋白（a）（Lp（a））和甘油三酸酯（TG）的血液浓度成反比。VLDL粒径越大,载脂蛋白E和apoE2/E2基因型的受试者中富含VLDL的存在越大，Lp(a)浓度越低。这种逆关联的机制是未知的。该分析的目的是通过比较不同的血脂异常来评估以西班牙动脉粥样硬化学会（SEA）注册表中包含的脂质单位治疗的患者的Lp（a）-TG相关性。
方法：在2023年3月31日之前在登记处登记的年龄≥18岁的5000名受试者，包括Lp（a）浓度数据和未经治疗的完整血脂谱信息。
结果：平均年龄为53.0±14.0岁，48%的女性9.5%的受试者（n=502）患有糖尿病，22.4%（n=1184）肥胖。中位TG水平为130mg/dL（IQR88.0-210）和Lp（a）55.0nmol/L（IQR17.9-156）。当TG值超过300mg/dL时，Lp（a）浓度与TG浓度呈负相关。TG>1000mg/dL的受试者显示Lp（a）的最低水平，17.9nmol/L，TG<300mg/dL的受试者的平均Lp（a）浓度为60.1nmol/L。在没有糖尿病或肥胖的受试者中，Lp(a)-TG的负相关尤其重要(p<0.001)。如果TG>1000mg/dL，则TG<300mg/dL和22.0nmol/L的Lp（a）中位数为58.3nmol/L。在患有糖尿病和肥胖的受试者中，TG和Lp(a)之间没有发现相关性，家族性高胆固醇血症的受试者也没有。在TG<300mg/dL的多因素联合高脂血症受试者中，Lp（a）为64.6nmol/L；在TG的300-399mg/dL范围内，Lp(a)下降到38。8nmol/L，当TG>1000mg/dL时，最高可达22.3nmol/L。
结论：我们的结果表明，在无糖尿病的受试者中，TG浓度>300mg/dL时，Lp（a）-TG呈负相关，肥胖和无家族性高胆固醇血症。我们的研究结果表明,在那些由于肝脏过度产生VLDL而导致的高甘油三酯血症中，Lp(a)的形成减少，与那些富含TG的脂蛋白的外周分解代谢减少不同。
方法：在2023年3月31日之前在登记处登记的年龄≥18岁的5000名受试者，包括Lp（a）浓度数据和未经治疗的完整血脂谱信息。
结果：平均年龄为53.0±14.0岁，48%的女性9.5%的受试者（n=502）患有糖尿病，22.4%（n=1184）肥胖。中位TG水平为130mg/dL（IQR88.0-210）和Lp（a）55.0nmol/L（IQR17.9-156）。当TG值超过300mg/dL时，Lp（a）浓度与TG浓度呈负相关。TG>1000mg/dL的受试者显示Lp（a）的最低水平，17.9nmol/L，TG<300mg/dL的受试者的平均Lp（a）浓度为60.1nmol/L。在没有糖尿病或肥胖的受试者中，Lp(a)-TG的负相关尤其重要(p<0.001)。如果TG>1000mg/dL，则TG<300mg/dL和22.0nmol/L的Lp（a）中位数为58.3nmol/L。在患有糖尿病和肥胖的受试者中，TG和Lp(a)之间没有发现相关性，家族性高胆固醇血症的受试者也没有。在TG<300mg/dL的多因素联合高脂血症受试者中，Lp（a）为64.6nmol/L；在TG的300-399mg/dL范围内，Lp(a)下降到38。8nmol/L，当TG>1000mg/dL时，最高可达22.3nmol/L。
结论：我们的结果表明，在无糖尿病的受试者中，TG浓度>300mg/dL时，Lp（a）-TG呈负相关，肥胖和无家族性高胆固醇血症。我们的研究结果表明,在那些由于肝脏过度产生VLDL而导致的高甘油三酯血症中，Lp(a)的形成减少，与那些富含TG的脂蛋白的外周分解代谢减少不同。
