Serum Concentration Of Lp Research Articles

Serum Lipoprotein(a) Levels and Their Association with Atherosclerotic Cardiovascular Disease in Japan.

To investigate the distribution of lipoprotein(a) (Lp(a)) and its association with atherosclerotic cardiovascular disease (ASCVD) in Japanese patients at high risk for ASCVD using a health insurance database. Between July 2013 and June 2021, patients eligible for ASCVD prevention according to the 2017 Japan Atherosclerosis Society (JAS) guidelines with documented Lp(a) test results were extracted from the Medical Data Vision claims database and divided into three groups: primary prevention high-risk (Group I), secondary prevention (Group II) and secondary prevention high-risk (Group III). Data on lipid levels, cardiovascular morbidity risk factors and lipid-lowering treatments were extracted. Of 700,580 patients with documented low-density lipoprotein cholesterol (LDL-C), 2,967 (0.42%) were tested for Lp(a). In 2,170 eligible patients, the median [interquartile range] serum concentration of Lp(a) was 13.9 [7.5-24.6] mg/dL, with 151 patients (7.0%) above the recommended risk threshold of ≥ 50 mg/dL. Lp(a) levels increased with risk across all prevention groups. Being in the highest Lp(a) quintile (Q5) was associated with an increased frequency of ASCVD (28.9% versus 18.9% in the lowest quintile (Q1) for unstable angina; 18.7% versus 10.1% for myocardial infarction; 27.9% versus 17.0% for ischemic stroke). In the secondary prevention groups, the proportion of patients meeting an LDL-C target of ＜70 mg/dL decreased from 30.2% in Q1 to 19.0% in Q5 for Group II and from 32.9% to 16.3% for Group III. Despite a high prevalence of Lp(a) ≥ 50mg/dL in Japanese patients at high risk for ASCVD, it found that the Lp(a) testing rate was very low.

Association between serum lipoprotein(a) and mildly reduced eGFR: a cross-sectional study

Lipoprotein(a) [Lp(a)] is a risk factor for cardiovascular disease (CVD) and aortic stenosis. However, the data on the relationship between Lp(a) and mildly reduced estimated glomerular filtration rate (eGFR) has been disputed. This study was conducted to assess the relationship between Lp(a) concentrations and mildly reduced eGFR in healthy subjects.This community-based, cross-sectional study enrolled 1,064 volunteers aged ≥ 40 years who lived in Yonghong Community, Zhonglou District, Changzhou, China, between December 2016 and December 2017. A mildly reduced eGFR was defined as eGFR between 60 and 90 mL/min/1.73m2. A standardized questionnaire and biochemical measurements were used to gather information about participants. The serum concentration of Lp(a) was determined using the latex-enhanced immunoturbidimetric test. Of the total study population, 34.8% (n = 370) were men, and the mean age was 66.8 ± 8.5 years. A significant association existed between Lp(a) levels and the risk of mildly reduced eGFR. Individuals with the highest tertile of Lp(a) had higher odds of mildly reduced eGFR after adjusting for various confounders (adjusted odds ratio [OR]: 1.80, 95% confidence interval [CI]: 1.24–2.60, P = 0.0025) compared to those with the lowest tertile of Lp(a). Multivariable logistic regression of studies in which Lp(a) was presented as continuous variables showed consistent results (adjusted OR: 1.23 for 1-SD increment of Ln-Lp(a), 95% CI: 1.05–1.43). Subgroup analyses showed that study characteristics such as age, sex, obesity, diabetes, and hypertension status did not significantly affect the association (P for all interactions > 0.05). These results suggest that higher serum Lp(a) level was an independent risk factor for mildly reduced eGFR.

Atherosclerosis of brachiocephalic arteries and arterial stiffness in patients with breast cancer

Te study involved 43 patients with newly diagnosed breast cancer (BC) (II-III stage) with overexpression of HER2; median age 50 (40;57) years. All patients underwent neoadjuvant drug therapy with antracyclines, taxanes and trastuzumab followed by surgery, radiation and hormone therapy according to the indications. Before anticancer therapy the general clinical examination was conducted and lipid profle, plasma lipoprotein (a) [Lp(a)] level, titres of autoantibodies IgM and IgG to lipoproteins and their oxidized derivatives were estimated. Te vascular wall stiffness (pulse wave velocity on the carotid-femoral (PWVcf) and shoulder-ankle (PWVsa) segments, the central pressure, carotid intima-media thickness (CIMT) and the degree of stenosis of the brachiocephalic arteries) were determined at baseline and at each stage of anticancer therapy. Te atherosclerosis progression was determined if the new stenosis (≥15%) or increase of preexisting stenosis (≥5%) were revealed; CIMT increase ≥ 0.1 mm. Te parameters of cellular immunity (peripheral blood lymphocyte phenotyping via direct immunofluorescence and flow cytometry), lipid spectrum parameters, serum concentration of Lp (a), autoantibodies IgM and IgG against lipoproteins and their oxidized derivatives, as well as PWVсf and PWVsa were assessed in 17 BC patients before the onset of neoadjuvant therapy and in 20 healthy women. BC patients and healthy women were comparable in traditional cardiovascular risk factors but differed in PWVsa and PWVcf levels (p<0.05). In BC patients the activation of T-cell immunity with the stimulation of both subpopulations with pro-inflammatory and regulatory properties was observed (p<0.05). Te direct correlations between the content of activated T-lymphocytes (T-act), T-helpers (T) 1 and PWVsa (p<0.05), as well as T-act, T1 and T2 and PWVcf (p<0.05) were revealed in the general group. Te decrease of systolic blood pressure (SBP), central SBP (SBPc), central diastolic blood pressure (DBPc), PWVcf and PWVsa levels accompanied with a temporary heart rate increase were observed during anticancer therapy; SBP, SBPc, PWVcf levels restored by the end of the follow-up period. Te CIMT increase was detected in 22 (51%), and the atherosclerosis progression in 26 (60%) BC patients during anticancer therapy. Lp (a) level above 12.8 mg/dl was associated with CIMT increase (p<0.05). Age > 48 years and radiation therapy were risk factors for CIMT increase and atherosclerosis progression (p<0.05), respectively. Te vascular stiffness is increased in BC patients, which is associated with the activation of effector subpopulations of T-lymphocytes and the elevation of circulating level of both pro-atherogenic and anti-atherogenic T-cells. Te level of Lp (a) above 12.8 mg/dl is associated with atherosclerosis progression, which requires further research. Age and radiation therapy are the risk factors for atherosclerosis progression during anticancer therapy.

Lipoprotein(a), type 2 diabetes and nephropathy; the mystery continues

Lipoprotein(a), type 2 diabetes and nephropathy; the mystery continues

Lipoprotein(a) as a risk factor for coronary artery disease in hemodialysis patients

We studied whether lipoprotein(a) [Lp(a)] is an independent risk factor for coronary artery disease (CAD) in hemodialysis (HD) patients. A serum concentration of Lp(a) was measured in 212 patients with chronic glomerulonephritis and 56 patients with diabetic nephropathy (a total of 268 patients). The causes of death during five years of follow-up were studied and classified into either cardiovascular or noncardiovascular events. The mortality of these 268 HD patients during the observation period was 26.1%. Seventy-eight percent were due to cardiovascular events. Those who died of cardiovascular events had significantly higher serum Lp(a) levels than those died of noncardiovascular events. The relative risk of death from CAD was 0.71 in HD patients with a Lp(a) concentration above 30 mg/dl. This study indicates that the serum Lp(a) levels are independent indicators of the future risk of death from CAD in HD patients.

Effects of chemotherapy-induced castration on serum lipids and apoproteins in premenopausal women with node-positive breast cancer.

The purpose of this study was to determine the effect of adjuvant chemotherapy on serum lipids and lipoproteins in premenopausal nonmetastatic breast cancer patients. Fifty-nine premenopausal breast cancer patients were treated with adjuvant chemotherapy comprising cyclophosphamide, methotrexate, and 5-fluorouracil. Levels of serum FSH, LH, and estradiol; fasting plasma levels of total cholesterol, high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL), triglyceride, and apolipoprotein A-I, A-II, and B levels; and lipoprotein(a) [Lp(a)] were measured before treatment and 12 months after the beginning of chemotherapy. The changes in serum lipids after chemotherapy correlated significantly to changes in menstruation. Total cholesterol, LDL, and HDL cholesterol levels increased significantly only in patients with chemotherapy-induced ovarian dysfunction. Changes in apo B paralleled those in LDL and apo A-I and A-II HDL cholesterol. The serum concentration of Lp(a) increased significantly only in patients who developed permanent amenorrhea. There were no significant changes in triglyceride levels. Chemotherapy per se has no effect on serum lipids unless associated with induction of ovarian dysfunction. Ovarian failure after chemotherapy has an unfavorable effect on serum total and LDL cholesterol, apo B, and Lp(a) levels, but a favorable effect on HDL cholesterol.

Low lipoprotein (a) levels during acute viral hepatitis

High serum concentrations of lipoprotein (a) [Lp(a)] are considered a risk factor for premature atherosclerosis. Besides apolipoprotein B-100, Lp(a) consists of apolipoprotein (a) [apo(a)], which shows a remarkable size polymorphism. The serum concentration of Lp(a) is considerably influenced by this apo(a) phenotype. Because Lp(a) is synthesized in the liver, we wondered whether and to what extent Lp(a) levels might be affected by acute liver disease. We compared Lp(a) serum concentrations in 74 patients (54% male, 46% female; mean age, 46 years) with acute viral hepatitis (32, 28, and 14 with hepatitis A, B, and C, respectively) with those in 404 healthy controls (57% men, 43% women; mean age, 47 years). In addition, the intraindividual course of Lp(a) concentration during and after acute hepatitis was followed in a subgroup of 23 patients (15, 6, and 2 with hepatitis A, B, and C, respectively). During acute hepatitis, median Lp(a) concentrations in the patient group were significantly diminished compared with controls (7 vs. 17 mg/dL;P < .0001, Mann-Whitney test). Any bias by an unequal isoform distribution was excluded because there was no significant difference in the isoform distribution between patients and controls (P > .10, chi2 test). Furthermore, the decrease in Lp(a) concentration during acute hepatitis was independent of the molecular weight of the apo(a) isoform. Longitudinally observed patients showed a marked increase in Lp(a) concentration during convalescence (7 to 32 mg/dL;P < .0001, Wilcoxon test). Our results show that acute hepatitis is associated with decreased Lp(a) serum levels. Further studies are needed to evaluate whether Lp(a) serum concentration might be clinically useful as a parameter of liver function. (Hepatology 1996 Dec;24(6):1334-7)

The relationship between lipoprotein(a) and low density lipoprotein receptors during the treatment of hyperthyroidism.

To determine whether the low density lipoprotein (LDL) receptor pathway is involved in the catabolism of plasma lipoprotein (a) [Lp(a)], serum lipids, Lp(a), and LDL receptor activity were measured in seven patients with hyperthyroidism before and after methimazole treatment given hyperthyroidism is associated with enhanced LDL receptor activity. LDL receptor activity in patients was estimated by the equation using the serum concentrations of apolipoprotein (apo) B and C-II. When euthyroidism was achieved after treatment, not only did serum total cholesterol, high density lipoprotein-cholesterol, apo B, and LDL-cholesterol (LDL-Ch) levels rise, but Lp(a) significantly increased and calculated LDL receptor activity significantly decreased. The changes in LDL receptor activity were significantly correlated with the changes in LDL-Ch as expected, but not with changes in Lp(a). These results suggest that the serum concentration of Lp(a) is lowered in hyperthyroidism, probably by a mechanism other than the enhanced activity of the LDL receptor, and that the LDL receptor pathway is involved in the catabolism of Lp(a) to a limited extent.

Serum lipoprotein(a) [Lp(a)] in alcoholic men: Effect of withdrawal

This study examines the effect of alcohol withdrawal on lipoprotein(a) [Lp(a)] in 24 male, middle-aged chronic alcohol abusers admitted for withdrawal therapy. Serum concentration of Lp(a) was determined before and during the first 3 weeks of abstinence. The changes in three sialylated proteins [Lp(a), α1-antitrypsin (α1-AT), and haptoglobin (Hp)] and in desialylated transferrin (CDT) were also determined in 14 patients. After the 3 weeks of withdrawal therapy, the mean and median Lp(a) concentrations increased ( p = 0.0001). The changes in Lp(a) levels were not related to the changes in dietary intake nor to the decrease in total HDL, HDL 3, HDL 2 cholesterol, Apo A-I, and Apo B. In the subgroup of 14 chronic alcohol abusers, Lp(a) levels increased parallel with Hp and α1-AT, whereas CDT decreased. It is concluded that the impact of alcohol on sialylated proteins may be one of the mechanisms responsible for the increase in plasma Lp(a) after alcohol withdrawal.

Lipoprotein (a) levels in children and young adults: the influence of physical activity. The Cardiovascular Risk in Young Finns Study

A high lipoprotein(a) (Lp(a)) level is an independent and predominantly genetically determined risk factor for coronary heart disease and other vascular diseases. We studied the levels of Lp(a) and the influence of physical activity on Lp(a) in the young Finnish population. The study cohort comprised children and young adults aged 9, 12, 15, 18, 21 and 24 years (n = 2464) participating in a large multicenter follow-up study of cardiovascular risk factors in children and young adults. Data were available on physical activity, anthropometric variables, serum Lp(a), insulin and lipid levels. A physical activity index was calculated based on several physical activity variables. Lp(a) was determined by radioimmunoassay with a detection threshold of 3 mg/dl. Differences were assessed with non-parametric statistical analyses. The observed range of Lp(a) was from < 3 to 90.8 mg/dl. The distribution of Lp(a) was highly skewed as 88% of the population (89% males and 87% females) had Lp(a) concentrations less than 25 mg/dl. A total of 35% of the subjects had Lp(a) levels less than 3 mg/dl. There were no significant differences in Lp(a) levels with respect to age or gender. The serum concentration of Lp(a) was statistically significantly correlated with the level of physical activity. Other behavioral variables studied did not have a significant contribution to the variability of Lp(a) levels. These results demonstrate that levels of Lp(a) are not related to age, gender or many of the known coronary heart disease risk factors. However, physical activity is associated with favorable Lp(a) levels, as high levels of Lp(a) (> 25 mg/dl) were less frequent in the physically most active subjects.

Serum Lp(a) lipoprotein concentration and outcome of thrombolytic treatment for myocardial infarction.

Lp(a) lipoprotein has structural homology with plasminogen and has been shown to inhibit plasminogen activation in vitro. To determine whether the serum concentration of Lp(a) lipoprotein present when streptokinase was given in acute myocardial infarction influenced the outcome as judged by electrocardiographic methods. Serum Lp(a) lipoprotein concentration was measured in 135 consecutive patients admitted with a diagnosis of acute myocardial infarction who received streptokinase treatment. Recovery from myocardial injury was assessed by the reduction in the sum of ST segment elevation measured from the J point (STJ) in the electrocardiogram immediately before streptokinase was given compared with that three hours later. The serum Lp(a) lipoprotein concentrations were measured within 12 hours of the onset of symptoms of myocardial infarction and were higher than in healthy reference populations. Recovery from myocardial infarction could be assessed from the STJ in 116 patients (86% of the series). Those in whom it could not had bundle branch block, left ventricular hypertrophy, did not survive three hours, or had started intravenous nitrate treatment or some other clinical procedure before or at the time the second electrocardiogram was to be recorded. Patients with reductions in STJ after streptokinase that were > 4 mm (the median decrease) had mean (range) serum Lp(a) lipoprotein concentrations of 41.0 (0.8-220) mg/dl and those with a smaller reduction in STJ had concentrations of 29.1 (1.7-151) mg/dl. The difference was not statistically significant. In this study Lp(a) lipoprotein concentration did not significantly influence the outcome of thrombolytic treatment with streptokinase.

Serum lipoprotein (a) in renal transplant recipients receiving cyclosporin monotherapy

Coronary heart disease is more common in patients with chronic renal failure and is a major cause of death after renal transplantation. Elevated serum lipoprotein (a) (Lp(a)) is a known risk factor for coronary heart disease in the general population. We measured the serum concentration of Lp(a) in 58 renal transplant recipients (40 male, 18 female) on cyclosporin monotherapy, and in 58 age- and sex-matched controls. Serum Lp(a) was significantly elevated in the transplant patients with a median of 27.5 (range < 0.8-140.3) mg/dl compared to 7.6 (range < 0.8-87.4) mg/dl in controls (P < 0.001). Total serum cholesterol, low-density lipoprotein cholesterol, and total triglyceride concentrations were also significantly raised (P < 0.001) in the transplant recipients. The increased serum Lp(a) may contribute to the increased cardiovascular morbidity associated with renal transplantation.

Lp(a) lipoprotein in patients with arterial insufficiency of the lower extremities

The serum concentration of Lp(a) lipoprotein was determined in 66 patients with peripheral arterial insufficiency of the lower extremities (PAI) and 164 controls. The mean level was higher among the patients than among the controls (236 +/- 248 vs. 129 +/- 159 mg/l, p = 0.01), and values above 300 mg/l were more common among the patients (22/66 vs. 21/164, p less than 0.001). The difference between the 26 female patients and the 94 female controls was statistically significant (280 +/- 268 vs. 118 +/- 141 mg/l, p less than 0.001), but not the difference between the 40 male patients and the 70 male controls (208 +/- 235 vs. 142 +/- 182 mg/l). A high Lp(a) lipoprotein level was not associated with a high LDL-cholesterol level, and there was no significant correlation between the serum levels of Lp(a) lipoprotein and triglycerides++, total cholesterol or HDL-cholesterol. The results indicate, that high Lp(a) lipoprotein levels may be a risk factor for PAI in women.

Diverging effects of cholestyramine on apolipoprotein B and lipoprotein Lp(a): A dose-response study of the effects of cholestyramine in hypercholesterolaemia

Nineteen hypercholesterolaemic patients were randomly treated with either 16 or 8 g cholestyramine with a changeover after 6 weeks for a second 6-week period. During a third consecutive 6-week period all patients received 4 g cholestyramine daily. The low density lipoprotein (LDL) cholesterol and triglyceride concentrations decreased significantly (−11%, −21% and −26% for LDL cholesterol on 4, 8 and 16 g, respectively) with a dose-response effect. However, the increase from 8 g to 16 g only caused a modest additional reduction of the lipid levels. The serum concentration of apolipoprotein (apo) B was correlated to the LDL cholesterol and decreased similarly in a dose-response fashion. However, the average reduction of apo B was less pronounced (−4%, − 13% and −17% on 4, 8 and 16 g of cholestyramine, respectively) resulting in a significant change of the apo, B/LDL cholesterol ratio during treatment. There was a significant increase of the high density lipoprotein (HDL) cholesterol concentration, which was similar at all dose levels. Also, the apo A-1 concentration in serum increased significantly but the relative decrease was less pronounced than that of HDL cholesterol, causing a significant decrease of the apo A-I/HDL cholesterol ratio. The apo A-11 concentration in serum was unchanged or slightly decreased and the apo A-1/apo A-II ratio increased significantly. The lipoprotein (a) [Lp(a)] distribution was markedly skewed before treatment, without any significant correlations between the serum concentrations of Lp(a) and other lipid or apolipoprotein concentrations. The serum concentration of Lp(a) was not affected by treatment with cholestyramine and there was no significant correlation between the change of Lp(a) and the change in LDL cholesterol or apo B. The absence of effect on Lp(a) concentrations in serum by cholestyramine treatment may indicate that the major route of Lp(a) metabolism is not identical with that of LDL.

Serum Concentrations of Lp(a) and Other Lipoprotein Parameters in Heavy Alcohol Consumers

The serum concentration of lipoprotein Lp(a) and of other lipoproteins of 64 individuals consuming more than 200 g of ethanol per day for several years was measured. 42 of the propositi with no clinical signs of alcoholic liver cirrhosis (ALC) had an apoAI/apoAII ratio twice as high as the control group. The apoAI values of the consumers of alcohol were higher and the HDL-C and Lp(a) levels were lower than those of the control group. 22 alcohol drinkers with ALC exhibited strikingly reduced values of all serum lipids and lipoproteins and the lowest Lp(a) concentrations of all. It is suggested that alcohol drinking lowers serum Lp(a) what might be an additional reason why this group of people seems to be a lower risk of atherosclerosis.