scholarly journals Lipoprotein(a) Levels in Thyroid Disorders

2013 ◽  
Vol 59 (2) ◽  
pp. 81-84 ◽  
Author(s):  
Cristina Corina Pop-Radu ◽  
Mirela Gliga

Abstract Objective: The aim of this study was to assess the serum levels of Lipoprotein(a) [Lp(a)] in subjects with thyroid disorders, as well as to investigate their relationship with lipid profile and the markers of thyroid function and autoimmunity, admitting that elevated Lp(a) levels and dyslipidemia caused by thyroid disorders synergistically increased the atherogenic process. Methods: This study enrolled 38 subjects with hypothyroidism, 30 with hyperthyroidism and 55 with euthyroidism. The following parameters were measured: Lp(a), apolipoprotein AI (apo AI), apolipoprotein B (apo B), total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), very-low-density lipoprotein (VLDL), thyroid stimulating hormone (TSH), free thyroxine (FT4), triiodothyronine (T3), thyroid-peroxidase antibody (TPO-Ab). Results: Lp(a) was found with increased mean serum levels in hypothyroid subjects (483.28 ± 281.55 mg/L). Hyperthyroid subjects showed normal levels (253.13 ± 94.29 mg/L) of Lp(a), but significantly lower than those with hypothyroidism and slightly increased levels in the euthyroid subjects (305 ± 100.44 mg/L). In hypothyroidism a significant positive correlation between Lp(a) and TSH, apo B, TC, TG, TC/HDL, VLDL levels and a negative correlation with FT4, T3 and apo AI/B (p < 0.05) was observed. No correlations were found between serum Lp(a) levels, lipids profile and thyroid function parameters in hyperthyroid subjects, neither with TPO-Ab. Conclusions: The association of hypothyroidism with increased levels of Lp(a) seems to increase the already high cardiovascular risk in the hypothyroid subjects, while increased levels of Lp(a) represents independently a relevant cardiovascular risk factor.

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Maria do Sameiro-Faria ◽  
Michaela Kohlova ◽  
Sandra Ribeiro ◽  
Petronila Rocha-Pereira ◽  
Laetitia Teixeira ◽  
...  

We evaluated the potential cardiovascular risk protection of bilirubin in hemodialysis (HD) patients. An enlarged set of studies were evaluated in 191 HD patients, including hematological study, lipid profile, iron metabolism, nutritional, inflammatory markers, and dialysis adequacy. The TA duplication screening in the UDP-glucuronosyltransferase 1 A1 (UGT1A1) promoter region was also performed. TheUGT1A1genotype frequencies in HD patients were 49.2%, 42.4%, and 8.4% for 6/6, 6/7, and 7/7 genotypes, respectively. Although no difference was found inUGT1A1genotype distribution between the three tertiles of bilirubin, significant differences were found with increasing bilirubin levels, namely, a decrease in platelet, leukocyte, and lymphocyte counts, transferrin, oxidized low-density lipoprotein (ox-LDL), ox-LDL/low-density lipoprotein cholesterol ratio, apolipoprotein (Apo) A, Apo B, and interleukin-6 serum levels and a significant increased concentration of hemoglobin, hematocrit, erythrocyte count, iron, transferrin saturation, Apo A/Apo B ratio, adiponectin, and paraoxonase 1 serum levels. After adjustment for age these results remained significant. Our data suggest that higher bilirubin levels are associated with beneficial effects in HD patients, by improving lipid profile and reducing the inflammatory grade, which might contribute to increase in iron availability. These results suggest a potential cardiovascular risk protection of bilirubin in HD patients.


2018 ◽  
Vol 40 (33) ◽  
pp. 2775-2781 ◽  
Author(s):  
Lotte C A Stiekema ◽  
Erik S G Stroes ◽  
Simone L Verweij ◽  
Helina Kassahun ◽  
Lisa Chen ◽  
...  

AbstractAimsSubjects with lipoprotein(a) [Lp(a)] elevation have increased arterial wall inflammation and cardiovascular risk. In patients at increased cardiovascular risk, arterial wall inflammation is reduced following lipid-lowering therapy by statin treatment or lipoprotein apheresis. However, it is unknown whether lipid-lowering treatment in elevated Lp(a) subjects alters arterial wall inflammation. We evaluated whether evolocumab, which lowers both low-density lipoprotein cholesterol (LDL-C) and Lp(a), attenuates arterial wall inflammation in patients with elevated Lp(a).Methods and resultsIn this multicentre, randomized, double-blind, placebo-controlled study, 129 patients {median [interquartile range (IQR)]: age 60.0 [54.0–67.0] years, Lp(a) 200.0 [155.5–301.5] nmol/L [80.0 (62.5–121.0) mg/dL]; mean [standard deviation (SD)] LDL-C 3.7 [1.0] mmol/L [144.0 (39.7) mg/dL]; National Cholesterol Education Program high risk, 25.6%} were randomized to monthly subcutaneous evolocumab 420 mg or placebo. Compared with placebo, evolocumab reduced LDL-C by 60.7% [95% confidence interval (CI) 65.8–55.5] and Lp(a) by 13.9% (95% CI 19.3–8.5). Among evolocumab-treated patients, the Week 16 mean (SD) LDL-C level was 1.6 (0.7) mmol/L [60.1 (28.1) mg/dL], and the median (IQR) Lp(a) level was 188.0 (140.0–268.0) nmol/L [75.2 (56.0–107.2) mg/dL]. Arterial wall inflammation [most diseased segment target-to-background ratio (MDS TBR)] in the index vessel (left carotid, right carotid, or thoracic aorta) was assessed by 18F-fluoro-deoxyglucose positron-emission tomography/computed tomography. Week 16 index vessel MDS TBR was not significantly altered with evolocumab (−8.3%) vs. placebo (−5.3%) [treatment difference −3.0% (95% CI −7.4% to 1.4%); P = 0.18].ConclusionEvolocumab treatment in patients with median baseline Lp(a) 200.0 nmol/L led to a large reduction in LDL-C and a small reduction in Lp(a), resulting in persistent elevated Lp(a) levels. The latter may have contributed to the unaltered arterial wall inflammation.


Spinal Cord ◽  
2021 ◽  
Author(s):  
Peter Francis Raguindin ◽  
Gion Fränkl ◽  
Oche Adam Itodo ◽  
Alessandro Bertolo ◽  
Ramona Maria Zeh ◽  
...  

Abstract Study design Systematic review and meta-analysis. Objective To determine the difference in cardiovascular risk factors (blood pressure, lipid profile, and markers of glucose metabolism and inflammation) according to the neurological level of spinal cord injury (SCI). Methods We searched 5 electronic databases from inception until July 4, 2020. Data were extracted by two independent reviewers using a pre-defined data collection form. The pooled effect estimate was computed using random-effects models, and heterogeneity was calculated using I2 statistic and chi-squared test (CRD42020166162). Results We screened 4863 abstracts, of which 47 studies with 3878 participants (3280 males, 526 females, 72 sex unknown) were included in the meta-analysis. Compared to paraplegia, individuals with tetraplegia had lower systolic and diastolic blood pressure (unadjusted weighted mean difference, −14.5 mmHg, 95% CI −19.2, −9.9; −7.0 mmHg 95% CI −9.2, −4.8, respectively), lower triglycerides (−10.9 mg/dL, 95% CI −19.7, −2.1), total cholesterol (−9.9 mg/dL, 95% CI −14.5, −5.4), high-density lipoprotein (−1.7 mg/dL, 95% CI −3.3, −0.2) and low-density lipoprotein (−5.8 mg/dL, 95% CI −9.0, −2.5). Comparing individuals with high- vs. low-thoracic SCI, persons with higher injury had lower systolic and diastolic blood pressure (−10.3 mmHg, 95% CI −13.4, −7.1; −5.3 mmHg 95% CI −7.5, −3.2, respectively), while no differences were found for low-density lipoprotein, serum glucose, insulin, and inflammation markers. High heterogeneity was partially explained by age, prevalent cardiovascular diseases and medication use, body mass index, sample size, and quality of studies. Conclusion In SCI individuals, the level of injury may be an additional non-modifiable cardiovascular risk factor. Future well-designed longitudinal studies with sufficient follow-up and providing sex-stratified analyses should confirm our findings and explore the role of SCI level in cardiovascular health and overall prognosis and survival.


1994 ◽  
Vol 67-68 ◽  
pp. 175-190 ◽  
Author(s):  
Jörg Kreuzer ◽  
Marcia B. Lloyd ◽  
Dean Bok ◽  
Gunther M. Fless ◽  
Angelo M. Scanu ◽  
...  

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