Monitoring of up to 15 years effects of lipoprotein apheresis on lipids, biomarkers of inflammation, and soluble endoglin in familial hypercholesterolemia patients

. 2021 Feb 27 ; 16 (1) : 110. [epub] 20210227

Jazyk angličtina Země Anglie, Velká Británie Médium electronic

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/pmid33640001
Odkazy

PubMed 33640001
PubMed Central PMC7913462
DOI 10.1186/s13023-021-01749-w
PII: 10.1186/s13023-021-01749-w
Knihovny.cz E-zdroje

BACKGROUND: Lipoprotein apheresis (LA) is considered as an add-on therapy for patients with familial hypercholesterolemia (FH). We aimed to analyze the data collected in the last 15 years from FH patients treated with LA, to elucidate the benefit of this procedure with respect to plasma lipids, biomarkers of inflammation, and endothelial dysfunction and soluble endoglin. RESULTS: 14 patients (10 heterozygous FH patients (HeFH), 4 homozygous FH patients (HoFH)) were treated by long-term lipoprotein apheresis. Lipid levels were examined, and ELISA detected biomarkers of inflammation and soluble endoglin. Paired tests were used for intergroup comparisons, and a linear regression model served to estimate the influence of the number of days patients were treated with LA on the studied parameters. LA treatment was associated with a significant decrease of total cholesterol (TC), LDL-C, HDL-C, and apoB, in both HeFH and HoFH patients, after single apheresis and in a long-term period during the monitored interval of 15 years. Biomarkers of inflammation and endothelial dysfunction were reduced for soluble endoglin, hsCRP, and MCP-1, and sP-selectin after each procedure in some HeFH and HoFH patients. CONCLUSIONS: LA treatment up to 15 years, reduced cholesterol levels, levels of biomarkers related to endothelial dysfunction, and inflammation not only after each procedure but also in the long-term evaluation in FH patients. We propose that long-term LA treatment improves lipid profile and endothelial dysfunction in familial hypercholesterolemia patients, suggesting a promising improvement in cardiovascular prognosis in most FH patients.

Zobrazit více v PubMed

Kastelein JJP, Reeskamp LF, Hovingh GK. Familial hypercholesterolemia: the most common monogenic disorder in humans. J Am Coll Cardiol. 2020;75:2567–2569. doi: 10.1016/j.jacc.2020.03.058. PubMed DOI

Abifadel M, Elbitar S, El Khoury P, et al. Living the PCSK9 adventure: from the identification of a new gene in familial hypercholesterolemia towards a potential new class of anticholesterol drugs. Curr Atheroscler Rep. 2014;16:439. doi: 10.1007/s11883-014-0439-8. PubMed DOI

Alnouri F, Athar M, Al-Allaf FA, et al. Novel combined variants of LDLR and LDLRAP1 genes causing severe familial hypercholesterolemia. Atherosclerosis. 2018;277:425–433. doi: 10.1016/j.atherosclerosis.2018.06.878. PubMed DOI

Kim YR, Han KH. Familial hypercholesterolemia and the atherosclerotic disease. Korean Circ J. 2013;43:363–367. doi: 10.4070/kcj.2013.43.6.363. PubMed DOI PMC

Nordestgaard BG, Chapman MJ, Humphries SE, et al. Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease: consensus statement of the European Atherosclerosis Society. Eur Heart J. 2013;34:3478–3490a. doi: 10.1093/eurheartj/eht273. PubMed DOI PMC

Cenarro A, Etxebarria A, de Castro-Orós I, et al. The p. Leu167del mutation in APOE gene causes autosomal dominant hypercholesterolemia by down-regulation of LDL receptor expression in hepatocytes. J Clin Endocrinol Metab. 2016;101:2113–2121. doi: 10.1210/jc.2015-3874. PubMed DOI

Civeira F, Plana N. Treatment of heterozygous familial hypercholesterolemia in children and adolescents: an unsolved problem. Revista Española de Cardiología (Engl Ed) 2017;70:423–424. doi: 10.1016/j.rec.2017.02.008. PubMed DOI

Creider J, Hegele R. Clinical evaluation for genetic and secondary causes of dyslipidemia. In: Elsevier (ed) Clinical lipidology, 2nd ed. Philadelphia (USA), 2015, p. 128–34.

Bambauer R, Bambauer C, Lehmann B, et al. LDL-apheresis: technical and clinical aspects. Sci World J; 2012. PubMed PMC

Blaha V, Blaha M, Lanska M, et al. Lipoprotein apheresis in the treatment of dyslipidemia–the Czech Republic Experience. Physiol Res. 2017;66:S91. doi: 10.33549/physiolres.933584. PubMed DOI

Stefanutti C, Zenti MG. Lipoprotein apheresis and PCSK9-inhibitors. Impact on atherogenic lipoproteins and anti-inflammatory mediators in familial hypercholesterolaemia. Curr Pharm Des. 2018;24:3634–3637. doi: 10.2174/1381612824666181025115658. PubMed DOI

Blaha V, Blaha M, Solichova D, et al. Antioxidant defense system in familial hypercholesterolemia and the effects of lipoprotein apheresis. Atheroscler Suppl. 2017;30:159–165. doi: 10.1016/j.atherosclerosissup.2017.05.002. PubMed DOI

Chepelenko GV. Pathogenesis of atherosclerosis in patients with lipid metabolism disturbances: hypothesis on cholesterol utilization and atheromatous plaque formation. Angiol Sosud Khir. 2003;9:20–25. PubMed

Ridker PM, Silvertown JD. Inflammation, C-reactive protein, and atherothrombosis. J Periodontol. 2008;79:1544–1551. doi: 10.1902/jop.2008.080249. PubMed DOI

Hajilooi M, Sanati A, Ahmadieh A, et al. Circulating ICAM-1, VCAM-1, E-selectin, P-selectin, and TNFRII in patients with coronary artery disease. Immunol Invest. 2004;33:263–275. doi: 10.1081/IMM-120037275. PubMed DOI

Szabolcs MJ, Cannon PJ, Thienel U, et al. Analysis of CD154 and CD40 expression in native coronary atherosclerosis and transplant associated coronary artery disease. Virchows Arch. 2000;437:149–159. doi: 10.1007/s004280000215. PubMed DOI

Blaha M, Krejsek J, Blaha V, et al. Selectins and monocyte chemotactic peptide as the markers of atherosclerosis activity. Physiol Res. 2004;53:273–278. PubMed

Schoonderwoerd MJA, Goumans MTH, Hawinkels L. Endoglin: beyond the endothelium. Biomolecules. 2020 doi: 10.3390/biom10020289. PubMed DOI PMC

Blann AD, Wang JM, Wilson PB, et al. Serum levels of the TGF-beta receptor are increased in atherosclerosis. Atherosclerosis. 1996;120:221–226. doi: 10.1016/0021-9150(95)05713-7. PubMed DOI

Blaha M, Cermanova M, Blaha V, et al. Elevated serum soluble endoglin (sCD105) decreased during extracorporeal elimination therapy for familial hypercholesterolemia. Atherosclerosis. 2008;197:264–270. doi: 10.1016/j.atherosclerosis.2007.04.022. PubMed DOI

Vicen M, Vitverova B, Havelek R, et al. Regulation and role of endoglin in cholesterol-induced endothelial and vascular dysfunction in vivo and in vitro. FASEB J. 2019 doi: 10.1096/fj.201802245R. PubMed DOI

Strasky Z, Vecerova L, Rathouska J, et al. Cholesterol effects on endoglin and its downstream pathways in ApoE/LDLR double knockout mice. Circ J. 2011;75:1747–1755. doi: 10.1253/circj.CJ-10-1285. PubMed DOI

Rathouska J, Vecerova L, Strasky Z, et al. Endoglin as a possible marker of atorvastatin treatment benefit in atherosclerosis. Pharmacol Res. 2011;64:53–59. doi: 10.1016/j.phrs.2011.03.008. PubMed DOI

Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Atherosclerosis. 2019;290:140–205. doi: 10.1016/j.atherosclerosis.2019.08.014. PubMed DOI

Adults EPoDEaToHBCi. Executive summary of the third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA: J Am Med Assoc. 2001;285: 2486–97. 10.1001/jama.285.19.2486. PubMed

Parham JS, Goldberg AC. Mipomersen and its use in familial hypercholesterolemia. Expert Opin Pharmacother. 2019;20:127–131. doi: 10.1080/14656566.2018.1550071. PubMed DOI PMC

Bruckert E, Gallo A. Is lomitapide a life-saving drug in homozygous familial hypercholesterolemia. Eur J Prev Cardiol. 2017;24:1841–1842. doi: 10.1177/2047487317734387. PubMed DOI

Kroon AA, Van’Hof MA, Demacker PN, et al. The rebound of lipoproteins after LDL-apheresis Kinetics and estimation of mean lipoprotein levels. Atherosclerosis. 2000;152:519–526. doi: 10.1016/s0021-9150(00)00371-3. PubMed DOI

Beliard S, Gallo A, Duchene E, et al. Lipoprotein-apheresis in familial hypercholesterolemia: Long-term patient compliance in a French cohort. Atherosclerosis. 2018;277:66–71. doi: 10.1016/j.atherosclerosis.2018.08.007. PubMed DOI

Kolovou G, Hatzigeorgiou G, Mihas C, et al. Changes in lipids and lipoproteins after selective LDL apheresis (7-year experience) Cholesterol. 2012;2012:976578. doi: 10.1155/2012/976578. PubMed DOI PMC

Makino H, Harada-Shiba M. Long-term effect of low-density lipoprotein apheresis in patients with homozygous familial hypercholesterolemia. Therapeutic Apher Dial. 2003;7:397–401. doi: 10.1046/j.1526-0968.2003.00073.x. PubMed DOI

Masaki N, Tatami R, Kumamoto T, et al. Ten-year follow-up of familial hypercholesterolemia patients after intensive cholesterol-lowering therapy. Int Heart J. 2005;46:833–843. doi: 10.1536/ihj.46.833. PubMed DOI

Orsoni A, Saheb S, Levels JH, et al. LDL-apheresis depletes apoE-HDL and pre-beta1-HDL in familial hypercholesterolemia: relevance to atheroprotection. J Lipid Res. 2011;52:2304–2313. doi: 10.1194/jlr.P016816. PubMed DOI PMC

Neumann CL, Schulz EG, Hagenah GC, et al. Lipoprotein apheresis – More than just cholesterol reduction? Atheroscler Suppl. 2013;14:29–32. doi: 10.1016/j.atherosclerosissup.2012.10.017. PubMed DOI

Higashi Y, Noma K, Yoshizumi M, et al. Endothelial function and oxidative stress in cardiovascular diseases. Circ J. 2009;73:411–418. doi: 10.1253/circj.CJ-08-1102. PubMed DOI

van Wijk DF, Sjouke B, Figueroa A, et al. Nonpharmacological lipoprotein apheresis reduces arterial inflammation in familial hypercholesterolemia. J Am Coll Cardiol. 2014;64:1418–1426. doi: 10.1016/j.jacc.2014.01.088. PubMed DOI

Utsumi K, Kawabe M, Hirama A, et al. Effects of selective LDL apheresis on plasma concentrations of ICAM-1, VCAM-1 and P-selectin in diabetic patients with arteriosclerosis obliterans and receiving maintenance hemodialysis. Clin Chim Acta. 2007;377:198–200. doi: 10.1016/j.cca.2006.09.026. PubMed DOI

Kobayashi S, Oka M, Moriya H, et al. LDL-apheresis reduces P-Selectin, CRP and fibrinogen – possible important implications for improving atherosclerosis. Ther Apher Dial. 2006;10:219–223. doi: 10.1111/j.1744-9987.2006.00332.x. PubMed DOI

Sampietro T, Tuoni M, Ferdeghini M, et al. Plasma cholesterol regulates soluble cell adhesion molecule expression in familial hypercholesterolemia. Circulation. 1997;96:1381–1385. doi: 10.1161/01.CIR.96.5.1381. PubMed DOI

Empen K, Otto C, Brödl UC, et al. The effects of three different LDL-apheresis methods on the plasma concentrations of E-selectin, VCAM-1, and ICAM-1. J Clin Apher. 2002;17:38–43. doi: 10.1002/jca.10010. PubMed DOI

Pulawski E, Mellwig KP, Brinkmann T, et al. Influence of single low-density lipoprotein apheresis on the adhesion molecules soluble vascular cellular adhesion molecule-1, soluble intercellular adhesion molecule-1, and P-selectin. Ther Apher. 2002;6:229–233. doi: 10.1046/j.1526-0968.2002.00405.x. PubMed DOI

Dlouha D, Blaha M, Blaha V, et al. analysis of circulating miRNAs in patients with familial hypercholesterolaemia treated by LDL/Lp(a) apheresis. Atheroscler Suppl. 2017;30:128–134. doi: 10.1016/j.atherosclerosissup.2017.05.037. PubMed DOI

Rathouska J, Jezkova K, Nemeckova I, et al. Soluble endoglin, hypercholesterolemia and endothelial dysfunction. Atherosclerosis. 2015;243:383–388. doi: 10.1016/j.atherosclerosis.2015.10.003. PubMed DOI

Blazquez-Medela AM, Garcia-Ortiz L, Gomez-Marcos MA, et al. Increased plasma soluble endoglin levels as an indicator of cardiovascular alterations in hypertensive and diabetic patients. BMC Med. 2010;8:86. doi: 10.1186/1741-7015-8-86. PubMed DOI PMC

Gallardo-Vara E, Gamella-Pozuelo L, Perez-Roque L, et al. Potential role of circulating endoglin in hypertension via the upregulated expression of BMP4. Cells. 2020 doi: 10.3390/cells9040988. PubMed DOI PMC

Vitverova B, Blazickova K, Najmanova I, et al. Soluble endoglin and hypercholesterolemia aggravate endothelial and vessel wall dysfunction in mouse aorta. Atherosclerosis. 2018;271:15–25. doi: 10.1016/j.atherosclerosis.2018.02.008. PubMed DOI

Dlouha D, Blaha M, Blaha V, et al. analysis of circulating miRNAs in patients with familial hypercholesterolaemia treated by LDL/Lp (a) apheresis. Atherosclerosis Supplements. 2017;30:128–134. doi: 10.1016/j.atherosclerosissup.2017.05.037. PubMed DOI

Vaverkova H, Tichy L, Karasek D, et al. A case of autosomal recessive hypercholesterolemia caused by a new variant in the LDL receptor adaptor protein 1 gene. J Clin Lipidol. 2019;13:405–410. doi: 10.1016/j.jacl.2019.02.003. PubMed DOI

Blaha M, Cermanova M, Blaha V, et al. Safety and tolerability of long lasting LDL-apheresis in familial hyperlipoproteinemia. Ther Apher Dial. 2007;11:9–15. doi: 10.1111/j.1744-9987.2007.00450.x. PubMed DOI

Solichova D, Melichar B, Blaha V, et al. Biochemical profile and survival in nonagenarians. Clin Biochem. 2001;34:563–569. doi: 10.1016/S0009-9120(01)00261-2. PubMed DOI

Blaha M, Kostal M, Lanska M, et al. The decrease of mean platelet volume after extracorporeal LDL-cholesterol elimination. Atheroscler Suppl. 2013;14:77–81. doi: 10.1016/j.atherosclerosissup.2012.10.019. PubMed DOI

Blaha M, Zadak Z, Blaha V, et al. Extracorporeal LDL cholesterol elimination (25 years of experience in CZ) Atheroscler Suppl. 2009;10:17–20. doi: 10.1016/S1567-5688(09)71804-5. PubMed DOI

Blaha M, Pecka M, Urbankova J, et al. Activity of thrombocytes as a marker of sufficient intensity of LDL-apheresis in familial hypercholesterolaemia. Transfus Apher Sci. 2004;30:83–87. doi: 10.1016/j.transci.2003.11.002. PubMed DOI

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...