Position of lipoprotein apheresis in present
Authors:
Vladimír Bláha 1; Milan Bláha 2; Miriam Lánská 2; Eduard Havel 1; Pavel Vyroubal 1; Zdeněk Zadák 1; Michal Vrablík 3; Jan Piťha 4; Pavel Žák 2; Luboš Sobotka 1
Authors place of work:
III. interní gerontometabolická klinika LF UK a FN Hradec Králové, přednosta prof. MUDr. Luboš Sobotka, CSc.
1; IV. interní hematologická klinika LF UK a FN Hradec Králové, přednosta doc. MUDr. Pavel Žák, CSc.
2; Centrum preventivní kardiologie III. interní kliniky 1. LF UK a VFN Praha, přednosta prof. MUDr. Štěpán Svačina, DrSc., MBA
3; Institut klinické a experimentální medicíny Praha, ředitel MUDr. Aleš Herman, Ph. D.
4
Published in the journal:
Vnitř Lék 2015; 61(11): 958-964
Category:
Reviews
Summary
Lipoprotein apheresis (LA) is an effective treatment method the patients with severe hypercholesterolemia, resistant to the standard therapy. LA is an extracorporeal elimination technique, which specifically removes low density lipoprotein (LDL) cholesterol from the circulation. At present, lipoprotein apheresis, combined with high-dose statin and ezetimibe therapy, is the best available means of treating patients with homozygous and statin refractory heterozygous familial hypercholesterolaemia (FH). However, the extent of cholesterol-lowering achieved is often insufficient to meet the targets set by current guidelines. The recent advent of new classes of lipid-lowering agents provides new hope that the latter objective may now be achievable. These compounds act either by reducing low density lipoprotein (LDL) cholesterol production by inhibiting apolipoprotein B synthesis with an antisense oligonucleotide (mipomersen), or by inhibiting microsomal triglyceride transfer protein (lomitapid), or by enhancing LDL catabolism via monoclonal antibody-mediated inhibition of the activity of proprotein convertase subtilisin/kexin 9 (PCSK9 – alirocumab, evolocumab etc). The promising is the combination of LDL-apheresis with new drugs, namely for its potential to further decrease of LDL-cholesterol between apheresis. Depending on the outcome of current trials, it seems likely that these compounds, used alone or combined with lipoprotein apheresis, will markedly improve the management of refractory FH.
Key words:
alirocumab – atherosclerosis – cardiovascular disease – evolocumab – hypercholesterolemia –lipoprotein apheresis – lomitapid – mipomersen
Zdroje
1. Stein EA. Drug and alternative therapies for hyperlipidemia. Atherosclerosis 1994;108(Suppl): S105–S116.
2. 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(3): 219–223.
3. Bláha V, Bláha M, Lánská M et al. LDL-aferéza v léčbě familiárních hyperlipoproteinemií. Vnitř lék 2014; 60(11): 970–976.
4. Stefanutti C, Morozzi C, Petta A. Lipid and low-density-lipoprotein apheresis. Effects on plasma inflammatory profile and on cytokine pattern in patients with severe dyslipidemia. Cytokine 2011; 56(3): 842–849.
5. de Gennes JL, Touraine R, Maunand B et al. Homozygous cutaneo-tendinous forms of hypercholesteremic xanthomatosis in an exemplary familial case. Trial of plasmapheresis an heroic treatment. Bull Mem Soc Med Hôp Paris 1967; 118: 1377–1402.
6. Turnberg LA, Mahoney MP, Gleeson MH et al. Plasmapheresis and plasma exchange in the treatment of hyperlipaemia and xanthomatous neuropathy in patients with primary biliary cirrhosis. Gut 1972; 13(12): 976–981.
7. Thompson GR, Lowenthal R, Myant NB. Plasma exchange in the management of homozygous familial hypercholesterolaemia. Lancet 1975; 1(7918): 1208–1211.
8. Berger GM, Miller JL, Bonnici F et al. Continuous flow plasma exchange in the treatment of homozygous familial hypercholesterolemia. Am J Med 1978; 65(2): 243–51.
9. King ME, Breslow JL, Lees RS. Plasma-exchange therapy of homozygous familial hypercholesterolemia. N Engl J Med 1980; 302(26): 1457–1459.
10. Lupien PJ, Moorjani S, Awad J. A new approach to the management of familial hypercholesterolaemia: removal of plasmacholesterol based on the principle of affinity chromatography. Lancet. 1976; 1(7972): 1261–1265.
11. Stoffel W, Borberg H, Greve V. Application of specific extracorporeal removal of low density lipoprotein in familial hypercholesterolaemia. Lancet 1981; 2(8254): 1005–1007.
12. Thompson GR. Lipoprotein apheresis. Curr Opin Lipidol 2010; 21(6): 487–491.
13. Winters JL. American society for apheresis guidelines on the use of apheresis in clinical practice: Practical, concise, evidence-based recommendations for the apheresis practitioner. J Clin Apher 2014; 29(4): 191–193.
14. Bosch T, Schmidt B, Blumenstein M et al. Lipid apheresis by hemoperfusion: in vitro efficacy and ex vivo biocompatibility of a new low-density lipoprotein adsorber compatible with human whole blood. Artif Organs 1993; 17(7): 640–652.
15. Richter WO, Donner MG, Schwandt P. Three low density lipoprotein apheresis techniques in treatment of patients with familial hypercholesterolemia: a long-term evaluation. Ther Apher 1999; 3(3): 203–208.
16. Cashin-Hemphill L, Noone M, Abbott JF et al. Low-density lipoprotein apheresis therapy during pregnancy. Am J Cardiol 2000; 86(10): 1160.
17. Bláha V, Bláha M, Lánská M et al. Lipoproteinová aferéza. Aktuality z vnitřního lékařství. Axonite CZ, Praha 2015.
18. Naoumova RP, Thompson GR, Soutar AK. Currentmanagement of severe homozygous hypercholesterolaemias. Curr Opin Lipidol 2004; 15(4): 413–22.
19. Gagné C, Gaudet D, Bruckert E et al. Efficacy and safety of ezetimibe coadministered with atorvastatin or simvastatin in patients with homozygous familial hypercholesterolemia. Circulation 2002; 105(21): 2469–2475.
20. Gordon BR. Incorporation of low-density lipoprotein apheresis into the treatment programof patientswith severe hypercholesterolemia. Curr Atheroscler Rep 2000; 2(4): 308–313.
21. Raal FJ, Pilcher GJ, Panz VR et al. Reduction in mortality in subjects with homozygous familial hypercholesterolemia associated with advances in lipid-lowering therapy. Circulation 2011; 124(20): 2202–2207.
22. Bilheimer DW, Goldstein JL, Grundy SM et al. Liver transplantation to provide low-density-lipoprotein receptors and lower plasma cholesterol in a child with homozygous familial hypercholesterolemia. N Engl J Med 1984; 311(26): 1658–1664.
23. Van Craeyveld E, Jacobs F, Gordts SC, De Geest B. Gene therapy for familial hypercholesterolemia. Curr Pharm Des 2011; 17(24): 2575–2591.
24. Yamamoto A, Harada-Shiba M et al. The effect of ezetimibe on serum lipids and lipoproteins in patients with homozygous familial hypercholesterolemia undergoing LDL-apheresis therapy. Atherosclerosis 2006; 186(1): 126–131.
25. Raal FJ, Santos RD, Blom DJ et al. Mipomersen, an apolipoprotein B synthesis inhibitor, for lowering of LDL cholesterol concentrations in patients with homozygous familial hypercholesterolaemia: a randomised, double-blind, placebo-controlled trial. Lancet 2010; 375(9719): 998–1006.
26. Cuchel M, Meagher EA, du Toit Theron H et al. Efficacy and safety of a microsomal triglyceride transfer protein inhibitor in patients with homozygous familial hypercholesterolaemia: a single-arm, open-label, phase 3 study. Lancet 2013; 381(9860): 40–46.
27. Stein EA, Honarpour N, Wasserman SM et al. Effect of the proprotein convertase subtilisin/kexin 9 monoclonal antibody, AMG145, in homozygous familial hypercholesterolemia. Circulation 2013; 128(19): 2113–2120.
28. Vogt A, Parhofer KG. The potential of mipomersen, an ApoB synthesis inhibitor, to reduce necessity for LDL-apheresis in patients with heterozygous familial hypercholesterolemia and coronary artery disease. Expert Opinion on Pharmacotherapy 2013; 14(6): 691–697.
29. Stefanutti C, Blom DJ, Averna MR et al. The lipid-lowering effects of lomitapid are unaffected by adjunctive apheresis in patients with homozygous familial hypercholesterolaemia A post-hoc analysis of a Phase 3, single-arm, open-label trial. Atherosclerosis 2015; 240(2): 408–414.
30. Bruckert E, Blaha V, Stein EA et al. Trial Assessing Long-Term Use of PCSK9 Inhibition in Patients with Genetic LDL Disorders (TAUSSIG): Efficacy and Safety in Patients with Familial Hypercholesterolemia Receiving Lipid Apheresis. Circulation 2014; 130: A17016.
31. Tavori H, Giunzioni I, Linton MF et al. Loss of plasma proprotein convertase subtilisin/kexin 9 (PCSK9) after lipoprotein apheresis. Circ Res 2013; 113(12):1290–1295.
32. Stefanutti C, Thompson GR. Lipoprotein Apheresis in the Management of Familial Hypercholesterolaemia: Historical Perspective and Recent Advances. Curr Atheroscler Rep 2015; 17(1): 465. Dostupné z DOI: <http://doi 10.1007/s11883–014–0465–6>.
Štítky
Diabetology Endocrinology Internal medicineČlánok vyšiel v časopise
Internal Medicine
2015 Číslo 11
Najčítanejšie v tomto čísle
- Clinical importance of basal insulin analogues and insulin Toujeo® 300 units/ml
- Atherosclerosis: from etiology to its possible influencing
- Position of lipoprotein apheresis in present
- Practical approach to statin intolerance