This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https: //www. Creative Commons Attribution – Non Commercial (unported, v. License (http: //creativecommons. By accessing the work you hereby accept the Terms. Non- commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Abstract. This review reports the current situation with respect to therapeutic options (lifestyle and drugs) reducing the concentrations of atherogenic low- density lipoprotein cholesterol (LDL- C) and lipoprotein(a) (Lp. Three lipoprotein apheresis (LA) principles have been realized: precipitation, filtration, and adsorption. Available LA methods are herein described in detail – major components, pumps, extracorporeal volume, treated volume, and anticoagulation. General features of all LA methods as well as pleotropic effects are elaborated. Indications for LA therapy are quoted: homozygous familial hypercholesterolemia (HCH), severe HCH, and isolated elevation of Lp(a) and progress of atherosclerotic disease. A major focus is on the evidence of the effect of LA on cardiovascular outcome data, and the most important publications are cited in this context. The best studies have been performed in patients with elevated Lp(a) in whom cardiovascular events were reduced by more than 8. Donation FAQs. Each apheresis donation procedure takes about one-and-one-half to. Donating Apheresis Plasma. Plasma is needed by patients in our community every day! Make your appointment at schedule.bloodworksnw.org or by calling 1-800-398-7888. Major adverse effects and contraindications are listed. The impact of an LA therapy on patient quality of life and the requirements they have to fulfill are also highlighted. Finally, the future role of LA in treating high- risk patients with high LDL- C and/or high Lp(a) is discussed. It is probable that the significance of LA for treating patients with elevated LDL- C will decrease (with the exception of homozygous familial HCH) due to the application of PCSK9 inhibitors. The antisense oligonucleotide against apolipoprotein(a) could replace LA in patients with high Lp(a), provided positive outcome data are generated. Keywords: LDL cholesterol, lipoprotein(a), lipid- lowering therapy, lipoprotein apheresis, cardiovascular outcome. Video abstract. Download video file.(1. You can get help in planning your diet after transplant from your doctor and dietitian. Diet and Transplantation. Common Organ Donation and Transplantation Terms. Apheresis Plan For Autologous and Allogeneic Donors Patient Label Here 13. Apheresis Plan For Autologous and Allogeneic Donors. M, avi)Introduction to current management strategies for patients with severe hypercholesterolemia and elevated lipoprotein(a)Severe hypercholesterolemia (HCH) and elevation of lipoprotein(a) (Lp. It must be admitted, however, that the effect of an optimal diet on low- density lipoprotein cholesterol (LDL- C) levels in severe HCH is rather limited (a 5% reduction is realistic with almost no reduction in patients with homozygous familiar HCH), and no effect of diet on Lp(a) concentrations has been observed. Physical activity does not exert an action on either parameter. Nonsmoking is of great relevance – the combination of the discussed metabolic disturbances and cigarette smoking is highly atherogenic. In patients who have already developed atherosclerotic lesions (either documented by imaging techniques or having suffered from cardiovascular events), drug therapy is required. In HCH patients, the drugs of first choice are statins. Usually, one starts with a low dose and – when this is tolerated, but the effect is not sufficient – the physician then prescribes a higher dose (Figure 1. A). Statins differ with respect to their effectiveness: atorvastatin and rosuvastatin are more potent. According to European Guidelines, an LDL- C target should be aimed for. In patients with proven atherosclerosis, LDL- C should be lowered to < 1. L. If this target cannot be reached, either ezetimibe or a bile- acid sequestrant (or both) should be added to the statin. For high- risk patients whose LDL- C levels remain very far from the target despite the proposed drug treatment (or in patients with an intolerance to statins or the other suggested drugs),3 a new option is available: PCSK9 inhibitors. These can also be combined with a statin and help, in many patients, to lower LDL- C very effectively. The antisense oligonucleotide mipomersen represents an alternative therapeutic approach but is associated with a rather high rate of adverse effects and is only approved for use in the USA (not in Europe). In patients with homozygous familial HCH, the MTP inhibitor, lomitapide can be administered – usually in addition to a lipoprotein apheresis (LA) treatment. In these patients, PCSK9 inhibitors either show a limited effect on LDL- C levels or no effect (depending on the residual function of the LDL receptors). Therapeutic steps in treating patients with (A) high LDL- C or (B) high Lp(a). The next step is undertaken after at least a 3- month period in which the efficiency of the ongoing drug therapy is determined. PCSK9 inhibitors are prescribed only after 1 year of application of other lipid- lowering drugs (when the latter are tolerated). The situation with respect to Lp(a) is quite different (Figure 1.
B). Statins do not affect Lp(a) concentrations (some studies have even shown an increase); other lipid- lowering drugs are also ineffective. The general policy for treating patients with high Lp(a) is to optimize other risk factors such as LDL- C (as already mentioned), diabetes, hypertension, and lifestyle. PCSK9 inhibitors reduce Lp(a) levels up to 3. Lp(a) concentrations, this effect is much less or even absent. An elevation of Lp(a) represents no indication for the administration of PCSK9 inhibitors, but these drugs could be used in patients with a parallel elevation of LDL- C. Mipomersen reduces Lp(a) as well. In several large placebo- controlled studies, statins have been shown to effectively reduce the morbidity and mortality of cardiovascular diseases, reducing new events by 3. However, there remain patients who develop new events despite taking a statin. One possible reason for this could be that in many patients LDL- C target levels have not been reached. It is quite well accepted that the incidence of new events will be lower when LDL- C levels are lower. Ezetimibe added to a statin led to a further reduction in new events. No data with respect to the occurrence of cardiovascular events have been published for bile- acid sequestrants. For PCSK9 inhibitors, preliminary results point to their effectiveness in this respect, but the first controlled long- term study performed in more than 2. At present, no effective drug therapy is available for Lp(a) – nicotinic acid was withdrawn from the market in Europe after two studies showed no positive effect on cardiovascular events and a rather high rate of adverse events (AEs). In one study, a new antisense oligonucleotide against apolipoprotein(a) has been shown to decrease Lp(a) very effectively. Review of clinical utility, recommendations, patient selection, and implementation of LAThe position of LA within the therapeutic regimen of lipid disorders is always at the end (Figure 1). Only high- risk patients are considered candidates for this extracorporeal treatment. LA does not play a major role in primary prevention, with the exception of homozygous familial HCH (when patients are at an extremely high risk to develop atherosclerosis). In 1. 96. 7, de Gennes et al. HCH. In the 1. 97. LA methods were developed, first in Japan and then in Germany. The major aim of all available LA methods is to eliminate atherogenic LDL and Lp(a) particles from the blood, but other lipoproteins such as very LDL and high- density lipoprotein (HDL) are also being removed. Some LA methods eliminate the lipoproteins from plasma – the first step is the separation of plasma either by filtration or by centrifugation. Other methods use whole blood (Figure 2). Principles of available LA methods. After plasma separation, there are different techniques that can be used to remove atherogenic lipoproteins (names of the LA systems given; Figure 2 and Table 1). Second filter that retains the lipoproteins (and also other proteins): Lipidfiltration and membrane filtration optimized novel extracorporeal treatment (MONET). Addition of a large amount of heparin and an acetate buffer – at p. H 5. 1. 2, lipoproteins are precipitated (and also fibrinogen); the excess of heparin is then removed by a heparin adsorber, and the p. H is normalized by a bicarbonate dialysis: heparin- induced extracorporeal LDL precipitation (HELP). Antibodies against apolipoprotein B (apo. B) that are bound to sepharose; each patient has his/her own two columns that are at first loaded with plasma (the plasma is guided to the second column, while the first column is regenerated; both columns are loaded and regenerated alternatively); the regeneration starts: a glycine buffer separates the antigen from the antibodies, the antigen is washed out by a fluid, and the p. H is normalized using a phosphate buffer: Thera. Sorb. This system allows single- needle handling. The Pocard LDL columns use the same principle. Dextran sulfate bound to cellulose with a negatively charged surface binding apo. B containing lipoproteins: Liposorber LA- 1. There are two whole blood LA methods on the market (names of the systems given). Polyacrylate- coated polyacrylamide beads with a negatively charged surface binding apo. B containing lipoproteins: direct adsorption of lipoproteins (DALI). Dextran sulfate bound to cellulose with a negatively charged surface binding apo. B containing lipoproteins: Liposorber D. The following issues apply to all LA methods. Blood is usually obtained by venous puncture and returned via a vein at the contralateral arm. When the venous situation in a given patient is very poor, an arteriovenous fistula has to be established. Part of the blood is extracorporeal during the session. Duration of an LA session is between 1. Usually, the blood flow during the session is between 8. L/min. Anticoagulation is always needed, either with heparin or with citrate (or both; Table 1). Apheresis Units 0. However, it looks like you listened to.
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