Lipoprotein apheresis

Thompson, Gilbert R.

doi:10.1097/mol.0b013e32833e13fd

Cited by 46 publications

(32 citation statements)

References 28 publications

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“…This study compared retrospective events from the lipid-lowering phase with prospective events in the apheresis phase, with limitations inherent using such an approach. Nevertheless, it provides the best evidence yet that lowering of Lp(a) is beneficial [61]. If confirmed by further studies, it would fulfill Koch's second postulate for Lp(a).…”

Section: Koch's Postulate For Lp(a)supporting

confidence: 52%

Lipoprotein(a): Reloaded

Kronenberg

Utermann

2011

Curr Cardiovasc Risk Rep

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Section: Koch's Postulate For Lp(a)supporting

confidence: 52%

Lipoprotein(a): Reloaded

Kronenberg

Utermann

2011

Curr Cardiovasc Risk Rep

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“…LA involves the extracorporeal removal of LDL and lipoprotein from whole blood or plasma. The previous term for LA was 'LDL apheresis,' but this was considered inappropriate because the procedure removes not only LDL, but also chylomicron, VLDL, and lipoprotein (a) [4] . Recent advances in technology have allowed direct adsorption of these lipoproteins from the blood.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Follow-Up of a Homozygous Familial Hypercholesterolemic Patient Receiving Regular Double Filtration Plasmapheresis - Case Report and Literature Review

Tsai

Wu²,

Shu³

et al. 2016

Blood Purif

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Homozygous familial hypercholesterolemia (HoFH) is a very rare condition (1 case per 1 million people) with a dismal outcome due to inevitable coronary artery disease that occurs when left untreated. Lipoprotein apheresis (LA), previously known as low-density lipoprotein (LDL) apheresis, is very effective in reducing LDL-cholesterol (LDL-C) if HoFH is refractory to aggressive drug therapy and diet control. In this study, we report a case with HoFH, who presented with xanthomata over the 4 limbs when she was 3 years old. When she was 11 years old, she began treatment with semi-selective LA with double filtration plasmapheresis (DFPP) once per week because HoFH was refractory to high-dose statin and diet control. LDL-C was reduced from 8.2 ± 0.9 to 2.69 ± 0.75 mmol/l (reduction rate = 67.3 ± 6.1%). The xanthomata over the 4 limbs were nearly completely resolved after 2 years of DFPP. Two years later, after the initiation of DFPP, we performed coronary angiography and echocardiography for regular checkup in the absence of chest pain, and the result was negative. To date (11 years after initiation of DFPP), she has not complained of any chest pain, shown intolerance to exercise, or exhibited ST-T change on electrocardiography. At the age of 20, multidetector computed tomography showed no significant stenosis over the coronary arteries. At the most recent follow-up visit, she was found to have good heart function and no xanthomata. LA is effective in the treatment of HoFH when drug therapy and diet control fail. With this treatment, pre-existing xanthomata can regress and coronary artery disease can be prevented.

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“…23 LDL apheresis significantly lowers LDL-C and is considered the standard of care for patients with HoFH. 24 This procedure reduces the risk of coronary heart disease in patients with heterozygous FH. 25 However, drawbacks of apheresis include limited availability, high cost, procedure duration, and the need to maintain adequate vascular access.…”

Section: Discussionmentioning

confidence: 99%

“…25 However, drawbacks of apheresis include limited availability, high cost, procedure duration, and the need to maintain adequate vascular access. 24 There are also no prospective randomized studies demonstrating improved survival with apheresis, and despite apheresis, HoFH patients still develop extensive aortic calcification. 26 Prospective studies in non-HoFH populations have consistently shown a significant reduction in cardiovascular events and total mortality when LDL-C is reduced by 24% to 30%.…”

Section: Discussionmentioning

confidence: 99%

Reduction in Mortality in Subjects With Homozygous Familial Hypercholesterolemia Associated With Advances in Lipid-Lowering Therapy

et al. 2011

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Background-Homozygous familial hypercholesterolemia is an inherited disorder caused by mutations in both low-density lipoprotein receptor alleles, which results in extremely elevated plasma low-density lipoprotein cholesterol concentrations and very early morbidity and mortality due to cardiovascular disease. Methods and Results-To evaluate the impact of advances in lipid-lowering (predominantly statin) therapy on cardiovascular disease morbidity and mortality in a large cohort of patients with homozygous familial hypercholesterolemia, the records of 149 patients (81 females, 68 males) from 2 specialized lipid clinics in South Africa were evaluated retrospectively. Homozygous familial hypercholesterolemia was diagnosed by confirmation of mutations in genes affecting low-density lipoprotein cholesterol or by clinical criteria. A Cox proportional hazard model with time-varying exposure was used to estimate the risk of death and major adverse cardiovascular events among statin-treated patients compared with statin-naive patients. The hazard ratio for benefit from lipid therapy, calculated with the Cox proportional hazards model for the end point of death, was 0.34 (95% confidence interval 0.14 -0.86; Pϭ0.02), and for the end point of major adverse cardiovascular events, it was 0.49 (95% confidence interval 0. Clinical Perspective on p 2207The frequency of FH throughout the world has been estimated at 1 in 500 people in the less severe heterozygous form and at 1 per 1 million people in the more severe homozygous form. 1 In South African white Afrikaners, there is a much higher prevalence of heterozygous and homozygous FH, estimated at 1:100 and 1:30 000, respectively. 3 This high prevalence is due to a founder effect that occurred when a limited number of LDL receptor mutations were introduced by Dutch families who settled in the Cape Province during the second half of the seventeenth century. 4 Until the 1980s, treatment of FH was limited to a low-fat diet and minimally effective lipid-modifying agents. Lipidlowering drug therapy changed radically in the 1990s with the introduction of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, or statins, a drug class that is remarkably effective in lowering LDL-C. 5 Multiple ranContinuing medical education (CME) credit is available for this article. Go to http://cme.ahajournals.org to take the quiz. The aims of the present study were to assess the impact of modern lipid-lowering therapy, predominantly statin therapy, on all-cause and cardiovascular mortality in a large cohort of HoFH patients who have been followed up for up to 40 years at 2 specialized lipid treatment centers in South Africa. Methods PatientsThis study was a retrospective cohort design that reviewed data from July 1972, the time of inception of the first specialized lipid clinics in South Africa, to March 2009. Medical records of HoFH subjects were reviewed to establish genetic and phenotypic data, anthropometric measures, and data on cardiovascular events and lipidlowering drug...

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Lipoprotein apheresis

Abstract: Lipoprotein apheresis seems to be going through a growth spurt, presumably reflecting better implementation of treatment guidelines or a broadening of indications for its use.

Cited by 46 publications

References 28 publications

Lipoprotein(a): Reloaded

Lipoprotein(a): Reloaded

Long-Term Follow-Up of a Homozygous Familial Hypercholesterolemic Patient Receiving Regular Double Filtration Plasmapheresis - Case Report and Literature Review

Reduction in Mortality in Subjects With Homozygous Familial Hypercholesterolemia Associated With Advances in Lipid-Lowering Therapy

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