Targeting the Role of Lipoprotein (a) in Stroke

Mazhar, Zahra; Hughes, Andrew; Garelnabi, Mahdi

doi:10.2174/1871529x17666170421150028

Cited by 8 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lp(a) has been considered as an LDL-like particle but its metabolism is different from LDL. Currently, there are clear relationships between risk of cerebral infarction and high Lp(a) concentration in plasma [16]. There is also evidence of a sustained and independent association between Lp(a) levels and the risk of sudden cardiac death [17].…”

Section: Discussionmentioning

confidence: 99%

A Novel Mutation in the Kringle IV Domain of LPA gene leading to Familial Hyperlipoproteinemia

Zhang

Wang

et al. 2019

Preprint

View full text Add to dashboard Cite

Background This study aims to investigate the clinical characterization and causative genetic defect of a four-generation Chinese Han family with hyperlipoproteinemia. Methods The combined use of next-generation sequencing and qPCR technique was performed to investigate genetic pathology of familial hyperlipoproteinemia. Results The clinical manifestations of the family members include hyperlipoproteinemia, early-onset hypertension, coronary heart disease, lipoma, cerebral infarction and even sudden death, and a novel heterozygous deletion of 3-16 exon of LPA gene was identified to be causative for the symptoms in the family. Conclusions A novel deletion in the LPA gene was identified in a Chinese family associated with hyperlipoproteinemia, which expands the spectrum of the LPA mutation and its associated phenotype. Keywords Copy number variation; Hyperlipoproteinemia; Kringle IV; Lipoprotein(a); LPA;

show abstract

Section: Discussionmentioning

confidence: 99%

A Novel Mutation in the Kringle IV Domain of LPA gene leading to Familial Hyperlipoproteinemia

Zhang

Wang

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…Elevated Lp(a) blood concentrations and genetypes were associated with increased risk of aortic valve stenosis in the population, with concentration > 90 mg/ dL predicting a threefold increased risk [34]. Future investigations and potential research projects must clarify the role of Lp(a) in stroke [35].…”

Section: Pathophysiology Of Dyslipoproteinemiamentioning

confidence: 99%

Dyslipoproteinemia therapy with lipoprotein-apheresis and/or human monoclonal antibodies

Bambauer¹,

Schiel²

2019

Trends Med

View full text Add to dashboard Cite

The prognosis of patients suffering from severe dyslipoproteinemia, sometimes combined with elevated lipoprotein (a) (Lp(a)), and coronary artery disease (CAD) refractory to diet and lipid-lowering drugs has been improved by the introduction of the lipoprotein-apheresis, and the human monoclonal antibodies (HMA) in different studies. All severe forms of dyslipoproteinemia can be treated successfully with these methods alone or in combination. Different lipoprotein-apheresis systems are available which reduce LDL cholesterol, Lp(a), triglycerides and others: cascade filtration or lipoproteinfiltration, immunoadsorption, heparin-induced LDL precipitation, dextran sulfate LDL adsorption, LDL hemoperfusion, and/or different HMA. There is a strong correlation between dyslipoproteinemia and atherosclerosis. Besides the elimination of other risk factors in severe dyslipoproteinemia therapeutic strategies focus on a drastic reduction of serum lipoproteins. In such patients in whom the maximum drug therapy failed, lipoprotein-apheresis (LA) is indicated. Technical and clinical aspects of these different lipoproteinapheresis methods and results of the application of HMA are shown here. The published data clearly demonstrate that treatment with lipoprotein-apheresis in patients suffering from severe dyslipoproteinemia refractory to conservative therapy are effective and safe in long application. A disadvantage is the high costs and the expensive technologies of the different lipoprotein-apheresis methods. The costs of the therapy with HMA are lower than the costs of the lipoprotein-apheresis but larger studies are necessary to show what method could be preferred.

show abstract

“…N-acetylcysteine has been shown to induce a dose-dependent reduction in Lp(a) levels about seven percent by causing dissociation of the Apo A by cleavage of disulfide bonds [54]. Very high levels of Lp(a) can only be normalized by lipoprotein-apheresis (LA), and/or with the therapy of the proprotein convertase subtilisin/kexin type 9 (PCSK9) with evolocumab as a fully HMA which is directed against human PCSK9 [55,56]. Evolocumab up regulates LDL receptors causing increased catabolism of LDL and the reduction of LDL and is higher than of Lp(a) blood concentrations [57].…”

Section: Nephrogenic Systemic Fibrosis (Nsf)mentioning

confidence: 99%

Therapeutic Apheresis and Human Monoclonal Antibodies in Non-Immunologic Diseases. TA, HMA in non-immunologic diseases

2023

JCEI

View full text Add to dashboard Cite

Non-immunologic diseases such as nephrological, blood diseases, dyslipoproteinemia, cancer, infections, intoxications etc. have often a severe course or a bad prognosis. Since more than 45 years, therapeutic apheresis has led in combination with other therapies to a steady increase in survival rates. Therapeutic apheresis is indicated in the most of the non-immunologic diseases, and in all antibody-mediated diseases. Since the introduction of hollow fiber membranes, a complete separation of the corpuscular components, pathologic substances, antibodies, toxins etc. is reached. The mortality rate of severe non-immunologic diseases is reduced by therapeutic apheresis. Other new therapies are various human monoclonal antibodies alone or in combination with therapeutic apheresis. The pathological aspects, the first-line and second-lines therapies for non-immunologic such as nephrological, neurological, gastroenterological, hematological diseases, and others are shown. The guidelines of the Apheresis Applications Committee of the American Society for Apheresis are cited. Therapeutic apheresis and/or human monoclonal antibodies have shown to effectively cure severe diseases without immunologic origin.

show abstract

Targeting the Role of Lipoprotein (a) in Stroke

Cited by 8 publications

References 0 publications

A Novel Mutation in the Kringle IV Domain of LPA gene leading to Familial Hyperlipoproteinemia

A Novel Mutation in the Kringle IV Domain of LPA gene leading to Familial Hyperlipoproteinemia

Dyslipoproteinemia therapy with lipoprotein-apheresis and/or human monoclonal antibodies

Therapeutic Apheresis and Human Monoclonal Antibodies in Non-Immunologic Diseases. TA, HMA in non-immunologic diseases

Contact Info

Product

Resources

About