China
Africa
Explore chapters and articles related to this topic
Nature of Flow of a Liquid
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Both low high-density (Stamos and Rosenson, 1999) and high low-density (Rosenson and Lowe, 1998) lipoprotein levels are associated with elevated plasma viscosity. In patients with hyperlipoproteinemia, the risk can be reduced by aggressive lipid-lowering therapy (Braunwald, 1997a; Braunwald, 1997b). Low-density lipoprotein (LDL) immunophoresis is an excellent therapeutic option in patients with familial hypercholesterolemia: long-term LDL apheresis treatment is known to reduce plasma LDL cholesterol and plasma viscosity (Otto et al., 2002). Agents such as statins and gembibrozil that lower LDL and triglycerides, respectively, improve cardiovascular risk and may lower plasma viscosity (Stein and Rosenson, 1998; Banyai et al., 2001). C-reactive protein, a sensitive indicator of inflammation and cardiovascular risk, is positively associated with plasma fibrinogen and viscosity (Mendall et al., 2000) and is significantly reduced by pravastatin (Ridker et al., 1999). Also, hormone replacement therapy improves cardiovascular risk by lowering plasma viscosity in postmenopausal women (Rosenson et al., 1998).
Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Treatment is focused on preventing atherosclerotic cardiovascular disease (ASCVD) from developing. This includes atherosclerosis-related acute coronary syndromes, peripheral artery disease, stroke, and transient ischemic attack. Treatment is required as secondary prevention for ASCVD and as primary prevention for some patients without ASCVD. There is controversy about treating children, since diet changes can be difficult, and adult heart disease is not proven to be effectively prevented by previous treatment during childhood. For some children with elevated LDL, the American Academy of Pediatrics does recommend treatment. If a child has heterozygous familial hypercholesterolemia, he or she should be treated initially at ages 8–10. For those with homozygous familial hypercholesterolemia, premature death must be prevented by diet changes, medications, and often, LDL apheresis. Treatments start as soon as the diagnosis is made.
Familial hypercholesterolemia
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
Homozygotes are generally resistant to the drugs and diet that are effective in heterozygotes, but those with some functional receptor activity may respond. The most practical and effective approach to the treatment of most homozygotes has been the removal of LDL by plasmapheresis or LDL apheresis [20, 87]. These procedures lower blood concentrations of cholesterol appreciably, and xanthomas have been observed to regress, as have lesions in the coronary arteries, which were limiting flow. Currently, this appears to be the treatment of choice [88]. LDL apheresis was found to decrease levels of ferritin, transferrin, and vitamin B12 significantly, and some patients became mildly anemic, but there was no change in plasma iron saturation or folic acid [89].
Therapeutic apheresis in kidney diseases: an updated review
Published in Renal Failure, 2022
Yi-Yuan Chen, Xin Sun, Wei Huang, Fang-Fang He, Chun Zhang
LDL-A is a novel technique used for the treatment of nephrotic syndrome (NS), especially focal segmental glomerulosclerosis (FSGS), which selectively removes lipoprotein particles from the blood with the reinfusion of the remaining components (Figure 1(D)) [8]. There are four different techniques of LDL apheresis: IAS, dextran sulfate cellulose adsorption, heparin extracorporeal LDL precipitation, and direct adsorption of lipoprotein using hemoperfusion. All of these techniques are used for familial hypercholesterolemia, but only dextran sulfate cellulose adsorption can be used for drug-resistant NS [8]. The machine first separates plasma from the rest of the blood, and then, the Liposorber filter removes the LDL, very-low-density lipoproteins, Lipoprotein (a), and triglycerides from the plasma. Finally, the hemocytes and purified plasma are returned to the patients. Low blood pressure is the most common adverse effect associated with LDL-A.
Novel emerging therapies in atherosclerosis targeting lipid metabolism
Published in Expert Opinion on Investigational Drugs, 2020
Manasvi Gupta, Colin Blumenthal, Subhankar Chatterjee, Dhrubajyoti Bandyopadhyay, Vardhmaan Jain, Carl J Lavie, Salim S. Virani, Kausik K Ray, Wilbert S Aronow, Raktim K Ghosh
Homozygous familial hypercholesterolemia (HoFH) is an autosomal dominant disease characterized by remarkably high LDL-C levels (>500 mg/dL) leading to early onset of ASCVD. Lomitapide is an inhibitor of microsomal triglyceride transfer protein (MTTP), which plays a crucial role in the assembly and secretion of VLDL by transferring TGs onto apo B. Since VLDL is eventually modified over time to form LDL, reduced production of VLDL will also reduce LDL-C levels. It was initially marketed for use in this patient population and was shown to reduce total cholesterol by 58.4%, LDL-C by 50.9%, TG by 65.2%, and apoB by 55.6% from the baseline values at 4 weeks [34]. In a larger trial which led to the FDA approval of the drug for the same indication, 40 mg lomitapide was shown to reduce the LDL-C level in patients with HoFH population and a baseline LDL-C of 336 ± 112 mg/dl by almost 38% at 78 weeks. These results were comparable to outcomes of LDL apheresis, with the added advantage of oral daily administration. As seen in previous trial, total cholesterol, apoB, and TG levels were also found to be lower in the population treated with lomitapide compared to placebo [35].
Successful treatment of cholesterol crystal embolism with anti-proprotein convertase subtilisin/kexin type 9 (PCSK9) antibody: a case report
Published in Renal Failure, 2020
Junki Morino, Keiji Hirai, Shohei Kaneko, Saori Minato, Katsunori Yanai, Yuko Mutsuyoshi, Hiroki Ishii, Momoko Matsuyama, Taisuke Kitano, Mitsutoshi Shindo, Akinori Aomatsu, Haruhisa Miyazawa, Kiyonori Ito, Yuichiro Ueda, Susumu Ookawara, Yoshiyuki Morishita
Statins have been reported to decrease the risk of developing end-stage renal disease in patients with CCE [17]. In this case, however, statin therapy did not prevent progression of renal dysfunction. There is no difference in efficacy and safety among strong statins including pitavastatin which this patient was taking [18]. Therefore, we did not change pitavastatin to another statin. Steroid therapy has been shown to have reno-protective effects on CCE [2], although it also can induce various adverse events such as gastrointestinal bleeding, hyperglycemia, infections, osteoporosis, and cardiovascular events [4]. LDL-apheresis has been shown to improve renal function in CCE patients [3], but it has also been reported to induce several serious adverse events, including bleeding, shock, and allergic reactions. LDL-apheresis also requires extracorporeal circulation with the use of a plasma component separator and a specific LDL adsorption column [5].