Summary GlobalData's clinical trial report, "Dysbetalipoproteinemia
(Type III Hyperlipoproteinemia) Global Clinical Trials Review, H1, 2014" provides data on the Dysbetalipoproteinemia
(Type III Hyperlipoproteinemia) clinical trial scenario.
5 mmol/L (400 mg/dL), in familial dysbetalipoproteinemia
, or when there is abnormal VLDL composition.
Non-denaturing polyacrylamide gradient gel electrophoresis for the diagnosis of dysbetalipoproteinemia
The hereditary types of hyperlipoproteinemia are familial lipoprotein lipase deficiency and/or apoprotein C-II deficiency (type I or V), familial hypercholesterolemia (type IIa or IIb), familial dysbetalipoproteinemia
type III), familial hypertriglyceridemia (type IV), and combined hypercholesterolemia (type IIa, IIb, and/or IV) (table).
Remnant-like particle cholesterol levels in patients with dysbetalipoproteinemia
or coronary artery disease.
Simvastatin is indicated to: reduce elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), and triglycerides (TG); to increase high-density lipoprotein cholesterol (HDL-C) in patients with primary hyperlipidemia (Fredrickson type IIa, heterozygous familial and nonfamilial) or mixed dyslipidemia (Fredrickson type IIb); to reduce elevated TG in patients with hypertriglyceridemia (Fredrickson type lV hyperlipidemia); to reduce elevated TG and VLDL-C in patients with primary dysbetalipoproteinemia
(Fredrickson type lll hyperlipidemia); and to reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (e.
(type III hyperlipoproteinemia) requires 2 copies of the binding defective APOE E2 allele.
Characterization of human very low density lipoproteins containing two electrophoretic populations: double pre-beta lipoproteinemia and primary dysbetalipoproteinemia
Homozygosity for apo E2 is the cause of familial dysbetalipoproteinemia
(Fdis[beta]), an autosomal, recessively transmitted disease in which reduced catabolism leads to dyslipemic phenotype type III, a characteristic accumulation of chylomicrons and VLDL remnants.
Pravachol(R) is also indicated as adjunctive therapy to diet for the treatment of patients with elevated serum triglyceride levels (Fredrickson Type IV) and for the treatment of patients with primary dysbetalipoproteinemia
(Fredrickson Type III) who do not respond adequately to diet.
Inclusion criteria Active patient at the lipid clinic--chart not archived Diagnosis of possible, probable, or definite HFH Over 18 years of age at last clinic visit Exclusion criteria Homozygous HFH Secondary causes of dyslipidemia, including diabetes mellitus, hypothyroidism, renal disease, hepatic disease, drug-induced dyslipidemia, and HIV TGs [greater than or equal to] 3 mmol/L (applied for patients meeting criteria for possible or probable HFH criteria only) Concomitant diagnosis of another heritable dyslipidemia such as dysbetalipoproteinemia
No available Lp(a) data Table 3.
Zocor(R) is indicated to reduce elevated total-C, LDL-C, Apo B, and TG, and to increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Fredrickson types IIa and IIb), for the treatment of patients with hypertriglyceridemia (Fredrickson type IV hyperlipidemia), for the treatment of patients with primary dysbetalipoproteinemia
(Fredrickson type III hyperlipidemia), and is also indicated to reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (e.