A severe type of hyperlipidemia, sometimes familial, that is characterized by the elevation of both plasma CHYLOMICRONS and TRIGLYCERIDES contained in VERY-LOW-DENSITY LIPOPROTEINS. Type V hyperlipoproteinemia is often associated with DIABETES MELLITUS and is not caused by reduced LIPOPROTEIN LIPASE activity as in HYPERLIPOPROTEINEMIA TYPE I .
An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.
An inherited condition due to a deficiency of either LIPOPROTEIN LIPASE or APOLIPOPROTEIN C-II (a lipase-activating protein). The lack of lipase activities results in inability to remove CHYLOMICRONS and TRIGLYCERIDES from the blood which has a creamy top layer after standing.
A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.
Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.
'Blood Protein Disorders' refer to conditions characterized by an abnormal amount, structure, or function of proteins present in the blood, including immunoglobulins, coagulation factors, complement components, and transport proteins, which can lead to various clinical manifestations such as immune dysfunction, bleeding disorders, or metabolic imbalances.
A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).
A fibrillar collagen found widely distributed as a minor component in tissues that contain COLLAGEN TYPE I and COLLAGEN TYPE III. It is a heterotrimeric molecule composed of alpha1(V), alpha2(V) and alpha3(V) subunits. Several forms of collagen type V exist depending upon the composition of the subunits that form the trimer.
One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.
A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.
Conditions with excess LIPIDS in the blood.
A condition marked by the development of widespread xanthomas, yellow tumor-like structures filled with lipid deposits. Xanthomas can be found in a variety of tissues including the SKIN; TENDONS; joints of KNEES and ELBOWS. Xanthomatosis is associated with disturbance of LIPID METABOLISM and formation of FOAM CELLS.
A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.
Triglycerides are the most common type of fat in the body, stored in fat cells and used as energy; they are measured in blood tests to assess heart disease risk, with high levels often resulting from dietary habits, obesity, physical inactivity, smoking, and alcohol consumption.
Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.
A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.
A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.
Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.
A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.
A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.
Electrophoresis applied to BLOOD PROTEINS.
A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.
Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.

A case of hypothyroidism and type 2 diabetes associated with type V hyperlipoproteinemia and eruptive xanthomas. (1/23)

Primary hypothyroidism and type 2 diabetes are both typically associated with the increased level of triglycerides. To date, there have been only a few case reports of type 2 diabetes patients with both type V hyperlipoproteinemia and eruptive xanthomas, but there have been no reports of hypothyroidism patients associated with eruptive xanthomas. We report here on a case of a 48-yr old female patient who was diagnosed with type 2 diabetes and primary hypothyroidism associated with both type V hyperlipoproteinemia and eruptive xanthomas. We found rouleaux formation of RBCs in peripheral blood smear, elevated TSH, and low free T4 level, and dyslipidemia (total cholesterol 18.1 mM/L, triglyceride 61.64 mM/L, HDL 3.0 mM/L, and LDL 2.54 mM/L). She has taken fenofibrate, levothyroxine, and oral hypoglycemic agent for 4 months. After treatment, both TSH level and lipid concentration returned to normal range, and her yellowish skin nodules have also disappeared.  (+info)

High frequency of Fredrickson's phenotypes IV and IIb in Brazilians infected by human immunodeficiency virus. (2/23)

BACKGROUND: Human immunodeficiency virus (HIV) infection is very prevalent in Brazil. HIV therapy has been recently associated with coronary heart disease (CHD). Dyslipidemia is a major risk factor for CHD that is frequently described in HIV positive patients, but very few studies have been conducted in Brazilian patients evaluating their lipid profiles. METHODS: In the present work, we evaluated the frequency and severity of dyslipidemia in 257 Brazilian HIV positive patients. Two hundred and thirty-eight (93%) were submitted to antiretroviral therapy (224 treated with protease inhibitors plus nucleoside reverse transcriptase inhibitors, 14 treated only with the latter, 12 naive and 7 had no records of treatment). The average time on drug treatment with antiretroviral therapy was 20 months. None of the patients was under lipid lowering drugs. Cholesterol, triglyceride, phospholipid and free fatty acids were determined by enzymatic colorimetric methods. Lipoprotein profile was estimated by the Friedewald formula and Fredrickson's phenotyping was obtained by serum electrophoresis on agarose. Apolipoprotein B and AI and lipoprotein "a" were measured by nephelometry. RESULTS: The Fredrickson phenotypes were: type IIb (51%), IV (41%), IIa (7%). In addition one patient was type III and another type V. Thirty-three percent of all HIV+ patients presented serum cholesterol levels >or= 200 mg/dL, 61% LDL-cholesterol >or= 100 mg/dL, 65% HDL-cholesterol below 40 mg/dL, 46% triglycerides >or= 150 mg/dL and 10% have all these parameters above the limits. Eighty-six percent of patients had cholesterol/HDL-cholesterol ratio >or= 3.5, 22% increased lipoprotein "a", 79% increased free fatty acids and 9% increased phospholipids. The treatment with protease inhibitors plus nucleoside reverse transcriptase inhibitors increased the levels of cholesterol and triglycerides in these patients when compared with naive patients. The HDL-cholesterol (p = 0.01) and apolipoprotein A1 (p = 0.02) levels were inversely correlated with the time of protease inhibitor therapy while total cholesterol levels had a trend to correlate with antiretroviral therapy (p = 0.09). CONCLUSION: The highly varied and prevalent types of dyslipidemia found in Brazilian HIV positive patients on antiretroviral therapies indicate the urgent need for their early diagnosis, the identification of the risk factors for CHD and, when needed, the prompt intervention on their lifestyle and/or with drug treatment.  (+info)

Isolation and characterization of an apoA-II-containing lipoprotein (LP-A-II:B complex) from plasma very low density lipoproteins of patients with Tangier disease and type V hyperlipoproteinemia. (3/23)

Previous studies have shown that very low density lipoproteins (VLDL) from patients with Tangier disease are less effective as a substrate for human milk lipoprotein lipase (LPL) than VLDL from normal controls as assessed by measuring the first order rate constant (k1) of triglyceride hydrolysis. Tangier VLDL also has a higher content of apolipoprotein (apo) A-II than normal VLDL. To explore the possible relationship between the relatively high concentration of apoA-II in VLDL and low k1 values, Tangier VLDL were fractionated on an anti-apoA-II immunosorber. The retained fraction contained a newly identified triglyceride-rich lipoprotein characterized by the presence of apolipoproteins A-II, B, C-I, C-II, C-III, D, and E (LP-A-II:B:C:D:E or LP-A-II:B complex), whereas the unretained fraction consisted of previously identified triglyceride-rich apoB-containing lipoproteins free of apoA-II. In VLDL from patients with Tangier disease or type V hyperlipoproteinemia, the LP-A-II:B complex accounted for 70-90% and 25-70% of the total apoB content, respectively. The LP-A-II:B complexes had similar lipid and apolipoprotein composition; they were poor substrates for LPL as indicated by their low k1 values (0.014-0.016 min-1). In contrast, the apoA-II-free lipoproteins present in unretained fractions were effective substrates for LPL with k1 values equal to or greater than 0.0313 min-1. These results indicate that triglyceride-rich lipoproteins consist of several apoB-containing lipoproteins, including the LP-A-II:B complex, and that lipoprotein particles of similar size and density but distinct apolipoprotein composition also possess distinct metabolic properties.  (+info)

Interaction between variant apolipoproteins C-II and E that affects plasma lipoprotein concentrations. (4/23)

The genes for apolipoprotein (apo) C-II, a cofactor for activation of lipoprotein lipase, and apo E, a ligand for receptor-mediated uptake of triglyceride-rich lipoproteins, are physically linked on chromosome 19q13.1. In a large Caribbean Caucasian family, several individuals had clinical features of the complete absence of lipoprotein lipase activity and were homozygous for a DNA frameshift mutation of apo C-II, imparting functional inactivity to the mutant protein. Plasma from heterozygous carriers of this mutation, when compared with plasma from relatives who were noncarriers, had significantly diminished capacity to activate lipoprotein lipase in vitro. We also observed in heterozygotes for this mutation a wide range of serum lipid and lipoprotein levels. When age and sex were taken into account, the presence of a single apo E allele encoding the E4 isoform occurring in individuals with a single mutant apo C-II allele was strongly associated with higher levels of cholesterol, triglycerides, very low density lipoprotein cholesterol, and non-high density lipoprotein cholesterol when compared with those of relatives who carried neither or only one variant allele. This suggests that a single genetic mutation that usually has a recessive effect on lipoprotein metabolism can have an interactive effect on lipid phenotype when it is coinherited with a single mutation at another gene whose product affects the same metabolic pathway.  (+info)

Diagnosis and management of type I and type V hyperlipoproteinemia. (5/23)

Both type I and type V hyperlipoproteinemia are characterized by severe hypertriglyceridemia due to an increase in chylomicrons. Type I hyperlipoproteinemia is caused by a decisive abnormality of the lipoprotein lipase (LPL)- apolipoprotein C-II system, whereas the cause of type V hyperlipoproteinemia is more complicated and more closely related to acquired environmental factors. Since the relationship of hypertriglyceridemia with atherosclerosis is not as clear as that of hypercholesterolemia, and since type I and V hyperlipoproteinemia are relatively rare, few guidelines for their diagnosis and treatment have been established; however, type I and V hyperlipoproteinemia are clinically important as underlying disorders of acute pancreatitis, and appropriate management is necessary to prevent or treat such complications. Against such a background, here we propose guidelines primarily concerning the diagnosis and management of type I and V hyperlipoproteinemia in Japanese.  (+info)

Apolipoprotein E2-Dunedin (228 Arg replaced by Cys): an apolipoprotein E2 variant with normal receptor-binding activity. (6/23)

Homozygosity for the apolipoprotein (apo) E variant apoE2(158 Arg----Cys) invariably gives rise to dysbetalipoproteinemia, and when associated with obesity or a gene for hyperlipidemia, results in type III hyperlipoproteinemia. The association of the E2/2 phenotype with type IV/V hyperlipoproteinemia rather than type III hyperlipoproteinemia in identical twin brothers led us to investigate the primary structure of their apoE. Lipoprotein electrophoresis on agarose gels confirmed the presence of increased very low density lipoproteins (VLDL) and chylomicrons but little, if any, beta-VLDL, indicating that these subjects did not have dysbetalipoproteinemia. When the apoE from these twins was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis on a system that can distinguish apoE2(158 Arg----Cys) from all other known apoE variants, it gave rise to two components. One had the unique mobility of apoE2(158 Arg----Cys), and one migrated in the position of the other variants of apoE (and normal apoE3), indicating that the brothers were heterozygous for apoE2(158 Arg----Cys) and a second apoE2 isoform. Cysteamine modification and isoelectric focusing showed that, like apoE2(158 Arg----Cys), the second apoE2 isoform also contained two cysteine residues. The structural mutation in the second apoE2 isoform was determined by peptide sequencing. Like normal apoE3, this variant had arginine at position 158, but differed from apoE3 by the substitution of cysteine for arginine at position 228. Total apoE isolated from the brothers had the same receptor-binding activity in a competitive binding assay as a 1:1 mixture of normal apoE3 and apoE2(158 Arg----Cys).(ABSTRACT TRUNCATED AT 250 WORDS)  (+info)

A case of hypopituitarism and type V hyperlipidemia. (7/23)

A 29-year-old woman developed hypopituitarism following removal of a pituitary chromophobe adenoma, and this was complicated by type V hyperlipidemia and obesity.  (+info)

Accumulation of an apoE-poor subfraction of very low density lipoprotein in hypertriglyceridemic men. (8/23)

Studies were undertaken to investigate the mechanism of the marked accumulation of an apoE-poor very low density lipoprotein (VLDL) subfraction in untreated Type IV and IIb hypertriglyceridemic subjects. Heparin-Sepharose chromatography was used to separate large VLDL (Sf 60-400) from fasted subjects, into an apoE-poor, unbound fraction and an apoE-rich, bound fraction. As a percent of total VLDL protein, the apoE-poor fraction comprised 40 +/- 4% of total VLDL in hypertriglyceridemic subjects versus 25% in normal subjects. Compared to the apoE-rich, bound fraction, this apoE-poor material was found to have a 5-fold lower ratio of apoE to apoC (0.20 +/- 0.06 vs 0.91 +/- 0.18, P less than 0.005), but a 1.5-fold higher ratio of triglyceride to protein (11.41 +/- 0.85 vs 7.97 +/- 0.77, P less than 0.01). In addition, the apoE-poor fraction was found to be enriched 2-fold in apoB-48 (10.30 +/- 2.41% vs 5.73 +/- 1.59% of total apoB, P less than 0.005) compared to the apoE-rich fraction, suggesting that the apoE-poor fraction contains more chylomicron remnants. The amount of this apoE-poor VLDL was markedly reduced following a reduction in VLDL triglyceride levels (a decrease from 40 +/- 4% to 21 +/- 2% of VLDL protein following a 50% reduction in VLDL triglyceride levels). The large VLDL from Type I, III, and V hyperlipoproteinemic subjects subfractionated using heparin-Sepharose showed an equal distribution of apoE between the two fractions in contrast with the Type IV and IIb subjects. The separation of VLDL from Type I, III, and V subjects using heparin-Sepharose involves a mechanism other than apoE binding. Separation in the latter likely results from apoB-100 binding to heparin, as opposed to apoE binding of VLDL from Type IV and IIb subjects.  (+info)

Hyperlipoproteinemia Type V is a rare genetic disorder characterized by an excess of lipids (fats) in the blood. It is caused by mutations in genes responsible for the metabolism of lipoproteins, which are particles that transport fat molecules, such as cholesterol and triglycerides, throughout the body.

In Hyperlipoproteinemia Type V, there is a significant increase in the levels of both chylomicrons (lipoprotein particles that carry dietary lipids) and very low-density lipoproteins (VLDLs, lipoprotein particles that carry endogenous lipids produced by the liver). This results in extremely high levels of triglycerides and moderately elevated levels of cholesterol in the blood.

Individuals with Hyperlipoproteinemia Type V are at an increased risk for developing pancreatitis (inflammation of the pancreas), eruptive xanthomas (small, yellowish bumps on the skin caused by cholesterol deposits), and hepatosplenomegaly (enlargement of the liver and spleen). The diagnosis is typically made based on clinical presentation, family history, and laboratory tests that measure lipid levels. Treatment often involves dietary modifications, weight loss, exercise, and medications to lower lipid levels in the blood.

Hyperlipoproteinemia Type III, also known as Broad Beta Disease or Remnant Hyperlipidemia, is a genetic disorder characterized by an increased level of chylomicron remnants and intermediate-density lipoproteins (IDL) in the blood. This results in elevated levels of both low-density lipoprotein (LDL), or "bad" cholesterol, and triglycerides, and decreased levels of high-density lipoprotein (HDL), or "good" cholesterol. The condition can lead to premature atherosclerosis and an increased risk for cardiovascular disease. It is caused by mutations in the APOE gene, which encodes the apolipoprotein E protein, leading to abnormal clearance of lipoproteins from the blood.

Hyperlipoproteinemia Type I, also known as Familial Lipoprotein Lipase Deficiency, is a rare genetic disorder characterized by an absence or deficiency of the enzyme lipoprotein lipase. This enzyme is responsible for breaking down chylomicrons, which are large lipoprotein particles that transport dietary triglycerides from the intestines to the liver and peripheral tissues.

As a result of this deficiency, chylomicrons accumulate in the bloodstream, leading to elevated levels of triglycerides (hypertriglyceridemia) and chylomicrons (chylomiconemia). This condition can cause eruptive xanthomas, which are collections of lipid-laden foam cells that form under the skin, and recurrent pancreatitis, which is inflammation of the pancreas.

Hyperlipoproteinemia Type I is inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene, one from each parent, to develop the condition. Treatment typically involves a low-fat diet and medications to reduce triglyceride levels.

Hyperlipoproteinemia Type IV is a genetic disorder characterized by an increased level of very low-density lipoproteins (VLDL) in the blood. This leads to elevated levels of triglycerides, which are a type of fat found in the blood. The condition is also sometimes referred to as "Fredrickson Type IV."

People with Hyperlipoproteinemia Type IV have an increased risk of developing pancreatitis, a potentially life-threatening inflammation of the pancreas, due to high levels of triglycerides. They may also have an increased risk of cardiovascular disease due to elevated levels of VLDL and other atherogenic lipoproteins.

The condition is usually inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the disorder if one parent has it. However, some cases may be caused by mutations in multiple genes or by environmental factors such as obesity, diabetes, and excessive alcohol consumption.

Treatment for Hyperlipoproteinemia Type IV typically involves lifestyle modifications such as weight loss, exercise, and dietary changes to reduce triglyceride levels. In some cases, medication may be necessary to control the condition.

Hyperlipoproteinemias are medical conditions characterized by elevated levels of lipoproteins in the blood. Lipoproteins are particles that consist of proteins and lipids, which are responsible for transporting all fat molecules, such as cholesterol and triglycerides, around the body within the water outside cells. These lipids cannot dissolve in the blood, so they must be carried by these lipoprotein particles.

There are several types of hyperlipoproteinemias, classified based on the type of lipoprotein that is elevated and the pattern of inheritance. The most commonly recognized classification system is the Fredrickson classification, which includes five main types:

1. Type I - characterized by an excess of chylomicrons, a type of lipoprotein that carries dietary lipids, leading to extremely high levels of triglycerides in the blood. This rare disorder is usually caused by genetic mutations.
2. Type II - divided into two subtypes:
a. Type IIa - characterized by elevated LDL (low-density lipoprotein), or "bad" cholesterol, levels and often associated with premature cardiovascular disease. This condition can be caused by genetic factors, lifestyle choices, or both.
b. Type IIb - marked by increased levels of both LDL cholesterol and VLDL (very low-density lipoprotein), which leads to elevated triglycerides and cholesterol in the blood. This subtype can also be influenced by genetic factors, lifestyle choices, or both.
3. Type III - known as broad beta disease or remnant removal disease, this condition is characterized by an abnormal accumulation of remnant particles from VLDL and IDL (intermediate-density lipoprotein) metabolism, leading to increased levels of both cholesterol and triglycerides. This disorder can be caused by genetic mutations or secondary factors like diabetes, obesity, or hypothyroidism.
4. Type IV - characterized by elevated VLDL particles and high triglyceride levels in the blood. This condition is often associated with metabolic syndrome, obesity, diabetes, and alcohol consumption.
5. Type V - marked by increased VLDL and chylomicrons (lipoprotein particles that transport dietary lipids) in the blood, leading to extremely high triglyceride levels. This rare condition can be caused by genetic factors or secondary factors like diabetes, obesity, alcohol consumption, or uncontrolled lipid absorption.

It is important to note that these types are not mutually exclusive and can coexist in various combinations. Additionally, lifestyle choices such as diet, exercise, smoking, and alcohol consumption can significantly impact lipoprotein levels and contribute to the development of dyslipidemia (abnormal lipid levels).

Blood protein disorders refer to a group of medical conditions that affect the production or function of proteins in the blood. These proteins are crucial for maintaining the proper functioning of the body's immune system, transporting nutrients, and preventing excessive bleeding. Some examples of blood protein disorders include:

1. Hemophilia: A genetic disorder caused by a deficiency or absence of clotting factors in the blood, leading to prolonged bleeding and poor clot formation.
2. Von Willebrand disease: A genetic disorder characterized by abnormal or deficient von Willebrand factor, which is necessary for platelet function and proper clotting.
3. Dysproteinemias: Abnormal levels of certain proteins in the blood, such as immunoglobulins (antibodies) or paraproteins, which can indicate underlying conditions like multiple myeloma or macroglobulinemia.
4. Hypoproteinemia: Low levels of total protein in the blood, often caused by liver disease, malnutrition, or kidney disease.
5. Hyperproteinemia: Elevated levels of total protein in the blood, which can be caused by dehydration, inflammation, or certain types of cancer.
6. Hemoglobinopathies: Genetic disorders affecting the structure and function of hemoglobin, a protein found in red blood cells that carries oxygen throughout the body. Examples include sickle cell anemia and thalassemia.
7. Disorders of complement proteins: Abnormalities in the complement system, which is a group of proteins involved in the immune response, can lead to conditions like autoimmune disorders or recurrent infections.

Treatment for blood protein disorders varies depending on the specific condition and its severity but may include medications, transfusions, or other medical interventions.

Hyperlipoproteinemia Type II, also known as Fredrickson Type II or Familial Combined Hyperlipidemia, is a genetic disorder characterized by elevated levels of low-density lipoprotein (LDL) cholesterol and/or triglycerides in the blood. This condition can lead to an increased risk of developing cardiovascular diseases such as atherosclerosis and coronary artery disease.

The disorder is caused by mutations in several genes involved in lipid metabolism, including APOB, LDLR, PCSK9, and APOE. These genetic defects result in impaired clearance of LDL particles from the bloodstream, leading to their accumulation and increased risk of cardiovascular disease.

Individuals with Hyperlipoproteinemia Type II typically have elevated levels of both LDL cholesterol and triglycerides, although some may only have one or the other elevated. The disorder can present at any age, but it is often diagnosed in adulthood during routine cholesterol screening.

Treatment for Hyperlipoproteinemia Type II typically involves lifestyle modifications such as a heart-healthy diet, regular exercise, and weight loss. Medications such as statins, ezetimibe, and PCSK9 inhibitors may also be prescribed to lower LDL cholesterol levels and reduce the risk of cardiovascular disease.

Collagen Type V is a specific type of collagen, which is a protein that provides structure and strength to connective tissues in the body. Collagen Type V is found in various tissues, including the cornea, blood vessels, and hair. It plays a crucial role in the formation of collagen fibers and helps regulate the diameter of collagen fibrils. Mutations in the genes that encode for Collagen Type V can lead to various connective tissue disorders, such as Ehlers-Danlos syndrome and osteogenesis imperfecta.

Apolipoprotein E2 (ApoE2) is one of the three major isoforms of the apolipoprotein E (ApoE) protein, which is a component of lipoproteins that are involved in the transport and metabolism of cholesterol and other fats in the body. ApoE is produced by the APOE gene, which has three common alleles: ε2, ε3, and ε4.

The ApoE2 protein is encoded by the ε2 allele of the APOE gene. Compared to the other two isoforms (ApoE3 and ApoE4), ApoE2 has a different amino acid at position 112, where it has a cysteine instead of an arginine. This difference affects the protein's ability to interact with other molecules involved in lipid metabolism, such as the low-density lipoprotein receptor (LDLR).

Individuals who inherit two copies of the ε2 allele (ε2/ε2) have a higher risk of developing type III hyperlipoproteinemia, also known as dysbetalipoproteinemia, which is characterized by elevated levels of cholesterol and triglycerides in the blood due to impaired clearance of remnant lipoproteins. However, not all people with the ε2/ε2 genotype develop type III hyperlipoproteinemia, and other genetic and environmental factors may contribute to the development of this condition.

It's worth noting that having one or two copies of the ε2 allele has been associated with a reduced risk of developing Alzheimer's disease, although the mechanism by which ApoE2 protects against Alzheimer's is not fully understood.

VLDL (Very Low-Density Lipoproteins) are a type of lipoprotein that play a crucial role in the transport and metabolism of fat molecules, known as triglycerides, in the body. They are produced by the liver and consist of a core of triglycerides surrounded by a shell of proteins called apolipoproteins, phospholipids, and cholesterol.

VLDL particles are responsible for delivering fat molecules from the liver to peripheral tissues throughout the body, where they can be used as an energy source or stored for later use. During this process, VLDL particles lose triglycerides and acquire more cholesterol, transforming into intermediate-density lipoproteins (IDL) and eventually low-density lipoproteins (LDL), which are also known as "bad" cholesterol.

Elevated levels of VLDL in the blood can contribute to the development of cardiovascular disease due to their association with increased levels of triglycerides and LDL cholesterol, as well as decreased levels of high-density lipoproteins (HDL), which are considered "good" cholesterol.

Hyperlipidemias are a group of disorders characterized by an excess of lipids (fats) or lipoproteins in the blood. These include elevated levels of cholesterol, triglycerides, or both. Hyperlipidemias can be inherited (primary) or caused by other medical conditions (secondary). They are a significant risk factor for developing cardiovascular diseases, such as atherosclerosis and coronary artery disease.

There are two main types of lipids that are commonly measured in the blood: low-density lipoprotein (LDL) cholesterol, often referred to as "bad" cholesterol, and high-density lipoprotein (HDL) cholesterol, known as "good" cholesterol. High levels of LDL cholesterol can lead to the formation of plaques in the arteries, which can narrow or block them and increase the risk of heart attack or stroke. On the other hand, high levels of HDL cholesterol are protective because they help remove LDL cholesterol from the bloodstream.

Triglycerides are another type of lipid that can be measured in the blood. Elevated triglyceride levels can also contribute to the development of cardiovascular disease, particularly when combined with high LDL cholesterol and low HDL cholesterol levels.

Hyperlipidemias are typically diagnosed through a blood test that measures the levels of various lipids and lipoproteins in the blood. Treatment may include lifestyle changes, such as following a healthy diet, getting regular exercise, losing weight, and quitting smoking, as well as medication to lower lipid levels if necessary.

Xanthomatosis is a medical term that refers to the condition characterized by the presence of xanthomas, which are yellowish, fat-laden deposits that form under the skin or in other tissues. These deposits consist of lipids, such as cholesterol and triglycerides, and immune cells called macrophages, which have engulfed the lipids.

Xanthomas can occur in various parts of the body, including the eyelids, tendons, joints, and other areas with connective tissue. They may appear as small papules or larger nodules, and their size and number can vary depending on the severity of the underlying disorder.

Xanthomatosis is often associated with genetic disorders that affect lipid metabolism, such as familial hypercholesterolemia, or with acquired conditions that cause high levels of lipids in the blood, such as diabetes, hypothyroidism, and certain liver diseases. Treatment typically involves addressing the underlying disorder and controlling lipid levels through dietary changes, medications, or a combination of both.

Apolipoprotein E (ApoE) is a protein involved in the metabolism of lipids, particularly cholesterol. It is produced primarily by the liver and is a component of several types of lipoproteins, including very low-density lipoproteins (VLDL) and high-density lipoproteins (HDL).

ApoE plays a crucial role in the transport and uptake of lipids in the body. It binds to specific receptors on cell surfaces, facilitating the delivery of lipids to cells for energy metabolism or storage. ApoE also helps to clear cholesterol from the bloodstream and is involved in the repair and maintenance of tissues.

There are three major isoforms of ApoE, designated ApoE2, ApoE3, and ApoE4, which differ from each other by only a few amino acids. These genetic variations can have significant effects on an individual's risk for developing certain diseases, particularly cardiovascular disease and Alzheimer's disease. For example, individuals who inherit the ApoE4 allele have an increased risk of developing Alzheimer's disease, while those with the ApoE2 allele may have a reduced risk.

In summary, Apolipoprotein E is a protein involved in lipid metabolism and transport, and genetic variations in this protein can influence an individual's risk for certain diseases.

Triglycerides are the most common type of fat in the body, and they're found in the food we eat. They're carried in the bloodstream to provide energy to the cells in our body. High levels of triglycerides in the blood can increase the risk of heart disease, especially in combination with other risk factors such as high LDL (bad) cholesterol, low HDL (good) cholesterol, and high blood pressure.

It's important to note that while triglycerides are a type of fat, they should not be confused with cholesterol, which is a waxy substance found in the cells of our body. Both triglycerides and cholesterol are important for maintaining good health, but high levels of either can increase the risk of heart disease.

Triglyceride levels are measured through a blood test called a lipid panel or lipid profile. A normal triglyceride level is less than 150 mg/dL. Borderline-high levels range from 150 to 199 mg/dL, high levels range from 200 to 499 mg/dL, and very high levels are 500 mg/dL or higher.

Elevated triglycerides can be caused by various factors such as obesity, physical inactivity, excessive alcohol consumption, smoking, and certain medical conditions like diabetes, hypothyroidism, and kidney disease. Medications such as beta-blockers, steroids, and diuretics can also raise triglyceride levels.

Lifestyle changes such as losing weight, exercising regularly, eating a healthy diet low in saturated and trans fats, avoiding excessive alcohol consumption, and quitting smoking can help lower triglyceride levels. In some cases, medication may be necessary to reduce triglycerides to recommended levels.

Lipoproteins are complex particles composed of multiple proteins and lipids (fats) that play a crucial role in the transport and metabolism of fat molecules in the body. They consist of an outer shell of phospholipids, free cholesterols, and apolipoproteins, enclosing a core of triglycerides and cholesteryl esters.

There are several types of lipoproteins, including:

1. Chylomicrons: These are the largest lipoproteins and are responsible for transporting dietary lipids from the intestines to other parts of the body.
2. Very-low-density lipoproteins (VLDL): Produced by the liver, VLDL particles carry triglycerides to peripheral tissues for energy storage or use.
3. Low-density lipoproteins (LDL): Often referred to as "bad cholesterol," LDL particles transport cholesterol from the liver to cells throughout the body. High levels of LDL in the blood can lead to plaque buildup in artery walls and increase the risk of heart disease.
4. High-density lipoproteins (HDL): Known as "good cholesterol," HDL particles help remove excess cholesterol from cells and transport it back to the liver for excretion or recycling. Higher levels of HDL are associated with a lower risk of heart disease.

Understanding lipoproteins and their roles in the body is essential for assessing cardiovascular health and managing risks related to heart disease and stroke.

Apolipoprotein E3 (ApoE3) is one of the three major isoforms of apolipoprotein E (ApoE), a protein involved in the metabolism of lipids, particularly cholesterol. ApoE is produced by the APOE gene, which has three common alleles: ε2, ε3, and ε4. These alleles result in three main isoforms of the protein: ApoE2, ApoE3, and ApoE4.

ApoE3 is the most common isoform, found in approximately 77-78% of the population. It has a slightly different amino acid sequence compared to ApoE2 and ApoE4, which can affect its function. ApoE3 is thought to play a neutral or protective role in the risk of developing Alzheimer's disease and cardiovascular diseases, although some studies suggest that it may have a mildly favorable effect on lipid metabolism compared to ApoE4.

Familial Combined Hyperlipidemia (FCH) is a genetic disorder characterized by high levels of cholesterol and/or fats (lipids) in the blood. It is one of the most common inherited lipid disorders, affecting approximately 1 in 200 to 1 in 500 people.

FCH is caused by mutations in several genes involved in lipid metabolism, including the APOB, LDLR, and PCSK9 genes. These genetic defects lead to increased levels of low-density lipoprotein (LDL) cholesterol, triglycerides, or both in the blood.

Individuals with FCH may have elevated levels of total cholesterol, LDL cholesterol, and/or triglycerides, which can increase their risk for premature atherosclerosis and cardiovascular disease. The condition often presents in early adulthood and may manifest as mixed hyperlipidemia (high levels of both LDL cholesterol and triglycerides) or isolated hypercholesterolemia (high levels of LDL cholesterol only).

Familial combined hyperlipidemia is typically managed with lifestyle modifications, such as a heart-healthy diet, regular exercise, and weight management. Medications, such as statins, may also be prescribed to lower lipid levels and reduce the risk of cardiovascular disease. Regular monitoring of lipid levels is essential for effective management and prevention of complications associated with FCH.

Cholesterol is a type of lipid (fat) molecule that is an essential component of cell membranes and is also used to make certain hormones and vitamins in the body. It is produced by the liver and is also obtained from animal-derived foods such as meat, dairy products, and eggs.

Cholesterol does not mix with blood, so it is transported through the bloodstream by lipoproteins, which are particles made up of both lipids and proteins. There are two main types of lipoproteins that carry cholesterol: low-density lipoproteins (LDL), also known as "bad" cholesterol, and high-density lipoproteins (HDL), also known as "good" cholesterol.

High levels of LDL cholesterol in the blood can lead to a buildup of cholesterol in the walls of the arteries, increasing the risk of heart disease and stroke. On the other hand, high levels of HDL cholesterol are associated with a lower risk of these conditions because HDL helps remove LDL cholesterol from the bloodstream and transport it back to the liver for disposal.

It is important to maintain healthy levels of cholesterol through a balanced diet, regular exercise, and sometimes medication if necessary. Regular screening is also recommended to monitor cholesterol levels and prevent health complications.

Lipoprotein lipase (LPL) is an enzyme that plays a crucial role in the metabolism of lipids. It is responsible for breaking down triglycerides, which are the main constituent of dietary fats and chylomicrons, into fatty acids and glycerol. These products are then taken up by cells for energy production or storage.

LPL is synthesized in various tissues, including muscle and fat, where it is attached to the inner lining of blood vessels (endothelium). The enzyme is activated when it comes into contact with lipoprotein particles, such as chylomicrons and very-low-density lipoproteins (VLDL), which transport triglycerides in the bloodstream.

Deficiencies or mutations in LPL can lead to various metabolic disorders, including hypertriglyceridemia, a condition characterized by high levels of triglycerides in the blood. Conversely, overexpression of LPL has been associated with increased risk of atherosclerosis due to excessive uptake of fatty acids by macrophages and their conversion into foam cells, which contribute to plaque formation in the arteries.

Apolipoproteins are a group of proteins that are associated with lipids (fats) in the body and play a crucial role in the metabolism, transportation, and regulation of lipids. They are structural components of lipoprotein particles, which are complexes of lipids and proteins that transport lipids in the bloodstream.

There are several types of apolipoproteins, including ApoA, ApoB, ApoC, ApoD, ApoE, and others. Each type has a specific function in lipid metabolism. For example, ApoA is a major component of high-density lipoprotein (HDL), often referred to as "good cholesterol," and helps remove excess cholesterol from cells and tissues and transport it to the liver for excretion. ApoB, on the other hand, is a major component of low-density lipoprotein (LDL), or "bad cholesterol," and plays a role in the delivery of cholesterol to cells and tissues.

Abnormal levels of apolipoproteins or dysfunctional forms of these proteins have been linked to various diseases, including cardiovascular disease, Alzheimer's disease, and metabolic disorders such as diabetes. Therefore, measuring apolipoprotein levels in the blood can provide valuable information for diagnosing and monitoring these conditions.

Low-density lipoproteins (LDL), also known as "bad cholesterol," are a type of lipoprotein that carry cholesterol and other fats from the liver to cells throughout the body. High levels of LDL in the blood can lead to the buildup of cholesterol in the walls of the arteries, which can increase the risk of heart disease and stroke.

Lipoproteins are complex particles composed of proteins (apolipoproteins) and lipids (cholesterol, triglycerides, and phospholipids) that are responsible for transporting fat molecules around the body in the bloodstream. LDL is one type of lipoprotein, along with high-density lipoproteins (HDL), very low-density lipoproteins (VLDL), and chylomicrons.

LDL particles are smaller than HDL particles and can easily penetrate the artery walls, leading to the formation of plaques that can narrow or block the arteries. Therefore, maintaining healthy levels of LDL in the blood is essential for preventing cardiovascular disease.

Chylomicrons are a type of lipoprotein that are responsible for carrying dietary lipids, such as triglycerides and cholesterol, from the intestines to other parts of the body through the lymphatic system and bloodstream. They are the largest lipoproteins and are composed of an outer layer of phospholipids, free cholesterol, and apolipoproteins, which surrounds a core of triglycerides and cholesteryl esters. Chylomicrons are produced in the intestinal mucosa after a meal containing fat, and their production is stimulated by the hormone cholecystokinin. Once in the bloodstream, chylomicrons interact with other lipoproteins and enzymes to deliver their lipid cargo to various tissues, including muscle and adipose tissue, where they are used for energy or stored for later use.

Blood protein electrophoresis (BPE) is a laboratory test that separates and measures the different proteins in the blood, such as albumin, alpha-1 globulins, alpha-2 globulins, beta globulins, and gamma globulins. This test is often used to help diagnose or monitor conditions related to abnormal protein levels, such as multiple myeloma, macroglobulinemia, and other plasma cell disorders.

In this test, a sample of the patient's blood is placed on a special gel and an electric current is applied. The proteins in the blood migrate through the gel based on their electrical charge and size, creating bands that can be visualized and measured. By comparing the band patterns to reference ranges, doctors can identify any abnormal protein levels or ratios, which may indicate underlying medical conditions.

It's important to note that while BPE is a useful diagnostic tool, it should be interpreted in conjunction with other clinical findings and laboratory tests for accurate diagnosis and management of the patient's condition.

Apolipoprotein C (apoC) is a group of proteins that are associated with lipoproteins, which are complex particles composed of lipids and proteins that play a crucial role in the transport and metabolism of lipids in the body. There are three main types of apoC proteins: apoC-I, apoC-II, and apoC-III.

ApoC-I is involved in the regulation of lipoprotein metabolism and has been shown to inhibit the activity of cholesteryl ester transfer protein (CETP), which is an enzyme that facilitates the transfer of cholesteryl esters from high-density lipoproteins (HDL) to low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL).

ApoC-II is a cofactor for lipoprotein lipase, an enzyme that hydrolyzes triglycerides in chylomicrons and VLDL, leading to the formation of smaller, denser lipoproteins. A deficiency in apoC-II can lead to hypertriglyceridemia, a condition characterized by elevated levels of triglycerides in the blood.

ApoC-III is also involved in the regulation of lipoprotein metabolism and has been shown to inhibit the activity of lipoprotein lipase and CETP. Elevated levels of apoC-III have been associated with an increased risk of cardiovascular disease, possibly due to its effects on lipoprotein metabolism.

In summary, apolipoprotein C is a group of proteins that are involved in the regulation of lipoprotein metabolism and have important roles in the transport and metabolism of lipids in the body.

VLDL, or very low-density lipoproteins, are a type of lipoprotein that carries triglycerides and cholesterol from the liver to other parts of the body. Cholesterol is a fatty substance found in the blood, and VLDL contains both triglycerides and cholesterol.

Cholesterol itself cannot dissolve in the blood and needs to be transported around the body by lipoproteins, which are protein molecules that encapsulate and carry fat molecules, such as cholesterol and triglycerides, through the bloodstream. VLDL is one of several types of lipoproteins, including low-density lipoproteins (LDL) and high-density lipoproteins (HDL).

Elevated levels of VLDL in the blood can contribute to the development of atherosclerosis, a condition characterized by the buildup of plaque in the arteries, which can increase the risk of heart disease and stroke. Therefore, maintaining healthy levels of VLDL and other lipoproteins is an important part of overall cardiovascular health.

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Feussner G, Feussner V, Hoffmann MM, Lohrmann J, Wieland H, März W (1998). "Molecular basis of type III hyperlipoproteinemia in ... Defects in APOE result in familial dysbetalipoproteinemia aka type III hyperlipoproteinemia (HLP III), in which increased ... December 1996). "Apo E variants in patients with type III hyperlipoproteinemia". Atherosclerosis. 127 (2): 273-282. doi:10.1016 ... September 1992). "Apolipoprotein E1 Lys-146----Glu with type III hyperlipoproteinemia". Biochimica et Biophysica Acta. 1128 (1 ...
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... hyperlipoproteinemia type IV MeSH C18.452.339.750.495 - hyperlipoproteinemia type V MeSH C18.452.339.750.552 - lipoprotein ... hyperlipoproteinemia type IV MeSH C18.452.648.556.484 - hyperlipoproteinemia type III MeSH C18.452.648.556.490 - ... hyperlipoproteinemia type IV MeSH C18.452.648.556.495 - hyperlipoproteinemia type V MeSH C18.452.648.556.500 - ... hyperlipoproteinemia type IV MeSH C18.452.339.500.851 - hypertriglyceridemia MeSH C18.452.339.750 - hyperlipoproteinemia MeSH ...
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The metabolic syndrome quintuples the risk of type 2 diabetes mellitus. Type 2 diabetes is considered a complication of ... Singer P (May 1977). "[Diagnosis of primary hyperlipoproteinemias]". Zeitschrift für die Gesamte Innere Medizin und Ihre ... HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease (CVD), type 2 ... Metabolic syndrome can lead to several serious and chronic complications, including type-2 diabetes, cardiovascular diseases, ...
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The phenotypes include types I, IIa, IIb, III, IV, and V dyslipidemias. Familial hypertriglyceridemia is considered a type IV ... Primary hyperlipoproteinemia Familial apoprotein CII deficiency Skin lesion Ripatti P, Rämö JT, Mars NJ, Fu Y, Lin J, Söderlund ... Familial hypertriglyceridemia (type IV familial dyslipidemia) is a genetic disorder characterized by the liver overproducing ... 1 November 2009). "A polygenic basis for four classical Fredrickson hyperlipoproteinemia phenotypes that are characterized by ...
... type III hyperlipoproteinemia (HLP) having the apolipoprotein (apo) E2/2 phenotype were studied to determine the occurrence of ... Genetics of type III hyperlipoproteinemia G Feussner 1 , S Piesch, J Dobmeyer, C Fischer ... Genetics of type III hyperlipoproteinemia G Feussner et al. Genet Epidemiol. 1997. ... Genetics of hyperlipoproteinemia type III. Utermann G, Vogelberg KH, Steinmetz A, Schoenborn W, Pruin N, Jaeschke M, Hees M, ...
Home / Products tagged "Type III hyperlipoproteinemia". Type III hyperlipoproteinemia. Showing the single result ...
Type I hyperlipoproteinemia (pure hyperchylomicronemia). To make a definitive diagnosis of type I hyperlipidemia, a deficiency ... Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal metabolism. Scriver ... Feussner G, Piesch S, Dobmeyer J, Fischer C. Genetics of type III hyperlipoproteinemia. Genet Epidemiol. 1997. 14(3):283-97. [ ... Pathogenesis of type III hyperlipoproteinemia (dysbetalipoproteinemia). Questions, quandaries, and paradoxes. J Lipid Res. 1999 ...
Hyperlipoproteinemia Type IIa (Elevated LDL) and Hyperlipoproteinemia Type IIb (Elevated LDL + VLDL); plus renal, liver and ... Usual Adult Dose for Hyperlipoproteinemia Type IIb (Elevated LDL + VLDL). Initial: 20 mg-500 mg orally once daily at bedtime. ... Usual Adult Dose for Hyperlipoproteinemia Type IIa (Elevated LDL). Initial: 20 mg-500 mg orally once daily at bedtime. ... Usual Adult Dose for Hyperlipoproteinemia. Initial: 20 mg-500 mg orally once daily at bedtime. Maintenance: 20 mg-500 mg to 40 ...
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14.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) 14.5 Homozygous Familial Hypercholesterolemia 14.6 ... 1.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia). CRESTOR is indicated as an adjunct to diet for the ... adult patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.4) •. adult ... 1.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) 1.5 Adult Patients with Homozygous Familial ...
14.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) 14.5 Homozygous Familial Hypercholesterolemia 16 HOW ... 1.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia). Rosuvastatin tablets are indicated as an adjunct to diet ... 1.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) 1.5 Adult Patients with Homozygous Familial ... 14.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia). In a randomized, multicenter, double-blind crossover study ...
14.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) 14.5 Homozygous Familial Hypercholesterolemia 16 HOW ... 1.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia). Rosuvastatin calcium tablets are indicated as an adjunct to ... 1.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) 1.5 Adult Patients with Homozygous Familial ... 14.4 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia). In a randomized, multicenter, double-blind crossover study ...
Type III Hyperlipoproteinemia. ApoE. Individuals with family history or clinical symptoms of CVD. Diagnosis of Type III ... Diabetes, Type II. TCF7L2. General population. Predictive testing/risk assessment. ,Menopause, Early. Fragile X or FMR1. Women ... Diabetes, Type II. pPARG2. 1) Individuals with clinical suspicion or family history of diabetes; 2) General population. 1) ... Individuals with clinical suspicion of Hereditary hemorrhagic telangiectasia type 2 (HHT2). Diagnosis. ...
... frequently observed in type I and V hyperlipoproteinemias but rarely observed in patients with type IV hyperlipoproteinemia. ... frequently observed in type I and V hyperlipoproteinemias but rarely observed in patients with type IV hyperlipoproteinemia. ... frequently observed in type I and V hyperlipoproteinemias but rarely observed in patients with type IV hyperlipoproteinemia. ... frequently observed in type I and V hyperlipoproteinemias but rarely observed in patients with type IV hyperlipoproteinemia. ...
Type I hyperlipoproteinemia; Familial chylomicronemia; Familial LPL deficiency. Images. *. Coronary artery disease ...
Hyperlipoproteinemia Type II / diagnosis* * Hyperlipoproteinemia Type II / genetics * Male * Middle Aged * Primary Health Care ...
Hyperlipoproteinemia, type I MedGen: C0023817 OMIM: 238600 GeneReviews: Familial Lipoprotein Lipase Deficiency ... Severe mutations that cause LPL deficiency result in type I hyperlipoproteinemia, while less extreme mutations in LPL are ... Gene type. protein coding. RefSeq status. REVIEWED. Organism. Homo sapiens Lineage. Eukaryota; Metazoa; Chordata; Craniata; ... Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels.. EBI GWAS Catalog. EBI GWAS ...
Drug therapy is not indicated for patients with Type I hyperlipoproteinemia, who have elevations of chylomicrons and plasma ... Some Type IV patients with triglycerides under 1000 mg/dL may, through dietary or alcoholic indiscretion, convert to a Type V ... If a woman receiving nicotinic acid for primary hypercholesterolemia (Types IIa or IIb) becomes pregnant, the drug should be ... If a woman being treated with nicotinic acid for hypertriglyceridemia (Types IV or V) conceives, the benefits and risks of ...
Genetic Testing Registry: Hyperlipoproteinemia, type I Genetic and Rare Diseases Information Center. *Familial lipoprotein ...
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Type IV and Type V hyperlipidemia. EXCLUSION CRITERIA: Inability to provide informed consent.. --Back to Top-- ... Type: No longer recruiting/follow-up only Gender: Male & Female Min Age: 2 Max Age: 99 ... Type III Hyperlipoproteinemia; Plasma Lipoproteins Condition(s). Evaluation of Plasma Lipoproteins Investigational Drug(s) ...
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has a disorder known as type 1 hyperlipoproteinemia. *has severe liver disease, kidney disease, or gallbladder disease ... Talk to your doctor about the risks and benefits of taking the two types of medications together. ... has had a sunburn type reaction after taking any fibrate medication or ketoprofen ...
Type III hyperlipoproteinemia (dysbetalipoproteinemia): the role of apolipoprotein E in normal and abnormal metabolism. Scriver ... Feussner G, Piesch S, Dobmeyer J, Fischer C. Genetics of type III hyperlipoproteinemia. Genet Epidemiol. 1997. 14(3):283-97. [ ... Pathogenesis of type III hyperlipoproteinemia (dysbetalipoproteinemia). Questions, quandaries, and paradoxes. J Lipid Res. 1999 ... Modulation of the type III hyperlipoproteinemic phenotype by estrogen and occurrence of spontaneous atherosclerosis. J Biol ...
Nephrology, Rheumatology, Hematology 1. Inherited kidney disease (polycystic kidney disease - autosomal dominant type, type IV ... Hyperlipoproteinemia and dyslipoproteinemia (classification, diagnosis, treatment) 26. Metabolic syndrome 27. Imaging and ... 0/0/0. 4 credit(s). Type of Completion: zk (examination).. Taught in person.. Teacher(s). prof. MUDr. Zdeněk Adam, CSc. ( ... Acute and chronic viral hepatitis (type A, B, C, D, E and other viral infections of the liver) 21. Jaundice - pathophysiology ...
Hyperlipoproteinemia Type II (Familial Hypercholesterolemia) 01/2013. 1. Hypercholesterolemia 01/2013. 1. Acute Coronary ...
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Hyperlipoproteinemia Type II* / chemically induced Actions. * Search in PubMed * Search in MeSH ...
is now FDA approved for the diagnosis of type III hyperlipoproteinemia. or dysbetalipoproteinemia as well as for CHD risk ... THE ROLE OF NONESTERIFIED FATTY ACIDS IN THE PATHOGENESIS OF THE INSULIN RESISTANCE OF TYPE 2 DIABETES MELLITUS. ... Type 2 diabetes is associated with a two-fold increased risk for CHD. In most studies, the relative risk of CHD is greater in ... In 14 data sets taken from placebo-controlled, randomized trials in patients with type 2 diabetes, an average of 3.7 g of w3 FA ...
Hyperlipoproteinemia (Type V),e,,,1,0,1,,, 409,20756,Read Directions,z,,,1,1,2,,, 410,16331,Amniotic Fluid Color,c,,AMN; ... Hyperlipoproteinemia (Type IV),e,,,1,0,1,,, 516,10337,Serous Cystadenocarcinoma,o,1462,,1,0,1,,, 517,29992,Assault - Other ... Hyperlipoproteinemia (Type I),e,,,1,0,1,,, 2392,10440,Malignant Chondroblastoma,o,1404,,1,0,1,,, 2393,10439,Chondroblastoma,y, ... Firearm Type,z,,,1,1,2,,, 3346,13453,Cesarean Section for CPD,c,,,1,1,2,,, 3347,9771,Polyphagia,e,8703,,0,0,0,,, 3349,14710, ...
Soybean-protein diet in the treatment of type-II hyperlipoproteinaemia. Lancet 1977;1:275-7. ... Low-carbohydrate-diet score and risk of type 2 diabetes in women. Am J Clin Nutr 2008;87:339-46. ... Regular consumption of nuts is associated with a lower risk of cardiovascular disease in women with type 2 diabetes. J Nutr ... Walnut consumption is associated with lower risk of type 2 diabetes in women. J Nutr 2013;143:512-18. ...
Migratory polyarthritis in familial hypercholesterolemia (type II hyperlipoproteinemia). Arthritis Rheum. 1968 Jun. 11(3):385- ...
  • Lipoprotein disorders (also referred to as Lipid disorders, or Dyslipidemias, or Dyslipoproteinemias ) were first classified in 1967 into different phenotypes by Fredrickson according to the type of lipoproteins that are affected. (wikidoc.org)
  • Hyperlipoproteinemias generally cause elevations in the affected lipids/lipoproteins and hypolipoproteinemia s generally cause reductions in the affected lipids/lipoproteins. (wikidoc.org)
  • Hyperlipoproteinemia type III is one disease characterized by elevated triglycerides and beta-very low-density lipoproteins. (genebase.com)
  • Type IIb hyperlipoproteinemia is caused by mutation in the receptor-binding domain of APOLIPOPROTEIN B-100 which is a major component of LOW-DENSITY LIPOPROTEINS and VERY-LOW-DENSITY LIPOPROTEINS resulting in reduced clearance of these lipoproteins. (nih.gov)
  • Distribution of apolipoprotein(a) in the plasma from patients with lipoprotein lipase deficiency and with type III hyperlipoproteinemia. (jci.org)
  • Biophysical analysis of apolipoprotein E3 variants linked with development of type III hyperlipoproteinemia. (harvard.edu)
  • Hyperlipoproteinemia type II, also known as familial hypercholesterolemia (FH), is a genetic condition characterized by high cholesterol concentrations, specifically elevated levels of low-density lipoprotein (LDL), often referred to as bad cholesterol. (imarcgroup.com)
  • Type IV hyperlipoproteinemia is the most typical form of hyperlipidemia, marked by hypertriglyceridemia and moderate hypercholesterolemia. (industryarc.com)
  • AROAPOC-3 is an antisense rnai oligonucleotide commercialized by Arrowhead Pharmaceuticals , with a leading Phase III program in Familial Chylomicronemia (Type I Hyperlipoproteinemia). (pharmaceutical-technology.com)
  • We have determined the phenotype, concentration, and distribution of apo(a) in plasma from patients with lipoprotein lipase (LPL) deficiency (type I hyperlipoproteinemia, n = 14), in apo E 2/2 homozygotes with type III hyperlipoproteinemia (n = 12) and in controls (n = 16). (jci.org)
  • Hyperlipoproteinemia type 1 is caused due to deficiency of lipoprotein lipase. (openpr.com)
  • Fatty liver hepatitis and type 5 hyperlipoproteinemia in juvenile diabetes mellitus. (nih.gov)
  • A 28-year-old man with poorly controlled juvenile-onset diabetes mellitus presented with jaundice and type 5 hyperlipoproteinemia . (nih.gov)
  • This review will summarize the updated research progress on APOE functions and its role in Alzheimer's disease, Parkinson's disease, cardiovascular diseases, multiple sclerosis, type 2 diabetes mellitus, Type III hyperlipoproteinemia, vascular dementia, and ischemic stroke. (dovepress.com)
  • 3 In this review, we discuss the biological functions of human APOE and its role in Alzheimer's disease (AD), Parkinson's disease (PD), cardiovascular diseases (CVD), multiple sclerosis (MS), type 2 diabetes mellitus (T2DM), vascular dementia (VD), and ischemic (occlusive) stroke (IS). (dovepress.com)
  • Orlistat also helps in reducing blood pressure and prevents the onset of type 2 diabetes in obese people. (openpr.com)
  • As apoE2 binds defectively to LDL receptors, apoE2 homozygosity can precipitate type III hyperlipoproteinemia, however, only occurs when another condition, including: diabetes, oestrogen deficiency, hypothyroidism, or obesity, leads to the overproduction of VLDL or fewer LDL receptors, overwhelming the limited ability of apoE2 to mediate the clearance of triglyceride-rich and cholesterol-rich β-VLDL. (randox.com)
  • 2. Uncontrolled or newly diagnosed (=3 months since diagnosis) Type 2 diabetes mellitus as determined by the Principal Investigator. (who.int)
  • 300 mg/dL or those who have type 3 hyperlipoproteinemia owing to an increased secretion of triglyceride-rich particles, which can produce marked hypertriglyceridemia in some cases. (medscape.com)
  • Considering apo(a) type, the plasma concentration of apo(a) was normal in type III patients but significantly reduced in LPL deficiency. (jci.org)
  • However, APOE2 carriers could develop type III hyperlipoproteinemia and exhibit increased risk of cerebrovascular diseases and neurological disorders. (j-alz.com)
  • Who is working on investigational drugs for Hyperlipoproteinemia Type IV? (drugpatentwatch.com)
  • Drugs and a special diet may help, but the chance of a cure is uncertain because the person with Type V risks developing pancreatitis. (pharmacy-online.ca)
  • Xanthomas commonly associated with hypercholesterinaemia and increased levels of LDL (low density lipoprotein) in type II and type III hyperlipoproteinaemia and in secondary hyperlipidaemia. (dermis.net)
  • Hyperlipoproteinemia has been thought to be a major risk factor for coronary arterial disease, which is frequently associated with patients with primary gout. (go.jp)
  • If there is no contributing problem, the primary treatment for Types II, III, and IV is often dietary management - namely restricting cholesterol intake. (pharmacy-online.ca)
  • Additionally, the emerging application of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors via subcutaneous injections to enhance treatment adherence compared to several other injectable medications is expected to drive the hyperlipoproteinemia type II market during the forecast period. (imarcgroup.com)
  • 10-year Global patient forecast for Hyperlipoproteinemia Type 1. (blueprintorphan.com)
  • SLx-4090 is used to treat high blood fat level mostly observed in hyperlipoproteinemia type 1 patients. (openpr.com)
  • In the previous study we demonstrated that type IIb and IV hyperlipoproteinemia coexist frequently in gouty patients. (go.jp)
  • The plasma lipoprotein composition of six patients with mixed hyperlipoproteinemia (MH) was investigated in a study of influence of apoprotein content and lipase activities on mechanisms of plasma triglyceride (TG) production and removal. (utmb.edu)
  • The 7 major hyperlipoproteinemia type II markets are expected to exhibit a CAGR of 7.07% during 2023-2033. (imarcgroup.com)
  • The most effective treatment for Type V hyperlipoproteinemia is often weight reduction and long-term maintenance of a low-fat diet. (pharmacy-online.ca)
  • Secondly, Fredrickson's classification of hyperlipoproteinemia s took into consideration the elevation in chylomicrons , LDL , VLDL but did not include abnormalities in HDL levels. (wikidoc.org)
  • According to the report the United States has the largest patient pool for hyperlipoproteinemia type II and also represents the largest market for its treatment. (imarcgroup.com)
  • Orlistat is used for the treatment of hyperlipoproteinemia type 1. (openpr.com)
  • IMARC Group's new report provides an exhaustive analysis of the hyperlipoproteinemia type II market in the United States, EU5 (Germany, Spain, Italy, France, and United Kingdom) and Japan. (imarcgroup.com)
  • This report provides comprehensive information on the therapeutic development for Post-Operative Pain, complete with comparative analysis at various stages, therapeutics assessment by drug target, mechanism of action (MoA), route of administration (RoA) and molecule type, along with latest updates, and featured news and press releases. (powershow.com)
  • Pain, complete with comparative analysis at various stages, therapeutics assessment by drug target, mechanism of action (MoA), route of administration (RoA) and molecule type, along with latest updates, and featured news and press releases. (powershow.com)
  • Xanthomas are one of types of skin lesions that may occur in this situation. (wikipedia.org)
  • Fasting blood samples were obtained initially and at monthly intervals following institution of a low fat, low carbohydrate, Type V diet. (utmb.edu)
  • The rising cases of genetic mutations, which can affect the body's ability to efficiently remove LDL cholesterol from the blood, thereby leading to its accumulation, are primarily driving the hyperlipoproteinemia type II market. (imarcgroup.com)
  • The contents of these tape files are presented in the Outline of Items and Codes for each record type. (cdc.gov)
  • One hundred forty-seven relatives of 43 patients with "classical" type III hyperlipoproteinemia (HLP) having the apolipoprotein (apo) E2/2 phenotype were studied to determine the occurrence of hyperlipidemia and the presence of further possible genes for lipoprotein disorders in these families. (nih.gov)
  • Nicotinic acid is also indicated as adjunctive therapy for the treatment of adult patients with very high serum triglyceride levels (Types IV and V hyperlipidemia) † who present a risk of pancreatitis and who do not respond adequately to a determined dietary effort to control them. (rxlist.com)
  • Plasma triglyceride levels greater than 150 mg/dl - includes patients with deficiency of lipoprotein lipase, hepatic lipase or apoC-II, dysbetalipoproteinemia, Type IV and Type V hyperlipidemia. (nih.gov)
  • Even without a definitive diagnosis from the workup, treatment of presumed dysbetalipoproteinemia may proceed, because other lipid disorders, such as type IIb hyperlipidemia produce similar elevations in cholesterol and triglyceride levels and will respond to the same medical interventions. (medscape.com)
  • Hyperlipoproteinemia kind V, also called blended hyperlipoproteinemia familial or blended hyperlipidemia, is very similar to sort I, but with high VLDL in addition to chylomicrons. (7red.com)
  • A severe type of hyperlipidemia, sometimes familial, that is characterized by the elevation of both plasma CHYLOMICRONS and TRIGLYCERIDES contained in VERY-LOW-DENSITY LIPOPROTEINS. (bvsalud.org)
  • The only procedure that reliably distinguishes between a mixed hyperlipoproteinemia (increased LDL cholesterol and triglycerides) and type III hyperlipoproteinemia (increased IDL) is beta quantification (lipoprotein electrophoresis). (medscape.com)
  • Niacor ( niacin ), also called nicotinic acid, is a B vitamin (vitamin B3) used to treat and prevent a lack of natural niacin in the body, and to lower cholesterol and triglycerides (types of fat) in the blood. (rxlist.com)
  • Some Type IV patients with triglycerides under 1000 mg/dL may, through dietary or alcoholic indiscretion, convert to a Type V pattern with massive triglyceride elevations accompanying fasting chylomicronemia, but the influence of nicotinic acid therapy on the risk of pancreatitis in such situations has not been adequately studied. (rxlist.com)
  • Drug therapy is not indicated for patients with Type I hyperlipoproteinemia, who have elevations of chylomicrons and plasma triglycerides, but who have normal levels of VLDL. (rxlist.com)
  • Hyperlipoproteinemia type III occurs due to the diminished metabolism of cholesterol and triglycerides in the blood. (cardiovasculardna.com)
  • Apo E levels are measured for diagnosing hyperlipoproteinemia in patients with increase plasma triglycerides and cholesterol. (meridianbioscience.com)
  • It works by blocking the production of certain types of cholesterol, especially the type known as triglycerides . (pocketpills.com)
  • Both type I and II of DM are risk factors for coronary artery disease (4) but type I patients presents cardiovascular diseases in younger ages than type II (5). (ispub.com)
  • Coronary artery lesions are classified regarding their complexity into three major types, according to the classification by American College of Cardiology (ACC) and American Heart Association (AHA) (8). (ispub.com)
  • Atorvastatin is used to treat high cholesterol, and to lower the risk of stroke, heart attack, or other heart complications in people with type 2 diabetes, coronary heart disease, or other risk factors. (cue-state-photography.de)
  • Also often known as broad beta illness or dysbetalipoproteinemia, the commonest trigger for this type is the presence of ApoE E2/E2 genotype. (7red.com)
  • We report a case of eruptive xanthoma with type IV hyperlipoproteinemia and Koebner phenomenon in a 28-year-old Korean male. (elsevierpure.com)
  • However, only a small proportion of people carrying this genotype actually develop hyperlipoproteinemia, so other genetic, environmental or hormonal factors are also thought to play a role. (cardiovasculardna.com)
  • If the direct LDL cholesterol is significantly lower than the calculated LDL cholesterol, a diagnosis of type IIIhyperlipoproteinemia is likely. (medscape.com)
  • type II is similar but is an X-linked disorder. (theodora.com)
  • The defective binding of apolipoprotein (apo) E2 to lipoprotein receptors, an underlying cause of type III hyperlipoproteinemia, results from replacement of Arg 158 with Cys, disrupting the naturally occurring salt bridge between Asp 154 and Arg 158. (rcsb.org)
  • It is a hyperlipoproteinemia type II A, diagnosed by: elevated serum low-density lipoprotein cholesterol (LDLc) with normal high-density lipoprotein cholesterol (HDLc), clinical aspect (xanthodermia), clear serum at direct examination. (hovawartclub.hu)
  • Clinical features of Mexican patients with Mucopolysaccharidosis type I. (geneticsmr.com)
  • Patients should avoid alcohol and estrogen in certain types of hyperlipoproteinemias. (medscape.com)
  • Besides homozygosity for a receptor binding-defective isoform of apo E (apo E2), additional genes for familial lipoprotein disorders might operate in the pathogenesis of type III HLP. (nih.gov)
  • Specialized lipid centers should be contacted if type IIb or III must be confirmed. (medscape.com)
  • Hyperlipoproteinemia sort II is further classified into sorts IIa and IIb, depending mainly on whether elevation in the triglyceride stage occurs in addition to LDL ldl cholesterol. (7red.com)
  • Its bitter tasting leaves have been used in traditional medicine and contain labdane-type diterpene lactone andrographolide. (nih.gov)
  • Xanthomas are one of types of skin lesions that may occur in this situation. (wikipedia.org)
  • Each type of medication will also be imprinted with a unique code. (pfotenengel-ev.de)