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A General Clinical And Medical Overview Of Hyperlipidemias As Metabolic Disorders II

Updated on February 18, 2014

Hypercholesterolemia

Source
Source

Hyperlipidemia

Hyperlipidemias may be primary or secondary. In the primary hyperlipidemias, genetic factors may be prominent. Environmental factors such as obesity, high saturated fat diet, and smoking aggravate the disorder. Primary hyperlipidemias may be further classified into three groups.

Group I: This consists of hypercholesterolemia (280 to 400 mg/dl, 7 to 10 mmol/liter) with a clear serum, normal triglyceride levels, and increase in LDL (beta lipoproteins). In the majority of cases, environmental factors like high saturated fat diet and smoking are seen to aggravate the condition. For a long time, the condition is asymptomatic, but 50% develop Ischemic heart disease by the age of 50 years.

The condition occurs as an autosomally dominant inherited disorder in 5% of subjects. They show very high serum cholesterol levels (320 – 640 mg per dl in heterozygotes and 640- 1280 mg/dl in homozygotes). Xanthomas and arthritis are common. Xanthomas are deposits of cholesterol seen as yellowish nodular masses to several centimeters. They develop insidiously and are painless. The common types are xanthoma tendinosum (over the tendo- Achilles, extensor tendons of the hand, etc), xanthoma tuberosum over the boney prominences (around the elbow, knees, iliac crest, etc), xanthoma planum (plaque-like), striate xanthoma along the palmar creases, or as popular eruptions (eruptive xanthoma). Soometimes, they ulcerate and discharge greasy material. Some may be calcified. Histology shows collections of lipid-laden cells.

Many subjects may show xanthelasma. These are yellowish plaque-like lesions seen on the medial aspects of the upper and lower eyelids. Though these show a strong association with hypercholesterolemia, they may also be seen in persons with normal cholesterol levels. Corneal arcus occurs as a grayish ring along the periphery of the cornea. A clear zone of cornea can be seen outside the arcus and this feature distinguishes corneal arcus from other lesions like Kayser-Fleischer ring. Corneal arcus is seen to develop in the majority of persons with age, but premature occurrence of arcus has been associated with the presence of hypercholesterolemia, especially LDL, cholesterol.

Group II: Consists of chylomicronemia and this results from the deficiency of extrahepatic lipoprotein lipase. This is rare.

Fredrickson’s Classification

Lipoprotein pattern
Lipoprotein
Group
Type 1
Chylomicron
Group III
Type 2a
LDL
Group I
Type 2b
LDL and VLDL
 
Type 3
remnants
Group II
Type 4
VLDL
 
Type 5
VLDL and Chylomicrons
 
Fredrcikson has suggested a classification which includes six groups based on the serum levels of lipids and lipoproteins, estimated in the fasting state.

Secondary Hyperlipidemias

Secondary hyperlipoproteinamias out-number the primary types. In the majority of cases, LDL cholesterol is increased in the serum. The risk of coronary, cerebral, renal and peripheral arterial disease are high irrespective of the primary cause and this risk can be brought down by appropriate therapy.

The seconday types are seen in diabetes mellitus, hypothyroidism, nephrotic syndrome, biliary obstruction, pancreatitis or as a side effect of drugs such as estrogens and corticosteroids. In all subjects with hyperlipidemias, primary causes should be looked for and attended to.

Smoking Aggravates Hyperlipidemia

In the majority of cases, environmental factors like high saturated fat diet and smoking are seen to aggravate the condition. For a long time, the condition is asymptomatic, but 50% develop Ischemic heart disease by the age of 50 years.
In the majority of cases, environmental factors like high saturated fat diet and smoking are seen to aggravate the condition. For a long time, the condition is asymptomatic, but 50% develop Ischemic heart disease by the age of 50 years. | Source

Management Of Primary Hyperlipidemia

Many cases can be controlled by dietary management. Excess weight should be reduced. Groups I and II benefit by the avoidance of dietary cholesterol and restriction of fat to supply less than 30% of the total calories. Lipids should be supplied as polyunsaturated fats. Foods such as egg yolk, butter, margarine, hydrogenated oils, lard, suet, cakes and biscuits made with these fats, whole milk, cream, fatty meat, chocolates, coconut oils and foods fried in saturated fats should be avoided. Some cases show an abnormal elevation of serum lipids with the intake of alcohol and refined carbohydrates. Such cases benefit by restriction of alcohol and refined carbohydrates. Group II hyperlipidemia respond to reduction of fat below 25% of their dietary intake.

Drug therapy: Drugs are employed when dietary measures alone are inadequate. Cholestyramine, which is an anion exchange resin, in a daily dose of 16 to 32g in 3 to 4 divided doses helps to control the hyperlipidemia in group acids and cholesterol. It is very effective in type 2 hyperlipidemia, but is contraindicated in types 3, 4 and 5.

Clofibrate, which is a branched chain fatty acid, reduces VLDL and it is effective in lowering plasma triglycerides in types 3 and 4. When given in doses of 0.5g, 3-4 times a day. Clofibrate is indicated in severe hyperlipidemia where the risk of atheromatous occlusions, xanthomatosis and pancreatitis is high (Frederickson’s type III, IV and V). Adverse side effects of clofibrate include gastrointestinal upset, increased incidence of cholelithiasis, and increased frequency of malignant neoplasms. Nictoinic acid in a dose of 0.5 to 1g thrice daily augments the lipid lowering effects of other drugs in groups I and II hyperlipidemias.

Fredrickson’s Classification

Lipoprotein pattern
Lipoprotein
Group
Type 1
Chylomicron
Group III
Type 2a
LDL
Group I
Type 2b
LDL and VLDL
 
Type 3
remnants
Group II
Type 4
VLDL
 
Type 5
VLDL and chylomicrons
 
Fredrcikson has suggested a classification which includes six groups based on the serum levels of lipids and lipoproteins, estimated in the fasting state.

Secondary hyperlipidemias

Secondary hyperlipoproteinamias out-number the primary types. In the majority of cases, LDL cholesterol is increased in the serum. The risk of coronary, cerebral, renal and peripheral arterial disease are high irrespective of the primary cause and this risk can be brought down by appropriate therapy.

The seconday types are seen in diabetes mellitus, hypothyroidism, nephrotic syndrome, biliary obstruction, pancreatitis or as a side effect of drugs such as estrogens and corticosteroids. In all subjects with hyperlipidemias, primary causes should be looked for and attended to.

Management Of Primary Hyperlipidemia

Many cases can be controlled by dietary management. Excess weight should be reduced. Groups I and II benefit by the avoidance of dietary cholesterol and restriction of fat to supply less than 30% of the total calories. Lipids should be supplied as polyunsaturated fats. Foods such as egg yolk, butter, margarine, hydrogenated oils, lard, suet, cakes and biscuits made with these fats, whole milk, cream, fatty meat, chocolates, coconut oils and foods fried in saturated fats should be avoided. Some cases show an abnormal elevation of serum lipids with the intake of alcohol and refined carbohydrates. Such cases benefit by restriction of alcohol and refined carbohydrates. Group II hyperlipidemia respond to reduction of fat below 25% of their dietary intake.

Drug therapy: Drugs are employed when dietary measures alone are inadequate. Cholestyramine, which is an anion exchange resin, in a daily dose of 16 to 32g in 3 to 4 divided doses helps to control the hyperlipidemia in group acids and cholesterol. It is very effective in type 2 hyperlipidemia, but is contraindicated in types 3, 4 and 5.

Clofibrate, which is a branched chain fatty acid, reduces VLDL and it is effective in lowering plasma triglycerides in types 3 and 4. When given in doses of 0.5g, 3-4 times a day. Clofibrate is indicated in severe hyperlipidemia where the risk of atheromatous occlusions, xanthomatosis and pancreatitis is high (Frederickson’s type III, IV and V). Adverse side effects of clofibrate include gastrointestinal upset, increased incidence of cholelithiasis, and increased frequency of malignant neoplasms. Nictoinic acid in a dose of 0.5 to 1g thrice daily augments the lipid lowering effects of other drugs in groups I and II hyperlipidemias.

© 2014 Funom Theophilus Makama

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