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Lipoprotein disorders
The major classes of lipoproteins are chylomicrons, very-low-density
lipoproteins (VLDL), intermediate-density lipoproteins (IDL),
low-density lipoproteins (LDL), and high-density lipoproteins (HDL).
Disorders that affect lipid metabolism may be caused by defects in the
structural proteins of lipoprotein particles, in the cell receptors
that recognize the various types of lipoproteins, or in the enzymes
that break down fats. As a result of such defects, lipids may become
deposited in the walls of blood vessels, which can lead to
atherosclerosis (a disease characterized by abnormal thickening and
hardening of the walls of the arteries).
Familial
hypercholesterolemia is an autosomal dominant disease that is caused by
the deficiency of the LDL receptor on the surface of cells in the liver
and other organs. As a result, cholesterol is not moved into the cells.
Under normal conditions, when enough cholesterol is present in the
cell, feedback mechanisms signal enzymes to cease cholesterol
synthesis. In familial hypercholesterolemia, these enzymes are relieved
of feedback inhibition, thus inducing the production of still more
cholesterol. The disease is characterized by early coronary vascular
disease, strokes, and fatty deposits on the tendons. Blood cholesterol
levels are very high from birth, and LDL cholesterol is also elevated.
Treatment is by a low-cholesterol diet and drugs that inhibit
cholesterol synthesis or increase its excretion in the gastrointestinal
tract.
If a person with familial hypercholesterolemia is
homozygous for the condition, severe vascular disease starts in early
childhood, and heart attacks are usual by the age of 20. Similar
symptoms are present in familial dysbetalipoproteinemia
(hyperlipoproteinemia type III), which may be inherited as an autosomal
recessive or autosomal dominant condition (that is, if the trait has
been inherited from both parents). In this disorder, which manifests in
adulthood, increased blood cholesterol and triglycerides are present
due to an abnormality of a constituent of lipoproteins called
apoprotein E. Treatment is similar to that required for familial
hypercholesterolemia.
A deficiency of microsomal transfer
protein causes abetalipoproteinemia, an autosomal recessive condition
characterized by the virtual absence of VLDL and LDL. Triglycerides
accumulate in the gastrointestinal tract and liver, and there are low
blood levels of cholesterol, HDL cholesterol, and triglycerides.
Persons with abetalipoproteinemia have severe fat malabsorption and
develop neurological symptoms including unsteady gait, retinal defects,
and nerve damage due to the deficiency of vitamin E.
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