section 20.3
Lipoprotein-Associated Disorders
TABLE 20-6
Plasma Levels o f Cholesterol and Risk o f Atherosclerosis in Adults
Cholesterol Level
Moderate Risk
High Risk
LDL <100
< 2 0 0
(5.20 mmol/L)
< 1 0 0
(2.60 mmol/L)
40-59 mg/dl
(1.03-1.53 mmol/L)
Cardioprotective: >60 mg/dl
(1.55 mmol/L)
200-239 mg/dl
(5.2-6.20 mmol/L)
130-159 mg/dl
(3.35-4.10 mmol/L)
>240 mg/dl
(>6.20 mmol/L)
>160 mg/dl
(>4.15 mmol/L)
<40 mg/dl
(1.03 mmol/L)
*LDL level 100-129 mg/dl considered near optimal/above optimal.
The Total Plasma and LDL-Cholesterol Levels in Children and Adolescents from Families with Hypercholes-
terolemia or Premature Cardiovascular Disease
Cholesterol Level
<170 mg/dl
(<4.42 mmol/L)
< 1 0 0
(<2.6 mmol/L)
170-199 mg/dl
(4.42-5.17 mmol/L)
110-129 mg/dl
(2.86-3.35 mmol/L)
> 2 0 0
(52 mmol/L)
>130 mg/dl
(>3.38 mmol/L)
TABLE 20-7
Examples o f Secondary Causes That Can Alter Plasma
Lipoprotein Levels
Acute Illnesses
Surgical procedures
Viral illness
Myocardial infarction
Acute inflammatory disorders
Chronic Conditions
Diabetes mellitus
Thyroid disease
Nephrotic syndrome
Liver disease
Commonly Prescribed Drugs
/3-Adrenergic blocking agents
important to initiate lifestyle changes that include weight
loss in obese individuals, dietary modifications (e.g., re-
duced saturated fat intake including
-fatty acids),
exercise, avoidance of tobacco, and moderate alcohol
consumption. Individuals who are homozygous for a
slow oxidizing alcohol dehydrogenase gene (ADH3)
have higher HDL-cholesterol levels and a lower risk
of myocardial infarction. In the absence of positive re-
sults with lifestyle therapy, the pharmacological agents
for increasing HDL cholesterol levels includes niacin
and estrogen in postmenopausal women. Modest in-
creases in HDL cholesterol levels are also observed
with HMG-CoA reductase inhibitors and fibric acids.
Another factor that regulates HDL cholesterol lev-
els is the plasma level of cholesteryl ester transfer pro-
tein (CETP). CETP, a hydrophobic glycoprotein (M.W.
741,000), facilitates the transfer of cholesteryl esters in
HDL and triacylglycerols in LDL and VLDL (see above).
In CETP deficiency due to a point mutation (G ->• A)
in a splice donor site that prevents normal processing of
mRNA, the plasma HDL cholesterol levels of affected in-
dividuals are markedly high, with decreased LDL choles-
terol. In the affected families, there was no evidence
of premature atherosclerosis and, in fact, there was a
trend toward longevity. These observations support the
role of CETP and the antiatherogenic property of HDL.
However, not all factors that elevate HDL levels may be
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