section 20.3 
Lipoprotein-Associated Disorders
447
TABLE 20-6
Plasma Levels o f Cholesterol and Risk o f Atherosclerosis in Adults
Cholesterol Level
Desirable
Moderate Risk
High Risk
Total
LDL <100 
HDL
< 2 0 0
mg/dl 
(5.20 mmol/L)
< 1 0 0
mg/dl*
(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
Acceptable
Borderline
High
Total
LDL
<170 mg/dl 
(<4.42 mmol/L) 
< 1 0 0
mg/dl 
(<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
mg/dl 
(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 
Bums
Myocardial infarction 
Acute inflammatory disorders
Chronic Conditions
Diabetes mellitus 
Thyroid disease 
Uremia
Nephrotic syndrome 
Liver disease
Commonly Prescribed Drugs
Diuretics
Progestins
Androgens
/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 
trans
-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
 
    
