lipoproteins. This would account for the increased levels of triglyceride and the increased number of VLDL and LDL particles. Another effect of long chain free fatty acids is to increase hepatic lipase on the surface of hepatic cells. Hepatic lipase hydrolyzes triglyceride and phospholipid in LDL and HDL, decreasing the size of each particle. However, Cholesteryl Ester Transfer Protein (CETP) also contributes to this lipoprotein remodeling process; whether hepatic lipase or CETP has the predominant effect on the size and density of LDL and HDL particles depends on the triglyceride content of VLDL and the secretion rate of VLDL.


TYPES OF DYSLIPIDEMIA


Primary dyslipidemia: Several monogenic disorders have been defined that lead to different type of dyslipidemias (Table 3), but for many cases, the etiology is polygenic. These disorders affect plasma lipoprotein levels by overproduction of lipoproteins and/or decreased clearance.
Increased LDL cholesterol level Increased triglyceride level Decreased HDL cholesterol level
∙ Diabetes mellitus
∙ Hypothyroidism
∙ Nephrotic syndrome
∙ Obstructive liver disease
∙ Drugs
  Anabolic steroids

Progestins

ß blockers (without intrinsis sympathom-imetic action)
∙ Alcoholism
∙ Diabetes mellitus
∙ Hypothyr-oidism
∙ Obesity
∙ Renal insufficiency
∙ Drugs
  ß blockers (without intrinsis sympathom-imetic action)

Bill acidbinding resins

Estrogens

Ticlopidine (Ticlid)
∙ Cigarette smoking
∙ Diabetes mellitus
∙ Hypertriglyc-eridemia
∙ Menopause
∙ Obesity
∙ Puberty (in males)
∙ Uremia
∙ Drug
  Anabolic steroids

ß blockers (without intrinsis sympathom-imetic action)

Progestins
Schaefer EJ. Diagonosis and management of lipoprotein disorders. In: Rifkind BM, ed. Drug treatment of hyperlipidemia. New York: Dekker, 1991:17-52.

Table 4: Causes of Secondary Dyslipidemia

Management of Dyslipidemia in Adults: SYED M. AHMED, M.D. MPH, DR. P.H. MARK E. CLASEN, MD, PH.D,
& JOHN F. DONNELLY, M.D. Wright State University School of Medicine, Dayton, Ohio
Name

Liporotein(s)
in Excess

 Possible Causes
Possible Causes		 Clinical Significance Treatment Options
Hypercholesterolemia 1) Nutritional
2) Genetic (less active
     LDL receptor)		 Decreased LDL clearance from circulation HMG-CoA reductase
inhibitors, bile acid
sequestrants, nicotinic acid
Polygenic LDL
Familial LDL 3) Genetic Homozygous Heterozygous
 (defective gene for the LDL receptor)		 Decreased LDL clearance from circulation Homozygous (Probucol) Heterozygous (HMG-CoA reductase inhibitors, bile acid sequestrants, or combination of both)
Hypertriglyceridemia Excessive consumption Caloric
Alcohol		 Increased VLDL secretion from liver Diet modification, nicotinic acid, fibric acids
Diet induced VLDL
Primary hypertriglyceridemia VLDL Onten associated with other medical problems
  Obesity
  Diabetes		 Increased production of trilycerides and VLDL particles (decreased HDL particles, increased small LDL particles=>atherogenic) Weight loss, diet modification, tight control of blood glucose levels, HMG-CoA reductase inhibitors, nicotinic acid, fibric acids
Secondary hypertriglyceridemia VLDL Often secondary to other medical problems
  Obesity
  Diabetes
  Nephrotic syndrome		 Increased production of triglycerides and VLDL particles Weight loss, tight control of blood glucose levels, HMG-CoA reductase inhibitors, nicotinic acid, fibric acids, acids, bile-acid sequestrants
Mixed Hyperlipidemias Genetic (overproduction of apolipoprotein B-100) Increased production of VLDL particles => elevated triglyceride levels HMG-CoA reductase inhibitors, nicotinic acid, fibric-acids derivatives
Familial combined hyperlipidemia VLDL & LDL
Lipoprotein lipase deficiency Chylomicron & VLDL Genetic (deficency of lipoprotein lipase enzyme) Reduced ability of delipidize triglyceride molecules from VLDL and chylomicron particles HMG-CoA reductase inhibitors, fibric acids derivative, niacin
Table 3: Types of Dyslipidemia

Peggy K. Han: Current Pathophysiology, Classification, Diagnosis, and Treatment Options of Dyslipidemia, 2003