Initial attempts to maintain an appropriate serum lipid profile should always
include dietary and behavioral modifications. These steps remain the mainstay
for the management of all patients with hyperlipidemia. However, many
patients will require lipid-lowering medications to achieve and maintain lipid
levels.
Bile acid Sequestrants
The bile acid sequestrants bind bile acids in the intestinal tract and
interfere with reabsorption. This results in decreased return of bile acids to
the liver, increased endogenous synthesis of bile acids and enhanced degradation
of cholesterol. This in turn results in decreased hepatic cholesterol,
increased hepatic LDL receptor synthesis and expression, and enhanced clearance
of LDL cholesterol from the blood. The net result is commonly a 15 to 20
percent reduction in serum cholesterol. Cholestyramine and colestipol are
both well tolerated in divided doses. Constipation and indigestion are
relatively common side effects that may limit patient compliance. These resins
may also interfere with the uptake of numerous medications and this should be
considered prior to initiation of therapy in patients taking cardiac and other
medications.
Niacin
Niacin (nicotinic acid) inhibits the hepatic secretion of very low-density
lipoprotein (VLDL) cholesterol and lowers serum VLDL and LDL cholesterol, and
may raise HDL cholesterol. The most common side effects include flushing and
itching.
Fibric Acids
Fibric acid derivatives have a variety of effects on lipid metabolism that
result in significant improvements in the lipid profile. These include
reductions in VLDL cholesterol and triglycerides, and an increase in HDL
cholesterol. Intolerable side effects occur rarely. Patients may experience
nonspecific gastrointestinal symptoms and weight gain. Myopathy is a rare
but serious complication that typically accompanies the use of multiple lipid-
lowering medications. Gemfibrozil is commonly prescribed at a dose of 600mg
taken twice a day.
Hydroxy-Methyl-Glutaryl Coenzyme A Reductase Inhibitors
The current mainstay of medical treatment of hyperlipidemia is a group of drugs
that interfere with the actions of hydroxy-methyl-glutaryl coenzyme A (HMG CoA)
reductase. The HMG CoA reductase inhibitors block cholesterol synthesis in the
liver, resulting in the increased uptake of serum LDL cholesterol. This results
in predictable and dose-related decrements in serum LDL cholesterol. Side
effects include gastrointestinal discomfort, liver toxicity, and myopathy.
