Pharmacology for Dentistry

Antihyperlipidemic Agents 197

hypercholesterolemia and mixed
dyslipidemias. Atorvastatin also reduces
VLDL-cholesterol and TG and produces
variable increases in HDL-cholesterol and
apolipoprotein A1. Atorvastatin reduces
LDL-cholesterol in patients with familial
hyper-cholesterolemia (FH).

Atorvastatin is generally well tolerated.
Adverse effects include constipation,
flatulence, dyspepsia, abdominal pain,
headache, nausea, myalgia, diarrhoea,
asthenia and insomnia.

Dose related and reversible elevated
serum ALT levels have also been reported.

Elevated serum CPK levels have been
reported in some patients but only rarely
patients have concurrent muscle pain,
tenderness or weakness.

It is indicated as an adjunct to diet to
reduce elevated total cholesterol, LDL-
cholesterol and TG levels in patients with
primary hypercholesterolemia, diabetic
dyslipidaemia or mixed hyperlipidemia,
hypertriglyceridemia, dysbetalipo-
proteinemia and familial hypercholester-
olemia.

PRAVASTATIN

Pravastatin sodium besides increasing
LDL cholesterol catabolism, also inhibits
LDL-cholesterol production by inhibiting
hepatic synthesis of VLDL-cholesterol, the
LDL-cholesterol precursor. These effects
result in a reduction of total cholesterol,
LDL-cholesterol, VLDL-cholesterol,
apolipoprotein B and trigly-cerides, whilst
increasing (HDL-cholesterol) and
apolipoprotein A. It has little effect on
cholesterol synthesis in other tissues.

Pravastatin is administered orally in the
active form and is rapidly absorbed, with

peak plasma levels occurring 1 to 1.5 hours

after dosing. Pravastatin undergoes

extensive first-pass extraction in the liver,

which is its primary site of action. It is 50%

bound to plasma proteins.

Adverse effects include rash, myalgia,

headache, non-cardiac chest pain; rarely

nausea/vomiting, diarrhoea and fatigue

may occur.

Pravastatin is indicated as an adjunct to

diet in patients with primary

hypercholesterolemia, mixed dyslipidemia,

elevated serum triglyceride levels and

primary dysbetalipoproteinemia who do not

respond adequately to diet.

FIBRIC ACID DERIVATIVES

These activate lipoprotein lipase which is

a key enzyme in degradation of VLDL

resulting in lower circulating triglycerides.

These drugs lower triglyceride levels by 20-

50% with 10-15% decrease in LDL

cholesterol and a 10-15% increase in HDL

cholesterol.

CLOFIBRATE

It has a specific action on type III

hyperlipo-proteinemia and also reduces

VLDL and LDL but because of its association

with a small increase in risk of gastrointestinal

and hepatobiliary neoplasia, it is seldom used.

GEMFIBROZIL

Gemfibrozil reduces plasma

triglycerides by 40 to 55% by decreasing the

concentration of VLDL. Its effectiveness is

less in lowering LDL.

It also decrease hepatic synthesis and

secretion of VLDL. The lowering of