Statins are HMG-CoA reductase inhibitors that prevent cholesterol synthesis and increase LDL catabolism. They are absorbed following oral intake but undergo hepatic metabolism, with absorption affected by food intake and elimination primarily through bile and feces. Rosuvastatin and pitavastatin are the most potent at lowering LDL cholesterol, while lovastatin and fluvastatin are the least potent. Potential adverse effects of statins include myopathy and rhabdomyolysis, which can be increased by drug interactions. Other interactions can occur with anticoagulants, oral contraceptives, and other drugs. Studies have found differing effects of individual statins on kidney function and risk of kidney damage. Thrombocytopenia and pancre

1. By: Ala’a F. Hassan/Clinical pharmacy unit
Action: all are HMG CoA reductase inhibitors that prevents
the 1st enzymatic step of de-novo cholesterol synthesis as
well as increase LDL catabolism(increase surface LDL
receptors on cells)
Absorption: pravastatin & fluvastatin are completely
absorbed following oral intake while only 30-50%
absorbance reported with lovastatin & Simvastatin
food intake was found to increase lovastatin absorption
while decrease (fluvastatin, atrovastatin & pravastatin)
bioavailablities still rosuvastatin & simvastatin absorption
is unaffected by food
Undergo marked hepatic 1st pass extraction (lovastatin &
simvastatin are prodrugs) with t1l2 ranges from 1-3 hr
(fluvastatin ,pravastatin & simvastatin) up to 19 hr with
rosuvastatin; peak plasma concentration achieved within
4hrs mostly
Elimination: principally excretion via bile & feces despite
urinary elimination also occurs(with pravastatin &
rosuvastatin mostly as unchanged drugs)

2. Statins dosing chart & potency
So pitavastain was found to be highly potent for lowering LDLc
followed by rosuvastatin, atrovastatin, simvastatin &
pravastatin though the lest potent agent were lovastatin &
fluvastatin
Adverse effects & Interactions
i. Cholesterol is an essential structural component of cells, a
precursor for steroid hormones, vitamin D metabolites and
bile acids, and an important factor in neural myelinization
and brain growth so possible side effects of statins on
growth, pubertal development and endocrinologic functions
have restricted their use in children during the prepubertal
stage, Furthermore since fat-soluble vitamins are
transported by lipoproteins, their reduction by statins has
been suspected to lead to vitamin deficiencies.
ii. The most serious adverse effect associated with statins
therapy is myopathy, which may progress to fatal or
nonfatal rhabdomyolysis which is increased with renal
insufficiency & intake of drugs as cyclosporine, antifungals,

3. erythromycin, clarithromycin, fucidic acid, gemfibrozil,
niacin, colchicin, nicotinic acid & anti arrythmics
iii. Statins found to enhance coumarins anticoagulant effect
while dcrease warfarin effect
iv. Other interaction reported with antacid(reduces
rosuvastatin absorption) ,ethnylestradiol as well as
glibinclamide & digoxin (plasma concentration Increased
by fluvastatin & atorvastain respectively), bosentan
(increases statin plasma concentration
v. Effects of statins on urinary protein excretion and kidney
function found atrovastatin to be protective and
Rosuvastatin was unprotective and possibly harmful, in
diabetic and nondiabetic patients[Allegations were made
that patients taking low doses of rosuvastatin were at
greater risk of developing serious kidney damage specially
with fibrates as fenofibrate, and rhabdomyolysis than those
taking other statins]
vi. There are few reports of statins induced thrombocytopenia
with pathophysiologic mechanisms of two major categories:
decreased platelet production via marrow suppression and
peripheral platelet clearance, usually by one of several
possible immune mechanisms
vii. Other studies report pancreatitis induced by atrovastatin,
rosuvastatin, simvastatin, pravastatin, fluvastatin and
lovastatin.