Here's what the LIPITOR advertisement states.......
LIPITOR CAN HELP YOU GET TO GOAL
Do you know your cholesterol numbers? Do you have a cholesterol goal? It's important to get your cholesterol checked regularly. If your numbers are high, diet and exercise are the first step. But if you still haven't reached your goal, ask your doctor or healthcare provider if LIPITOR is right for you.
OVER 10 MILLION PEOPLE HAVE TAKEN LIPITOR
LIPITOR had been proven effective in clinical studies: LIPITOR, with diet and exercise, lowered LDL (bad) cholesterol 39-60%, total cholesterol 29-45%, and triglycerides 19-37%.
LIPITOR IS TAKEN ONCE A DAY
LIPITOR is taken once a day, at any time, with or without food. Side effects are usually mild and temporary. In clinical studies, less than 2% of people taking LIPITOR stopped due to adverse side effects. LIPITOR is generally well tolerated. The most commonly reported side effects include constipation, flatulence, dyspepsia, and abdominal pain.
Only your doctor or healthcare provider can determine if LIPITOR is right for you. Some people should not take LIPITOR, including those with liver disease or possible liver problems, women who are nursing, pregnant, or may become pregnant, or people who are allergic to any of the ingredients in LIPITOR.
It's important to tell your doctor about any medications you are currently taking to avoid possible serious drug interactions. Your doctor may perform simple blood tests to monitor liver function before and during treatment.
If you are taking LIPITOR, tell your doctor about any unusual muscle pain or weakness, as this could be a sign of serious side effects. (Please see news article "Bayer Yanks Cholesterol Drug After 40 Deaths")
And now for the (very) small print........
*Please note that the following has been excerpted from the preceding Lipitor® advertisement and emphasis has been added.
Nutrients Depleted: Coenzyme Q10
U.S. Brand Names: Lipitor®
Use: Adjunct to diet for the reduction of elevated total and LDL-cholesterol levels in patients with hypercholesterolemia (type IIa, IIb, and IIc); used in hypercholesterolemic patients without clinically evident heart disease to reduce the risk of myocardial infarction, to reduce the risk for revascularization, and reduce the risk of death due to cardiovascular causes.
Pregnancy and Lactation: Artherosclerosis is a chronic process and discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy or primary hypercholesterolemia. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Since HMG-CoA reductase inhibitors decrease cholesterol synthesis and possible the synthesis of other biologically active substances derived from cholesterol, they may cause fetal harm when administered to pregnant women. Therefore, HMG-CoA reductase inhibitors are contraindicated during pregnancy and in nursing mothers. ATORVASTATIN SHOULD BE ADMINISTERED TO WOMEN OF CHILDBEARING AGE ONLY WHEN SUCH PATIENTS ARE HIGHLY UNLIKELY TO CONCEIVE AND HAVE BEEN INFORMED OF THE POTENTIAL HAZARDS. If the patient becomes pregnant while taking this drug, therapy should be discontinued and the patient apprised of the potential hazard to the fetus.
Contraindications: Active liver disease or unexplained persistent elevations of serum transaminases. Hypersensitivity to any component of this medication.
Liver Damage: HMG-CoA reductase inhibitors, like some other lipid-lowering therapies, have been associated with biochemical abnormalities of liver function. Persistent elevations (greater than 3 times the upper limit of normal [ULN] occurring on 2 or more occasions) in serum trasaminases occurred in 0.7% of patients who received atorvastatin in clinical trials. The incidence of these abnormalities was 0.2%, 0.2%, 0.6%, and 2.3% for 10, 20, 40, and 80 mg, respectively. One patient in clinical trials developed jaundice. Increases in liver function tests (LFT) in other patients were not associated with jaundice or other clinical signs or symptoms. Upon dose reduction, drug interruption, or discontinuation, transaminase levels returned to near pretreatment levels without sequealae. Eighteen of 30 patients with persistent LFT elevations continued treatment with a reduced dose of atorvastatin. It is recommended that liver function tests be performed prior to and at 12 weeks following both the initiation of therapy and any elevation of dose, and periodically (eg, semiannually) thereafter. Liver enzyme changes generally occur in the first 3 months of treatment with atorvastatin. Patients who develop increased transaminase levels should be monitored until the abnormalities resolve. Should an increase in ALT or AST of greater than 3 times ULN persist, reduction of dose or withdrawal of atorvastatin is recommended. Atorvastatin should be used with cuation in patients who consume substantial quantities of alcohol and/or have have a history of liver disease. Active liver disease or unexplained persistent transaminase elevations are contraindications to the use of atorvastatin.
Skeletal Muscle: Rhabdomyolysis with acute renal failure secondary to myoglobinuria has been reported with other drugs in this class. (Please see news article "Bayer Yanks Cholesterol Drug After 40 Deaths".) Uncomplicated myalgia has been reported in atorvastatin-treated patients. Myopathy, defined as muscle aches or muscle weakness in conjunction with increases in creatine phosphokinase (CPK) values greater than 10 times ULN, should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevation of CPK. Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particually if accompanied by malaise or fever. Atorvastatin therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed or suspected. The risk of myopathy during treatment with other drugs in this class is increased with concurrent administration of cyclosporine, fibric acid derivatives, erthromycin, niacin, or azole antifungals. Physicians considering combined therapy with atorvastatin and fibric acid derivatives, erythromycin, immunosuppressive drugs, azole antifungals, or lipid-lowering doses of niacin should carefully weigh the potential benefits and risks and should carefully monitor patients for any signs or symptoms of muscle pain, tenderness, or weakness, particurally during the initial months of therapy and during any periods of upward dosage titration of either drug. Periodic creatine phosphokinase (CPK) determinations may be considered in such situations, but there is no assurance that such monitoring will prevent the occurence of severe myopathy. Atorvastatin therapy should be temporarily withheld or discontinued in any patient with an acute, serious condition suggestive of a myopathy or having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (eg, severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures.
General: Before instituting therapy with atorvastatin, an attempt should be made to control hypercholesterolemia with appropriate diet, exercise, and weight reduction in obese patients, and to treat other underlying medical problems.
Information for Patients: Patients should be advised to report promptly unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever.
Drug Interactions: The risk of myopahty during treatment with other drugs of this class is increased with concurrent administration of cyclosporine, fibric acid derivatives, niacin (nictonic acid), erythromycin, azole antifungals.
Endocrine Function:HMG-CoA reductase inhibitors interfere with cholesterol synthesis and theoretically might blunt adrenal and/or gonadal steroid production. Clinical studies have shown that atorvastatin does not reduce basal plasma cortisol concentration or impair adrenal reserve. The effects of HMG-CoA reductase inhibitors on male fertility have not been sutdied in adequate numbers of patients. The effects, if any, on the pituitary gonadal axis in premenopausal women are unknow. Caution should be exercised if an HMG-CoA reductase inhibitor is administered concomitantly with drugs that may decrease the levels or activity of endogenous steroid hormones, such as ketoconazole, spironolactone, and cimetidine.
CNS toxicity: Brain hemorrhage was seen in a female dog treated for 3 months at 120 mg/kg/day. Brain hemorrhage and optic nerve vacuolation were seen in another female dog that was sacrificed in moribund condition after 11 weeks of escalating doses up to 280 mg/kg/day. The 120 mg/kg dose resulted in a systemic exposure approximately 16 times the human plasma area-under-the-curve (AUC, 0-24 hours) based on the maximum human dose of 80 mg/day. A single tonic convulsion was seen in each of 2 male dogs (one treated at 10 mg/kg/day) in a 2-year study. No CNS lesions have been observed in mice after chronic treatment for up to 2 years at doses up to 400 mg/kg/day or in rats at doses up to 100 mg/day. These doses were 6 to 11 times (mouse) and 8 to 16 times (rat) the human AUC (0-24) based on the maximum recommended human dose of 80 mg/day. CNS vascular lesions, characterized by perivascular hemorrhages, edema, and mononuclear cell infiltration of perivascular spaces, have been observed in dogs treated with other members of this class. A chemically similar drug in this class produced optic nerve degeneration (Wallerian degeneration of retinogeniculate fibers) in clinically normal dogs in a dose-dependent fashion at a dose that produced plasma drugs levels about 30 times higher than the mean drug level in humans taking the highest recommended dose.
Carcinogenesis, Mutagenesis, Impairment of Fertility: In a 2-year carcinogenicity study in rats at dose levels of 10, 30, and 100 mg/kg/day, 2 rare tumors were found in muscle un high-dose females: in one, there was a rhabdomyosarcoma and, in another, there was a fibrosarcoma. This dose represents a plasma AUC (0-24) value of approximately 16 times the mean human plasma drug exposure after an 80 mg oral dose. A 2-year carcinogenicity study in mice given 100, 200, or 400 mg/kg/day resulted in a significant increase in liver adenomas in high-dose males and liver carcinomas in high-dose females. These findings occurred at plasma AUC (0-24) values of approximately 6 times the mean human plasma drug exposure after an 80 mg oral dose. In vitro, atorvastatin was not mutagenic or clastogenic in the following tests
More than 1% experience:
Central nervous system: Headache
Gastrointestinal: Diarrhea, flatulence, abdominal pain (2% to 3%)
Neuromuscular & skeletal: Myalgia (1% to 5%)
Less than 1% experience: Giddiness, euphoria, mild confusion, impaired short-term memory, mild LFT increases, pharyngitis, rhinitis
Overdose/Toxicology: Few symptoms are anticipated. Treatment is supportive.