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Atorvastatin (Systemic)


VA CLASSIFICATION
Primary: CV601

Commonly used brand name(s): Lipitor.

Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).



Category:


Antihyperlipidemic—

HMG-CoA reductase inhibitor—

Indications

Accepted

Hyperlipidemia (treatment)—Atorvastatin is indicated as an adjunct to diet to reduce elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (apo B), and triglyceride (TG) concentrations in patients with primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Fredrickson Types IIa and IIb) {01}.
—Atorvastatin is also indicated to reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments, such as low-density lipoprotein apheresis, or if such treatments are unavailable {01}.
—For additional information on initial therapeutic guidelines related to the treatment of hyperlipidemia, see Appendix III.


Pharmacology/Pharmacokinetics

Physicochemical characteristics:
Molecular weight—
    1209.42 {01}

Mechanism of action/Effect:

3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors competitively inhibit the enzyme that catalyzes the conversion of HMG-CoA to mevalonate, the rate-limiting step in cholesterol biosynthesis {01}. The primary site of action of HMG-CoA reductase inhibitors is the liver, which is the principal site of cholesterol synthesis and low-density lipoprotein clearance {01}. Cholesterol and triglycerides circulate in the bloodstream as part of lipoprotein complexes {01}. These complexes are composed of high-density lipoprotein (HDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL) {01}. In the liver, triglycerides (TG) and cholesterol are incorporated into VLDL, which is released into the plasma for transport to the peripheral tissues {01}. LDL is formed from VLDL and is catabolized primarily through the LDL receptor {01}. Elevated plasma concentrations of total cholesterol (total-C), LDL-cholesterol (LDL-C), and apoliproprotein B (apo B) promote human atherosclerosis and are risk factors for developing cardiovascular disease {01}. Increased plasma concentrations of HDL-C are associated with decreased cardiovascular risk {01}. Atorvastatin lowers plasma cholesterol and lipoprotein concentrations by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface to enhance uptake and catabolism of LDL {01}. Atorvastatin also reduces LDL production and the number of LDL particles {01}. Atorvastatin reduces total-C, LDL-C, and apo B in patients with homozygous and heterozygous familial hypercholesterolemia (FH), nonfamilial forms of hypercholesterolemia, and mixed dyslipidemia {01}. Atorvastatin also reduces VLDL-C and TG and produces variable increases in HDL-C and apolipoprotein A-1 {01}.

Absorption:

Atorvastatin is rapidly absorbed, the extent of absorption increasing in proportion to the dose {01}. The absolute bioavailability of atorvastatin is approximately 12% {01}. Atorvastatin has a low systemic availability due to pre-systemic clearance in the gastrointestinal mucosa and/or hepatic first-pass metabolism {01}. Food decreases the rate and extent of absorption by approximately 25% and 9%, respectively; although, LDL-C reduction is similar when atorvastatin is given with or without food {01}. The concentration of atorvastatin in plasma (C max) and the area under the plasma concentration–time curve (AUC) are lower by approximately 30% following evening administration when compared with morning administration {01}. However, LDL-C reduction is the same, regardless of the time of day of administration {01}. Grapefruit juice in large amounts, has been shown to interfere with the metabolism of atorvastatin, causing increases in Cmaxand AUC {02}{03}. It is recommended that atorvastatin not be administered with large amounts of grapefruit juice{02}.

Distribution:

Mean volume of distribution (Vol D)—Approximately 565 L {01}.

Protein binding:

Very high (³ 98%) {01}.

Biotransformation:

Atorvastatin undergoes extensive hepatic and/or extra-hepatic metabolism to form ortho- and parahydroxylated derivatives and various beta-oxidation products {01}. It does not appear to undergo enterohepatic recirculation {01}. Atorvastatin and its ortho- and parahydroxylated metabolites were found to have equal inhibitory effects on HMG-CoA reductase in vitro {01}. The active metabolites are responsible for approximately 70% of the inhibition of HMG-CoA reductase {01}. Studies in vitro suggest that atorvastatin is metabolized by the cytochrome P450 3A4 isozyme {01}.

Half-life:


Elimination:

Approximately 14 hours {01}.


Time to peak concentration:

1 to 2 hours {01}.

Elimination:
    Primarily fecal (biliary) {01}.
    Renal: < 2% {01}.


In dialysis—
        Although studies have not been performed, atorvastatin is not expected to be removed significantly by hemodialysis because of its extensive binding to plasma proteins {01}.



Precautions to Consider

Carcinogenicity

In a 2-year study in mice, doses of 100, 200, or 400 mg per kg (mg/kg) of body weight per day resulted in a marked increase in liver adenomas in male mice given high doses and liver carcinomas in female mice given high doses {01}. These events occurred at area under the plasma concentration–time curve (AUC [0-24]) values of approximately six times the mean human plasma drug exposure after an 80-mg oral dose {01}.

In a 2-year study in rats, doses of 10, 30, and 100 mg/kg per day resulted in rare muscle tumors {01}. Rhabdomyosarcoma occurred in one female rat given high doses and fibrosarcoma occurred in another female rat given high doses {01}. The high dose represents an AUC (0–24) value of approximately 16 times the mean human plasma drug exposure after an 80-mg oral dose {01}.

Mutagenicity

No evidence of mutagenicity or clastogenicity was found in in vitro tests, with and without metabolic activation, including the Ames test with Salmonella typhimurium and Escherichia coli , the HGPRT forward mutation assay in Chinese hamster lung cells, the chromosomal aberration assay in Chinese hamster lung cells, or in the in vivo mouse micronucleus test {01}.

Pregnancy/Reproduction
Fertility—
No changes in fertility were observed in studies in rats given doses of up to 175 mg/kg (15 times the human exposure) of atorvastatin {01}. In 2 of 10 rats given 100 mg/kg per day for 3 months (16 times the human exposure at the 80-mg dose), aplasia and aspermia in the epididymis resulted {01}. Testis weights were significantly decreased with 30 and 100 mg/kg doses and epididymal weight was lower at 100 mg/kg {01}. Doses of 100 mg/kg per day given to male rats for 11 weeks prior to mating resulted in decreases in sperm motility and spermatid head concentration and increases in the number of abnormal sperm {01}. No adverse effects were observed on semen parameters or in reproductive organ histopathology in dogs given doses of 10, 40, or 120 mg/kg for 2 years {01}.

Pregnancy—
Atorvastatin therapy is contraindicated in pregnant women because it decreases cholesterol synthesis and possibly the synthesis of other biologically active substances, such as steroids and cell membranes, that are derived from cholesterol and are essential for fetal development {01}.

There have been rare reports of congenital anomalies following intrauterine exposure to HMG-CoA reductase inhibitors {01}. Severe congenital bone deformities, tracheo-esophageal fistula, and anal atresia (VATER association) were reported in a baby born to a woman who took the HMG-CoA reductase inhibitor lovastatin with dextroamphetamine sulfate during the first trimester of pregnancy {01}. Atorvastatin should not be administered to women of childbearing potential when they are highly likely to conceive {01}. If a woman becomes pregnant during atorvastatin therapy, the medication should be discontinued and the patient advised of the potential hazards to the fetus {01}.

In rats, atorvastatin crosses the placenta and reaches a concentration in fetal liver tissue equal to that in maternal plasma {01}. No evidence of teratogenicity was found in rats given doses of up to 300 mg/kg per day or in rabbits given doses of up to 100 mg/kg per day {01}. These doses represent 30 and 20 times, respectively, the human exposure based on body surface area (mg/m 2) {01}.

Studies in rats given 20, 100, or 225 mg/kg per day, from gestation day 7 through lactation day 21 (weaning), have shown decreased pup survival at birth, neonate, weaning, and maturity in pups of mothers given doses of 225 mg/kg per day {01}. On days 4 and 21, body weight was decreased in pups of mothers given doses of 100 mg/kg per day; body weight was decreased at birth and at days 4, 21, and 91 in pups of mothers given 225 mg/kg per day {01}. Pup development was delayed, as determined by rotorod performance (mothers given 100 mg/kg per day) and acoustic startle (mothers given 225 mg/kg per day) {01}. Development was also delayed in pinnae detachment and eye opening (mothers given 225 mg/kg per day) {01}. These doses represent 6 times (100 mg/kg) and 22 times (225 mg/kg) the human exposure at 80 mg per day {01}.

FDA Pregnancy Category X {01}.

Breast-feeding

While it is not known whether atorvastatin is distributed into breast milk, atorvastatin is contraindicated in women who are breast-feeding because inhibition of cholesterol synthesis may cause serious adverse effects in the nursing infant {01}. Atorvastatin is distributed into the milk of lactating rats {01}. Plasma and liver atorvastatin concentrations in nursing rat pups have reached 50% and 40%, respectively, of that in the mother's milk {01}.

Pediatrics

Appropriate studies on the relationship of age to the effects of atorvastatin have not been performed in the pediatric population {01}. However, eight pediatric patients (none younger than 9 years of age) with homozygous familial hypercholesterolemia (FH) were treated with atorvastatin at doses of up to 80 mg per day for 1 year {01}. No clinical or biochemical abnormalities were reported in these patients {01}.


Geriatrics


Use of atorvastatin in patients 65 years of age and older has not demonstrated geriatrics-specific problems that would limit the usefulness of atorvastatin in the elderly. Safety and efficacy of atorvastatin in 221 patients ³ 70 years of age given doses of up to 80 mg per day were similar to those in younger patients {01}. However, in healthy subjects ³ 65 years of age, atorvastatin plasma concentrations (C max) are higher and the AUC is greater by approximately 40% and 30%, respectively, compared with those in younger adults {01}. Reduction of low-density lipoprotein cholesterol (LDL-C) is comparable to that in younger patients given equal doses of atorvastatin {01}.


Pharmacogenetics

There is no clinically significant difference in LDL-C reduction with atorvastatin between men and women, although plasma concentrations of atorvastatin in women are approximately 20% higher for C max and 10% lower for AUC, compared with those in men {01}.

Surgical

Atorvastatin therapy should be temporarily withheld or discontinued in any patient having a risk factor, such as major surgery, predisposing to the development of renal failure secondary to rhabdomyolysis {01}.

Drug interactions and/or related problems
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):


Note: Combinations containing any of the following medications, depending on the amount present, may also interact with this medication.

Alcohol, substantial use of {01}    (elevations in transaminase values may occur {01})


Antacids, aluminum and magnesium hydroxide–containing {01}    (plasma concentrations decreased by approximately 35% when atorvastatin was administered concurrently with an aluminum and magnesium hydroxide–containing antacid; however, reduction of LDL-C was not altered {01})


» Azole antifungals {01} or
» Erythromycin {01} or
» Gemfibrozil {01} or
» Grapefruit juice in large amounts{02}{03}or    (concurrent use with large amounts of grapefruit juice has been reported to significantly increase the serum concentrations and the area under the plasma concentration-time curve (AUC){02}{03}. In a study with 12 subjects, administration of grapefruit juice double-strength 200 mL three times a day resulted in a Cmax decrease of about 24% of active atorvastatin compounds. An increase in AUC of active atorvastatin compounds was about 23%. The time to C max(tmax) was increased from 1 hour to 4 hours. Grapefruit juice or other grapefruit products in large doses should not be taken before or after administration of atorvastatin{02})


» Immunosuppressants, especially cyclosporine {01} or
» Niacin (nicotinic acid) {01}    (increased risk of myopathy, such as rhabdomyolysis, with concurrent administration {01}; inhibition of cytochrome P450 3A4 isozyme [the enzyme responsible for atorvastatin metabolism] by erythromycin may increase atorvastatin plasma concentrations by approximately 40% with concurrent administration {01})


Colestipol {01}    (concurrent use may decrease plasma concentrations of atorvastatin by approximately 25% {01}; however, LDL-C reduction may be greater with combination therapy than with either medication given alone {01})


Contraceptives, oral {01} , such as:
Ethinyl estradiol {01}
Norethindrone {01}    (concurrent administration may increase AUC for ethinyl estradiol and norethindrone by approximately 20% and 30%, respectively {01})


Digoxin {01}    (concurrent administration may increase steady-state digoxin plasma concentrations by approximately 20% {01})


Medications that may decrease the concentrations or activity of endogenous steroid hormones {01} , such as:
Cimetidine {01}
Ketoconazole {01}
Spironolactone {01}    (HMG-CoA reductase inhibitors interfere with cholesterol synthesis and could possibly blunt adrenal and/or gonadal steroid production {01}; concurrent administration with these drugs may further decrease concentrations and/or inhibit the activity of endogenous steroid hormones {01})



Laboratory value alterations
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

With physiology/laboratory test values
Creatine kinase (CK), serum {01}    (increases of CK > 10 times the upper limit of normal [ULN], accompanied by muscle aches or weakness, are associated with myopathy, such as rhabdomyolysis {01}; atorvastatin should be discontinued if marked elevations of creatine kinase occur {01})


Transaminases, serum {01}    (elevations in liver enzyme values usually occur within the first 3 months of treatment {01}; persistent increases [> three times ULN, occurring on two or more occasions] in transaminase values occurred in 0.7% of patients in clinical trials {01}; elevations in transaminase values are not usually associated with clinical signs or symptoms, although one patient in clinical trials developed jaundice {01}; if elevations in aspartate aminotransferase [AST (SGOT)] or alanine aminotransferase [ALT (SGPT)] are > three times the ULN and persist, atorvastatin dosage should be reduced or discontinued {01}; patients should be monitored until the abnormal values are resolved {01})


Medical considerations/Contraindications
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)— not necessarily inclusive (» = major clinical significance).


Except under special circumstances, this medication should not be used when the following medical problems exist:
» Hepatic disease, active {01} , including
» Alcoholic liver disease, chronic {01}
» Childs-Pugh Index grade A disease {01}
» Childs-Pugh Index grade B disease {01} or
» Elevations of transaminase values, unexplained, persistent {01}    (the presence of hepatic disease may increase atorvastatin plasma concentrations {01}. Plasma concentrations are significantly increased in patients with chronic alcoholic liver disease {01}. In patients with Childs-Pugh Index grade A disease, C max and AUC are each fourfold greater {01}. In patients with Childs-Pugh Index grade B disease, C max and AUC are approximately sixteen- and elevenfold greater, respectively)


» Hypersensitivity to atorvastatin {01}
Risk-benefit should be considered when the following medical problems exist
» Electrolyte, endocrine, or metabolic disorders, severe {01} or
» Hypotension {01} or
» Infection, severe acute {01} or
» Seizures, uncontrolled {01} or
» Surgery, major {01} or
» Trauma {01}    (these conditions may predispose a patient to the development of renal failure, secondary to rhabdomyolysis {01}; atorvastatin should be discontinued or temporarily withheld {01})


Hepatic disease, history of {01}    (elevations in transaminase values may occur {01})



Patient monitoring
The following may be especially important in patient monitoring (other tests may be warranted in some patients, depending on condition; » = major clinical significance):

Creatine kinase (CK), serum {01}    (periodic determinations recommended in patients who develop muscle pain, tenderness, or weakness during therapy or if concurrently receiving azole antifungals, erythromycin, gemfibrozil, immunosuppressive drugs such as cyclosporine, or niacin {01})


» Hepatic function determinations {01}    (recommended prior to initiation of treatment and at 6 and 12 weeks of treatment or at a dosage increase, and periodically, such as every 6 months, thereafter {01})


» Lipid concentrations, serum {01} , primarily:
Low-density lipoprotein cholesterol (LDL-C) {01} and, if not available
Total cholesterol (total-C) {01}     (determinations recommended within 2 to 4 weeks after initiation or at a dosage adjustment of atorvastatin {01})




Side/Adverse Effects

Note: Brain hemorrhage was seen in a female dog given 120 mg per kg of body weight (mg/kg) per day of atorvastatin for 3 months {01}. This dose represents approximately 16 times the human area under the plasma concentration–time curve (AUC [0-24]) based on the maximum human dose of 80 mg per day {01}. Brain hemorrhage and optic nerve vacuolation were seen after 11 weeks in another female dog given atorvastatin in escalating doses of up to 280 mg/kg per day {01}.
In a 2-year study in male dogs, a single tonic convulsion was seen in two dogs; one had been given 10 mg/kg per day and the other had been given 120 mg/kg per day of atorvastatin {01}.
Central nervous system vascular lesions, characterized by perivascular hemorrhages, edema, and mononuclear cell infiltration of perivascular spaces, have been observed in dogs treated with other HMG-CoA reductase inhibitors {01}.
Optic nerve degeneration (Wallerian degeneration of retinogeniculate fibers) was reported in dogs given a chemically similar drug at plasma concentrations 30 times higher than mean plasma concentrations in humans administered the highest recommended human dose {01}.

The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)—not necessarily inclusive:

Those indicating need for medical attention
Incidence less frequent or rare
    
Muscle disorders, such as leg cramps{01}
myalgia, uncomplicated{01} (muscle pain), myopathy and/or rhabdomyolysis{01} (fever; muscle cramps, pain, stiffness, or weakness; unusual tiredness), and myositis{01} (inflammation of muscle)

Note: The degradation of muscle occurs in rhabdomyolysis, resulting in the release of myoglobin into the urine, which can lead to acute renal failure {01}. Myopathy and/or rhabdomyolysis should be considered if symptoms occur in conjunction with creatine kinase (CK) value increases > 10 times the upper limit of normal {01}. The risk of myopathy increases when HMG-CoA reductase inhibitors are administered with azole antifungals, erythromycin, gemfibrozil, immunosuppressants such as cyclosporine, or niacin {01}. Patients should be monitored during the first months of therapy and during dosage increases of either drug, and should report immediately any unexplained symptoms of muscle pain, tenderness, or weakness, especially if accompanied by fever or malaise {01}.




Those indicating need for medical attention only if they continue or are bothersome
Incidence less frequent
    
Abdominal pain{01}
    
constipation{01}
    
diarrhea{01}
    
dyspepsia{01} (heartburn; indigestion; stomach discomfort)
    
flatulence{01} (belching; excessive gas)
    
skin rash{01}





Overdose
For more information on the management of overdose or unintentional ingestion, contact a Poison Control Center (see Poison Control Center Listing ).

Treatment of overdose
Treatment is symptomatic and supportive {01}.

Supportive care—Patients in whom intentional overdose is confirmed or suspected should be referred for psychiatric consultation.


Patient Consultation
As an aid to patient consultation, refer to Advice for the Patient, Atorvastatin (Systemic) .

In providing consultation, consider emphasizing the following selected information (» = major clinical significance):

Before using this medication
»   Conditions affecting use, especially:
Hypersensitivity to atorvastatin

Pregnancy—Contraindicated during pregnancy or in women planning to become pregnant in the near future





Breast-feeding—Contraindicated in women who are breast-feeding



Surgical
Increased risk of development of renal failure secondary to rhabdomyolysis with major surgery
Other medications, especially azole antifungals; erythromycin; gemfibrozil; immunosuppressants, such as cyclosporine; niacin; or grapefruit juice in large amounts{02}{03}
Other medical problems, especially active hepatic disease, including chronic alcoholic liver disease, Childs-Pugh Index grade A disease and Childs-Pugh Index grade B disease; hypotension; major surgery; severe acute infection; severe electrolyte, endocrine, or metabolic disorders; trauma; uncontrolled seizures; or unexplained persistent elevations of transaminase values

Proper use of this medication
Compliance with therapy; taking medication at the same time each day to maintain the antihyperlipidemic effect

Compliance with prescribed diet during treatment

» Proper dosing
Missed dose: Taking as soon as possible; not taking if almost time for next dose; not doubling doses

» Proper storage

Precautions while using this medication
Regular visits to physician to check progress

Notifying physician immediately if pregnancy is suspected because of possible harm to the fetus

Caution if any kind of surgery (including dental surgery) or emergency treatment is required

Not taking over-the-counter niacin preparations without consulting physician because of increased risk of rhabdomyolysis

Not using alcohol excessively because elevations of liver enzymes may occur

Notifying physician immediately if unexplained muscle pain, tenderness, or weakness occurs, especially if accompanied by unusual tiredness or fever {01}


Side/adverse effects
Signs of potential side effects, especially muscle disorders, such as leg cramps, uncomplicated myalgia, myopathy and/or rhabdomyolysis, and myositis


General Dosing Information
Clinical response to atorvastatin is seen within 2 weeks, and maximum response is usually achieved within 4 weeks and maintained during long-term therapy {01}.

Prior to starting atorvastatin therapy, secondary causes for hypercholesterolemia, such as poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease, other medication therapy, and alcoholism should be excluded and a lipid profile performed to measure total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) {01}.

Atorvastatin may be used with colestipol or cholestyramine for additive antihyperlipidemic effects {01}.

Diet/Nutrition
Prior to treatment with atorvastatin, control of hypercholesterolemia with diet, exercise, weight reduction in obese patients, and treatment of underlying medical problems should be attempted {01}. The patient should be placed on a standard cholesterol-lowering diet before receiving atorvastatin and should continue on this diet during treatment with atorvastatin {01}.

Atorvastatin may be taken with or without food {01}.

Grapefruit juice and grapefruit products in large doses should not be taken before or after administration of atorvastatin or the dose of atorvastatin should be reduced accordingly in order to avoid significant increases in plasma drug concentrations and the area under the atorvastatin plasma concentration-time curve (AUC){02}{03}.

For additional information on initial therapeutic guidelines related to the treatment of hyperlipidemia, see Appendix III .


Oral Dosage Forms

ATORVASTATIN CALCIUM TABLETS

Usual adult dose
Heterozygous familial and nonfamilial hypercholesterolemia and mixed dyslipidemia (Fredrickson Types IIa and IIb)
Oral, initially 10 mg once a day {01}. The dosage range is 10 to 80 mg once a day, to be administered at any time of the day, with or without food {01}. After initiation or titration of atorvastatin, lipid concentrations should be measured within 2 to 4 weeks and the dosage adjusted accordingly {01}.

Note: The goal of therapy is to lower LDL-C {01}. The National Cholesterol Education Program (NCEP) recommends that LDL-C concentrations be used to initiate and assess treatment response {01}. Only if LDL-C concentrations are not available should total-C be used to monitor therapy {01}.


Homozygous familial hypercholesterolemia
Oral, 10 to 80 mg a day {01}.

Note: Atorvastatin should be used in these patients as an adjunct to other lipid-lowering treatments, such as LDL apheresis, or if such treatments are unavailable {01}.



Usual adult prescribing limits
80 mg a day {01}.

Usual pediatric dose
Homozygous familial hypercholesterolemia
Dosage has not been established.


Strength(s) usually available
U.S.—


10 mg (Rx) [Lipitor (film-coated)]


20 mg (Rx) [Lipitor (film-coated)]


40 mg (Rx) [Lipitor (film-coated)]

Packaging and storage:
Store at controlled room temperature between 20 and 25 °C (68 and 77 °F) {01}.

Auxiliary labeling:
Do not take other medications without your doctor's advice



Developed: 10/29/1997
Revised: 08/07/2000



References
  1. Lipitor package insert (Parke-Davis—US), New 12/96, Rec 3/97, Rev 1/97, Rec 7/97.
  1. Lilja J, Kivisto KT, Neuvonen PJ. Grapefruit juice increases serum concentrations of atorvastatin and has no effect on pravastatin. Clin Pharmacol Ther 1999; 66:118–127.
  1. Personal Communication: Ana Aymes, Drug Information Services, Parke-Davis, July 2000.

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