After a comprehensive review of all available data, the FDA is requesting all statin manufacturers to remove the contraindication in the prescribing information against using statins in pregnant patients. Although statin therapy should be discontinued in most pregnant patients, health care providers should consider the ongoing therapeutic needs of the individual patient, especially patients at very high risk of cardiovascular events during pregnancy, such as patients with homozygous familial hypercholesterolemia or those with established cardiovascular disease. Additionally, breastfeeding is still not recommended in patients taking a statin; health care providers should determine whether it is better to temporarily stop statin therapy while breastfeeding or to continue statin therapy and not have the patient breastfeed. If ongoing statin treatment is necessary, infant formula and other alternatives are available. The FDA expects that removing the contraindication will enable health care providers and patients to make individual decisions about benefit and risk, especially for those at very high risk of heart attack or stroke.
Further information is available at https://www.fda.gov/drugs/drug-safety-and-availability/fda-requests-removal-strongest-warning-against-using-cholesterol-lowering-statins-during-pregnancy.
Note: Use in conjunction with lifestyle modification (eg, diet, exercise). When choosing to initiate therapy and selecting dose intensity, consider the following: age, baseline LDL cholesterol (LDL-C), 10-year atherosclerotic cardiovascular disease (ASCVD) risk, risk-enhancing factors, potential adverse effects, and drug interactions. Pitavastatin is considered a moderate-intensity statin at doses of 1 to 4 mg/day (generally reduces LDL-C by ~30% to 49%). If LDL-C must be lowered ≥50%, select an alternative high-intensity statin (atorvastatin or rosuvastatin). Assess response ~1 to 3 months after initiation of therapy or dose adjustment and every 3 to 12 months thereafter (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
Heterozygous familial hypercholesterolemia:
Note: Use of pitavastatin should be limited to patients unable to tolerate a high-intensity statin (atorvastatin or rosuvastatin). Multiple lipid-lowering therapies may be needed if statin monotherapy is not effective. Referral to a lipid specialist should be considered if treatment goals are not met (ACC/AHA [Grundy 2019]; Rosenson 2021).
Patients unable to tolerate high-intensity therapy:
Moderate-intensity therapy: Oral: 1 to 4 mg once daily (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
Prevention of atherosclerotic cardiovascular disease (off-label use):
Note: If LDL-C goal (eg, percent reduction or absolute goal) is not met with the initial dose, may consider up-titration to a maximum of 4 mg/day based on estimated 10-year ASCVD risk (see ACC/AHA ASCVD Risk Estimator Plus online), LDL-C response, and tolerability. If LDL-C goal is not met with maximally tolerated dose, consider switching to a high-intensity statin (atorvastatin or rosuvastatin); additional lipid-lowering therapy may be warranted (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
Primary prevention:
Patients without diabetes, age 40 to 75 years, and LDL-C 70 to 189 mg/dL:
ASCVD 10-year risk 5% to <7.5%:
Note: Depending on baseline LDL-C and presence of risk-enhancing factors, consider statin therapy after shared decision-making with patient. Some experts suggest shared decision-making if ASCVD 10-year risk is 5% to 10%; however, in patients with a baseline LDL-C ≥160 mg/dL, statin therapy is usually recommended (Pignone 2020).
Moderate-intensity therapy: Oral: 1 to 4 mg once daily to reduce LDL-C by 30% to 49% (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
ASCVD 10-year risk ≥7.5% to <20%:
Note: Depending on baseline LDL-C and presence of risk-enhancing factors, consider statin therapy after shared decision-making with patient. Some experts suggest initiating moderate-intensity statin therapy in most patients if ASCVD 10-year risk is >10% to <20% and LDL-C is >100 mg/dL (Pignone 2020).
Moderate-intensity therapy: Oral: 1 to 4 mg once daily to reduce LDL-C by 30% to 49%; higher risk patients with multiple risk-enhancing factors may benefit from high-intensity statin therapy (ie, with atorvastatin or rosuvastatin) to reduce LDL-C by ≥50% (ACC/AHA [Grundy 2019]).
ASCVD 10-year risk ≥20% (alternative agent):
Note: Use of pitavastatin should be limited to patients unable to tolerate a high-intensity statin (ACC/AHA [Grundy 2019]).
Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):
Moderate-intensity therapy: Oral: 1 to 4 mg once daily (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
Patients with diabetes:
Age 40 to 75 years without additional ASCVD risk factors :
Moderate-intensity therapy: Oral: 1 to 4 mg once daily to reduce LDL-C by 30% to 49% (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
ASCVD 10-year risk ≥20% or multiple ASCVD risk factors (alternative agent) :
Note: Use of pitavastatin should be limited to patients unable to tolerate a high-intensity statin (ACC/AHA [Grundy 2019]).
Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):
Moderate-intensity therapy: Oral: 1 to 4 mg once daily (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
Patients with LDL-C ≥190 mg/dL and age 20 to 75 years (regardless of ASCVD risk estimate or coexisting diabetes mellitus) (alternative agent):
Note: Use of pitavastatin should be limited to patients unable to tolerate a high-intensity statin (ACC/AHA [Grundy 2019]).
Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):
Moderate-intensity therapy: Oral: 1 to 4 mg once daily (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
Secondary prevention in patients with established ASCVD (eg, coronary heart disease, cerebrovascular disease [ischemic stroke or transient ischemic attack], peripheral arterial disease) (alternative agent):
Note: Use of pitavastatin should be limited to patients unable to tolerate a high-intensity statin (ACC/AHA [Grundy 2019]). Patients with high-risk ASCVD may require additional therapies to achieve LDL-C goal (eg, <70 mg/dL or <50 mg/dL if very high risk) (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]; Rosenson 2020).
Patients unable to tolerate high-intensity therapy (eg, appropriate doses of atorvastatin or rosuvastatin):
Moderate-intensity therapy: Oral: 1 to 4 mg once daily (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
GFR ≥60 mL/minute/1.73 m2: There are no dosage adjustments provided in the manufacturer’s labeling.
GFR 15 to 59 mL/minute/1.73 m2 (not receiving hemodialysis): Initial: 1 mg once daily; maximum: 2 mg/day
ESRD receiving hemodialysis: Initial: 1 mg once daily; maximum: 2 mg/day
Contraindicated in active liver disease or in patients with unexplained persistent elevations of serum transaminases.
(For additional information see "Pitavastatin: Pediatric drug information")
Note: Dosage should be individualized according to the baseline LDL-C level, the recommended goal of therapy, and patient response; adjustments should be made at intervals of 4 weeks. Lifestyle changes are recommended to be implemented for at least 6 to 12 months before beginning pharmacotherapy (AACE [Jellinger 2017]). Pitavastatin is available in 2 salt forms (calcium and magnesium); dosing expressed as mg of pitavastatin base.
Heterozygous familial hypercholesterolemia (HeFH): Children ≥8 years and Adolescents: Livalo (pitavastatin calcium): Oral: Initial: 2 mg once daily; evaluate lipids after 4 weeks and titrate dose accordingly; maximum daily dose: 4 mg/day; lipid levels should be evaluated 4 weeks after any dose adjustment.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Dosing adjustment for toxicity: Muscle symptoms (potential myopathy): Children ≥8 years and Adolescents: Discontinue use until symptoms can be evaluated; check CPK level; based on experience in adult patients, also evaluate patient for conditions that may increase the risk for muscle symptoms (eg, hypothyroidism; reduced renal or hepatic function; rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases). Upon resolution (symptoms and any associated CPK abnormalities), resume the original dose or consider a lower dose of pitavastatin and retitrate. If muscle symptoms recur, discontinue pitavastatin use. After muscle symptom resolution, may then reinitiate a different statin at an initial low dose; gradually increase if tolerated. Based on experience in adult patients, if muscle symptoms or elevated CPK persists for 2 months in the absence of continued statin use, consider other causes of muscle symptoms. If determined to be due to another condition aside from statin use, may resume statin therapy at the original dose (NHLBI 2011; ACC/AHA [Stone 2014]).
Children ≥8 years and Adolescents: Livalo: There are no pediatric-specific recommendations (has not been established); based on experience in adult patients, dosage reductions should be considered.
Children ≥8 years and Adolescents: Livalo: Contraindicated in active liver disease or in patients with unexplained persistent elevations of serum transaminases.
Refer to adult dosing.
Severe muscle symptoms or fatigue: Promptly discontinue use; evaluate CPK, creatinine, and urinalysis for myoglobinuria (ACC/AHA [Stone 2014]).
Mild to moderate muscle symptoms: Discontinue use until symptoms can be evaluated; evaluate patient for conditions that may increase the risk for muscle symptoms (eg, hypothyroidism, reduced renal or hepatic function, rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases). Upon resolution, resume the original or lower dose of pitavastatin. If muscle symptoms recur, discontinue pitavastatin use. After muscle symptom resolution, may then use a low dose of a different statin; gradually increase if tolerated. In the absence of continued statin use, if muscle symptoms or elevated CPK continues after 2 months, consider other causes of muscle symptoms. If determined to be due to another condition aside from statin use, may resume statin therapy at the original dose (ACC/AHA [Stone 2014]).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral, as calcium:
Livalo: 1 mg, 2 mg, 4 mg
Tablet, Oral, as magnesium [strength expressed as base]:
Zypitamag: 1 mg [DSC], 2 mg, 4 mg
No
Administer with or without food; may take without regard to time of day.
Oral: Administer without regard to food or time of day; take at the same time each day.
Heterozygous familial hypercholesterolemia (Livalo [pitavastatin calcium] only): As an adjunctive therapy to diet to reduce elevated total cholesterol, LDL-C, and apo B in children and adolescents ≥8 years of age.
Heterozygous familial hypercholesterolemia: As an adjunctive therapy to diet to reduce elevated total cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (apo B), and triglycerides, and to increase high-density lipoprotein cholesterol in adults with primary hyperlipidemia.
Primary and secondary prevention of atherosclerotic cardiovascular disease
Pitavastatin may be confused with atorvastatin, fluvastatin, lovastatin, nystatin, pravastatin, rosuvastatin, simvastatin
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
1% to 10%:
Gastrointestinal: Constipation (4%), diarrhea (3%)
Neuromuscular & skeletal: Back pain (4%), myalgia (2% to 3%)
Frequency not defined:
Central nervous system: Headache
Dermatologic: Pruritus, skin rash, urticaria
Endocrine & metabolic: Increased serum glucose
Hepatic: Increased serum alkaline phosphatase, increased serum bilirubin, increased serum transaminases
Hypersensitivity: Hypersensitivity reaction
Infection: Influenza
Neuromuscular & skeletal: Arthralgia, increased creatine phosphokinase in blood specimen
Respiratory: Nasopharyngitis
<1%, postmarketing, and/or case reports: Abdominal distress, abdominal pain, amnesia, angioedema, asthenia, cognitive dysfunction, confusion, depression, dizziness, dyspepsia, elevated glycosylated hemoglobin, erectile dysfunction, fatigue, forgetfulness, hepatic failure, hepatitis, hypoesthesia, immune-mediated necrotizing myopathy, insomnia, interstitial pulmonary disease, jaundice, malaise, memory impairment, muscle spasm, myopathy, nausea, peripheral neuropathy, rhabdomyolysis
Hypersensitivity to pitavastatin or any component of the formulation; active liver disease, including unexplained persistent elevations of hepatic transaminase levels; pregnancy; lactation; coadministration with cyclosporine
Concerns related to adverse effects:
• Diabetes mellitus: Increases in HbA1c and fasting blood glucose have been reported; however, the benefits of statin therapy far outweigh the risk of dysglycemia. Optimize lifestyle measures including exercise, maintaining a healthy body weight, and making healthy food choices.
• Hepatotoxicity: Elevations in serum transaminases have been reported; elevations were transient and resolved or improved on continued therapy or after a brief interruption in therapy in most cases. Postmarketing reports of fatal and nonfatal hepatic failure have been reported and are rare. If serious hepatotoxicity with clinical symptoms and/or hyperbilirubinemia or jaundice occurs during treatment, interrupt therapy promptly. Consider baseline and periodic liver enzyme tests, as clinically indicated. Ethanol may enhance the potential of adverse hepatic effects; instruct patients to avoid excessive ethanol consumption.
• Hypersensitivity: Hypersensitivity reactions, including rash, pruritus, and urticaria, have been reported.
• Myopathy/Rhabdomyolysis: Myopathy with CPK >10 times the ULN and rhabdomyolysis (sometimes fatal) with or without acute renal failure secondary to myoglobinuria have been reported; patients should be monitored closely. This risk is dose-related (doses >4 mg) and is increased with concurrent use of colchicine, erythromycin, fibrates, niacin (doses ≥1 g/day), or rifampin. If concurrent use is warranted, consider lower starting and maintenance doses of pitavastatin; use is contraindicated with cyclosporine and not recommended with gemfibrozil. Use caution in patients ≥65 years of age, uncontrolled hypothyroidism, and renal impairment; these patients are predisposed to myopathy. Immune-mediated necrotizing myopathy (IMNM) associated with HMG-CoA reductase inhibitors use has also been reported rarely. Patients should be instructed to report unexplained muscle pain, tenderness, weakness, or brown urine, particularly if accompanied by malaise or fever or if muscle signs and symptoms persist after discontinuing pitavastatin. Temporarily withhold therapy in any patient with an acute, serious condition suggestive of myopathy or predisposing to the development of renal failure secondary to rhabdomyolysis (eg, sepsis; shock; severe hypovolemia; major surgery; trauma; severe metabolic, endocrine, electrolyte disorders; uncontrolled epilepsy). Discontinue therapy if markedly elevated CPK levels occur or myopathy is diagnosed/suspected; consider treatment with immunosuppressants and additional neuromuscular and serologic testing. Prior to initiating a different HMG-CoA reductase inhibitor consider risk of IMNM; monitor closely.
Disease-related concerns:
• Hepatic impairment: Use is contraindicated in patients with active liver disease or unexplained persistent elevations of serum transaminases; use with caution in patients who consume large amounts of ethanol or have a history of liver disease.
• Myasthenia gravis: May rarely worsen or precipitate myasthenia gravis (MG); monitor for worsening MG if treatment is initiated (AAN [Narayanaswami 2021]).
• Renal impairment: Use with caution in patients with renal impairment; these patients are predisposed to myopathy and rhabdomyolysis. Dosage adjustment required in patients with GFR <60 mL/minute/1.73 m2 including end-stage renal disease receiving hemodialysis.
Special Populations:
• Elderly: Use with caution in patients ≥65 years of age; these patients are predisposed to myopathy and rhabdomyolysis.
• Surgical patients: The manufacturer recommends temporary discontinuation for elective major surgery, acute medical or surgical conditions, or in any patient experiencing an acute or serious condition predisposing to renal failure (eg, sepsis; shock; severe hypovolemia; trauma; severe metabolic, endocrine, electrolyte disorders; uncontrolled epilepsy). Based on current research and clinical guidelines, HMG-CoA reductase inhibitors should be continued in the perioperative period for noncardiac and cardiac surgery (ACC/AHA [Fleisher 2014]; ACC/AHA [Hillis 2011]). Perioperative discontinuation of statin therapy is associated with an increased risk of cardiac morbidity and mortality.
Other warnings/precautions:
• Appropriate use: The effect on cardiovascular morbidity and mortality has not been determined.
• Hyperlipidemia: Secondary causes of hyperlipidemia should be ruled out prior to therapy.
Substrate of CYP2C8 (minor), CYP2C9 (minor), OATP1B1/1B3 (SLCO1B1/1B3), UGT1A3, UGT2B7; Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Acipimox: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy
Asunaprevir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy
Bezafibrate: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Bezafibrate may increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). More specifically, bezafibrate may increase the serum concentration of fluvastatin Management: Avoid use of bezafibrate and HMG-CoA reductase inhibitors (statins) unless strictly indicated due to the increased of muscle toxicity (including rhabdomyolysis). In patients who may be predisposed to myopathy, concomitant use is contraindicated. Risk D: Consider therapy modification
Ciprofibrate: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Management: Avoid the use of HMG-CoA reductase inhibitors and ciprofibrate if possible. If concomitant therapy is considered, benefits should be carefully weighed against the risks, and patients should be monitored closely for signs/symptoms of muscle toxicity. Risk D: Consider therapy modification
Clarithromycin: May increase the serum concentration of Pitavastatin. Risk C: Monitor therapy
Cobicistat: May increase the serum concentration of Pitavastatin. Risk C: Monitor therapy
Colchicine: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Colchicine may increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy
CycloSPORINE (Systemic): May increase the serum concentration of Pitavastatin. Risk X: Avoid combination
Daclatasvir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy
DAPTOmycin: HMG-CoA Reductase Inhibitors (Statins) may enhance the adverse/toxic effect of DAPTOmycin. Specifically, the risk of skeletal muscle toxicity may be increased. Management: Consider temporarily stopping statin (HMG-CoA reductase inhibitor) therapy prior to daptomycin. If daptomycin is used with a statin, creatine phosphokinase (CPK) monitoring could be considered. Risk D: Consider therapy modification
Eltrombopag: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy
Encorafenib: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy
Erythromycin (Systemic): May increase the serum concentration of Pitavastatin. Management: Limit pitavastatin to a maximum of 1 mg/day when used in combination with erythromycin. If this combination is used, monitor patients more closely for evidence of pitavastatin toxicity. Risk D: Consider therapy modification
Etravirine: May increase the serum concentration of Pitavastatin. Risk C: Monitor therapy
Fenofibrate and Derivatives: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy
Fosphenytoin-Phenytoin: May decrease the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Consider avoiding coadministration of fosphenytoin/phenytoin and statins. If combined, monitor for decreased therapeutic effects of statins if fosphenytoin/phenytoin is initiated/dose increased. Risk D: Consider therapy modification
Fostemsavir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest possible starting statin dose and monitor patients closely for statin-related adverse effects (eg, muscle aches and pains) during coadministration with fostemsavir. Risk D: Consider therapy modification
Fusidic Acid (Systemic): May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk for muscle toxicities, including rhabdomyolysis may be significantly increased. Management: Avoid concurrent use whenever possible. Use is listed as contraindicated in product characteristic summaries in several countries, although UK labeling suggests that use could be considered under exceptional circumstances and with close supervision. Risk X: Avoid combination
Gemfibrozil: May enhance the myopathic (rhabdomyolysis) effect of Pitavastatin. Gemfibrozil may increase the serum concentration of Pitavastatin. Risk X: Avoid combination
Glecaprevir and Pibrentasvir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest statin dose possible if combined with glecaprevir/pibrentasvir and monitor for increased statin effects/toxicities. Avoid concomitant use with atorva-, simva-, or lovastatin. Limit rosuvastatin to 10 mg daily and reduce pravastatin dose 50% Risk D: Consider therapy modification
Lanthanum: HMG-CoA Reductase Inhibitors (Statins) may decrease the serum concentration of Lanthanum. Management: Administer HMG-CoA reductase inhibitors at least two hours before or after lanthanum. Risk D: Consider therapy modification
Letermovir: May increase the serum concentration of Pitavastatin. Risk X: Avoid combination
Niacin: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy
Niacinamide: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy
Ombitasvir, Paritaprevir, Ritonavir, and Dasabuvir: May increase the serum concentration of Pitavastatin. Management: Canadian product labeling recommends use of the lowest pitavastatin dose with this combination. Risk C: Monitor therapy
Raltegravir: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy
Red Yeast Rice: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk X: Avoid combination
Repaglinide: HMG-CoA Reductase Inhibitors (Statins) may increase the serum concentration of Repaglinide. Risk C: Monitor therapy
RifAMPin: May increase the serum concentration of Pitavastatin. Management: Limit pitavastatin dose to a maximum of 2 mg/day with concurrent rifampin. Risk D: Consider therapy modification
Rupatadine: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk for increased CPK and/or other muscle toxicities may be increased. Risk C: Monitor therapy
Simeprevir: May increase the serum concentration of Pitavastatin. Risk C: Monitor therapy
Telithromycin: May increase the serum concentration of Pitavastatin. Risk C: Monitor therapy
Teriflunomide: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy
Trabectedin: HMG-CoA Reductase Inhibitors (Statins) may enhance the myopathic (rhabdomyolysis) effect of Trabectedin. Risk C: Monitor therapy
Voclosporin: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy
Voxilaprevir: May increase the serum concentration of Pitavastatin. Risk X: Avoid combination
Adequate contraception is recommended if an HMG-CoA reductase inhibitor is required in females of reproductive potential. Females planning a pregnancy should discontinue the HMG-CoA reductase inhibitor 1 to 2 months prior to attempting to conceive (AHA/ACC [Grundy 2019]).
Pitavastatin is contraindicated in pregnant females.
There are reports of congenital anomalies following maternal use of HMG-CoA reductase inhibitors in pregnancy; however, maternal disease, differences in specific agents used, and the low rates of exposure limit the interpretation of the available data (Godfrey 2012; Lecarpentier 2012). Cholesterol biosynthesis may be important in fetal development; serum cholesterol and triglycerides increase normally during pregnancy. The discontinuation of lipid lowering medications temporarily during pregnancy is not expected to have significant impact on the long term outcomes of primary hypercholesterolemia treatment.
Pitavastatin should be discontinued immediately if an unplanned pregnancy occurs during treatment.
It is not known if pitavastatin is present in breast milk. Due to the potential for serious adverse reactions in a breastfed infant, use while breastfeeding is contraindicated by the manufacturer.
Red yeast rice contains variable amounts of several compounds that are structurally similar to HMG-CoA reductase inhibitors, primarily monacolin K (or mevinolin) which is structurally identical to lovastatin; concurrent use of red yeast rice with HMG-CoA reductase inhibitors may increase the incidence of adverse and toxic effects (Lapi 2008; Smith 2003).
ACC/AHA Blood Cholesterol Guideline recommendations ( ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]):
Lipid panel (total cholesterol, HDL, LDL, triglycerides): Lipid profile (fasting or nonfasting) before initiating treatment. Fasting lipid profile should be rechecked 4 to 12 weeks after starting therapy and every 3 to 12 months thereafter. If 2 consecutive LDL levels are <40 mg/dL, consider decreasing the dose.
Hepatic transaminase levels: Baseline measurement of hepatic transaminase levels (AST and ALT); measure AST, ALT, total bilirubin, and alkaline phosphatase if symptoms suggest hepatotoxicity (eg, unusual fatigue or weakness, loss of appetite, abdominal pain, dark-colored urine or yellowing of skin or sclera) during therapy.
CPK: CPK should not be routinely measured. Baseline CPK measurement is reasonable for some individuals (eg, family history of statin intolerance or muscle disease, clinical presentation, concomitant drug therapy that may increase risk of myopathy). May measure CPK in any patient with symptoms suggestive of myopathy (pain, tenderness, stiffness, cramping, weakness, or generalized fatigue).
Evaluate for new-onset diabetes mellitus during therapy; if diabetes develops, continue statin therapy and encourage adherence to a heart-healthy diet, physical activity, a healthy body weight, and tobacco cessation.
If patient develops a confusional state or memory impairment, may evaluate patient for nonstatin causes (eg, exposure to other drugs), systemic and neuropsychiatric causes, and the possibility of adverse effects associated with statin therapy.
Manufacturer's labeling: Consider neuromuscular and serologic testing if immune-mediated necrotizing myopathy is suspected.
Treatment goals: May vary depending on clinical condition, different clinical practice guidelines, and expert opinion. Refer to clinical practice guidelines for specific treatment goals.
Inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis (reduces the production of mevalonic acid from HMG-CoA); this then results in a compensatory increase in the expression of LDL receptors on hepatocyte membranes and a stimulation of LDL catabolism. In addition to the ability of HMG-CoA reductase inhibitors to decrease levels of high-sensitivity C-reactive protein (hsCRP), they also possess pleiotropic properties including improved endothelial function, reduced inflammation at the site of the coronary plaque, inhibition of platelet aggregation, and anticoagulant effects (de Denus 2002; Ray 2005).
Distribution: Vd: ~148 L
Protein binding: >99%, primarily to albumin and alpha 1-acid glycoprotein
Metabolism: Hepatic, via UGT1A3 and UGT2B7; minimal metabolism via CYP2C9 and CYP2C8
Bioavailability: 51%
Half-life elimination: ~12 hours
Time to peak, plasma: ~1 hour
Excretion: Feces (79%); urine (15%)
Renal function impairment: Cmax and AUC were 60% and 102% higher in patients with GFR 30 to 59 mL/minute/1.73 m2 and 40% and 86% higher in patients with ESRD on hemodialysis, respectively.
Hepatic function impairment: Half-life was 15 and 10 hours for patients with moderate and mild impairment, respectively.
Geriatric: Cmax and AUC were 10% and 30% higher, respectively, in elderly patients compared with younger patients.
Gender: Cmax and AUC were 60% and 54% higher, respectively, in women compared with men.
Race: Cmax and AUC were 21% and 5% lower, respectively, in black patients compared with white patients.
Tablets (Livalo Oral)
1 mg (per each): $12.79
2 mg (per each): $12.79
4 mg (per each): $12.79
Tablets (Zypitamag Oral)
2 mg (per each): $9.30
4 mg (per each): $9.30
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