Pravastatin

Generic

Generic for Pravachol

ID: 60505016805

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Tablet

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10 mg

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TL;DR — Quick Summary

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INDICATIONS & USAGE SECTION DOSAGE & ADMINISTRATION SECTION SPL UNCLASSIFIED SECTION 2.5 Dosage and Administration Modifications Due to Drug Interactions DOSAGE FORMS & STRENGTHS SECTION

🩺What it's for

Pravastatin sodium tablets are indicated: To reduce the risk of myocardial infarction, myocardial revascularization procedures, and cardiovascular mortality in adults with elevated low-density lipoprotein cholesterol (LDL-C) without clinically evident coronary heart disease (CHD).

💊How to take it

Take orally once daily at any time of the day, with or without food (2.1). For patients that require a high-intensity statin or are unable to achieve their LDL-C goal receiving pravastatin sodium tablets 80 mg daily, prescribe alternative LDL-C-lowering treatment (2.1). Assess LDL-C when clinically appropriate, as early as 4 weeks after initiating pravastatin sodium tablets, and adjust the dosage if necessary (2.1).

ℹ️Common side effects

The following important adverse reactions are described below and elsewhere in the labeling: Myopathy and Rhabdomyolysis [see Warnings and Precautions (5.1)] Immune-Mediated Necrotizing Myopathy [see Warnings and Precautions ( 5.2 )] Hepatic Dysfunction [see Warnings and Precautions (5.3)] Increases in HbA1c and Fasting Serum Glucose Levels [see Warnings and Precautions (5.4)] In short-term clinical trials, the most commonly reported adverse reactions ( 2% and greater than placebo) were:…

⚠️Serious risks

Myopathy and Rhabdomyolysis: Risk factors include age 65 years or greater, uncontrolled hypothyroidism, renal impairment, concomitant use with certain other drugs, and higher pravastatin dosage. Discontinue pravastatin if markedly elevated CK levels occur or myopathy is diagnosed or suspected. Temporarily discontinue pravastatin in patients experiencing an acute or serious condition at high risk of developing renal failure secondary to rhabdomyolysis.

📋Interactions & cautions

In patients taking a bile acid sequestrant, administer pravastatin sodium tablets at least 1 hour before or 4 hours after the bile acid sequestrant [see Drug Interactions (7.2)]. Concomitant use of pravastatin sodium tablets with the following drugs requires dosage modifications of pravastatin sodium tablet s [see Warnings and Precautions (5.1) and Drug Interactions (7.1)]: Cyclosporine In patients taking cyclosporine, the recommended starting dosage is pravastatin sodium 10 mg once daily.

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The following adverse reactions have been identified during postapproval use of pravastatin. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. Musculoskeletal: myopathy, rhabdomyolysis, tendon disorder, polymyositis, immune-mediated necrotizing myopathy associated with statin use. Nervous System: dysfunction of certain cranial nerves (including alteration of taste, impairment of extraocular movement, facial paresis), peripheral nerve palsy. Rare postmarketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use. Cognitive impairment was generally nonserious, and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median of 3 weeks). There have been rare reports of new-onset or exacerbation of myasthenia gravis, including ocular myasthenia, and reports of recurrence when the same or a different statin was administered. Hypersensitivity: anaphylaxis, angioedema, lupus erythematosus-like syndrome, polymyalgia rheumatica, dermatomyositis, vasculitis, purpura, hemolytic anemia, positive ANA, ESR increase, arthritis, arthralgia, asthenia, photosensitivity, chills, malaise, toxic epidermal necrolysis, erythema multiforme (including Stevens-Johnson syndrome). Gastrointestinal: abdominal pain, constipation, pancreatitis, hepatitis (including chronic active hepatitis), cholestatic jaundice, fatty change in liver, cirrhosis, fulminant hepatic necrosis, hepatoma, fatal and non-fatal hepatic failure. Dermatologic: a variety of skin changes (e.g., nodules, discoloration, dryness of mucous membranes, changes to hair/nails), lichen planus. Renal: urinary abnormality (including dysuria, frequency, nocturia). Respiratory: dyspnea, interstitial lung disease. Psychiatric: nightmare. Reproductive: gynecomastia. Laboratory Abnormalities: liver function test abnormalities, thyroid function abnormalities.

Risk Summary Discontinue pravastatin when pregnancy is recognized. Alternatively, consider the ongoing therapeutic needs of the individual patient. Pravastatin decreases synthesis of cholesterol and possibly other biologically active substances derived from cholesterol; therefore, pravastatin may cause fetal harm when administered to pregnant patients based on the mechanism of action [see Clinical Pharmacology (12.1)]. In addition, treatment of hyperlipidemia is not generally necessary during pregnancy. Atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hyperlipidemia for most patients. Available data from case series and prospective and retrospective observational cohort studies over decades of use with statins in pregnant women have not identified a drug-associated risk of major congenital malformations. Published data from prospective and retrospective observational cohort studies with pravastatin use in pregnant women are insufficient to determine if there is a drug-associated risk of miscarriage (see Data). In animal reproduction studies, no evidence of fetal malformations was seen in pregnant rats or rabbits orally administered pravastatin during the period of organogenesis at doses that resulted in 10 times and 120 times, respectively, the human exposure at the maximum recommended human dose (MRHD) of 80 mg/day, based on body surface area (mg/m2). An imbalance in some fetal skeletal variations, increased offspring mortality, and developmental delays occurred when pregnant rats were exposed to 10 times to 12 times the MRHD during organogenesis to parturition (see Data). The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. Data Human Data A Medicaid cohort linkage study of 1,152 statin-exposed pregnant women compared to 886,996 controls did not find a significant teratogenic effect from maternal use of statins in the first trimester of pregnancy, after adjusting for potential cofounders including maternal age, diabetes mellitus, hypertension, obesity, and alcohol and tobacco use using propensity score-based methods. The relative risk of congenital malformations between the group with statin use and the group with no statin use in the first trimester was 1.07 (95% confidence interval 0.85 to 1.37) after controlling for confounders, particularly pre-existing diabetes mellitus. There were also no statistically significant increases in any of the organ-specific malformations assessed after accounting for cofounders. In the majority of pregnancies, statin treatment was initiated prior to pregnancy and was discontinued at some point in the first trimester when pregnancy was identified. Study limitations include reliance on physician coding to define the presence of a malformation, lack of control for certain confounders such as body mass index, use of prescription dispensing as verification for the use of a statin, and lack of information on non-live births. Animal Data Embryofetal and neonatal mortality was observed in rats given pravastatin during the period of organogenesis or during organogenesis continuing through weaning. In pregnant rats given oral gavage doses of 4 mg/kg/day, 20 mg/kg/day, 100 mg/kg/day, 500 mg/kg/day, and 1,000 mg/kg/day from gestation days 7 through 17 (organogenesis) increased mortality of offspring and increased cervical rib skeletal anomalies were observed at 100 mg/kg/day systemic exposure, 10 times the human exposure at 80 mg/day MRHD based on body surface area (mg/m2). In other studies, no teratogenic effects were observed when pravastatin was dosed orally during organogenesis in rabbits (gestation days 6 through 18) up to 50 mg/kg/day or in rats (gestation days 7 through 17) up to 1,000 mg/kg/day. Exposures were 10 times (rabbit) or 120 times (rat) the human exposure at 80 mg/day MRHD based on body surface area (mg/m2). In pregnant rats given oral gavage doses of 10 mg/kg/day, 100 mg/kg/day, and 1,000 mg/kg/day from gestation day 17 through lactation day 21 (weaning), developmental delays were observed at 100 mg/kg/day systemic exposure, corresponding to 12 times the human exposure at 80 mg/day MRHD, based on body surface area (mg/m2). In pregnant rats, pravastatin crosses the placenta and is found in fetal tissue at 30% of the maternal plasma levels following administration of a single dose of 20 mg/day orally on gestation day 18, which corresponds to exposure 2 times the MRHD of 80 mg daily based on body surface area (mg/m2).

Absorption Pravastatin is administered orally in the active form. Peak plasma pravastatin concentrations occurred 1 to 1.5 hours upon oral administration. Based on urinary recovery of total radiolabeled drug, the average oral absorption of pravastatin is 34% and absolute bioavailability is 17%. While the presence of food in the gastrointestinal tract reduces area under the concentration-time curve (AUC) and Cmax by 31% and 49%, respectively, the lipid-lowering effects of the drug are similar whether taken with or 1 hour prior to meals. Pravastatin plasma concentrations, including AUC, Cmax, and steady-state minimum (Cmin), are directly proportional to administered dose. Systemic bioavailability of pravastatin administered following a bedtime dose was decreased 60% compared to that following an AM dose. Despite this decrease in systemic bioavailability, the efficacy of pravastatin administered once daily in the evening, although not statistically significant, was marginally more effective than that after a morning dose. The coefficient of variation (CV), based on between-subject variability, was 50% to 60% for AUC. The geometric means of pravastatin Cmax and AUC following a 20 mg dose in the fasted state were 26.5 ng/mL and 59.8 ng*hr/mL, respectively. Steady-state AUCs, Cmax, and Cmin plasma concentrations showed no evidence of pravastatin accumulation following once or twice daily administration of pravastatin tablets. Distribution Approximately 50% of the circulating drug is bound to plasma proteins. Elimination Metabolism The major biotransformation pathways for pravastatin are: (a) isomerization to 6- epi pravastatin and the 3 -hydroxy isomer of pravastatin (SQ 31,906) and (b) enzymatic ring hydroxylation to SQ 31,945. The 3 -hydroxy isomeric metabolite (SQ 31,906) has 1/10 to 1/40 the HMG-CoA reductase inhibitory activity of the parent compound. Pravastatin undergoes extensive first-pass extraction in the liver (extraction ratio 0.66). Excretion Approximately 20% of a radiolabeled oral dose is excreted in urine and 70% in the feces. After intravenous administration of radiolabeled pravastatin to normal volunteers, approximately 47% of total body clearance was via renal excretion and 53% by non-renal routes (i.e., biliary excretion and biotransformation). Following single dose oral administration of 14C-pravastatin, the radioactive elimination t for pravastatin is 1.8 hours in humans and the elimination half-life (t ) for total radioactivity (pravastatin plus metabolites) is 77 hours. Specific Populations Renal Impairment A single 20 mg oral dose of pravastatin was administered to 24 patients with varying degrees of renal impairment (as determined by creatinine clearance). No effect was observed on the pharmacokinetics of pravastatin or its 3 -hydroxy isomeric metabolite (SQ 31,906). Compared to healthy subjects with normal renal function, patients with severe renal impairment had 69% and 37% higher mean AUC and Cmax values, respectively, and a 0.61 hour shorter t for the inactive enzymatic ring hydroxylation metabolite (SQ 31,945) [see Use in Specific Populations (8.6)]. Hepatic Impairment In a study comparing the kinetics of pravastatin in patients with biopsy confirmed cirrhosis (N=7) and normal subjects (N=7), the mean AUC varied 18-fold in cirrhotic patients and 5-fold in healthy subjects. Similarly, the peak pravastatin values varied 47-fold for cirrhotic patients compared to 6-fold for healthy subjects [see Use in Specific Populations (8.6)]. Geriatric In a single oral dose study using pravastatin 20 mg, the mean AUC for pravastatin was approximately 27% greater and the mean cumulative urinary excretion (CUE) approximately 19% lower in elderly men (65 to 75 years old) compared with younger men (19 to 31 years old). In a similar study conducted in women, the mean AUC for pravastatin was approximately 46% higher and the mean CUE approximately 18% lower in elderly women (65 to 78 years old) compared with younger women (18 to 38 years old). In both studies, Cmax, Tmax, and t values were similar in older and younger subjects [see Use in Specific Populations (8.5) ]. Pediatric After 2 weeks of once-daily 20 mg oral pravastatin administration, the geometric means of AUC were 80.7 (CV 44%) and 44.8 (CV 89%) ng*hr/mL for pediatric patients 8 to 11 years (N=14) and 12 to 16 years (N=10), respectively. The corresponding values for Cmax were 42.4 (CV 54%) and 18.6 ng/mL (CV 100%) for pediatric patients 8 to 11 years and 12 to 16 years, respectively. No conclusion can be made based on these findings due to the small number of samples and large variability [see Use in Specific Populations (8.4) ]. Drug-Drug Interactions Table 5: Effect of Coadministered Drugs on the Pharmacokinetics of Pravastatin Coadministered Drug and Dosing Regimen Pravastatin Dose (mg) Change in AUC Change in Cmax Cyclosporine 5 mg/kg single dose 40 mg single dose 282% 327% Clarithromycin 500 mg BID for 9 days 40 mg OD for 8 days 110% 128% Boceprevir 800 mg TID for 6 days 40 mg single dose 63% 49% Darunavir 600 mg BID/Ritonavir 100 mg BID for 7 days 40 mg single dose 81% 63% Colestipol 10 g single dose 20 mg single dose 47% 53% Cholestyramine 4 g single dose Administered simultaneouslyAdministered 1 hour prior to cholestyramineAdministered 4 hours after cholestyramine 20 mg single dose 40% 12% 12% 39% 30% 6.8% Cholestyramine 24 g OD for 4 weeks 20 mg BID for 8 weeks5 mg BID for 8 weeks10 mg BID for 8 weeks 51% 38% 18% 4.9% 23% 33% Fluconazole 200 mg IV for 6 days200 mg PO for 6 days 20 mg PO+10 mg IV20 mg PO+10 mg IV 34% 16% 33% 16% Kaletra 400 mg/100 mg BID for 14 days 20 mg OD for 4 days 33% 26% Verapamil IR 120 mg for 1 day andVerapamil ER 480 mg for 3 days 40 mg single dose 31% 42% Cimetidine 300 mg QID for 3 days 20 mg single dose 30% 9.8% Antacids 15 mL QID for 3 days 20 mg single dose 28% 24% Digoxin 0.2 mg OD for 9 days 20 mg OD for 9 days 23% 26% Probucol 500 mg single dose 20 mg single dose 14% 24% Warfarin 5 mg OD for 6 days 20 mg BID for 6 days 13% 6.7% Itraconazole 200 mg OD for 30 days 40 mg OD for 30 days 11% (compared to Day 1) 17% (compared to Day 1) Gemfibrozil 600 mg single dose 20 mg single dose 7.0% 20% Aspirin 324 mg single dose 20 mg single dose 4.7% 8.9% Niacin 1 g single dose 20 mg single dose 3.6% 8.2% Diltiazem 20 mg single dose 2.7% 30% Grapefruit juice 40 mg single dose 1.8% 3.7% BID = twice daily; OD = once daily; QID = four times daily Table 6: Effect of Pravastatin on the Pharmacokinetics of Coadministered Drugs Pravastatin Dosing Regimen Name and Dose Change in AUC Change in Cmax 20 mg BID for 6 days Warfarin 5 mg OD for 6 daysChange in mean prothrombin time 17% 0.4 sec 15% 20 mg OD for 9 days Digoxin 0.2 mg OD for 9 days 4.6% 5.3% 20 mg BID for 4 weeks10 mg BID for 4 weeks5 mg BID for 4 weeks Antipyrine 1.2 g single dose 3.0% 1.6% Less than 1% Not Reported 20 mg OD for 4 days Kaletra 400 mg/100 mg BID for 14 days No change No change BID = twice daily; OD = once daily

In a 2-year study in rats fed pravastatin at doses of 10, 30, or 100 mg/kg body weight, there was an increased incidence of hepatocellular carcinomas in males at the highest dose (p<0.01). These effects in rats were observed at approximately 12 times the human dose (HD) of 80 mg based on body surface area (mg/m2) and at approximately 4 times the HD, based on AUC. In a 2-year study in mice fed pravastatin at doses of 250 and 500 mg/kg/day, there was an increased incidence of hepatocellular carcinomas in males and females at both 250 and 500 mg/kg/day (p<0.0001). At these doses, lung adenomas in females were increased (p=0.013). These effects in mice were observed at approximately 15 times (250 mg/kg/day) and 23 times (500 mg/kg/day) the HD of 80 mg, based on AUC. In another 2-year study in mice with doses up to 100 mg/kg/day (producing drug exposures approximately 2 times the HD of 80 mg, based on AUC), there were no drug-induced tumors. No evidence of mutagenicity was observed in vitro, with or without rat-liver metabolic activation, in the following studies: microbial mutagen tests, using mutant strains of Salmonella typhimurium or Escherichia coli; a forward mutation assay in L5178Y TK +/ mouse lymphoma cells; a chromosomal aberration test in hamster cells; and a gene conversion assay using Saccharomyces cerevisiae. In addition, there was no evidence of mutagenicity in either a dominant lethal test in mice or a micronucleus test in mice. In a fertility study in adult rats with daily doses up to 500 mg/kg, pravastatin did not produce any adverse effects on fertility or general reproductive performance. No adverse effects were seen in juvenile rats dosed with 5 mg/kg/day pravastatin (5 times plasma exposure at the maximum recommended human dose [MRHD] of 80 mg based on AUC) in a study of pravastatin administered from postnatal days (PND) 4 through 80 at 5, 15 and 45 mg/kg/day. A PND 4 rat is generally comparable to a 3rd trimester human fetus with regards to neurologic development/myelination. At 15 mg/kg/day ( 20 times the MRHD), decreased body-weight gain was observed during the pre-weaning period and slight thinning of the corpus callosum was observed at the end of the drug-free recovery period (PND 132). Thinning of the corpus callosum was not associated with any inflammatory or degenerative changes in the brain. Impacts on neurobehavioral and learning endpoints were detected only at very high exposures (43 times the MRHD). No thinning of the corpus callosum was observed in rats dosed with pravastatin for 3 months beginning on PND 35 at 250 mg/kg/day. PND 35 in a rat is approximately equivalent to an 8 to 12-year-old human child.

Prevention of Coronary Heart Disease In the Pravastatin Primary Prevention Study (WOS), the effect of pravastatin on fatal and nonfatal CHD was assessed in 6,595 male patients 45 to 64 years of age, without a previous MI, and with LDL-C levels between 156 to 254 mg/dL. In this randomized, double-blind, placebo-controlled study, patients were treated with standard care, including dietary advice, and either pravastatin 40 mg daily (N=3,302) or placebo (N=3,293) and followed for a median duration of 4.8 years. Median (25th, 75th percentile) percent changes from baseline after 6 months of pravastatin treatment in Total-C, LDL-C, TG, and HDL-C were 20.3 ( 26.9, 11.7), 27.7 ( 36, 16.9), 9.1 ( 27.6, 12.5), and 6.7 ( 2.1, 15.6), respectively. Pravastatin significantly reduced the rate of first coronary events (either CHD death or nonfatal MI) by 31% (248 events in the placebo group [CHD death=44, nonfatal MI=204] versus 174 events in the pravastatin group [CHD death=31, nonfatal MI=143], p=0.0001 [see figure below]). The risk reduction with pravastatin was similar across the age range studied and throughout the range of baseline LDL cholesterol levels. Pravastatin also decreased the risk for undergoing myocardial revascularization procedures (coronary artery bypass graft [CABG] surgery or percutaneous transluminal coronary angioplasty [PTCA]) by 37% (80 vs 51 patients). Cardiovascular deaths were decreased by 32% (73 vs 50) and there was no increase in death from non-cardiovascular causes. Secondary Prevention of Cardiovascular Events In the LIPID study, the effect of pravastatin, 40 mg daily, was assessed in 9,014 patients (7,498 men; 1,516 women; 3,514 patients 65 years; 782 patients with diabetes) who had experienced either an MI (5,754 patients) or had been hospitalized for unstable angina pectoris (3,260 patients) in the preceding 3 to 36 months. Patients in this multicenter, double-blind, placebo-controlled study participated for an average of 5.6 years (median of 5.9 years) and at randomization had Total-C between 114 and 563 mg/dL (mean 219 mg/dL), LDL-C between 46 and 274 mg/dL (mean 150 mg/dL), TG between 35 and 2,710 mg/dL (mean 160 mg/dL), and HDL-C between 1 and 103 mg/dL (mean 37 mg/dL). At baseline, 82% of patients were receiving aspirin and 76% were receiving antihypertensive medication. Treatment with pravastatin significantly reduced the risk for total mortality by reducing coronary death (see Table 7). The risk reduction due to treatment with pravastatin on CHD mortality was consistent regardless of age. Pravastatin significantly reduced the risk for total mortality (by reducing CHD death) and CHD events (CHD mortality or nonfatal MI) in patients who qualified with a history of either MI or hospitalization for unstable angina pectoris. Table 7: LIPID - Primary and Secondary Endpoints Number (%) of Subjects Event Pravastatin 40 mg (N=4,512) Placebo (N=4,502) Risk Reduction p -value Primary Endpoint CHD mortality 287 (6.4) 373 (8.3) 24% 0.0004 Secondary Endpoints Total mortality 498 (11.0) 633 (14.1) 23% <0.0001 CHD mortality or nonfatal MI 557 (12.3) 715 (15.9) 24% <0.0001 Myocardial revascularization procedures (CABG or PTCA) 584 (12.9) 706 (15.7) 20% <0.0001 Stroke All-cause 169 (3.7) 204 (4.5) 19% 0.0477 Non-hemorrhagic 154 (3.4) 196 (4.4) 23% 0.0154 Cardiovascular mortality 331 (7.3) 433 (9.6) 25% <0.0001 In the CARE study, the effect of pravastatin, 40 mg daily, on CHD death and nonfatal MI was assessed in 4,159 patients (3,583 men and 576 women) who had experienced a MI in the preceding 3 to 20 months and who had normal (below the 75th percentile of the general population) plasma total cholesterol levels. Patients in this double-blind, placebo-controlled study participated for an average of 4.9 years and had a mean baseline Total-C of 209 mg/dL. LDL-C levels in this patient population ranged from 101 to 180 mg/dL (mean 139 mg/dL). At baseline, 84% of patients were receiving aspirin and 82% were taking antihypertensive medications. Median (25th, 75th percentile) percent changes from baseline after 6 months of pravastatin treatment in Total-C, LDL-C, TG, and HDL-C were 22 ( 28.4, 14.9), 32.4 ( 39.9, 23.7), 11 ( 26.5, 8.6), and 5.1 ( 2.9, 12.7), respectively. Treatment with pravastatin significantly reduced the rate of first recurrent coronary events (either CHD death or nonfatal MI), the risk of undergoing revascularization procedures (PTCA, CABG), and the risk for stroke or TIA (see Table 8). Table 8: CARE - Primary and Secondary Endpoints Number (%) of Subjects Event Pravastatin 40 mg (N=2,081) Placebo (N=2,078) Risk Reduction p -value Primary Endpoint CHD mortality or nonfatal MIa 212 (10.2) 274 (13.2) 24% 0.003 Secondary Endpoints Myocardial revascularization procedures (CABG or PTCA) 294 (14.1) 391 (18.8) 27% <0.001 Stroke or TIA 93 (4.5) 124 (6.0) 26% 0.029 a The risk reduction due to treatment with pravastatin was consistent in both sexes. Primary Hyperlipidemia In multicenter, double-blind, placebo-controlled studies of patients with primary hyperlipidemia, treatment with pravastatin in daily doses ranging from 10 to 40 mg consistently and significantly decreased Total-C, LDL-C, and TG (see Table 9). In a pooled analysis of 2 multicenter, double-blind, placebo-controlled studies of patients with primary hyperlipidemia, treatment with pravastatin at a daily dose of 80 mg (N=277) significantly decreased Total-C, LDL-C, and TG. The 25th and 75th percentile changes from baseline in LDL-C for pravastatin 80 mg were 43% and 30%. The efficacy results of the individual studies were consistent with the pooled data (see Table 9). Table 9: Primary Hyperlipidemia Trials: Dose Response of Pravastatin Once Daily Administration Dose Total-C LDL-C HDL-C TG Mean Percent Changes From Baseline After 8 Weeksa Placebo (N=36) -3% -4% +1% -4% 10 mg (N=18) -16% -22% +7% -15% 20 mg (N=19) -24% -32% +2% -11% 40 mg (N=18) -25% -34% +12% -24% Mean Percent Changes From Baseline After 6 Weeksb Placebo (N=162) 0% -1% -1% +1% 80 mg (N=277) -27% -37% +3% -19% a A multicenter, double-blind, placebo-controlled study. b Pooled analysis of 2 multicenter, double-blind, placebo-controlled studies. Hypertriglyceridemia The response to pravastatin in patients with hypertriglyceridemia (baseline TG >200 mg/dL and LDL-C <160 mg/dL) was evaluated in a subset of 429 patients from the CARE study. For pravastatin-treated subjects, the median (min, max) baseline TG level was 246 (200.5, 349.5) mg/dL (see Table 10). Table 10: Patients with Hypertriglyceridemia Median (25th, 75th percentile) % Change from Baseline Pravastatin 40 mg (N=429) Placebo (N=430) TG -21.1 (-34.8, 1.3) -6.3 (-23.1, 18.3) Total-C -22.1 (-27.1, -14.8) 0.2 (-6.9, 6.8) LDL-C -31.7 (-39.6, -21.5) 0.7 (-9.0, 10.0) HDL-C 7.4 (-1.2, 17.7) 2.8 (-5.7, 11.7) Non-HDL-C -27.2 (-34.0, -18.5) -0.8 (-8.2, 7.0) Dysbetalipoproteinemia The response to pravastatin in two double-blind crossover studies of 46 patients with genotype E2/E2 and dysbetalipoproteinemia is shown in Table 11. Table 11: Patients with Dysbetalipoproteinemia Median (min, max) % Change from Baseline Median (min, max) at Baseline (mg/dL) Median % Change (min, max) Pravastatin 40 mg (N=20) Study 1 Total-C 386.5 (245.0, 672.0) -32.7 (-58.5, 4.6) TG 443.0 (275.0, 1,299.0) -23.7 (-68.5, 44.7) VLDL-Ca 206.5 (110.0, 379.0) -43.8 (-73.1, -14.3) LDL-Ca 117.5 (80.0, 170.0) -40.8 (-63.7, 4.6) HDL-C 30.0 (18.0, 88.0) 6.4 (-45.0, 105.6) Non-HDL-C 344.5 (215.0, 646.0) -36.7 (-66.3, 5.8) a N=14 Median (min, max) at Baseline (mg/dL) Median % Change (min, max) Pravastatin 40 mg (N=26) Study 2 Total-C 340.3 (230.1, 448.6) -31.4 (-54.5, -13.0) TG 343.2 (212.6, 845.9) -11.9 (-56.5, 44.8) VLDL-C 145.0 (71.5, 309.4) -35.7 (-74.7, 19.1) LDL-C 128.6 (63.8, 177.9) -30.3 (-52.2, 13.5) HDL-C 38.7 (27.1, 58.0) 5.0 (-17.7, 66.7) Non-HDL-C 295.8 (195.3, 421.5) -35.5 (-81.0, -13.5) HeFH in Pediatric Patients Aged 8 Years and Above A double-blind, placebo-controlled study in 214 pediatric patients (100 males and 114 females) with heterozygous familial hypercholesterolemia (HeFH), aged 8 to 18 years was conducted for 2 years. The pediatric patients aged 8 to 13 years were randomized to placebo (N=63) or 20 mg of pravastatin daily (N=65) and the pediatric patients aged 14 to 18 years were randomized to placebo (N=45) or 40 mg of pravastatin daily (N=41). Inclusion in the study required an LDL-C level >95th percentile for age and sex and one parent with either a clinical or molecular diagnosis of familial hypercholesterolemia. The mean baseline LDL-C value was 239 mg/dL and 237 mg/dL in the pravastatin (range: 151 to 405 mg/dL) and placebo (range: 154 to 375 mg/dL) groups, respectively. Pravastatin significantly decreased plasma levels of LDL-C, Total-C, and ApoB in both pediatric age groups (see Table 12). The effect of pravastatin treatment in the 2 age groups was similar. Table 12: Lipid-Lowering Effects of Pravastatin in Pediatric Patients with Heterozygous Familial Hypercholesterolemia: Least-Squares Mean % Change from Baseline at Month 24 (Last Observation Carried Forward: Intent-to-Treat)a Pravastatin 2 0 mg ( Aged 8 to 13 years) N=65 Pravastatin 4 0 mg (Aged 14 to 18 years) N=41 Combined Pravastatin (Aged 8 to 18 years) N=106 Combined Placebo ( Aged 8 to 18 years) N=108 95% CI of the Difference Between Combined Pravastatin and Placebo LDL-C -26.04b -21.07b -24.07b -1.52 (-26.74, -18.86) TC -20.75b -13.08b -17.72b -0.65 (-20.40, -13.83) HDL-C 1.04 13.71 5.97 3.13 (-1.71, 7.43) TG -9.58 -0.30 -5.88 -3.27 (-13.95, 10.01) ApoB (N) -23.16b (61) -18.08b (39) -21.11b (100) -0.97 (106) (-24.29, -16.18) a The above least-squares mean values were calculated based on log-transformed lipid values. b Significant at p 0.0001 when compared with placebo. The mean achieved LDL-C was 186 mg/dL (range: 67 to 363 mg/dL) in the pravastatin group k to 236 mg/dL (range: 105 to 438 mg/dL) in the placebo group.

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