PRAVASTATIN SODIUM- pravastatin sodium_tablet

Pravastatin is a reversible inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts HMG-CoA to mevalonate, a precursor of cholesterol. Inhibition of HMG-CoA reductase by pravastatin accelerates the expression of LDL-receptors, followed by the uptake of LDL-C from blood to the liver, leading to a decrease in plasma LDL-C and total cholesterol. Sustained inhibition of cholesterol synthesis in the liver also decreases levels of very-low-density lipoproteins. The maximum LDL-C reduction of pravastatin sodium is usually achieved by 4 weeks and is maintained after that. Absorption max Pravastatin plasma concentrations, including AUC, C max min The coefficient of variation (CV), based on between-subject variability, was 50% to 60% for AUC. The geometric means of pravastatin C max Steady-state AUCs, C max min Distribution Elimination Metabolism Excretion Following single dose oral administration of 14 ½ ½ Specific Populations Renal Impairment max ½ [see Use in Specific Populations (8. 6) Hepatic Impairment [see Use in Specific Populations (8. 6) Geriatric max max ½ Use in Specific Populations (8. 5) Pediatric max [see Use in Specific Populations (8. 4) Drug-Drug Interactions Table 5: Effect of Coadministered Drugs on the Pharmacokinetics of Pravastatin Pravastatin Coadministered Drug and Dosing Regimen Dose (mg) Change in AUC Change in C max BID = twice daily; OD = once daily; QID = four times daily Cyclosporine 5 mg/kg single dose 40 mg single dose up arrow282% up arrow327% Clarithromycin 500 mg BID for 9 days 40 mg OD for 8 days up arrow110% up arrow128% Boceprevir 800 mg TID for 6 days 40 mg single dose up arrow63% up arrow49% Darunavir 600 mg BID/Ritonavir 100 mg BID for 7 days 40 mg single dose up arrow81% up arrow63% Colestipol 10 g single dose 20 mg single dose down arrow47% down arrow53% Cholestyramine 4 g single dose 20 mg single dose Administered simultaneously down arrow40% down arrow39% Administered 1 hour prior to cholestyramine up arrow12% up arrow30% Administered 4 hours after cholestyramine down arrow12% down arrow6. 8% Cholestyramine 24 g OD for 4 weeks 20 mg BID for 8 weeks 5 mg BID for 8 weeks 10 mg BID for 8 weeks down arrow51% down arrow38% down arrow18% up arrow4. 9% up arrow23% down arrow33% Fluconazole 200 mg IV for 6 days 20 mg PO+10 mg IV down arrow34% down arrow33% 200 mg PO for 6 days 20 mg PO+10 mg IV down arrow16% down arrow16% Kaletra 400 mg/100 mg BID for 14 days 20 mg OD for 4 days up arrow33% up arrow26% Verapamil IR 120 mg for 1 day and 40 mg single dose up arrow31% up arrow42% Cimetidine 300 mg QID for 3 days 20 mg single dose up arrow30% up arrow9. 8% Antacids 15 mL QID for 3 days 20 mg single dose down arrow28% down arrow24% Digoxin 0. 2 mg OD for 9 days 20 mg OD for 9 days up arrow23% up arrow26% Probucol 500 mg single dose 20 mg single dose up arrow14% up arrow24% Warfarin 5 mg OD for 6 days 20 mg BID for 6 days down arrow13% up arrow6. 7% Itraconazole 200 mg OD for 30 days 40 mg OD for 30 days up arrow11% (compared to Day 1) up arrow17% (compared to Day 1) Gemfibrozil 600 mg single dose 20 mg single dose down arrow7% down arrow20% Aspirin 324 mg single dose 20 mg single dose up arrow4. 7% up arrow8. 9% Niacin 1 g single dose 20 mg single dose down arrow3. 6% down arrow8. 2% Diltiazem 20 mg single dose up arrow2. 7% up arrow30% Grapefruit juice 40 mg single dose down arrow1. 8% up arrow3. 7% Table 6: Effect of Pravastatin on the Pharmacokinetics of Coadministered Drugs Pravastatin Dosing Regimen Name and Dose Change in AUC Change in C max BID = twice daily; OD = once daily 20 mg BID for 6 days Warfarin 5 mg OD for 6 days Change in mean prothrombin time up arrow17% up arrow0. 4 sec up arrow15% 20 mg OD for 9 days Digoxin 0. 2 mg OD for 9 days up arrow4. 6% up arrow5. 3% 20 mg BID for 4 weeks 10 mg BID for 4 weeks 5 mg BID for 4 weeks Antipyrine 1. 2 g single dose up arrow3% up arrow1. 6% up arrow Less than 1% Not Reported 20 mg OD for 4 days Kaletra 400 mg/100 mg BID for 14 days No change No change.

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). To reduce the risk of coronary death, myocardial infarction, myocardial revascularization procedures, stroke or transient ischemic attack, and slow the progression of coronary atherosclerosis in adults with clinically evident CHD. As an adjunct to diet to reduce LDL-C in adults with primary hyperlipidemia. As an adjunct to diet to reduce LDL-C in pediatric patients ages 8 years and older with heterozygous familial hypercholesterolemia (HeFH). As an adjunct to diet for the treatment of adults with: Primary dysbetalipoproteinemia. Hypertriglyceridemia. Pravastatin sodium tablets are an HMG-CoA reductase inhibitor (statin) indicated (1) 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).

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, and adjust the dosage if necessary (2. 1) Adults: recommended starting dosage is pravastatin sodium tablets 40 mg to 80 mg once daily. 2) Pediatric Patients (2. 3) aged 8 to 13 years, the recommended dosage is 20 mg once daily. aged 14 to 18 years, the recommended starting dosage is 40 mg once daily. Severe renal impairment: recommended starting dosage is pravastatin sodium 10 mg once daily. Recommended maximum pravastatin sodium tablets dosage is 40 mg once daily. 4) See full prescribing information for dosage modifications due to drug interactions (2. 5 7) Take pravastatin sodium tablets orally once daily as a single dose at any time of the day, with or without food. 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. Assess LDL-C when clinically appropriate, as early as 4 weeks after initiating pravastatin sodium tablets, and adjust the dosage if necessary. The recommended starting dosage is pravastatin sodium tablets 40 mg to 80 mg once daily. In pediatric patients aged 8 to 13 years, the recommended dosage is pravastatin sodium tablets 20 mg once daily. In pediatric patients aged 14 to 18 years, the recommended starting dosage is pravastatin sodium tablets 40 mg once daily. In patients with severe renal impairment, the recommended starting dosage is pravastatin sodium 10 mg once daily. The maximum recommended dosage of pravastatin sodium tablets in patients with severe renal impairment is 40 mg once daily [see Clinical Pharmacology (12. 3) The recommended dosage of pravastatin sodium tablets for patients with mild or moderate renal impairment is the same as patients with normal renal function. 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 tablets [see Warnings and Precautions (5. 1) Drug Interactions (7. 1) Cyclosporine Clarithromycin and Erythromycin.

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: musculoskeletal pain, nausea/vomiting, upper respiratory infection, diarrhea, and headache. 1) To report SUSPECTED ADVERSE REACTIONS, contact Glenmark Pharmaceuticals Inc. , USA at 1 (888) 721-7115 or FDA at 1-800-FDA-1088 or www. gov/medwatch Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice. In pravastatin sodium placebo-controlled clinical trials, 1313 patients (age range 20 to 76 years, 32% women, 93. 5% White, 5% Black, 0. 9% Hispanic, 0. 4% Asian, 0. 2% Other) with a median treatment duration of 14 weeks, 3. 3% of patients on pravastatin sodium and 1. 2% patients on placebo discontinued due to adverse reactions (regardless of causality). The most common adverse reactions that led to treatment discontinuation and occurred at an incidence greater than placebo were: hepatic transaminase elevations, nausea, anxiety/depression, and dizziness. Adverse reactions (regardless of causality) reported in >=2% of pravastatin sodium-treated patients in placebo-controlled trials of up to 8 months duration are identified in Table 1: Table 1: Adverse Reactions in >=2% of Patients Treated with Pravastatin (Any Dose) and at an Incidence Greater Than Placebo in Short-Term Placebo-Controlled Trials % Placebo N=411 % Any Dose N=902 Nausea/Vomiting 7. 4 Diarrhea 5. 7 Headache 4. 3 Upper Respiratory Infection 5. 9 Angina Pectoris 3. 5 CPK Increased 3. 1 Dizziness 3. 5 ALT Increased 1. 9 Chest Pain 1. 5 Myalgia 1. 3 Influenza 0. 7 2 g-GT Increased 1. 2 2 Adverse Reactions (regardless of causality) In pravastatin sodium placebo-controlled clinical trials, 21,483 patients (age range 24 to 75 years, 10. 3% women, 52. 3% White, 0. 8% Black, 0. 5% Hispanic, 0. 1% Asian, 0. 1% Other, 46. 1% not recorded) had a median treatment duration of 261 weeks. Adverse reactions (regardless of causality) were pooled from 7 double-blind, placebo-controlled trials (West of Scotland Coronary Prevention Study [WOS]; Cholesterol and Recurrent Events study [CARE]; Long-term Intervention with Pravastatin in Ischemic Disease study [LIPID]; Pravastatin Limitation of Atherosclerosis in the Coronary Arteries study [PLAC I]; Pravastatin, Lipids and Atherosclerosis in the Carotids study [PLAC II]; Regression Growth Evaluation Statin Study [REGRESS]; and Kuopio Atherosclerosis Prevention Study [KAPS]) involving a total of 10,764 patients treated with pravastatin sodium 40 mg and 10,719 patients treated with placebo. Patients were exposed to pravastatin sodium for a mean of 4 to 5. 1 years in WOS, CARE, and LIPID and 1. 9 years in PLAC I, PLAC II, KAPS, and REGRESS. Adverse reactions (regardless of causality) occurring in >=5% of patients treated with pravastatin sodium in these studies are identified in Table 2. Table 2: Adverse Reactions in >=5% of Patients Treated with Pravastatin 40 mg and at an Incidence Greater than Placebo in Long-Term Placebo-Controlled Trials Placebo (N=10,719) % of patients Pravastatin sodium (N=10,764) % of patients Musculoskeletal Pain 24. 9 Upper Respiratory Tract Infection 20. 2 Musculoskeletal Traumatism 9. 2 Chest Pain 9. 8 10 Influenza 9 9. 2 Fatigue 7. 2 Dizziness 6. 3 Rash (including dermatitis) 7. 2 Sinus Abnormality 6. 7 7 Muscle Cramp 4. 1 Adverse Reactions (regardless of causality) Laboratory Abnormalities Transient, asymptomatic eosinophilia has been reported. Eosinophil counts usually returned to normal despite continued therapy. Anemia, thrombocytopenia, and leukopenia have been reported with statins. The following adverse reactions have been identified during postapproval use of pravastatin sodium. 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: Nervous System: Hypersensitivity: Gastrointestinal: Dermatologic: Renal: Respiratory: Psychiatric: Reproductive: Laboratory Abnormalities:.

Acute liver failure or decompensated cirrhosis [see Warnings and Precautions (5. 3) Hypersensitivity to any pravastatin or any excipients in pravastatin sodium tablets. Hypersensitivity to pravastatin or any excipient in pravastatin sodium tablets (4) Acute liver failure or decompensated cirrhosis (4 5.

Pregnancy: May cause fetal harm (8. 1) Lactation: Breastfeeding not recommended during treatment with pravastatin sodium (8. 2) Risk Summary [see Clinical Pharmacology (12. 1) (see Data). 2 (see Data The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. 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 Animal Data 2 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 1000 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/m 2 In pregnant rats given oral gavage doses of 10, 100, and 1000 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/m 2 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/m 2 Risk Summary Because of the potential for serious adverse reactions in a breastfed infant, based on the mechanism of action, advise patients that breastfeeding is not recommended during treatment with pravastatin sodium [see Use in Specific Populations (8. 1) Clinical Pharmacology (12. 1) The safety and effectiveness of pravastatin sodium as an adjunct to diet to reduce LDL-C have been established in pediatric patients 8 years of age and older with HeFH. Use of pravastatin sodium for this indication is based on a double-blind, placebo-controlled clinical study in 214 pediatric patients (100 males and 114 females) 8 years of age and older with HeFH. Doses greater than 40 mg daily have not been studied in this population. The safety and effectiveness of pravastatin sodium have not been established in pediatric patients younger than 10 years of age with HeFH or in pediatric patients with other types of hyperlipidemia (other than HeFH). In clinical studies, 4,797 (36. 4%) pravastatin sodium-treated patients were aged 65 and older and 110 (0. 8%) were aged 75 and older. No significant differences in efficacy or safety were observed between geriatric patients and younger patients. Mean pravastatin AUCs are 25% to 50% higher in elderly subjects than in healthy young subjects, but mean maximum plasma concentration (C max max ½ [see Clinical Pharmacology (12. 3) Advanced age (>=65 years) is a risk factor for pravastatin sodium-associated myopathy and rhabdomyolysis. Dose selection for an elderly patient should be cautious, recognizing the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy and the higher risk of myopathy. Monitor geriatric patients receiving pravastatin sodium for the increased risk of myopathy [see Warnings and Precautions (5. 1) Renal impairment is a risk factor for myopathy and rhabdomyolysis. Monitor all patients with renal impairment for development of myopathy. In patients with severe renal impairment, the recommended starting dose is pravastatin sodium 10 mg once daily. The maximum recommended dosage in patients with severe renal impairment is pravastatin sodium 40 mg once daily. The recommended dosage for patients with mild or moderate renal impairment is the same as patients with normal renal function. [see Dosage and Administration (2. 4) Warnings and Precautions (5. 3) Pravastatin sodium shows a large inter-subject variability in pharmacokinetics in patients with liver cirrhosis [ Clinical Pharmacology (12. 3) [see Contraindications (4) Warnings and Precautions (5.

See full prescribing information for details regarding concomitant use of pravastatin sodium with other drugs that increase the risk of myopathy and rhabdomyolysis. 1) Bile Acid Sequestrants: in patients taking a bile acid sequestrant, administer pravastatin sodium at least 1 hour before or at least 4 hours after the bile acid sequestrant (7. 2) Pravastatin sodium is a substrate of the transport protein OATP1B1. Pravastatin sodium plasma levels can be significantly increased with concomitant administration of inhibitors of OATP1B1. Table 3 includes a list of drugs that increase the risk of myopathy and rhabdomyolysis when used concomitantly with pravastatin sodium and instructions for preventing or managing them [see Warnings and Precautions (5. 1) Clinical Pharmacology (12. 3) Table 3: Drug Interactions that Increase the Risk of Myopathy and Rhabdomyolysis with Pravastatin Sodium Gemfibrozil Clinical Impact: There is an increased risk of myopathy/rhabdomyolysis when pravastatin sodium is administered with gemfibrozil Intervention: Avoid concomitant use of gemfibrozil with pravastatin sodium. Cyclosporine Clinical Impact: The risk of myopathy and rhabdomyolysis is increased with concomitant use of cyclosporine with pravastatin sodium. Intervention: Initiate with a dosage of pravastatin sodium 10 mg once daily. Do not exceed pravastatin sodium 20 mg once daily [see Dosage and Administration (2. Select Macrolide Antibiotics Clinical Impact: The risk of myopathy and rhabdomyolysis is increased by concomitant use of clarithromycin or erythromycin with pravastatin sodium. Other macrolides (e. , azithromycin) have the potential to increase pravastatin sodium exposures and increase the risk of myopathy and rhabdomyolysis when used concomitantly. Intervention: For patients taking erythromycin or clarithromycin, do not exceed 40 mg pravastatin sodium once daily [see Dosage and Administration (2. Niacin Clinical Impact: Cases of myopathy and rhabdomyolysis have been observed with concomitant use of niacin with pravastatin sodium. Intervention: Consider if the benefit of using niacin concomitantly with pravastatin sodium outweighs the increased risk of myopathy and rhabdomyolysis. If concomitant use is decided, monitor patients for signs and symptoms of myopathy, particularly during initiation of therapy and during upward dose titration of either drug. Fibrates (other than Gemfibrozil) Clinical Impact: Fibrates may cause myopathy when given alone. The risk of myopathy and rhabdomyolysis is increased with concomitant use of fibrates with pravastatin sodium. Intervention: Consider if the benefit of using fibrates concomitantly with pravastatin sodium outweighs the increased risk of myopathy and rhabdomyolysis. Colchicine Clinical Impact: Cases of myopathy and rhabdomyolysis have been reported with concomitant use of colchicine with pravastatin sodium. Intervention: Consider if the benefit of using colchicine concomitantly with pravastatin sodium outweighs the increased risk of myopathy and rhabdomyolysis. Table 4 presents drug interactions that may decrease the efficacy of pravastatin sodium and instructions for preventing or managing them. Table 4: Drug Interactions that Decrease the Efficacy of Pravastatin Sodium Bile Acid Sequestrants Clinical Impact: Concomitant cholestyramine or colestipol administration decreased the mean exposure of pravastatin approximately 51% and 47%, respectively [see Clinical Pharmacology (12. Intervention: In patients taking a bile acid sequestrant, administer pravastatin sodium at least 1 hour before or at least 4 hours after the bile acid sequestrant [see Dosage and Administration (2.

OVERDOSAGE
No specific antidotes for pravastatin sodium are known. Contact Poison Control (1-800-222-1222) for latest recommendations.
NONCLINICAL TOXICOLOGY
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/m 2 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 Salmonella Typhimurium Escherichia coli Saccharomyces cerevisiae 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.
CLINICAL STUDIES
Prevention of Coronary Heart Disease th th Pravastatin sodium 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 sodium group [CHD death=31, nonfatal MI=143], p=0. 0001 [see figure below]). The risk reduction with pravastatin sodium was similar across the age range studied and throughout the range of baseline LDL cholesterol levels. Pravastatin sodium 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 Table 7: LIPID - Primary and Secondary Endpoints Number (%) of Subjects Event Pravastatin Sodium 40 mg (N=4512) Placebo (N=4502) Risk Reduction p Primary Endpoint CHD mortality 287 (6. 0004 Secondary Endpoints Total mortality 498 (11) 633 (14. 0001 CHD mortality or nonfatal MI 557 (12. 0001 Myocardial revascularization 584 (12. 0001 Stroke All-cause 169 (3. 0477 Non-hemorrhagic 154 (3. 0154 Cardiovascular mortality 331 (7. 0001 In the CARE study, the effect of pravastatin sodium, 40 mg daily, on CHD death and nonfatal MI was assessed in 4159 patients (3583 men and 576 women) who had experienced a MI in the preceding 3 to 20 months and who had normal (below the 75 th th th Table 8: CARE - Primary and Secondary Endpoints Number (%) of Subjects Event Pravastatin Sodium 40 mg (N=2081) Placebo (N=2078) Risk Reduction p Primary Endpoint CHD mortality or nonfatal MI The risk reduction due to treatment with pravastatin sodium was consistent in both sexes. 003 Secondary Endpoints Myocardial revascularization procedures (CABG or PTCA) 294 (14. 001 Stroke or TIA 93 (4. 5) 124 (6) 26% 0. 029 Primary Hyperlipidemia In a pooled analysis of 2 multicenter, double-blind, placebo-controlled studies of patients with primary hyperlipidemia, treatment with pravastatin sodium at a daily dose of 80 mg (N=277) significantly decreased Total-C, LDL-C, and TG. The 25 th th Table 9: Primary Hyperlipidemia Trials: Dose Response of Pravastatin Sodium Once Daily Administration Dose Total-C LDL-C HDL-C TG Mean Percent Changes From Baseline After 8 Weeks A multicenter, double-blind, placebo-controlled study. 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 Weeks Pooled analysis of 2 multicenter, double-blind, placebo-controlled studies. Placebo (N=162) 0% −1% −1% +1% 80 mg (N=277) −27% −37% +3% −19% Hypertriglyceridemia Table 10: Patients with Hypertriglyceridemia Median (25 th th Pravastatin 40 mg (N=429) Placebo (N=430) TG −21. 3) Total-C −22. 8) LDL-C −31. 7 (−9, 10) HDL-C 7. 7) Non-HDL-C −27. 2 (−34, −18. 2, 7) Dysbetalipoproteinemia Table 11: Patients with Dysbetalipoproteinemia Median (min, max) % Change from Baseline Median (min, max) Median % Change (min, max) Study 1 Total-C 386. 5 (245, 672) −32. 6) TG 443 (275, 1299) −23. 7) VLDL-C a 206. 5 (110, 379) −43. 3) LDL-C a 117. 5 (80, 170) −40. 6) HDL-C 30 (18, 88) 6. 4 (−45, 105. 6) Non-HDL-C 344. 5 (215, 646) −36. 8) a Median (min, max) Median % Change (min, max) Study 2 Total-C 340. 5, −13) TG 343. 8) VLDL-C 145 (71. 1) LDL-C 128. 5) HDL-C 38. 1, 58) 5 (−17. 7) Non-HDL-C 295. 5 (−81, −13. 5) HeFH in Pediatric Patients Aged 8 Years and Above th Pravastatin sodium significantly decreased plasma levels of LDL-C, Total-C, and ApoB in both pediatric age groups (see Table 12). The effect of pravastatin sodium treatment in the 2 age groups was similar. Table 12: Lipid-Lowering Effects of Pravastatin Sodium in Pediatric Patients with Heterozygous Familial Hypercholesterolemia: Least-Squares Mean % Change from Baseline at Month 24 (Last Observation Carried Forward: Intent-to-Treat) Pravastatin 20 mg (Aged 8 to 13 years) N=65 Pravastatin 40 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. 04 Significant at p<=0. 0001 when compared with placebo. 83) HDL-C 1. 01) ApoB (N) −23. 16 (61) −18. 08 (39) −21. 11 (100) −0. 97 (106) (−24. 18) The mean achieved LDL-C was 186 mg/dL (range: 67 to 363 mg/dL) in the pravastatin sodium group k to 236 mg/dL (range: 105 to 438 mg/dL) in the placebo group. Coronary Heart Disease Death or Nonfatal Myocardial Infarction Survival Distributions.

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