BACKGROUND: This study was designed to evaluate the clinical efficacy of pravastatin, HMG-CoA reductase inhibitor, in patients with hypercholesterolemia. Methods and RESULTS: Pravastatin 5 mg was administered twice daily for 12 weeks in twenty five patients(12 male, 13 female) with hypercholesterolemia(>240 mg/dl). Compared with pretreatment levels, pravastatin significantly decreased levels of total cholesterol(281+/-41mg/dl versus 218+/-31mg/dl) by 22% and LDL-cholesterol(199+/-46mg/dl versus 137+/-37mg/dl) by 31% with significantly decreased total-cholesterol/HDL-cholesterol ratio(7.1+/-3.0 versus 5.1+/-1.6) and LDL-cholesterol/HDL-cholesterol ratio(5.1+/-2.5 versus 3.3+/-1.4) (p<0.005, respectively). During pravastatin treatment, the level of Apo B(164+/-38mg/dl versus 123+/-20mg/dl) was decreased significantly by 24% with significantly decreased Apo B/Apo A-1 ratio(1.4+/-0.5 versus 1.0+/-0.3) (p<0.005, respectively). No serious side effects were found. CONCLUSIONS: Results from the present study show that pravastatin is an effective and well-tolerated cholesterol-lowering agent.
Humans ; Hypercholesterolemia* ; Male ; Oxidoreductases ; Pravastatin*

An open clinical trial was performed to test the efficacy and side effects of Pravastatin(Mevlotin(R)), HMG-CoA reductase inhibitor, administering 5mg twice daily for 12weeks in 30 patients of hypercholesterolemia in out patient clinics, Pusan National University Hospital. The total cholesterol, triglyceride and HDL-cholesterol were measured with enzyme methods and LDL-cholesterol was calculated indirectly by Friedewald formula. The result obtained were as follows: 1) The degree of change at the end points compared with baseline pretreatment levels were 26.1% fall in serum total cholesterol.36.6% fall in LDL-cholesterol, 20.8% fall in triglyceride and 14, 6% rise in HDL-cholesterol. And the rate of improvement more than moderate degree were 90.0% in total cholesterol(the fall of 10% or more), 53.3% in triglyceride (the fall 20% or more) and 33.3% in HDL-cholesterol(the rise of 7mg% or more). 2) The total cholesterol/HDL-cholesterol and LDL-cholesterol/HDL cholesterol ratios were decreased significantly from 6, 4+/-0.7 to 4.2+/-0.5(34.4%) and from 4.5+/-0.7 to 2.5 +/-0.4(44.4%) respectively. 3) The greatest fall in serum total cholesterol and LDL-cholesterol were observed in 2 weeks after administrating drug and thereafter fell gradually and maintained until 12 weeks of endpoint, but HDL-cholesterol showed significant rise from the 4 weeks of administration. On the other hand triglyceride showed remarkable fall in the measured values from the 4 weeks but statistical significance was observed only in 10 and 12 weeks after administration owing to wide individual variation of values. 4) There observed the tendency that the higher the initial pretreatment levels the greater the degree of fall in total cholesterol and triglyceride. 5) Neither side effects nor abnormal laboratory findings were shown during the period of observation. The results suggest that Pravastatin will be a useful and safe drug in the treatment of hyperlipidemia.
Busan ; Cholesterol ; Hand ; Humans ; Hypercholesterolemia* ; Hyperlipidemias ; Oxidoreductases ; Pravastatin ; Triglycerides

A new hypolipidemic drug, pravastatin, hydroxymethylglutaryl coenzyme A reductase inhibitor was administered to 33 patients with primary hyperlipidemia, 10mg daily for 8 weeks and sequential changes of lipid profile were analysed as follows. 1) Mean value at baseline period of total cholesterol, triglyceride, high and low density lipoprotein cholesterol were 260, 220, 51 and 163mg/dl respectively. 2) Total cholesterol showed 21% decrease at the end of 8 weeks and that of LDL-cholesterol were 30%. 3) Triglyceride decreased 16% at the end of 8 weeks and increment of HDL-cholesterol was 8% at the end of 8 weeks. 4) No serious side reactions were observed except one patient, who showed generalized skin rash which last 3 days and did not prevent further medication. In conclusion, pravastatin is a safe and useful hypolipidemic agent for the patient with primary hyperlipidemia.
Cholesterol ; Cholesterol, LDL ; Coenzyme A ; Exanthema ; Humans ; Hyperlipidemias* ; Oxidoreductases ; Pravastatin* ; Triglycerides

Effects of Pravastatin(Mevalotin(R)), a new HMG-CoA reductase inhibitor on the blood lipids were studied for the period of 3 months in 40 subjects with hypercholesterolemia more than 250mg/dl. Age of the subject was 50 years in average with range of 34 to 72 years. There were 22 cases of male and 18 cases of female. The cause of hyperlipidemia was not specified, but there were no case of liver, thyroid and renal disease. The 10mg of Preavastatin was given in devided doses in the morning and at bed time for 3 months. Serum LDL-cholesterol, total cholesterol, HDL-cholesterol, triglyceride and atherogenic index were measured before and after the medication in every month and following results were obtained. 1) Serum cholesterol decreased maximally at 2months after the medication with average decrease of LDL-cholesterol 79.8mg/dl(43%), serum total cholesterol 99.8mg/dl(34%) and the atherogenic index 3.0(45%). The decrease of total serum cholesterol was dependent on the pretreatment level. 2) The serum triglyceride decreased in average 81mg/dl(26%) in one month after the medication however the change was not statistically significant because of wide variation. 3) The HDL-cholesterol decreased in average 1.6mg/dl(4%) in one month and statistically significant. 4) The serum total cholesterol started to change in 3 days and tended to decrease with unstable variation up to the end of 2 weeks after the medication. In one month after cutting drug, there were slight increase of cholesterol but did not return to control value. 5) The significant effect of blood lipid lowering drug in non-specific hyperlipidemia should be evaluated when the changes are more than intra-individual variation of blood lipids. 6) There were only 2 cases of side effect with epigastric pain and fullness which subsided soon and there was no change in liver functions, serum creatinine and fasting blood sugar after the medication. In conclusion, the pravastatin is an excellent new lipid lowering drug with safety.
Blood Glucose ; Cholesterol ; Creatinine ; Fasting ; Female ; Humans ; Hypercholesterolemia ; Hyperlipidemias* ; Liver ; Male ; Oxidoreductases ; Pravastatin ; Thyroid Gland ; Triglycerides

BACKGROUND: Pravastatin, HMG-CoA reductase inhibitor, has been known to be the most effective drug in patients with hypercholesterolemia. We studied the effectiveness and side effects of this drug. METHODS: We studied twenty four patients(8 males, 16 females), with pravastatin 5mg bid for 8 weeks, whose fasting serum total cholesterol levels were higher than 240mg/dl on the first visit. Lipid profiles were checked at 2 weeks interval for 8 weeks and compared with baseline level individually. RESULTS: Among lipid profiles, pravastatin significantly decreased the total cholesterol from 282.8mg/dL to 224.5mg/dL(reduction rate, 21%), the LDL cholesterol from 197.2mg/dL to 143.8mg/dL(27%), the total cholesterol/HDL cholesterol ratio from 6.2 to 4.6(25%), and the LDL cholesterol/HDL cholesterol ratio from 4.1 to 2.7 (34%). These changes were statistically significant(p<0.05). Triglyceride and HDL cholesterol showed no significant changes compared to baseline levels during treatment. The clinical and laboratory findings after treatment did not show serious abnormalities except two patients who dropped out due to side effect such as constipation and skin eruption. CONCLUSION: Results from the present study show that short-term pravastatin therapy seems to be effective and safe in patients with hypercholesterolemia.
Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Constipation ; Fasting ; Humans ; Hypercholesterolemia ; Hyperlipidemias* ; Male ; Oxidoreductases ; Pravastatin* ; Skin ; Triglycerides

OBJECTIVETo prepare pravastatin sodium-loaded chitosan microspheres to allow sustained drug release.

METHODSThe drug-loaded chitosan microspheres were prepared by using genipin as the cross-linker. The influences of molecular weight of chitosan, volume ratio of oil and water, reaction temperature, and stirring speed on the formation of chitosan microspheres were investigated. The morphology of the microspheres was observed using scanning electron microscopy. The encapsulation efficiency, swelling ratio under different pH conditions, and in vitro drug release were measured.

RESULTSThe in vitro release of pravastatin sodium could last for at least 31 days. The drug release rate varied with the reaction condition. The drug entrapment efficiency of the microsphere was 54.7%. The optimal processing conditions were as follows: chitosan viscosity of 200-400 mPa·s, oil-water proportion of 10:1, stirring speed of 850 r/min, and reaction temperature at 40 degrees celsius;.

CONCLUSIONThe pravastatin sodium-loaded microspheres show good sustained drug release property, and the drug release rate can be modified by controlling the cross-linking time.

Chitosan ; Cross-Linking Reagents ; Delayed-Action Preparations ; Iridoids ; Microscopy, Electron, Scanning ; Microspheres ; Pravastatin ; chemistry

BACKGROUND: The effect of pravastatin on insulin resistance (IR) is controversial and poorly studied in prediabetes. METHODS: This study was performed in hyperglycemic patients at Saint Carollo Hospital from January 1, 2013 to December 31, 2015. Among them, we selected 40 patients (24 prediabetes and 16 new onset diabetes [NOD]) who had been treated with pravastatin 20 mg daily for 2 or 4 months and in whom fasting insulin and fasting glucose had been measured before and after administration of pravastatin. IR was defined as a fasting insulin level ≥ 12.94 µU/mL, homeostasis model for IR (HOMA-IR) ≥ 3.04 or quantitative insulin sensitivity check index (QUICKI) ≤ 0.32. RESULTS: Pravastatin treatment decreased total cholesterol and low-density lipoprotein cholesterol levels by 25.2% and 32.3% respectively (P = 0.000 for all), but did not affect fasting insulin level, HOMA-IR, or QUICKI in total, prediabetes, and NOD groups. Prevalence of IR was significantly different between prediabetes and NOD groups both before and after pravastatin treatment (0% versus 37.5%, P = 0.001), but pravastatin treatment did not affect the prevalence of IR in the prediabetes or NOD group. Fasting glucose level was not significantly different before and after pravastatin treatment in prediabetes (106.8 ± 6.4 mg/dL versus 103.8 ± 8.4 mg/dL, P = 0.223) but was significantly different in the NOD group (171.5 ± 70.1 mg/dL versus 124.4 ± 26.7 mg/dL, P = 0.017). CONCLUSION: Pravastatin treatment did not affect IR or fasting glucose level in hyperglycemic patients. Therefore, we suggest pravastatin can be prescribed to hypercholesterolemic patients with hyperglycemia.
Cholesterol ; Fasting ; Glucose ; Homeostasis ; Humans ; Hyperglycemia ; Insulin Resistance* ; Insulin* ; Lipoproteins ; Pravastatin* ; Prediabetic State ; Prevalence ; Saints

BACKGROUND: HMG-CoA reductase is known as a rate limiting enzyme in the synthesis of cholesterol. We studied the clinical efficacy and the side effects of pravastatin, a HMG-CoA reductase inhibitor, in patients with hypercholesterolemia. METHOD: Ten miligrams of pravastatin was administered once daily for 8 weeks in twenty five patients(7 male, 18 female) with hypercholesterolemia(>240mg/dl). Compared with pretreatment levels, pravastatin significantly decreased levels of total cholesterol(286+/-22 versus 234+/-27mg/dl, p<0.005) by 19%LDL-cholesterol(176+/-40 versus 144+/-33mg/dl, p<0.005) by 23% with significantly decreased levels of total cholesterol/HDL-cholesterol ratio(5.5+/-2.0 versus 4.8+/-1.5, p<0.05) and LDL-cholesterol/HDL-cholesterol ratio(3.4+/-1.2 versus 2.9+/-0.9, p<0.05). The level of HDL-cholesterol(52+/-17 versus 54+/-13mg/dl) and triglyceride(241+/-198 verus 178+/-111mg/dl) were not changed significantly. The side effects of pravastatin were mild and transient, including 1 case of headache, 1 dizziness, 1 facial flushing and 2 nausea. The laboratory tests including serum transaminases, uric acid, creatinine, creatine phosphokinase and blood glucose were not changed significant. CONCLUSION: Pravastatin 10mg as a single daily dose is as effective and safe as 5mg two times a day in patients with hypercholesterolemia.
Blood Glucose ; Cholesterol ; Creatine Kinase ; Creatinine ; Dizziness ; Flushing ; Headache ; Humans ; Hypercholesterolemia* ; Male ; Nausea ; Oxidoreductases ; Pravastatin* ; Transaminases ; Uric Acid

BACKGROUNG: It is controversial whether the use of HMG CoA reductase inhibitors (statins) is associated with an increased bone mineral density (BMD) in humans. The purpose of this study was to assess the influence of statins on BMD in Korean postmenopausal women. METHODS: Forty-four postmenopausal women (aged 54.3 5.8 years) were included. The statin users (n=24) were administered either simvastain, atorvastatin, pravastatin, or lovastatin. The control group (n=20) did not take statins. BMD of the spine were measured by dual-energy X-ray absorptiometry. Alkaline phosphatase (ALP) was tested as a bone marker. The data were analysed with two-sample t test and paired t-test. RESULTS:The mean annual spinal BMD changes of the study groups were 1.5 5.6% for statin users and 0.2 4.2% for control group. There was no statistically significant difference in mean annual spinal BMD changes (P=0.696). The mean annual ALP changes of the study groups were 5.6 18.1% for the statin users and 0.4 13.9% for the control group. There was no statistically significant difference in mean annual ALP changes (P=0.246). In each group, the spinal BMD significantly was not changed after 1 year (P>0.05). CONCLUSION: This study suggest that statins do not protect from bone loss in Korean postmenopausal women.
Absorptiometry, Photon ; Alkaline Phosphatase ; Bone Density ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors* ; Lovastatin ; Menopause ; Pravastatin ; Spine ; Atorvastatin Calcium

OBJECTIVETo observe the effects of pravastatin on the proliferation and invasion of human hepatocarcinoma HepG2 cell line.

METHODSThe effects of pravastatin on the proliferation, migration and invasion of HepG2 cells was observed by MTT assay, Boyden chamber assay and motility assay. p38 activity was measured, and the expression of p-p38, MKP-1, RhoC and MMP-2 was analyzed by Western blot.

RESULTSPravastatin inhibited the proliferation of HepG2 cells. The intracellular p38 activity and expressions of p-p38, RhoC and MMP-2 were decreased, while MKP-1 expression was elevated in pravastatin treated cells. In addition, pravastatin inhibited the invasion and motility.

CONCLUSIONPravastatin can inhibit the proliferation and invasion of HepG2 cells.

Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Hep G2 Cells ; Humans ; Matrix Metalloproteinase 2 ; metabolism ; Neoplasm Invasiveness ; Pravastatin ; pharmacology