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PubMed1999

Preoperative lipid-control with simvastatin reduces the risk of postoperative thrombocytosis and thrombotic complications following CABG.

OBJECTIVE: It has earlier been suggested that postoperative thrombocytosis frequently occur after coronary artery bypass grafting (CABG) and may be linked to lipid disturbances. A prospective randomized study was undertaken to evaluate if preoperative lipid-control, using HMG-CoA-reductase inhibitor (Zocor), simvastatin, reduces the risk of postoperative thrombocytosis. METHODS: Seventy-seven patients with symptomatic coronary artery disease and hypercholesterolemia (total cholesterol > or =6.2 mmol/l), planned for CABG where randomly assigned to; undergo CABG without preoperation lipid control (group I, n = 37) or undergo simvastatin-treatment (20 mg daily) to control their lipids (4 weeks) prior to CABG (group II, n = 40). RESULTS: Patient characteristics and operation data did not differ between the groups. Serum-cholesterol, cholesterol/HDL-cholesterol, LDL-cholesterol, Apolipoprotein A1 and Plasminogen were all significantly higher in group I patients compared with group II just prior to surgery. Other laboratory parameters did not differ. RESULTS: In group II, total cholesterol and cholesterol/HDL-cholesterol quota were significantly lowered by simvaststin (-2 and -29%, respectively). Postoperative thrombocytosis (platelet counts > or =400000/microl) occurred significantly more frequently in group I 81% (30/37) compared with 3% (1/40) in group II, P<0.0001. Myocardial infarction after the 7th postoperative day was more often diagnosed in group I, 14 vs. 0% in group II. Postoperative transient renal failure occurred also more frequently in group I, 24% compared with 8% in group II. Other postoperative complications and laboratory data did not differ. CONCLUSIONS: This study once again underlines the importance of lipid control using HMG-CoA-reductase inhibitors (e.g. Zocor) in patients with established coronary artery disease. For the first time it is shown that lipid-control with simvastatin prior to CABG reduces the risk of postoperative thrombocytosis, thus lowers the risk for thrombotic complications.

Aged↗
PubMed1991

Simvastatin but not pravastatin inhibits the proliferation of rat aorta myocytes.

The in vitro effect of simvastatin and pravastatin, two competitive inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, on the proliferation of rat aortic smooth muscle cells was investigated. Simvastatin, but not pravastatin, inhibited the replication of arterial myocytes in concentrations ranging between 0.01 microM and 10 microM. The inhibition, evaluated as cell number and nuclear incorporation of [3H]thymidine, was dose-dependent and completely prevented by addition of mevalonate (100 microM), confirming the role of mevalonate or its products in regulating cell division and growth. The present results provide evidence that simvastatin, in addition to its effect on cholesterol biosynthesis, interferes in vitro with other processes involved in atherogenesis.

Animals↗
PubMed2006

Randomized comparative study of the effects of treatment with once-daily, niacin extended-release/lovastatin and with simvastatin on lipid profile and fibrinolytic parameters in Taiwan.

Hyperlipidemia can be effectively treated either with niacin or HMG-CoA reductase inhibitor (statin), or a combination of both. Few reports showed the effects of the combination regimen with niacin and statin on hemostatic functions. We conducted a single-center, double-blind, double-dummy, randomized, two-arm study to assess the effects of the niacin extended-release/lovastatin therapy in a fixed-dose formulation and of simvastatin on lipid lowering and two fibrinolytic parameters, fibrinogen and d-dimer. All patients were enrolled according to NCEP-ATP III guidelines and underwent a placebo run-in period of 4 weeks before being randomized to either niacin extended-release/lovastatin tablets (500/20 mg) once daily (n = 36) or simvastatin capsule (20 mg) once daily (n = 34). After 16 weeks of treatment, both groups of patients showed significantly reduced low-density lipoprotein cholesterol and total cholesterol (LDL-C, p < 0.001 and < 0.001, respectively, p = 0.159 between the groups; TC, p < 0.001 and < 0.001, respectively, p = 0.018 between the groups). Both drugs were well tolerated. Only in the group treated with niacin extended-release/lovastatin was fibrinogen concentration significantly reduced after treatment (2.48 +/- 0.65 to 1.99 +/- 0.62 g/L, p = 0.008). No difference was found with d-dimer in either group. This study shows that both niacin extended-release/lovastatin and simvastatin are effective and well-tolerated lipid-lowering drugs in Taiwanese patients with dyslipidemia. A combinational treatment with niacin extended-release/lovastatin may provide additional benefit in fibrinolysis.

Aged↗
PubMed2001

Myositis, microvesicular hepatitis, and progression to cirrhosis from troglitazone added to simvastatin.

A 68-year-old woman, with type 2 diabetes mellitus, hypercholesterolemia, and prior long-term simvastatin therapy, self-resumed troglitazone after running out of metformin. She developed an acute severe hepatitis with microvesicular steatosis and mysositis. There was subsequent resolution of the myositis but progression of the hepatitis to symptomatic cirrhosis over a period of 12 weeks. Both troglitazone and simvastatin are metabolized by cytochrome P-450 3A4. Troglitazone typically induces metabolism of drugs metabolized by this cytochrome so that simple simvastatin toxicity seems less likely to have been involved. The association with myositis, the severity of the hepatitis with progression to cirrhosis, and the presence of microvesicular steatosis suggests altered mitochondrial metabolism, which has been described with each agent, as the underlying pathogenic mechanism. Although troglitazone (Rezulin) has been withdrawn from the market, other similar agents are available for therapy of type 2 diabetes mellitus. Increased awareness of a potential interaction between these two classes of drugs is warranted.

Aged↗
PubMed1992

Influence of age and gender on the plasma profiles of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitory activity following multiple doses of lovastatin and simvastatin.

The effects of age and of gender on the plasma profiles of HMG-CoA reductase inhibitors following separate once-a-day dosage regimens (17 days) of lovastatin (80 mg/day) and simvastatin (40 mg/day) were studied in hypercholesterolemic patients. In general, plasma concentrations of active and total HMG-CoA reductase inhibitors were higher in elderly individuals (age, 70 to 78 years) and in females for both drugs. However, the Tmax of these inhibitors was not significantly affected by either age or gender. Following the last dose of lovastatin, the mean steady-stage plasma concentrations of total and active HMG-CoA reductase inhibitors were 30-60% higher in the elderly than in young individuals (age, 19 to 30 years). Also, the mean plasma concentrations were 20-50% higher in female than in male patients. Similarly, following the last dose of simvastatin, the mean plasma concentrations of HMG-CoA reductase inhibitors were 40-60% higher in the elderly than in young patients and were 20-50% higher in female than in male patients. These age- and gender-related differences do not appear to be large enough to warrant modification of dosage regimens, because plasma concentrations of these inhibitors are not necessarily indicative of efficacy and the therapeutic windows for lovastatin and simvastatin are broad.

Adult↗
PubMed1999

Different effect of simvastatin and atorvastatin on key enzymes involved in VLDL synthesis and catabolism in high fat/cholesterol fed rabbits.

The effects of atorvastatin (3 mg kg(-1)) and simvastatin (3 mg kg(-1)) on hepatic enzyme activities involved in very low density lipoprotein metabolism were studied in coconut oil/cholesterol fed rabbits. Plasma cholesterol and triglyceride levels increased 19 and 4 fold, respectively, after 7 weeks of feeding. Treatment with statins during the last 4 weeks of feeding abolished the progression of hypercholesterolaemia and reduced plasma triglyceride levels. 3-Hydroxy-3-methyl-glutaryl Coenzyme A reductase, acylcoenzyme A:cholesterol acyltransferase, phosphatidate phosphohydrolase and diacylglycerol acyltransferase activities were not affected by drug treatment. Accordingly, hepatic free cholesterol, cholesteryl ester and triglyceride content were not modified. Simvastatin treatment caused an increase (72%) in lipoprotein lipase activity without affecting hepatic lipase activity. Atorvastatin caused a reduction in hepatic phospholipid content and a compensatory increase in CTP:phosphocholine cytidylyl transferase activity. The results presented in this study suggest that, besides the inhibitory effect on 3-hydroxy-3-methyl-glutaryl Coenzyme A reductase, simvastatin and atorvastatin may have additional effects that contribute to their triglyceride-lowering ability.

Acyl Coenzyme A↗
PubMed2005

Determinants of variable response to simvastatin treatment: the role of common variants of SCAP, SREBF-1a and SREBF-2 genes.

We investigated the effect of single-nucleotide polymorphisms in sterol regulatory element-binding factors-1a and -2 (SREBF-1a and SREBF-2) and SREBF cleavage-activating protein (SCAP) genes on lipid-lowering response to simvastatin. In all, 146 hypercholesterolemic patients of European descent were prospectively treated with simvastatin 20 mg/day for over 6 months. Of these 99 subjects completed the 6-month follow-up. Plasma lipids and lipoproteins were measured before and throughout the study. The mean percentage decrease in plasma total cholesterol (TC) was greater in subject carriers of SCAP 2386G allele compared with those homozygous for 2386A allele (-29.6+/-13.4 vs -22.1+/-13.8%, P=0.007). About 61% of the 2386G carriers were above-average responders for TC levels (DeltaTC -27.8%), whereas only 29% of 2386A homozygous reached this reduction (P=0.009). Our data suggest that the SCAP 2386A>G gene polymorphism was a significant predictor of TC and triglyceride responses to simvastatin treatment.

Adult↗
PubMed2004

Simvastatin promotes osteogenesis around titanium implants.

OBJECTIVES: Hydroxymethylglutaryl-coenzyme A reductase inhibitors, the so-called statins, have been widely used for hyperlipidemic patients, and it was recently reported that it promoted bone formation. In the present study, we examined the effect of simvastatin on the promotion of osteogenesis around titanium implants. MATERIALS AND METHODS: Ten 30-week-old rats received pure titanium implants in both tibiae, and were then divided into experimental and control groups. The experimental group was administered simvastatin daily. Thirty days later, all animals were killed and then specimens were prepared. The bone contact ratio (BCR) to the implant and bone density (BD) around the implant, as well as histological findings, were obtained. RESULTS: In the control group, newly formed bone could be seen around the implants. It was seen to be in direct contact with the implant surface, but otherwise unmineralized connective tissue was occasionally interposed. In the medullary canal, a scanty amount of bone trabeculae was observed. In the experimental group, in contrast, thicker bone trabeculae were abundantly seen in the medullary canal and showed a mesh-like structure. In the histometrical observations, both BCR and BD of the experimental group were significantly greater than those of the control group. CONCLUSION: The administration of simvastatin increases the value of both BCR and BD. This drug may have the potential to improve the nature of osseointegration.

Animals↗
PubMed2002

Influence of simvastatin, pravastatin, and BM 15.766 on neutral sterols in liver and testis of guinea pigs.

There is mounting evidence that specific sterol precursors of cholesterol are associated with reproductive functions. Testicular meiosis-activating sterol (T-MAS) and follicular fluid meiosis-activating-sterol (FF-MAS) are 2 cholesterol precursors found in reproductive organs of mammals, which are able to overcome meiotic arrest in vitro. This study investigates the influence of simvastatin and pravastatin, 2 inhibitors of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase, and BM 15.766, an inhibitor of 7-dehydrocholesterol reductase, on concentrations of neutral sterols in liver and testis of guinea pigs. Concentrations of T-MAS, lathosterol, and desmosterol were markedly higher in testis compared with liver. Simvastatin (150 mg/d) and pravastatin (150 mg/d and 350 mg/d) markedly reduced cholesterol precursors in liver. In contrast, T-MAS and desmosterol in testis remained unchanged, albeit other cholesterol precursors were reduced. BM 15.766 led to the accumulation of 7- and 8-dehydrocholesterol, both in liver and testis. However, concentrations of T-MAS in testis were not changed by BM 15.766. We conclude that treatment of guinea pigs with simvastatin, pravastatin, or BM 15.766, which simulates the biochemical defect of the Smith-Lemli-Opitz (SLO) syndrome, does not affect T-MAS concentrations in testis.

Animals↗
PubMed1996

Testicular function in hypercholesterolemic male patients during prolonged simvastatin treatment.

Simvastatin is a very effective hypocholesterolemic drug which, reducing cholesterol biosynthesis, can affect normal steroid hormone production. Testes require a continuous cholesterol supply for testosterone synthesis and this can be derived from low density lipoprotein receptor-mediated uptake or from de novo local synthesis. The aim of the study was to see if prolonged simvastatin treatment compromised endocrine testicular function both in basal conditions and after stimulation by human Chorionic Gonadotropin (hCG) (Profasi 5,000 Ul, i.m. at 8 a.m.). Free testosterone (FT) levels were determined at baseline and after 3, 6 and 12 months of simvastatin treatment (20 mg/day) in eight hypercholesterolemic patients. At the same time we performed a hCG stimulation test to evaluate testicular reserve. A significant reduction of FT, both basal and hCG-stimulated, was observed in the 6th and the 12th month of the study. However, FT levels remained in the normal range and no patient complained of gonadal function related symptoms. No significant change was observed in estradiol response to hCG test. Lastly, there was no variation in LH, FSH, progesterone, 17-OH-progesterone, androstenedione or dehydroepiandrosterone-sulphate levels. Our study concluded that the drug causes a mild decline in FT secretion without any clinical sign of testicular dysfunction.

Androgens↗
PubMed2003

Residual effects of lovastatin and simvastatin on urinary mevalonate excretions in patients with familial hypercholesterolemia.

3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG CoA) reductase inhibitors are widely used to decrease plasma cholesterol levels in patients with heterozygous familial hypercholesterolemia (FH) who are at increased risk of premature coronary artery disease. Tissue-culture and animal studies have indicated that administration of HMG CoA reductase inhibitors (eg, lovastatin, simvastatin, etc) induces a compensatory increase in the activity of HMG CoA reductase, both by increasing its synthesis and decreasing catabolism. To determine in human subjects whether cessation of therapy with this class of drugs leads to induction of HMG CoA reductase activity and above-normal rates of cholesterol biosynthesis, we measured urinary concentrations of mevalonic acid (an indicator of cholesterol biosynthesis) after the cessation of therapy with lovastatin and simvastatin (80 mg/day) in patients with heterozygous FH. Plasma concentrations of LDL increased promptly on discontinuation of reductase inhibitor therapy but did not increase above pretreatment levels at any point after drug discontinuation. Similarly, the 24-hour urinary excretion of mevalonic acid was reduced during treatment with lovastatin or simvastatin and increased promptly on discontinuation of drug but did not increase to levels exceeding those found at baseline when the patients were receiving dietary therapy only. We conclude that cessation of treatment with HMG CoA reductase inhibitors in patients with FH does not result in a rebound increase in cholesterol biosynthesis and that no rebound overshoot occurs in plasma concentrations of low-density-lipoprotein cholesterol.

Adult↗
PubMedDate not supplied

Long-term effect of simvastatin on the improvement of impaired myocardial flow reserve in patients with familial hypercholesterolemia without gender variance.

BACKGROUND: Impaired myocardial flow reserve (MFR) in patients with familial hypercholesterolemia (FH) without evidence of ischemia has been reported. However, it has not been clarified whether diminished MFR in such male or female patients with FH can be reversed by simvastatin. METHODS AND RESULTS: Sixteen patients with FH and 16 age-matched control subjects were studied. All patients were proved to have no evidence of exercise stress-induced myocardial ischemia. Baseline myocardial blood flow (MBF) and MBF during dipyridamole administration (MBF [DP]) were measured with positron emission tomography and nitrogen 13 ammonia; MFR was then calculated before and 9 to 15 months after therapy with simvastatin (5-10 mg/day). Total cholesterol level was significantly higher in patients with FH (277 +/- 49.0) than in control subjects (190 +/- 14.9) but was normalized after lipid-lowering therapy (205 +/- 40.3). Baseline MBF was comparable among FH patients before (77.6 +/- 11.6 mL/min/100 g) and after therapy (74.5 +/- 9.62 mL/min/100 g) and control subjects (78.5 +/- 29.9 mL/min/100 g). However, MBF (DP) in FH patients before therapy (178 +/- 50.9 mL/min/100 g) was significantly lower than that in control subjects (282 +/- 148 mL/min/100 g) and was significantly improved after therapy (228 +/- 91.6 mL/min/100 g, P <.05). In fact, there was no statistically significant difference in the MBF (DP) value in FH patients after therapy compared with that in control subjects (P =.09). MFR significantly improved after therapy in patients with FH (3.33 +/- 1.19 vs 2.27 +/- 0.625, P <.01) and was then statistically comparable to that in control subjects (3.54 +/- 1.11). Improvement of MFR was observed whether MBF (DP) before therapy was greater than or less than 200 mL/min/100 g. MFR was improved in both male and female patients with FH. There was a significant relationship between percent change in plasma total cholesterol concentration and percent change in MFR before and after lipid-lowering therapy (r = -0.57, P <.05). CONCLUSIONS: Diminished MFR in patients with FH without evidence of ischemia can be reversed by moderate- to long-term simvastatin therapy without gender variance.

Anticholesteremic Agents↗
PubMed1998

The sedimentable sterols in gallstone patients before and during ursodeoxycholic acid and simvastatin treatments.

BACKGROUND: The insoluble material in supersaturated bile is prerequisite for the formation of gallstones. We therefore studied the biliary precipitable and soluble cholesterol and noncholesterol sterols, including the cholesterol precursor sterols (including lanosterol and lathosterols), and the plant sterols campesterol and sitosterol, and cholestanol, which usually reflect cholesterol synthesis and absorption, respectively, before and after a 6-month treatment with ursodeoxycholic acid (UCDA), 15.4 +/- 4 mg/kg/day (standard error of the mean) or simvastatin (40 mg/day) in 21 patients with cholesterol gallstones, to obtain further information about the factors contributing to the formation of gallstones. METHODS: The sediment and supernatant fractions of duodenal bile samples were separated by ultracentrifugation and analyzed with gas-liquid chromatography. RESULTS: At the base line (n = 21) 50% +/- 3% of biliary cholesterol and a variable amount of the noncholesterol sterols (from 14% of lanosterol to 62% of cholestanol) were in the sediment fraction. The pattern of the noncholesterol sterols in the sediment resembled that of gallstones described previously. At base line body mass index was positively related to the percentage of precipitable cholesterol in bile (r = 0.46, P < 0.05), and the serum sitosterol proportion negatively related to the molar percentage of biliary cholesterol and positively to that of bile acids (r = -0.46 and r = 0.50, P < 0.05 for both). UDCA decreased the precipitable percentage of cholesterol from 46% to 31% (P < 0.03) and simvastatin from 57% to 42% (P = 0.05). Both drugs also decreased the precipitable percentages of lathosterols and cholestanol while increasing that of lanosterol. In relation to cholesterol, the sediment to supernatant ratios of all methylsterols were increased, whereas those of polar lathosterols tended to decrease during UDCA treatment. CONCLUSIONS: Patients with high body mass index have more precipitable cholesterol in their bile. Although both UDCA and simvastatin decreased the precipitable cholesterol, the bile still contained one-third of its cholesterol in the sedimentable form.

Adult↗
PubMed2005

Physico-chemical characterization and stability study of glassy simvastatin.

The objective of the present study was to investigate the glass forming capability of a model drug simvastatin. The glassy material produced by melt quench technique was subjected to physico-chemical characterization and subsequent stability and enthalpy relaxation study. The chemical stability of drug during preparation of glass was tested by High Performance Liquid Chromatography (HPLC) and Infrared (IR) spectroscopy. The presence of amorphous form was confirmed by DSC and XRPD. Surprisingly, glassy simvastatin was almost stable throughout the period of stability, inspite of its Tg being relatively low. The stability and very low enthalpy recovery of glassy simvastatin perhaps could be attributed to strong inter-molecular hydrogen bonding.

Anticholesteremic Agents↗
PubMed2006

The effect of high dose simvastatin on, platelet size in patients with, type 2 diabetes mellitus.

Statins reduce coronary heart disease risk by altering blood lipids and other mechanisms. One of the possible other mechanisms is through an effect on thrombosis. We assessed the effect of simvastatin 80 mg daily versus placebo given in a single blind crossover fashion on platelet size in response to standard ex vivo stimuli, a surrogate for platelet activation, in 12 subjects with type 2 diabetes and mixed dyslipidemia. Exposure to collagen, cold, and heat caused the expected changes in platelet volume. Contrary to our expectations, ex vivo platelet size during collagen and cold exposure increased by 2.6 and 1.7%, respectively (P < 0.05), during simvastatin treatment as opposed to the placebo period. We conclude that some of the effects of high dose simvastatin therapy on platelets may not necessarily be anti-atherogenic.

Blood Platelets↗
PubMed2006

Effects of celiprolol and simvastatin on the calculated risk of coronary heart disease (the Celisimva study).

OBJECTIVES: The most important risk factors for coronary heart disease are hypercholesterolemia, smoking and hypertension. To find out which treatment is more effective in modifying the total risk--lowering cholesterol concentration or using antihypertensive treatment--we conducted a parallel group placebo-controlled study. The goal of the study was to assess the effect of two drugs on the calculated CHD Framingham risk score in subjects with both moderate hypertension and moderate hypercholesterolemia. DESIGN: Celiprolol for hypertension and simvastatin for cholesterol-lowering were given as monotherapy or as combination treatment. The effects of the treatments on the CHD risk scores were calculated after 3 months. A total of 112 patients were randomized. RESULTS: The total CHD risk decreased in simvastatin and combination groups from 26% to 19% and from 26% to 17%, respectively. Celiprolol alone decreased the risk from 25% to 21%, which was not statistically different from placebo. CONCLUSIONS: It can be concluded that subjects with moderate hypercholesterolemia and hypertension benefit more from lipid-lowering treatment with simvastatin than from blood pressure-lowering with beta blocker celiprolol.

Aged↗
PubMed1992

A randomized placebo controlled trial on the effects of simvastatin, a HMG-CoA reductase inhibitor, on blood lipids and fibrinolytic parameters.

Coronary artery disease is frequently associated with disturbed blood lipids and with a deficient blood fibrinolytic capacity. In order to investigate a possible link between hypercholesterolemia and hypofibrinolysis, we have investigated the effect of simvastatin, a HMG-CoA reductase inhibitor, on blood lipids and fibrinolytic parameters in a double blind, randomized, placebo controlled study design. Twenty-four male patients, aged between 42 and 65 years, with angiographically confirmed coronary artery disease, were selected from a series of 731 consecutive patients on the basis of a fasting serum cholesterol level of more than 250 mg/dl and a plasma PAI-1 level of more than 60 ng/ml. Patients were randomly assigned to 20 mg of simvastatin daily (Group I), or placebo (Group II), for four weeks, followed by doubling of the dose for another four weeks. Blood samples were obtained at baseline and at 4 and 8 weeks. Groups I and II did not differ significantly at baseline. As expected, simvastatin produced a significant reduction in serum levels of total cholesterol (33 +/- 12 and 36 +/- 12 percent, mean +/- SD, after 4 and 8 weeks respectively, p less than 0.001 vs baseline), LDL-cholesterol (36 +/- 5 and 43 +/- 6 percent respectively, p less than 0.001 vs baseline) and apolipoprotein-B (20 +/- 29 and 23 +/- 30 percent respectively, p less than 0.05 vs baseline), whereas these parameters did not change significantly in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Efficacy of simvastatin for lowering cholesterol in non-insulin dependent diabetic patients with hypercholesterolemia.

Patients with non-insulin-dependent diabetes mellitus (NIDDM) are at high risk of cardiovascular disease for many reasons and especially due to the fact that dyslipidemias are more frequent in this group of patients. Fibrate derivatives are the drugs of choice when hypertriglyceridemia is the main lipid anomaly. When hypercholesterolemia is predominant, the use of resins and nicotinic acid has been advocated but these drugs are poorly tolerated on a long-term basis. We assessed the effect of simvastatin, a recent HMG-CoA reductase inhibitor in 12 NIDDM patients with hypercholesterolemia. After 4 weeks of placebo, which did not significantly modify the lipid values, patients were given simvastatin at increasing dosages (from 10 to a maximum of 40 mg daily) during 24 weeks. Compliance and clinical tolerance were excellent. There was no major biological side effect, but a significant deterioration of glucose control was noted at the end of the study. Simvastatin reduced total cholesterol by 28%, LDL-cholesterol by 36% and apo B by 31%. Concomitantly, there was an increase of HDL-cholesterol by 15%. This improvement of lipid profile persisted during the 24 weeks of treatment. Comparing the patients with pure hypercholesterolemia to those presenting combined hyperlipidemia, it was evident that the hypolipidemic effect was more marked in the diabetic subjects with combined hyperlipidemia.

Adult↗