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Biomedical subjects

S Mendoza

Publications and source records attributed to S Mendoza.

At least 19 recordsLinked to original sources

Effects of policosanol on patients with ischemic stroke: a pilot open study.

Stroke is a major health problem worldwide. Its pharmacological management includes thrombolytic therapy for the acute phase and antiplatelet drugs for stroke recovery and prevention. Statins can help in the acute phase and in preventing stroke in secondary prevention patients. Policosanol is a cholesterol-lowering drug with concomitant antiplatelet effects, with protective effects in stroke models. This observational study investigated the effects of policosanol (20 mg/day) administered during the acute phase and for 5 years later on the neurological recovery of patients with ischemic stroke treated with antiplatelets and vitamins. After hospital discharge, patients were followed up every 3 (first year) and 6 (thereafter) months. Neurological improvement was assessed with the modified Canadian Neurological Scale. Adverse events were recorded. Fifty patients were included; all completed the study. Neurological score improved throughout the study. No patient died, and most [40 (80.0%)] did not experience new vascular events; only one (2.0%) suffered a new stroke, and two (4.0%) suffered more than one transient ischemic attack. The time to the first recurrent event was 46.2 months. Policosanol persistently lowered serum total cholesterol, with such reduction correlating with the neurological improvement (R = 0.995253301). Triglycerides were unchanged. Treatment was well tolerated. Policosanol administered to patients suffering ischemic stroke treated with aspirin and vitamins showed good results on neurological outcomes and recurrent events. This study, however, has limitations, since it was open and uncontrolled, and patients also consumed aspirin and vitamins. New randomized, controlled studies are needed to assess the usefulness of policosanol in stroke management.

Aged↗

Epidemiology of transfusion-transmitted infections among multi-transfused patients in seven hospitals in Peru.

BACKGROUND: Transfusion-transmitted infections (TTIs) constitute a major health problem worldwide where routine screening of blood or blood products is improperly done, and where non-medical injecting medications and/or drug use are prevalent. Prevalence and risk factors vary by geographic location and by the specific TTI (including HIV-1, HBV, HCV and HTLV-I). OBJECTIVE: To determine the prevalence and risk factors associated with TTIs among a sample of multi-transfused adult patients in Peru. STUDY DESIGN: A cross-sectional multi-center study was conducted across seven major hospitals in Peru from February 2003 to September 2004. Self-reported behavior information (medical procedures, number of sexual partners, and drug use history) was analyzed, along with a review of exposure history from hospital medical records. Prevalences were calculated by TTI for different exposures, along with unadjusted and adjusted odds ratios for infection risk. RESULTS: Overall, 192 (54.7%) of 351 multi-transfused patients were found infected with one or more TTIs. Number of transfusion units, years of transfusion history (6 or more), and number of treatment facilities (2 or more) were associated with HCV infection. Hemodialysis history was a common risk factor associated with HBV, HCV and HTLV-I infection. HIV infection was associated only with total number of transfusion units received. CONCLUSIONS: High prevalences of HBV and HCV infection were found among Peruvian multi-transfused patients and were associated with a past history and number of blood transfusions, as well as with past hemodialysis procedures. TTIs continue to represent a significant public health problem in Peru. Continued vigilant attention to blood safety procedures, including universal screening and health care provider education, is recommended.

Adolescent↗

Effects of concurrent therapy with policosanol and omega-3 fatty acids on lipid profile and platelet aggregation in rabbits.

BACKGROUND: Policosanol is a mixture of high-molecular-weight aliphatic primary alcohols isolated from sugarcane wax with cholesterol-lowering and antiplatelet effects. Omega-3 fatty acids (FA) from fish oil can protect against coronary disease. An antiarrhythmic mechanism is emerging as the most convincing explanation for omega-3 FA cardiovascular protection, but triglyceride (TG)-lowering effects and inhibition of platelet function could play a role. In view of the effects of policosanol and omega-3 FA on lipid profile and platelet function, potential benefits of combined therapy were expected. OBJECTIVE: To investigate whether combined therapy with policosanol and omega-3 FA would offer some benefit, compared with policosanol or omega-3 FA alone, on serum lipid profile and platelet aggregation in rabbits. METHODS: Male rabbits were randomly distributed in four groups (n = 9 per group). A control group received vehicle, one group was treated with policosanol 5 mg/kg and one with omega-3 FA (eicosapentaenoic acid; EPA [47.0%], docosahexaenoic acid; DHEA [41%]) 250 mg/kg, and the fourth received policosanol 5 mg/kg + omega-3 FA 250 mg/kg. Treatments were orally administered for 60 days. Bodyweight, food consumption and animal behaviour were performed at baseline and study completion. RESULTS: Policosanol significantly lowered low-density lipoprotein cholesterol (LDL-C) [42.7%; p < 0.01] and total cholesterol (TC) [29.4%; p < 0.05], increased high-density lipoprotein (HDL-C) [15.4%; p < 0.05], but left TG levels unchanged. Omega-3 FA significantly lowered TG (47.1%; p < 0.05), but left TC, LDL-C and HDL-C unchanged. Combined therapy decreased LDL-C (38.7%; p < 0.05). Changes in TC, LDL-C and HDL-C obtained with combined therapy were greater (p < 0.05) than those with omega-3 FA, but similar to those with policosanol, whereas the opposite applied to TG reduction. No significant changes in lipid profile were observed in the control group. Policosanol and omega-3 FA significantly (p < 0.05) but moderately inhibited platelet aggregation induced with arachidonic acid (13.3% and 12.4%, respectively); combined therapy achieved greater inhibition (23.9%; p < 0.05). All groups showed similar food consumption and bodyweight gain. No toxic signs were observed in any animal. CONCLUSIONS: Concurrent therapy with policosanol 5 m/kg and omega-3 FA 250 mg/kg lowered LDL-C, TC and TG and increased HDL-C. All treatments inhibited platelet aggregation, but better effects were observed with policosanol + omega-3 FA compared with either treatment alone. Combined therapy was well tolerated. These results suggest that treatment with policosanol + omega-3 FA could be useful for regulating lipid profile and inhibiting platelet aggregation, but conclusive demonstration of such effects requires further experimental and clinical studies.

Animals↗

Effects of addition of policosanol to omega-3 fatty acid therapy on the lipid profile of patients with type II hypercholesterolaemia.

BACKGROUND: Policosanol is a mixture of higher aliphatic primary alcohols purified from sugar-cane wax. The mixture has cholesterol-lowering efficacy, its specific effects being to reduce serum total (TC) and low-density lipoprotein cholesterol (LDL-C), and to increase high-density lipoprotein cholesterol (HDL-C). The effects of policosanol on triglycerides (TG) are modest and inconsistent. Omega-3 fatty acids (FA) from fish oil protect against coronary disease, mainly through antiarrhythmic and antiplatelet effects. Omega-3 FA also have lipid-modifying effects, mostly relating to TG reduction. Thus, potential benefits could be expected from combined therapy with omega-3 FA and policosanol. OBJECTIVE: To investigate whether combined therapy with omega-3 FA + policosanol offers benefits compared with omega-3 FA + placebo with respect to the lipid profile of patients with type II hypercholesterolaemia. METHODS: This randomised, double-blind study was conducted in 90 patients with type II hypercholesterolaemia. After 5 weeks on a cholesterol-lowering diet, patients were randomised to omega-3 FA + placebo, omega-3 FA + policosanol 5 mg/day or omega-3 FA + policosanol 10 mg/day for 8 weeks. Omega-3 FA was supplied as 1g capsules (two per day); placebo and policosanol were provided in tablet form. Physical signs and laboratory markers were assessed at baseline and after 4 and 8 weeks on therapy. Drug compliance and adverse experiences (AEs) were assessed at weeks 4 and 8. The primary efficacy variable was LDL-C reduction; other lipid profile markers were secondary variables. RESULTS: After 8 weeks, omega-3 FA + policosanol 5 and 10 mg/day, but not omega-3 FA + placebo, significantly reduced LDL-C by 21.1% and 24.4%, respectively (both p < 0.0001). Omega-3 FA + policosanol 5 mg/day also significantly lowered TC (12.7%; p < 0.01) and TG (13.6%; p < 0.05), and significantly increased HDL-C (+14.4%; p < 0.001). Omega-3 FA + policosanol 10 mg/day significantly decreased TC (15.3%; p < 0.001) and TG (14.7%; p < 0.01), and significantly increased HDL-C (+15.5%; p < 0.0001). Omega-3 FA + placebo significantly reduced TG (14.2%; p < 0.05) but had no significant effect on other lipid profile variables. The proportion of randomised patients in the omega-3 FA + policosanol 5 or 10 mg/day groups that achieved LDL-C targets or reductions 15% was significantly greater than in the omega-3 FA + placebo group (p < 0.001). Combined therapy with omega-3 FA + policosanol 5 or 10 mg/day resulted in significantly greater changes in LDL-C, TC and HDL-C than treatment with omega-3 FA + placebo, but did not modify the TG response compared with the omega-3 FA + placebo group. Four patients (two in the omega-3 FA + placebo group and two in the omega-3 FA + policosanol 10 mg/day group) withdrew from the study; none of these withdrawals was due to AEs. Two patients reported mild AEs, namely nausea/headache (one in the omega-3 FA + placebo group) and heartburn (one in the omega-3 FA + policosanol 5 mg/day group). CONCLUSIONS: Policosanol 5 or 10 mg/day administered concomitantly with omega-3 FA 1 g/day improved LDL-C, TC and HDL-C, maintained the reduction in TG attributable to omega-3 FA monotherapy, and was well tolerated. Treatment with omega-3 FA + policosanol could be useful for regulating lipid profile in patients with type II hypercholesterolaemia, but further studies involving larger sample sizes are needed before definitive conclusions can be drawn.

Aged↗

Effects of D-003, a mixture of very long chain fatty acids purified from sugar cane wax, at 5 and 10 mg/day on platelet aggregation in healthy volunteers.

D-003 is a mixture of high molecular weight aliphatic primary acids purified from sugar cane wax with antiplatelet and cholesterol-lowering effects. Previous studies showed that D-003 (10-20 mg/day) administered for a short time inhibits platelet aggregation, 14 days being the longest duration investigated. This study was conducted to investigate the effects of D-003 (5 and 10 mg/day) for 30 days on platelet aggregation in normocholesterolemic subjects. This report shows the effects of D-003 on platelet aggregation to arachidonic acid (AA) (1.5 mM), collagen (2 microg/ml) and adenosine 5'-diphosphate ADP (2 microM) assessed at baseline and at treatment completion. Fifty-four subjects were randomized to placebo or D-003 (5 or 10 mg/day) for 30 days. Platelet aggregation to AA, collagen and ADP were assessed. D-003 at the lowest dose (5 mg/day) significantly but modestly inhibited (p < 0.01) platelet aggregation to AA (5.0%) and (p < 0.01) to collagen (7.5%). D-003 at 10 mg/day inhibited (p < 0.001) platelet aggregation to AA and collagen (p < 0.01) by 20.3% and 14.7%, respectively. ADP-induced aggregation, however, was unchanged. D-003 at 10 mg/day, but not at 5 mg/day, lowered (p < 0.01) plasma fibrinogen. D-003 (5 and 10 mg/day) reduced low-density lipoprotein cholesterol (LDL-C) by 17.7% and 26.4%, respectively, and total cholesterol (TC) by 14.5% and 18.5%, while at 10 mg/day, but not at 5 mg/day, it increased high-density lipoprotein cholesterol (HDL-C) by 9.6%. Triglycerides, however, were unchanged with D-003. No disturbances in safety indicators were induced with D-003. One subject (D-003 5 mg/day) discontinued the study and four patients (three taking D-003 and one taking placebo) reported adverse effects (AE) (headache in two patients taking D-003 and one patient taking placebo, and polyphagia in one patient taking D-003). In conclusion, D-003 (5-10 mg/day) for 30 days inhibited platelet aggregation to AA and collagen but not to ADP Therefore, the antiplatelet effect was present with the longer treatment, even at a dose of 5 mg/day. The cholesterol-lowering effects of D-003 were consistent with those expected for such a short treatment. In addition, D-003 at 10 mg/day significantly lowered plasma fibrinogen. The treatment was well tolerated.

Administration, Oral↗

The effect of D-003 (10 mg/day) on biochemical parameters of bone remodelling in postmenopausal women: a randomized, double-blind study.

Biphosphonates, which are antiresorptive agents used to treat osteoporosis, inhibit the mevalonate pathway, preventing protein prenylation and inhibiting osteoclast activity. Statins decrease cholesterol biosynthesis by blocking the mevalonate pathway and have been reported to have beneficial effects on bone. D-003 is a mixture of high molecular weight acids purified from sugarcane wax that inhibits cholesterol biosynthesis before mevalonate production. D-003 prevents bone loss and resorption in rats with osteoporosis induced with ovariectomy or corticoids. Biochemical markers of bone turnover are used to monitor the short-term efficacy of antiosteoporotic therapy. This randomized, double-blind, placebo-controlled study was undertaken to investigate the short-term effects of D-003 (10 mg/day) on biochemical markers of bone turnover in postmenopausal women with low bone mineral density (BMD). After 4 weeks on a low-fat diet, 34 women were randomized to D-003 (10 mg/day) or placebo for 6 months. Pre- and post-treatment samples were analyzed for urinary excretion of deoxypyridinoline (DPD)/creatinine (Cr), a marker of bone resorption, and serum bone specific alkaline phosphatase (BSAP), a marker of bone formation. The effects on lipid profile and safety indicators, as well as adverse events (AE), were investigated. D-003 (10 mg/day) lowered urinary excretion of tDPD/Cr versus baseline (20.6%) (p < 0.001) and placebo (33.7%) (p < 0.01), but did not modify serum BSAP. D-003 decreased low-density lipoprotein-cholesterol (LDL-C) (32.8%), total cholesterol (TC) (16.4%) and the TC/high-density lipoprotein-cholesterol (HDL-C) ratio (34.7%), increased HDL-C (30.3%) (p < 0.001) and did not modify triglycerides. The effects on these variables were significant as early as 3 months after treatment initiation. D-003 was well tolerated. Three patients (one in the placebo group and two in the D-003 group) withdrew from the study. Two of these withdrawals were due to AE: abdominal pain (placebo) and heartburn (D-003). Five patients (four in the placebo group [22.2%] and one in the D-003 group [6.3%]) reported mild AE. In conclusion, D-003 (10 mg/day) reduced urinary excretion of tDPD/Cr, a bone resorption marker and did not change serum BSAP, a bone formation marker, while it lowered cholesterol in study patients. These preliminary results suggest that D-003 could be useful in treating postmenopausal women with low BMD. However, the potential value of D-003 in treating or preventing osteoporosis deserves further clinical investigation.

Alkaline Phosphatase↗

Comparison of the effects of D-003, a mixture of high-molecular-weight aliphatic acids from sugarcane wax, and pravastatin on bones and osteoclast apoptosis of ovariectomized rats.

The mevalonate pathway is relevant in bone cells. Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the key enzyme of this route, stimulating osteoblast differentiation and activity. Pravastatin increases bone formation markers in postmenopausal women and bone density in diabetics. D-003 is a mixture of high-molecular-weight acids purified from sugarcane wax which inhibits cholesterol biosynthesis through HMG-CoA reductase regulation, preventing bone loss in osteoporosis induced with ovariectomy and prednisolone in rats. We investigated the effects of D-003 (50 mg/kg) and pravastatin (20 mg/kg) orally administered for 12 weeks to ovariectomized rats. Female rats were randomized in four groups (10 rats/group): two control groups treated with the vehicle, one false-operated (sham) and another ovariectomized (positive control), while two other groups received D-003 or pravastatin. Bone resorption and formation was studied through histomorphometry and apoptosis through immunohistochemistry. D-003 and pravastatin significantly (p < 0.001) prevented the changes of trabecular bone versus ovariectomized rats and (p < 0.001) the increase of the surface and number of osteoclasts versus ovariectomized controls. D-003 and pravastatin, however, did not modify osteoblast surfaces, a bone formation marker D-003 and pravastatin increased osteoclast apoptosis and reduced (p < 0.05) osteoblast and osteocyte apoptosis versus ovariectomized controls; D-003 was more effective (p < 0.05) than pravastatin. In conclusion, D-003 (50 mg/kg) orally administered for 12 weeks prevented bone loss and bone resorption in ovariectomized rats, increasing osteoclast apoptosis. The preventive effects of D-003 on bone loss and resorption in ovariectomized rats are comparable to those of pravastatin. Both drugs inhibited osteoblast apoptosis but failed to change osteoblast surface. The effects of D-003 on bone cell apoptosis were greater than those of pravastatin. Therefore, D-003 could be used to prevent or treat bone loss in postmenopausal women, but further animal studies and clinical trials are required to confirm the clinical relevance of this potential effect.

Animals↗

Effects of D-003 (5-200 mg/kg), a mixture of high molecular weight aliphatic acids from sugarcane wax, on bones and bone cell apoptosis in ovariectomized rats.

The mevalonate pathway is crucial for osteoclast function. D-003 is a mixture of high molecular weight acids purified from sugarcane wax, which inhibits cholesterol biosynthesis through HMG-CoA reductase regulation. D-003 administered at 50 and 200 mg/kg for 12 weeks prevented bone loss in ovariectomized rats, increasing osteoclast apoptosis. The present study investigated whether the effects of D-003 on bone resorption and osteoclast apoptosis are dose-dependent. Rats were randomized into seven groups (10 rats/group): two control groups orally treated with the vehicle, one false-operated (sham) and another ovariectomized group (positive control), while another four groups received D-003 (5, 25, 50 and 200 mg/kg). The effects on bone resorption and formation were studied through histomorphometry and the effects on apoptosis through immunohistochemistry. D-003 (5-200 mg/kg) dose-dependently and significantly prevented (p < 0.001) changes in trabecular bone and increase in osteoclast surface and number versus ovariectomized controls, leaving osteoblast surfaces unchanged. Across the dose range, D-003 significantly increased (p < 0.05) osteoclast apoptosis in a dose-dependent manner and reduced (p < 0.05) osteoblast and osteocyte apoptosis versus ovariectomized controls, but these effects did not show dose dependence. In conclusion, D-003 (5-200 mg/kg) orally administered at for 12 weeks prevented bone loss and bone resorption and increased osteoclast apoptosis in ovariectomized rats in a dose-dependent manner. These results are consistent with previous data, showing that D-003 administered at relatively low doses prevents bone loss induced with ovariectomy, which could be useful to prevent or treat bone loss in postmenopausal women. Further experimental and clinical studies, however, are needed to confirm these findings.

Animals↗

A comparison of the effects of D-003 and policosanol (5 and 10 mg/day) in patients with type II hypercholesterolemia: a randomized, double-blinded study.

The main goal of hypercholesterolemia management for coronary prevention is to reduce serum low-density lipoprotein cholesterol (LDL-C) levels. D-003 is a mixture of high molecular weight aliphatic acids purified from sugarcane wax, while policosanol is a cholesterol-lowering drug purified from the same source, consisting in a mixture of higher aliphatic alcohols. No previous comparative study of both drugs in humans has been reported. This randomized, double-blind study compares the efficacy and tolerability of D-003 and policosanol (5 and 10 mg/day) in patients with type II hypercholesterolemia. After a baseline period, 100 patients were randomized to D-003 or policosanol both at 5 mg/day and 10 mg/day, for 8 weeks. D-003 and policosanol 5 mg/day reduced (p < 0.0001) LDL-C by 26.9% and 20.9%, respectively. These reductions increased with 10 mg/day (35.1% for D-003, 25.1% for policosanol. The reductions of LDL-C achieved with D-003 5 mg/day and 10 mg/day were greater (p < 0.05 and p < 0.001, respectively) than with policosanol. The frequency of patients treated with D-003 (5 mg/day) reaching LDL-C reductions > or = 15% (22/25, 88%) was greater (p < 0.01) than with policosanol (5 mg/day) (19/25, 76%), and the same was true for D-003 10 mg/day (25/25, 100%) and policosanol (22/25, 88%; p < 0.01). D-003 and policosanol (5 mg/day) also lowered (p < 0.001) total cholesterol (TC) (16.2% and 13.5%, respectively), and increased high-density lipoprotein cholesterol (HDL-C) by 15.3% (D-003) and 6.7% (policosanol). At 10 mg/day, D-003 and policosanol reduced (p < 0.001) TC (21.3% and 16.0%, respectively), while HDL-C was increased by 17.3% and 9.8%, respectively, D-003 being more effective than policosanol. Treatments did not affect triglycerides. Both drugs were well tolerated, with D-003 tolerated as well as policosanol. Three patients discontinued the study, none due to adverse events (AEs). Seven patients (three from the D-003 group and four from the policosanol group) experienced mild AEs. In conclusion, D-003 (5 and 10 mg/day) administered to patients with type II hypercholesterolemia was more effective than policosanol in lowering LDL-C and TC, and in increasing HDL-C. D-003 could be useful for treating type II hypercholesterolemia, but this subject deserves further clinical research.

Aged↗

Effects of D-003, a mixture of high molecular weight aliphatic acids from sugar cane wax, on bones from ovariectomized rats.

Bisphosphonates inhibit bone resorption through mechanisms involving the metabolic pathway from mevalonate to cholesterol. Mevalonate is a precursor of the lipoids required for osteoclast activity and thus inhibition of its synthesis affects bone metabolism. Inhibitors of hydroxymethylglutaryl CoA (HMGCoA) reductase might increase experimentally new bone formation through a mevalonate-dependent effect. D-003 is a mixture of high molecular weight fatty acids isolated from sugar cane wax, which inhibits cholesterol biosynthesis through indirect regulation of HMGCoA reductase activity. This study was undertaken to determine whether D-003 could prevent bone loss in ovariectomized rats. Sprague Dawley female rats were ovariectomized or sham operated and were randomly distributed into five groups: a control ovariectomized and a sham (false-operated) group receiving Tween/H2O vehicle, a group treated with alendronate (3 mg/kg/day) and two groups treated with D-003 (50 and 200 mg/kg/day). Treatments were administered for 3 months. At sacrifice, bones were removed and histological variables of bone resorption and formation were studied by histomorphometry. Ovariectomy diminished trabecular number and thickness and increased trabecular gap, osteoclast number and surface. Alendronate and D-003 prevented a decrease in trabecular number and thickness as well as increases in trabecular separation, osteoclast number and surface compared with ovariectomized controls, thus preventing the bone loss and decreased bone resorption induced by ovariectomy, but failed to increase osteoblast surface compared with control ovariectomized rats. In conclusion, D-003 (50 and 200 mg/kg/day) prevented bone loss and decreased bone resorption in ovariectomized rats, which suggests that this substance could be promising in preventing or treating osteoporosis.

Administration, Oral↗

Policosanol prevents bone loss in ovariectomized rats.

Osteoporosis is characterized by reduced bone mass, abnormal bone architecture and increased fracture risk. Ovariectomy impairs bone mass and metabolism in rats and ovariectomized rats are considered as a suitable model of postmenopausal osteoporosis. Mevalonate is required for producing lipoids that are important in osteoclast activity and thus drugs affecting mevalonate production can prevent bone loss in rodents. Policosanol is a cholesterol-lowering drug isolated from sugar cane wax that inhibits cholesterol biosynthesis through an indirect regulation of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase activity. The purpose of this study was to determine whether policosanol could prevent bone loss in the bones of ovariectomized rats by comparing its effects with those induced by estradiol. Sprague Dawley female rats were randomly distributed in four groups: a sham-operated group treated with Tween/H2O vehicle and three groups of ovariectomized rats treated with 17beta-estradiol (30 microg/kg/day) or policosanol (50 and 200 mg/kg/day), respectively, for 3 months. At treatment completion the rats were sacrificed, their bones removed and variables of bone resorption and formation were investigated by histomorphometry. Ovariectomy increased trabecular separation but diminished the number and thickness of trabecules. Estradiol and policosanol prevented these effects compared with ovariectomized controls. Both treatments also prevented an increase in the number of osteoclasts and their surface area induced by ovariectomy. Estradiol, but not policosanol, significantly prevented an increase of osteoblast surface area compared with ovariectomized controls. In conclusion, policosanol prevented bone loss and decreased bone resorption in ovariectomized rats, suggesting that it should be potentially useful in preventing bone loss in postmenopausal women.

Administration, Oral↗

Effects of d-003, a new substance purified from sugar cane wax, on platelet aggregation and plasma levels of arachidonic acid metabolites in healthy volunteers.

D-003 is a mixture of very high molecular weight aliphatic acids purified from sugar cane wax showing cholesterol-lowering and antiplatelet effects proven in experimental and clinical studies. Experimental evidence indicates that inhibition of platelet aggregation induced by D-003 is associated with a reduction of thromboxane B2 (TxB2) and an increase of prostacyclin (Pgl2) serum levels. This double-blinded, randomized, placebo-controlled study was undertaken to investigate whether D-003 (20 mg/day) modifies serum levels of TxB2 and Pgl2 and inhibits platelet aggregation in human healthy volunteers. Thirty-one subjects were randomized to placebo or D-003 at 20 mg/day for 14 days. Serum levels of TxB2 and Pgl2 and platelet aggregation to arachidonic acid (AA) (1.75 mM) and collagen (1 microg/ml) were assessed. D-003 (20 mg/day) significantly reduced (p < 0.001) TxB2by 36.4% and increased Pgl2 serum levels by 31% compared with baseline, and these changes were different from placebo. As expected, D-003 significantly inhibited (p < 0.001) platelet aggregation to AA (81.9-65.6%) and to collagen (75.3-62.3%). No subject withdrew from the study. No drug-related disturbances were observed. We conclude that D-003 at 20 mg/day for 14 days significantly inhibited platelet aggregation to AA and collagen and reduced TxB2 and increased Pgl2 serum levels. These results are consistent with those observed in experimental models, indicating that the antiplatelet effect of D-003 is associated with the observed changes on the levels of AA metabolites. Further studies, however, should explore the mechanism involved in this action in greater depth.

Adult↗

Concomitant use of policosanol and beta-blockers in older patients.

Policosanol is a cholesterol-lowering drug with concomitant antiplatelet effects. It is safe and well tolerated, even in populations with high consumption of concomitant drugs. These data suggest that adverse events (AE) due to drug-to-drug interactions (DDI) with policosanol are not relevant. Experimental data indicate that potential DDI between policosanol and drugs metabolized through the cytochrome P450 hepatic system are not expected, but pharmacodynamic DDI cannot be excluded. Several clinical studies have shown that policosanol decreased arterial pressure compared with placebo, and a pharmacological interaction with beta-blockers was experimentally proven. Therefore, clinical DDI between policosanol and beta-blockers can be expected. This study investigated whether policosanol reinforces the antihypertensive effects of beta-blockers and/or whether this combination impairs some safety indicators or induces specific AE in older patients. After 5 weeks on a diet-only baseline period, 205 older hypercholesterolemic patients taking beta-blockers were randomized to policosanol 5 mg/day or placebo for 3 years. After 1 year on therapy, policosanol significantly reduced (p < 0.00001 versus placebo) low-density lipoprotein-cholesterol (LDL-C) (20.9%), total cholesterol (TC) (19.3%) and triglycerides (TG) (25.7%), whereas it increased (p < 0.01 and p < 0.001 versus placebo) high-density lipoprotein-cholesterol (HDL-C) levels (4.1%). Treatment effects did not to wear off during the 3-year follow-up. At study completion, policosanol lowered (p < 0.00001 versus placebo) LDL-C (34.3%), TC (23.2%) and TG (21.2%) and raised (p < 0.00001 versus placebo) HDL-C (12.3%). Thirty-one patients (15.1%) discontinued the study, 22 in the placebo group (20.6%) and nine in the policosanol group (9.2%). Of these, 20 patients (16 in the placebo group and four in the policosanol group) withdrew from the study due to AE. The frequency of serious adverse events (SAE), mostly vascular, in policosanol patients (3/98, 3.1%) was lower than in the placebo group (15/107, 14.0%). No impairment of safety indicators was observed. Nevertheless, reductions in systolic and diastolic blood pressure were observed in policosanol patients compared with those in the placebo group. The frequency of policosanol patients reporting mild or moderate AE (18/98, 18.4%) was also lower than in the placebo group (30/107, 28.0%). In conclusion, policosanol was well tolerated in elderly patients taking beta-block- ers and did not increase AE. Additional reduction of blood pressure and a lower frequency of SAE were observed in policosanol patients compared with those taking placebo. The cholesterol-lowering efficacy of policosanol was that expected. These results provide support that policosanol therapy added to hypercholesterolemic elderly individuals taking beta-blockers could provide additional benefits in lowering blood pressure; SAE were not more frequent in the policosanol group than in the placebo group and there was no increase in AE.

Adrenergic beta-Antagonists↗

Extracts from plants used in Mexican traditional medicine activate Ca(2+)-dependent chloride channels in Xenopus laevis oocytes.

The two-electrode voltage-clamp technique was employed to investigate the effects of chloroform-methanol (1:1) extracts derived from five medicinal plants on Xenopus laevis oocytes. When evaluated at concentrations of 1 to 500 microg/ml, the extracts prepared from the aerial parts of Baccharis heterophylla H.B.K (Asteraceae), Chenopodium murale L. (Chenopodiaceae), Desmodium grahami Gray (Leguminosae) and Solanum rostratum Dun (Solanaceae) produced concentration-dependent oscillatory inward currents in the oocytes, while the extract of Gentiana spathacea did not induce any response. The reversal potential of the currents elicited by the active extracts was -17 +/- 2 mV and was similar to the chloride equilibrium potential in oocytes. These ionic responses were independent of extracellular calcium. However, they were eliminated by overnight incubation with BAPTA-AM (10 microM), suggesting that the currents were dependent on intracellular Ca2+ increase. Thus the plant extracts activate the typical oscillatory Ca(2+)-dependent Cl- currents generated in the Xenopus oocyte membrane more probably via a mechanism that involves release of Ca2+ from intracellular reservoirs. These observations suggest that Xenopus oocyte electrophysiological recording constitutes a suitable assay for the study of the mechanisms of action of herbal medicines.

Animals↗

Effects of D-003, a mixture of long-chain aliphatic primary acids, fluvastatin and the combined therapy of D-003 plus fluvastatin on the lipid profile of normocholesterolemic rabbits.

D-003 is a mixture of long-chain aliphatic primary acids isolated from sugar cane wax with cholesterol-lowering effects proven in animals and healthy human volunteers. D-003 reduced serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) in rabbits, while it increased high-density lipoprotein cholesterol (HDL-C) and did not affect triglycerides. D-003 inhibits cholesterol synthesis by regulating, instead of directly inhibiting, hydroxamethylglutaryl-CoA (HMGCoA) reductase activity. Although the ways in which D-003 and statins inhibit cholesterol biosynthesis are not identical, the strong competitive inhibition of cholesterol biosynthesis induced by statins suggests that an enhanced decrease of LDL-C and TC caused by the combined therapy D-003 plus statins is not expected. Nevertheless, taking into account the differential effects of D-003 and statins in HDL-C and triglycerides in rabbits, potential benefits of such combined therapy on other lipid variables cannot been discarded. Fluvastatin is a statin that inhibits competitively HMGCoA reductase, like other members of this class. This study was undertaken to compare the cholesterol-lowering effects of D-003, fluvastatin and the combined therapy of D-003 plus fluvastatin in normocholesterolemic rabbits. Animals were randomly distributed into four groups of eight. One control group received the vehicle, two groups were treated with D-003 or fluvastatin at 5 mg/kg/day each, and the fourth group received the combined therapy of both drugs at 5 mg/kg/day each. Treatments were orally administered for 30 days. Body weight, food consumption and overall animal behavior were recorded to detect any warning sign resulting from combined therapy. After treatment, it was found that both D-003 and fluvastatin had significantly lowered LDL-C - D-003 by 81.5% (p < 0.01) and fluvastatin by 61.4% (p < 0.05). Combined therapy reduced LDL-C values (75.9%). Final values and percent changes reached in all groups were different from the control (p < 0.01). The reductions of TC were consistent with LDL-C decreases, so that D-003, fluvastatin and combined therapy significantly lowered TC by 48.4% (p < 0.01), 39.7% (p < 0.05) and 45.3%, respectively, values being different from those of the control (p < 0.01). The responses of LDL-C and TC to combined therapy were statistically similar, but less pronounced than those reached by D-003 alone. D-003 and combined therapy, but not fluvastatin alone, increased HDL-C (+21.5% and + 19.0%, respectively), these changes being significant versus the control (p < 0.05). In turn, fluvastatin and combined therapy, but not D-003 alone, lowered triglycerides (13.6% and 13.0%, respectively, p < 0.05 versus control). The effects of combined therapy on HDL-C were similar to those of D-003 alone, and the effects of combined therapy on triglycerides were similar to those of fluvastatin alone. The only advantage of combined therapy appears to be that it shows better effects on HDL-C than those of fluvastatin alone and better effects on triglycerides than D-003 alone. No significant changes in lipid profile were observed in the control group. All groups showed similar food consumption and body weight gain, health status being unaffected by the treatments. It is concluded that D-003 and fluvastatin at 5 mg/kg/day administered orally for 30 days to normocholesterolemic rabbits lowered LDL-C and TC, D-003 being more effective in increasing HDL-C and fluvastatin in lowering triglycerides. Combined therapy did not improve the response of LDL-C and TC with respect to monotherapies, but induced better responses of HDL-C and triglycerides than fluvastatin alone had on HDL-C or D-003 alone had on triglycerides.

Administration, Oral↗

Effect of D-003, a mixture of high molecular weight primary acids from sugar cane wax, on paracetamol-induced liver damage in rats.

D-003 is a mixture of very high molecular weight aliphatic primary acids purified from sugar cane (Saccharum officinarum, L) wax, in which the most abundant component is octacosanoic acid. Experimental studies have shown that D-003 not only shows cholesterol-lowering and antiplatelet effects, but also offers strong protection against plasma lipoprotein oxidation. Previous studies demonstrated that D-003 protected against the histological changes characteristic of Cl4C-induced hepatic injury in rats. The aim of the present study was to investigate the effects of D-003 in acute hepatotoxicity induced by paracetamol in rats. Male Sprague Dawley rats were randomly distributed in two experimental series of three experimental groups as follows: group 1--positive control rats (paracetamol-treated); groups 2 and 3--rats with liver damage induced by paracetamol and treated with D-003 at 5 and 25 mg/kg, respectively, and which also received paracetamol to induce liver injury. In experimental series 1, animals received paracetamol orally (600 mg/kg). In series 2, paracetamol was administered through the intraperitoneal route (200 mg/kg). Eighteen hours after paracetamol dosing, rats were anesthetized with ether and livers were removed for histopathological studies. In the two experimental series, D-003 at 5 and 25 mg/kg significantly (p < 0.01) decreased the percentage of turgent cells and hepatocytes with necrosis and increased the percentage of normal hepatocytes with respect to positive controls in a dose-dependent manner. Necrotic areas and inflammatory infiltrates were observed in the liver of nine out of ten (90%) positive controls. In turn, D-003 dramatically reduced both necrotic areas and inflammatory infiltrate and was present in only one out of ten (10%) animals treated in the two experimental series. No histological alterations in liver sections of negative controls were found. D-003 protected against the histological changes characteristic of paracetamol-induced hepatic injury in rats, in which the process of lipid peroxidation plays a major role. The relationship between this protective action of D-003 in this experimental model and its antioxidant effects needs to be further investigated before definitive conclusions are drawn.

Acetaminophen↗

Effect of D-003, a mixture of high molecular weight primary acids from sugar cane wax, on CL4C-induced liver acute injury in rats.

D-003 is a mixture of very high molecular weight aliphatic primary acids purified from sugar cane (Saccharum officinarum, L.) wax, in which octacosanoic acid is the most abundant component. Previous experimental studies have shown that D-003 not only shows cholesterol-lowering and antiplatelet effects, but also offers strong protection against plasma lipoprotein oxidation. Acute hepatotoxicity induced by CCL4 in rats has been related to an increased rate of lipid peroxidation, and different antioxidant compounds have been revealed to be effective in this model. The aim of this study was to investigate the effects of D-003 in acute hepatotoxicity induced by CCL4 in rats. Male Sprague Dawley rats were randomly distributed in four experimental groups as follows: group 1: negative control rats; group 2: positive control rats (CCL4-treated); groups 3 and 4 rats with liver damage induced by CCL4 and treated with D-003 at 25 and 100 mg/kg, respectively. Acute liver injury was induced by CCL4 suspended in olive oil and intraperitoneally administered at 1 ml/kg. Eighteen hours after CCL4 dosing, the rats were anesthetized with ether and their livers were removed for histopathological studies. D-003 at 25 and 100 mg/kg significantly (p < 0.01) decreased the percentage of ballooned cells and hepatocytes with lipidic inclusions and increased the percentage of normal hepatocytes compared with that in positive controls in a dose-dependent manner. The percent inhibitions of the occurrence of ballooned cells and hepatocytes with lipids were marked (75% and 50%, respectively) with the high dose (100 mg/kg). The percent of turgent hepatocytes was also significantly reduced compared with that in positive controls, but this effect was not dose-dependent. No histological alterations in the liver sections of negative controls were found. Necrotic areas and inflammatory infiltrate were observed in the liver of 7/8 (87.5%) of positive controls. In turn, D-003 dramatically reduced both necrotic areas and inflammatory infiltrate and was present in only 1/8 (12.5%) animals treated with D-003 25 mg/kg and in none (0%) of the animals treated with 100 mg/kg. D-003 protected against the histological changes characteristic of CCL4-induced hepatic injury in rats, in which the process of lipid peroxidation plays the main role. The relationship between this protective action of D-003 on this experimental model and its antioxidant effects needs to be further investigated before definitive conclusions are drawn.

Animals↗

High-performance liquid chromatography-based determination of total isothiocyanate levels in human plasma: application to studies with 2-phenethyl isothiocyanate.

Dietary and pharmacologic isothiocyanates (ITCs) may play a role in reducing the risk of certain cancers. The quantification of ITCs in humans is important both for epidemiological and pharmacokinetic studies. We describe a modification of an HPLC-based assay of urinary ITCs for use with human plasma. The assay utilizes the cyclocondensation reaction of 1,2-benzenedithiol with ITCs present in human plasma, followed by a two-step hexane extraction and analysis by HPLC using UV detection at 365 nm. The method shows linearity and reproducibility with human plasma over a range of 49-3003 nM phenethyl isothiocyanate (PEITC) (r(2) = 0.996 +/- 0.003). A similar degree of linearity was seen with two other biologically occurring conjugates of PEITC: PEITC--N-acetylcysteine (PEITC--NAC) and PEITC--glutathione (PEITC--GSH). The recovery of PEITC assessed on multiple days was 96.6 +/- 1.5% and was 100% for PEITC--GSH and PEITC--NAC. The reproducibility of the assay on multiday samplings showed a mean %CV of 6.5 +/- 0.3% for PEITC, 6.4 +/- 4.3 for PEITC--NAC and 12.3 +/- 3.9 for PEITC--GSH. In clinical studies, mean plasma ITC level of 413 +/- 193 nM PEITC equivalents was determined for a non-dietary-controlled group of 23 subjects. Multiday analysis data from pharmacokinetic plasma sets of 3 subjects taking a single dose of PEITC at 40 mg showed a good CV (range: 16-21%). The applicability of the methodology to pharmacokinetic studies of PEITC in humans is demonstrated.

Chromatography, High Pressure Liquid↗