Search PubMed⌕ Search

Biomedical subjects

M Fainaru

Publications and source records attributed to M Fainaru.

At least 19 recordsLinked to original sources
PubMed1999

Weight gain and insulin resistance during nicotine replacement therapy.

BACKGROUND: Although the cessation of smoking reduces the increased risk for ischemic heart disease, it is associated with marked weight gain and presumably insulin resistance, both of which heighten the risk of coronary heart disease. HYPOTHESIS: We investigated the isolated effect of nicotine on body weight and insulin resistance during smoking cessation. METHODS: Eleven healthy, middle-aged heavy smokers were studied. Insulin sensitivity was assessed by an insulin-enhanced, frequently sampled intravenous glucose tolerance test with minimal model analysis. The subjects were studied at baseline (last day of smoking) (phase 1), at the end of the 6-week nicotine replacement program (phase 2), and after 8 weeks without smoking or nicotine replacement (phase 3). RESULTS: The subjects started to gain weight during nicotine replacement (phase 2) (0.3 +/- 0.2 kg/week, mean +/- standard deviation) and continued to do so at a steady rate after nicotine replacement was stopped (0.2 +/- 0.2 kg/week) (p = 0.3). Insulin sensitivity decreased by 14 +/- 2.6% during nicotine replacement but increased by 16 +/- 5.1% (compared with phase 2) during phase 3, even though the weight gain continued (p = 0.047; 95% confidence interval: 0.05-5.73). CONCLUSIONS: Smoking cessation is associated with weight gain and improvement in insulin resistance. Nicotine is the main ingredient in cigarette smoke causing insulin resistance, but the withdrawal of another, unknown ingredient in cigarette smoke is responsible for the weight gain associated with smoking cessation.

Administration, Cutaneous↗
PubMed1999

Susceptibility of serum lipids to copper-induced peroxidation correlates with the level of high density lipoprotein cholesterol.

As a first step in evaluating the significance of our recently developed method of monitoring the kinetics of copper-induced oxidation in unfractionated serum, we recorded the kinetics of lipid oxidation in the sera of 62 hyperlipidemic patients and analyzed the correlation between oxidation and lipid composition of the sera [high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, and triglycerides]. We used six factors to characterize the kinetics of oxidation, namely, the maximal absorbance of oxidation products (ODmax), the maximal rate of their production (Vmax), and the time at which the rate was maximal (t(max)) at two wavelengths (245 nm, where 7-ketocholesterol and conjugated dienic hydroperoxides absorb intensely, and 268 nm, where the absorbance is mostly due to dienals). The major conclusions of our analyses are that: (i) Both ODmax and Vmax correlate positively with the sum of concentrations of the major oxidizable lipids, cholesterol, and cholesteryl esters. (ii). The value of t(max), which is a measure of the lag preceding oxidation and therefore reflects the resistance of the serum lipids to copper-induced oxidation, exhibits a negative correlation with HDL cholesterol. Although this finding accords with the observation of shorter lags for HDL than for LDL, it is apparently inconsistent with the role of HDL as an antirisk factor in coronary heart diseases.

Adult↗
PubMed1999

Comparison of hemostatic factors and serum malondialdehyde as predictive factors for cardiovascular disease in hemodialysis patients.

Hemodialysis (HD) patients have accelerated cardiovascular morbidity and mortality rates compared with the general population. Identifying the factors that predict major coronary events in this population can direct the focus on prevention. This cross-sectional study compares known and suspected cardiovascular risk factors in HD patients with and without prevalent cardiovascular disease (CVD). In 76 HD patients (prevalent CVD, 44 of 76 patients), serum lipid, lipoprotein, apolipoprotein (Apo), plasma fibrinogen, tissue plasminogen activator (TPA), plasminogen activator inhibitor (PAI-1), and factor VII levels were measured using standard kits. Serum malondialdehyde (MDA; a marker of oxidative stress) was measured using spectrophotometry. Predictor variables were compared using analysis of variance and chi-squared tests, as appropriate. CVD prevalence was modeled using multiple logistic regression analysis, and odds ratios (OR) were calculated. Serum lipid, lipoprotein, Apo, plasma TPA, PAI-1, and factor VII values did not differ significantly from laboratory norms or discriminate for prevalent CVD in HD patients. Plasma fibrinogen levels were significantly elevated in HD patients compared with laboratory norms (369.4 +/- 130.02 v 276.7 +/- 77.7 mg/dL; P < 0.0001) but were not significantly different in HD patients with and without prevalent CVD. Serum MDA levels, both before and after the midweek HD treatment, were significantly elevated in all HD patients compared with laboratory norms (pretreatment, 2.6 +/- 0.8 nmol/mL; posttreatment, 2.1 +/- 0.3 v 0.91 +/- 0.09 nmol/mL; P < 0.01) and were significantly elevated in HD patients with prevalent CVD versus those without (pretreatment, 2.8 +/- 0.6 v 2.4 +/- 0.4 nmol/mL; P < 0.01; posttreatment, 2.3 +/- 0.4 v 1.94 +/- 0.2 nmol/mL; P < 0.01). Only serum MDA levels, both before and after the midweek treatment, contributed to the explanation of variation in CVD prevalence. OR for CVD in the highest versus lowest tertile of pretreatment MDA level was 2.71 (95% confidence interval [CI], 1.42 to 5.19). ORs for CVD in the highest versus lowest tertile of posttreatment MDA level was 3.65 (95% CI, 1.6 to 8.32).

Adult↗
PubMed1999

Serum malondialdehyde and prevalent cardiovascular disease in hemodialysis.

BACKGROUND: Oxidative stress has been proposed as a mechanism by which the accelerated rate of cardiovascular disease (CVD) observed in maintenance hemodialysis (HD) patients may be explained. This study examined the effects of HD and CVD on serum malondialdehyde (MDA) levels as a marker of oxidative stress in HD patients with and without prevalent CVD. Serum MDA levels and CVD prevalence in HD were modeled. METHODS: Serum MDA was determined using spectrophotometry in HD patients (N = 76, 53 men and 23 women, mean age 63.8 years) immediately prior to and at the conclusion of one midweek HD treatment. Traditional CVD risk factors, including serum lipids, lipoproteins, apolipoproteins, and fibrinogen, were also measured, as were serum chemistry and dialysis adequacy. RESULTS: Mean serum MDA levels were significantly elevated in HD patients with prevalent CVD compared with those without, whereas serum lipoprotein and plasma fibrinogen levels did not differ between the two groups. Patients in the highest compared with the lowest tertile of postdialysis MDA were nearly four times as likely to have prevalent CVD, and serum MDA was the single strongest predictor of prevalent CVD in this patient population. CONCLUSIONS: These findings indicate the presence of oxidative stress in HD patients, and are consistent with the theory of oxidative stress as a factor in accelerated CVD in this population.

Aged↗
PubMed1998

Lipid oxidation in unfractionated serum and plasma.

In an attempt to develop an assay for the susceptibility of plasma lipids to oxidation, we have studied the kinetics of copper-induced oxidation in diluted serum and plasma prepared with different anticoagulants (heparin, citrate and EDTA) by monitoring the absorbance of oxidation-products at several wavelengths. These studies revealed the complex and interrelated effects of the water-soluble antioxidant ascorbic acid, citrate and chloride ions on the kinetics of copper-induced oxidation of plasma lipids. Specifically, the onset of oxidation induced by copper-citrate chelates is only slightly affected by chloride ions and is accelerated upon increasing the copper concentration. By contrast, in the absence of citrate, the lag preceding oxidation in diluted serum or plasma (but not the maximal rate of oxidation) depends markedly on the chloride concentration in the diluting medium. In the absence of Cl-, the lag preceding oxidation is a decreasing saturable function of copper concentration, whereas in a normal phosphate-buffered saline solution (PBS), the lag shows a biphasic dependence on copper concentration such that at copper concentrations above 10-30 microM (depending on the extent of plasma dilution), increasing the concentration of copper results in prolongation of the lag. This dependence of copper-induced oxidation on the concentration of copper is not observed for dialyzed serum unless ascorbic acid is added. Our interpretation of these results is that water-soluble reductants and chloride ions act synergistically to stabilize Cu+, on the expense of Cu2+. Quenching of free radicals by Cu+ may be responsible for the prolongation of the lag at high copper concentrations, with no reduction of the maximal rate of oxidation. In spite of the complex dependencies described above, spectrophotometric monitoring of the kinetics of oxidation of plasma lipids, under 'optimized conditions' (50-fold diluted serum, in PBS containing 720 microM sodium citrate and 100 microM copper), agrees with independent measurements of the consumption of polyunsaturated fatty acids. Hence, the spectroscopic method may become useful for evaluation of the susceptibility of plasma lipids to oxidation. This possibility, however, has yet to be elucidated through investigations of the correlation between the susceptibility of serum lipids to copper-induced oxidation in vitro and clinical factors of significance.

Anticoagulants↗
PubMed1998

LDL-associated phospholipase A does not protect LDL against lipid peroxidation in vitro.

The irreversible proteinase inhibitor Pefabloc (4-[2-aminoethyl] benzenesulfonyl fluoride) inactivates LDL-catalyzed hydrolysis of the short-chain fluorescent phospholipid C6-NBD-PC (1-acyl-2-(N-4-nitrobenzo-2-oxa-1,3-diazole)-aminocaproyl phosphatidylcholine). The dose-dependence of this inactivation is similar to that obtained previously for the inhibitory effect of Pefabloc on the hydrolysis of platelet activating factor (PAF) by the LDL-associated PAF acetylhydrolase (PAF-AH), in agreement with the notion that the hydrolysis of C6-NBD-PC and PAF is catalyzed by the same enzyme (LDL-associated phospholipase A; LDL-PLA). This conclusion is also supported by the finding that hydrolysis of C6-NBD-PC by LDL becomes inactivated by LDL oxidation only at late stages of the oxidation, similar to the effect of oxidation on the hydrolysis of PAF by the LDL-associated PAF-AH. Under conditions of complete inactivation of this enzyme towards C6-NBD-PC, the kinetics of lipid peroxidation, induced either by copper ions or by the free radical generator AAPH at varying doses of the prooxidant, was similar to that observed when the PLA was active (i.e., in the absence of Pefabloc). Hence, LDL-associated PLA (PAF-AH) does not protect LDL lipids from peroxidation. Similar results were obtained with fractionated LDL in albumin-containing buffer and for non-fractionated serum, in which copper-induced peroxidation was also not influenced by inactivation of the enzyme responsible for hydrolysis of C6-NBD-PC. Phospholipolysis of short chain phospholipids by LDL-PLA may still play a protective role against the toxic effects of oxidized phospholipids by reducing their internalization into cells (Schmitt et al. 1995).

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1998

Role of behaviour modification in the treatment of childhood obesity with the parents as the exclusive agents of change.

OBJECTIVE: This study examined the reduction in overweight and changes in eating-related behaviours in obese children treated with a family-based approach, in which the parents were the exclusive agents of change. Results were compared to the conventional approach in which children are responsible for their own weight loss. DESIGN: A one-year longitudinal prospective design was used. Participants were randomly allocated for the experimental (parents as the agents of change) or the conventional (children as the agents of change) intervention. METHODS: Sixty obese children (20% over ideal weight for age, height and gender) aged 6-11 y (mean+/-s.d. 9.2+/-1.0 y) were included in the study. Anthropometric measurements and biochemical tests were performed on the children and their parents before and after the programme, and both parents completed a sociodemographic and a family eating and activity habits questionnaire. Hour-long support/educational sessions were conducted by a clinical dietitian-14 sessions for the parents in the experimental intervention and 30 for the children in the conventional intervention. Individual sessions were held for members of both groups, when necessary. RESULTS: Significant differences were found between the two groups in the reduction of exposure to food stimuli and changes in eating habits (eating while standing, watching TV, reading or doing homework, eating following stress and eating between meals). Mean weight reduction (by percentile) was significantly greater in the experimental intervention group (parent-only treatment) in comparison to the conventional intervention group (child-only treatment). CONCLUSIONS: Treatment of childhood obesity with the parents as the exclusive agents of change, induces more behavioural changes as well as greater weight loss, than the conventional approach.

Behavior Therapy↗
PubMed1998

Parents as the exclusive agents of change in the treatment of childhood obesity.

BACKGROUND: Excessive weight in childhood is a serious public health concern because of its costly health consequences and its increasing prevalence. OBJECTIVE: Our objective was to compare the efficacy of a family-based approach for the treatment of childhood obesity, in which the parents served as the exclusive agents of change, with that of the conventional approach, in which the children served as the agents of change. DESIGN: This study had a randomized, longitudinal prospective design and lasted 1 y. Sixty obese children aged 6-11 y were randomly allocated to the experimental (parents as agents of change) or control (children as agents of change) group. Anthropometric and biochemical measurements were determined at the start and end of the study. A sociodemographic questionnaire and a family eating and activity habits questionnaire were completed by both parents. Hour-long support and educational sessions were conducted by a clinical dietitian: 14 sessions for the parents in the experimental group and 30 sessions for the children in the control group. RESULTS: The dropout rate was nine times greater in the control group (n = 9) than in the experimental group (n = 1). Mean percentile weight reduction was significantly (P < 0.03) higher in children in the experimental group (14.6%) than in the control group (8.1%). CONCLUSIONS: Treatment of childhood obesity with parents as the exclusive agents of change was superior to the conventional approach, as indicated by the dropout rate and the percentage weight loss of the children during the 1-y intervention.

Adult↗
PubMed1997

The effect of albumin on copper-induced LDL oxidation.

In an attempt to gain deeper understanding of the mechanism or mechanisms responsible for the protective effect of serum albumin against Cu(2+)-induced peroxidation of low density lipoprotein (LDL), we have examined the influence of the concentrations of bovine serum albumin (BSA), Cu2+ and LDL on the kinetics of peroxidation. Since the common method of monitoring the oxidation by continuous recording of the absorbance of conjugated dienes at 234 nm cannot be used at high BSA-concentrations because of the intensive absorption of BSA, we have monitored the time-dependent increase of absorbance at 245 nm. At this wavelength, conjugated dienes absorb intensely, whereas the background absorbance of BSA is low. Using this method, as well as the TBARS assay for determination of malondialdehyde, over a large range of BSA concentrations, we show that in many cases the influence of BSA on the kinetics of oxidation can be compensated for by increasing the concentration of copper. This reconciles the apparent contradiction between previously published data. Detailed studies of the kinetic profiles obtained under different conditions indicate that binding of Cu2+ to albumin plays the major role in its protective effect while other mechanisms contribute much less than copper binding. This conclusion is consistent with the less pronounced effect of BSA on the oxidation induced by the free radical generator AAPH. It is also shown that the copper-albumin complex is capable of inducing LDL oxidation, although the kinetics of the latter process is very different from that of copper-induced oxidation. Nevertheless, when compared to copper induced oxidation at similar concentration of the oxidation-promotor, the kinetics of oxidation induced by copper-albumin complex is very different and is consistent with a tocopherol mediated peroxidation, characteristic under low radical flux. Similar kinetics was observed for copper-induced oxidation only at much lower copper concentrations.

Amidines↗
PubMed1996

Diurnal heterogeneity in structure and function of low density lipoproteins of normolipidemic males.

Structural changes in low density lipoproteins (LDL) have been shown to alter their metabolism and atherogenic potential. We investigated the diurnal changes in size and composition of LDL in seven healthy, non-obese, normolipidemic male volunteers consuming a standard diet (14.5% protein, 31.9% fat, 53.6% carbohydrate and 383 mg cholesterol/day) and continuing their daily routine. The food was divided into three meals and three snacks, and blood samples were obtained at 7 AM (after 12 h fasting), noon, 8 PM, midnight and 3 AM. LDL were isolated by both sequential and density gradient ultracentrifugation (d = 1.019 - 1.050 g/ml), and analyzed for lipids, apolipoproteins, size, and affinity to LDL receptors. Diurnal LDL preparations differ from fasting LDL in both chemical and physical parameters. The former get richer in triglyceride (TG/cholesterol weight ratio 0.23 vs. 0.16), larger in diameter (21.2 +/- 0.2 vs. 22.4 +/- 0.1 nm), and enriched in a more buoyant fraction (74.0 +/- 4.6 vs. 41.9 +/- 3.8% of LDL cholesterol in d = 1.019 - 1.035 g/ml). These structural changes in LDL were associated with enhanced affinity to LDL receptors in both human skin fibroblasts and HepG2 cells, as demonstrated by competition experiments with fasting human 125I-LDL. The observed diurnal heterogeneity in both the structure and the function of LDL may be attributed to the absorptive state as it did not occur during prolonged fasting. These diurnal changes may be important for better understanding LDL metabolism in vivo and for the elucidation of the atherogenic process.

Adult↗
PubMed1995

Copper-induced lipid oxidation in unfractionated plasma: the lag preceding oxidation as a measure of oxidation-resistance.

In spite of the pathological significance of oxidation of plasma lipids, no method is currently available for the evaluation of the susceptibility of these lipids to oxidation in unfractionated plasma. Here we demonstrate that copper-induced oxidation of diluted plasma, in the presence of citrate can be monitored continuously by recording the absorbance at 245 nm. The kinetics of accumulation of oxidation products in unfractionated plasma is a sum of lipid oxidation products obtained in low and high density lipoproteins isolated from the same plasma. The kinetic profiles are reproducible and can be performed with plasma samples even after prolonged storage at 4 degrees C (up to two months) or after freezing and thawing of the plasma. Being simple and reproducible, yet correlating with the oxidizability of low and high density lipoproteins, this method can be used to evaluate the "oxidation resistance" of plasma lipids and thus serve as a standard index of the susceptibility of the plasma lipids of patients to oxidation-inflicted pathologies, including atherosclerosis.

Anticoagulants↗
PubMed1995

The effect of lovastatin on early restenosis.

The effect of lovastatin given before percutaneous coronary angioplasty (PTCA) on early restenosis was investigated in men with mild to moderate hypercholesterolemia. Thirty-four hypercholesterolemic patients (serum LDL cholesterol 130-200 mg/dL) undergoing their first PTCA completed a 6-month prospective, double-blind, placebo-controlled trial. Eighteen received lovastatin 20 mg/day (Lo group) and 16 placebo (P1 group), beginning 10 to 21 days before PTCA. All underwent a thallium-201 quantitative exercise test 5 to 7 days after PTCA. Endpoints for restenosis were either 50% narrowing of the dilated artery on coronary angiography, performed in symptomatic patients or, in asymptomatic patients, the appearance of newly developed reversible filling defects in the vascular territory of the dilated artery on a second thallium scan done 6 months after PTCA. The hypocholesterolemic change observed in the Lo group was not accompanied by a reduction in early restenosis risk. The authors conclude that effective hypocholesterolemic therapy before PTCA does not affect early restenosis rate in men with mild to moderate hypercholesterolemia.

Adult↗
PubMed1995

Oxidation of low density lipoprotein upon sequential exposure to copper ions.

Copper-induced LDL oxidation is characterized by an 'induction phase' (lag phase) during which the endogenous antioxidants are consumed, followed by a 'propagation phase' in which the LDL-associated polyunsaturated fatty acids are oxidized. Oxidation products may play an important role in the propagation of the oxidative process in the arterial intima as they increase the permeability of the damaged endothelium to various plasma components, including LDL. We therefore found it of interest to investigate the kinetics of LDL oxidation in vitro under conditions where LDL is sequentially exposed to Cu(2+)-induced oxidation. The results of our studies demonstrate that when native LDL is exposed to copper oxidation in a medium containing oxidized LDL, oxidation of the added LDL may be almost instantaneous. Furthermore, even when native LDL is added to 'oxidizing LDL' towards the end of the lag phase or during the propagation phase it becomes oxidized after a very short lag. This oxidation process, occurring in spite of the possible protective effect of the antioxidants present in the newly added LDL, indicates that although antioxidants prolong the latency period by preventing the formation of active free radicals, when such radicals are present in the system, oxidation propagates. These results lend strong support to the generally accepted paradigm regarding the mechanism of propagation of lipid oxidation. In view of the effect of oxidation products on the permeability of the endothelium, the observed shortening of the lag period may result in a vicious cycle, independent of the LDL-associated antioxidants, leading to continuing oxidation and foam cell formation.

Cations↗
PubMed1995

[International postgraduate training program in medicine: survey of 13 training courses, 1988-1994].

In 1988 an International Postgraduate Training Program in Medicine was established as a joint venture of the Tel Aviv University School of Continuing Medical Education and the Ministry for Foreign Affairs, Division of International Cooperation. During 1988-1994, 359 physicians participated. A survey of 271 graduates was carried out within 1-5 years following the completion of training, and 57% responded to our questionnaire. The program fulfilled the academic expectations of 78% of the trainees, and the practical clinical expectations of 80%. 95% graded the program as good-to-excellent from the sociocultural aspect. 75% and 67.5% of the trainees graded the program as good-to-excellent with regard to improvement in their theoretical and practical skills, respectively. Regretfully, only 45% have continued their ties with the host departments and only 11% have carried out joint research projects. These results imply that further attention should be paid to the trainees' real-time input, in order to increase satisfaction. Personal tutors should be nominated in each department, and should be adequately compensated. More emphasis should be given to initiation of bilateral research projects and maintenance of professional ties between the trainees and their host departments.

Attitude of Health Personnel↗
PubMed1994

Diurnal changes in plasma lipoproteins of free-living healthy men consuming a standard diet.

Although it is well established that plasma lipoproteins are involved in atherogenesis, most patients with coronary heart disease have normal or nearly normal fasting plasma lipid and lipoprotein levels. As most of the human life is spent in the fed state we elected to investigate the changes occurring in plasma lipids and lipoproteins during normal daily activities. We studied 12 healthy, normolipidemic and non-obese subjects on a standard diet divided into three meals and three snacks. This method was found to be accurate and reproducible in four subjects who underwent repeated studies. The major diurnal changes were observed in plasma triglyceride level and in the composition of plasma lipoproteins. The degree and pattern of these changes differed among subjects but was specific and constant for each individual. The extent of these diurnal changes, which correlated positively with fasting plasma triglyceride and inversely with plasma HDL2 levels, may play an important role in the pathogenesis of atherosclerosis.

Activities of Daily Living↗
PubMed1993

Heterogeneity in peritoneal transport during continuous ambulatory peritoneal dialysis and its impact on ultrafiltration, loss of macromolecules and plasma level of proteins, lipids and lipoproteins.

We investigated the effect of heterogeneity in the peritoneal transport of plasma proteins on dialysis efficiency and plasma levels of proteins, lipids and lipoproteins in 32 patients undergoing long-term continuous ambulatory peritoneal dialysis (CAPD; 9 females and 23 males, 18-76 years old). Eleven patients were studied on several occasions (at 0-42 months) and the remainder at 6-60 months on CAPD (n = 49). We have divided our patients arbitrarily into two equal groups according to their protein concentration in the peritoneal effluent at the end of an 8-hour cycle. Patients with a high peritoneal protein concentration (> or = 2 g/l/1.73 m2) have lower ultrafiltration capacity, higher glucose absorption rate and increased loss of most plasma proteins [including albumin, immunoglobulins (Ig), complement components and high-density lipoproteins (HDL)] compared to patients with a low peritoneal protein concentration (< 2 g/l/1.73 m2). Consequently, plasma levels of albumin, IgM and HDL were lower in patients with a high peritoneal protein concentration. The latter had also increased levels of plasma triglycerides and very-low-density lipoproteins. The difference observed in peritoneal transport between the groups could be ascribed only in part to the duration of CAPD treatment, and hence to the number of peritonitis episodes but not to medications. Therefore, we suggest that inherent constitutional factors may be responsible for some of the observed heterogeneity in the peritoneal transport of these patients which is already evident at the start of CAPD treatment. Patients with high peritoneal transport are exposed to an augmented atherogenic plasma lipid profile in addition to a reduction in dialysis efficiency (ultrafiltration failure). These patients may become prone also to nutritional and immunological disturbances. Therefore, we suggest taking these effects into consideration before choosing the appropriate dialysis modality in patients with increased peritoneal transport for plasma proteins.

Adolescent↗
PubMed1993

Efficacy and safety of pravastatin once daily in primary moderate hypercholesterolemia: the Israeli experience.

Seventy-seven hypercholesterolemic patients participated in a 26-week, multicenter, randomized, double-blind, placebo-controlled study that investigated the efficacy and safety of pravastatin therapy. All patients had primary moderate hypercholesterolemia (total cholesterol 200-300 mg/dl, at the end of a 6-week dietary run-in period) and two additional coronary risk factors. Pravastatin, 20-40 mg/day given at bedtime, reduced total cholesterol by 19-22%, LDL-cholesterol by 24-30%, triglycerides by 10-30% and increased HDL-cholesterol by 9-13%. The drug caused mild elevation in alanine aminotransferase and aspartate aminotransferase. Almost all these elevations were within normal limits and no patient was clinically symptomatic. No other significant differences were observed between the pravastatin and the placebo-treated groups with regard to other adverse effects and to patient compliance and withdrawal. It is concluded that pravastatin has a beneficial effect on the lipid profile and that the drug is safe and well tolerated.

Adult↗