Is normal pregnancy atherogenic?

Serum cholesterol, triacylglycerols and low-density lipoprotein (LDL) subfractions were determined in 120 primagravid women during normal gestation (40 in each trimester) and in 20 non-pregnant age-matched controls. LDL subfractions were determined by PAGE, and an LDL score was calculated. The higher the score, the smaller the subfractions. The objective of the study was to determine the effects of the hyperlipidaemia, high oestrogen concentrations and insulin resistance known to exist in normal pregnancy on LDL subfraction formation. Pregnant women had an increased mean serum cholesterol concentration [5.78 (S.D. 1.09) mmol/l] in the first trimester compared with the non-pregnant controls [5.11 (0.77) mmol/l; P<0.01]. The serum cholesterol concentration increased progressively throughout gestation to a mean of 8.14 (1.39) mmol/l in the third trimester (P<0.001 compared with the second trimester). Triacylglycerol concentrations in the first trimester were similar to those of controls, and there was a non-significant increase by the second trimester to 1.32 (0.44) mmol/l. However, by the third trimester the mean triacylglycerol concentration had doubled [2.58 (0.98) mmol/l; P<0.001 compared with the first and second trimester]. During gestation the LDL score increased dramatically, from 1.17 (0.39) during the first trimester to 2.01 (0.37) in the second trimester (P<0.001) to 2.73 (0.48) in the third trimester (P<0.001 compared with the second trimester). Thus an atherogenic lipid profile develops during normal gestation. The significance of these changes remains unclear, but thay may have important implications for mother and foetus.     

Mathematical evaluation of methods for estimation of the concentration of the major lipid components of human serum lipoproteins.

The concentration of total cholesterol and triglycerides in the three major lipoprotein classes of human serum was measured in 136 men, randomly selected from an industrial population, by a quantitative method of lipoprotein electrophoresis on agarose gel and of fractions separated by preparative ultracentrifugation. Correlation coefficients for the two estimates were 0.98 for triglycerides in very low-density lipoproteins, 0.93 for total cholesterol in low-density lipoproteins, and 0.75 for total cholesterol in high-density lipoproteins. Data obtained form the analyses of the ultracentrifugal fractions were used to develop regression equations that predict the concentrations of total cholesterol and triglycerides in the lipoprotein classes from their concentrations in whole serum. These equations take into account the inverse curvilinear relationship between total cholesterol in high-density lipoproteins and serum tiriglyceride concentration. When applied to a separate sample of 530 men, the predicted values for triglycerides in very low-density lipoproteins and total cholesterol in low-density lipoproteins correlated as well with ultracentrifugal values as did the electrophoretic estimates. However, for total cholesterol in high-density lipoproteins, the electrophoretic method was superior. Similar regression equations were developed from ultracentrifugal lipoprotein analyses in 158 women from the same industrial population. Although the concentration of total cholesterol in the low-density lipoproteins estimated by both electrophoresis and the regression equations agreed closely in most cases with the ultracentrifugal values, errors exceeded 10% with sufficient frequency to limit the value of the estimates for this purpose. In both men and women, the ratio of total cholesterol to triglycerides in high-density lipoproteins was a hyperbolic function of serum triglyceride concentration, suggesting that cholesteryl esters in the core of this lipoprotein are progressively replaced by triglycerides as the concentration of triglycerides in very low-density lipoproteins increases. This altered composition of nonpolar lipids accounts, at least in part, for the reduction of cholesterol in high-density lipoproteins in hyperlipemic individuals.     

n -- 3 fatty acid supplementation during pregnancy in women with allergic disease: effects on blood pressure, and maternal and fetal lipids

n--3 Fatty acids derived from fish oil reduce plasma triacylglycerols (triglycerides) and increase HDL-C (high-density lipoprotein cholesterol); however, the effect of n--3 fatty acid supplementation during pregnancy, a hyperlipidaemic state, remains unknown. We took the opportunity to investigate maternal lipid levels and blood pressure during and after pregnancy, and fetal lipid levels at birth, in a study that aimed primarily to examine the effect of fish oil supplementation during pregnancy on immune function in infants born to women with allergic disease. Eighty-three pregnant women who had allergic disease, but were otherwise healthy, completed the study. They were randomly allocated to receive fish oil or olive oil capsules, taken as 4 g/day, from 20 weeks of pregnancy until delivery. Compared with olive oil, fish oil supplementation did not alter triacylglycerols, total cholesterol, LDL-C (low-density lipoprotein cholesterol) or HDL-C during or after pregnancy. There was also no effect of fish oil on cord blood triacylglycerols, total cholesterol, LDL-C or HDL-C. Fish oil supplementation during pregnancy did not alter maternal blood pressure during or after pregnancy. The effects of fish oil on lipids and blood pressure in non-pregnant individuals appear to be lost when it is administered during pregnancy.     

Resolving hyperlipidemia after liver transplantation in a patient with primary sclerosing cholangitis

A 64-year-old man with primary sclerosing cholangitis (PSC) and resultant liver failure presented to our hospital with severe dyslipidemia (total cholesterol, 525 mg/dL; low-density lipoprotein (LDL) cholesterol, 489 mg/dL; high-density lipoprotein (HDL) cholesterol, 13 mg/dL; triglycerides, 114 mg/d) and coronary artery disease. The abnormal lipid profile of patients with cholestatic liver disease, such as PSC, includes an abnormal atherogenic LDL called lipoproteinX. The patient's dyslipidemia persisted despite treatment with a statin. Lipids normalized only after liver transplantation (total cholesterol, 135 mg/dL; LDL cholesterol, 60 mg/dL; high-density lipoprotein cholesterol, 48 mg/dL; triglycerides, 130 mg/dL). To the best of our knowledge, the dramatic improvement in the lipid profile after liver transplantation represents the first such published report for PSC. The recognition of dyslipidemia and atherosclerosis in those with cholestatic liver disease and the normalization of lipid profile after liver transplantation warrant further study. We present a review of dyslipidemia in cholestatic liver disease, its relationship to atherosclerosis, and its treatment.     

Effects of fish oil fatty acids on plasma lipids and lipoproteins and oxidant-antioxidant imbalance in healthy subjects.

The purpose of this study was to investigate the effect of eicosapentaenoic and docosahexaenoic acids on plasma lipids and lipoproteins, lipid peroxidation and antioxidant status in healthy humans. A total of 19 healthy volunteers consumed 6 g/day Maxepa fish oil for 3 weeks (1.8 g n-3 fatty acids/day). At baseline and at day 21, we evaluated plasma lipoproteins, plasma and low-density lipoprotein fatty acids, lipid peroxidation markers (malondialdehyde concentration, low-density lipoprotein peroxidation in vitro), and the content of a number of antioxidants (reduced and oxidized glutathione in whole blood, plasma and erythrocyte glutathione peroxidases, plasma vitamin E and beta carotene). Plasma concentrations of total cholesterol, triglycerides, phospholipids, low-density lipoprotein cholesterol and low-density lipoprotein size did not differ significantly after 3 weeks of supplementation. Adding the fish oil to the diet increased the concentration of n-3 very-long-chain polyunsaturated fatty acids and decreased the concentration of n-6 fatty acid and oleic acid in plasma and low-density lipoprotein. Eicosapentaenoic and docosahexaenoic acid supplementation caused elevated values of the high-density lipoprotein cholesterol due to an increment of the high-density lipoprotein 2 fraction and reduced low-density lipoprotein peroxidation rate in vitro. However, we observed an imbalance between oxidizable substrates and antioxidants with an increased lipid peroxidation, whereas the content of reduced glutathione and beta carotene decreased without any variation in vitamin E. Association of antioxidants with n-3 PUFA could prevent lipid peroxidation and enhance the antiatherogenic effects of n-3 polyunsaturated fatty acids.     

Cholesterol esterification rate and its relation to lipoprotein levels in plasma in normal human pregnancy

The lecithin:cholesterol acyl transfer (LCAT) reaction produces cholesteryl esters and lysolecithin in plasma. The rate of LCAT is related to the plasma lipoprotein concentrations. During pregnancy there are pronounced elevations of the lipid and lipoprotein concentrations. Therefore, we studied the LCAT rate and its relation to the lipid levels in plasma lipoproteins in 19 healthy women before conception, every sixth to eighth week during pregnancy, and 8 weeks after delivery. In the first part of gestation the mean molar LCAT rate (the amount of cholesteryl esters produced during a certain time, in micromoles per liter per hour) remained unchanged, whereas pronounced elevations were seen in the very low-density lipoprotein (VLDL), high-density lipoprotein (HDL), and HDL2 levels. The molar LCAT rate did not increase until the last trimester of pregnancy, when it reached a maximal 20% mean increase simultaneous with the maximal increase of the mean triglyceride and VLDL levels and a slight decline of the HDL2 elevation. The mean fractional LCAT rate (the part of unesterified cholesterol that is esterified during a certain time, in percent per hour) showed a continuous decrease from the fourteenth until the twenty-eighth week, simultaneous with a progressive rise of the mean cholesterol and low-density lipoprotein (LDL) concentrations. During pregnancy the molar LCAT rate was positively correlated to the VLDL concentration and negatively to the HDL2 level, and the fractional LCAT rate was negatively correlated to the LDL concentration.     

Five methods for determining low-density lipoprotein cholesterol compared

We evaluated three precipitation methods for determination of low-density lipoprotein cholesterol in serum and an indirect method involving the Friedewald formula (Clin Chem 18: 499-502, 1972) by comparison with results by ultracentrifugation. The results of all methods for 83 sera, including 59 hyperlipidemic type IIA, IIB, and IV sera agreed very well, at least for concentrations of serum triglycerides below 8 mmol/L. The accuracy of the Friedewald formula was confirmed in 285 other sera, including 66 sera with triglycerides content between 4.52 and 8.0 mmol/L. For type III sera, the precipitation methods produced similar values to those obtained with the Friedewald formula, all being much higher than the ultracentrifugation values. Density-gradient ultracentrifugation showed that the very-low-density lipoprotein remnants in type III sera almost completely coprecipitated with the low-density lipoproteins. The precipitation methods are not only accurate but also very precise (CV less than 5%); they can therefore be used in clinical laboratories to measure atherogenic low-density lipoproteins plus the remnants of very-low-density lipoproteins. However, when serum triglycerides and high-density lipoprotein cholesterol also are determined, the Friedewald formula is a reliable alternative.     

Serum lipoprotein profile in patients with cancer. A comparison with non-cancer subjects

The association of cancer with low serum total cholesterol is well established. Less clear is the relationship of cancer with the cholesterol distribution among the different lipoprotein classes. Conflicting results have been reported on low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and serum triglyceride levels in different types of tumor. Total serum cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and serum triglycerides were analyzed in 530 patients with newly diagnosed cancer (97 with hematological malignancies, 92 with tumor of the lung, 108 of the upper digestive system, 103 of colon, 32 of breast, and 98 of the genitourinary system) and in 415 non-cancer subjects. Anthropometric (body mass index) and biochemical (serum albumin) indices of nutritional status were also determined in all subjects. Total cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, serum albumin, and body mass index were significantly lower in cancer than in non cancer-subjects. The lowest values of total cholesterol, low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol were recorded in patients with hematological malignancies and the highest in patients with breast tumor. All the cancer groups, with the exception of women with breast cancer, showed significantly lower total cholesterol, low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol than age- and sex-matched non-cancer subjects. Multiple regression analysis with low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and triglycerides as dependent variables and sex, age, body mass index, albumin, and cancer (dummy variable) as independent variables, showed that cancer was independently associated with low levels of low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol and with high values of serum triglycerides. Total cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, serum triglycerides, body mass index and serum albumin were significantly lower in patients with metastatic than in patients with non-metastatic solid tumor. The significant difference in low-density lipoprotein-cholesterol and serum triglycerides between patients with metastatic and non-metastatic cancer was lost when lipoprotein cholesterol and serum triglyceride levels were adjusted for nutritional variables. The lipid profile in cancer patients is characterized by low low-density lipoprotein-cholesterol, low high-density lipoprotein-cholesterol and relatively high serum triglycerides. The abnormality is a common feature of both hematological and solid tumors and is not entirely explained by poor nutrition.     

Effects of fish oil fatty acids on plasma lipids and lipoproteins and oxidant-antioxidant imbalance in healthy subjects

The purpose of this study was to investigate the effect of eicosapentaenoic and docosahexaenoic acids on plasma lipids and lipoproteins, lipid peroxidation and antioxidant status in healthy humans. A total of 19 healthy volunteers consumed 6 g/day Maxepa® fish oil for 3 weeks (1.8 g n-3 fatty acids/day). At baseline and at day 21, we evaluated plasma lipoproteins, plasma and low-density lipoprotein fatty acids, lipid peroxidation markers (malondialdehyde concentration, low-density lipoprotein peroxidation in vitro), and the content of a number of antioxidants (reduced and oxidized glutathione in whole blood, plasma and erythrocyte glutathione peroxidases, plasma vitamin E and beta carotene). Plasma concentrations of total cholesterol, triglycerides, phospholipids, low-density lipoprotein cholesterol and low-density lipoprotein size did not differ significantly after 3 weeks of supplementation. Adding the fish oil to the diet increased the concentration of n-3 very-long-chain polyunsaturated fatty acids and decreased the concentration of n-6 fatty acid and oleic acid in plasma and low-density lipoprotein. Eicosapentaenoic and docosahexaenoic acid supplementation caused elevated values of the high-density lipoprotein cholesterol due to an increment of the high-density lipoprotein 2 fraction and reduced low-density lipoprotein peroxidation rate in vitro. However, we observed an imbalance between oxidizable substrates and antioxidants with an increased lipid peroxidation, whereas the content of reduced glutathione and beta carotene decreased without any variation in vitamin E. Association of antioxidants with n-3 PUFA could prevent lipid peroxidation and enhance the antiatherogenic effects of n-3 polyunsaturated fatty acids.     

Subtle changes in ADMA and l-arginine concentrations in normal pregnancies are unlikely to account for pregnancy-related increased flow-mediated dilatation

BACKGROUND: Our objective was to investigate whether serum concentrations of asymmetric dimethylarginine (ADMA) or l-arginine correlate to hyperlipidemia or endothelial function in normal pregnancy compared with the non-pregnant subjects. METHODS AND RESULTS: As a part of population-based, prospective cohort Cardiovascular Risk in Young Finns study conducted in Finland we examined 57 pregnant Finnish women throughout gestation and 62 control women matched for age and smoking. Serum glucose, triglycerides (TG), total cholesterol (TC), low-density cholesterol (LDL-C), high-density cholesterol (HDL-C) and ADMA, symmetric dimethylarginine (SDMA) and l-arginine were determined concomitantly with endothelium-dependent brachial artery flow-mediated dilation (FMD), measured by ultrasound. All serum lipid concentrations were significantly higher in pregnant women than in non-pregnant women (P < 0.001 for each). The mean serum ADMA concentration in pregnant women was significantly lower compared with the non-pregnant controls (0.513 micromol l(-1) +/- 0.0593 versus 0.577 micromol l(-1) +/- 0.0710, P < 0.001). Lowered ADMA concentrations did not correlate statistically to FMD in these healthy pregnant women but FMD was enhanced towards the end of pregnancy. CONCLUSIONS: ADMA and l-arginine concentrations fall in normal pregnancy despite marked hypercholesterolemia. Endothelium-dependent vasodilation is enhanced in normal pregnancy but is not statistically correlated to maternal serum ADMA or l-arginine concentrations.     

Effect of weight loss on serum lipoprotein(a) concentrations in an obese population.

To assess the distribution of serum concentrations of the atherogenic lipoprotein(a) [Lp(a)] in an obese population and the possible effects of weight reduction, we determined Lp(a) in 52 white, moderately obese subjects (16 men and 36 women). The subjects were participating in a weight-reduction program of diet, exercise, and behavior modification plus combination anorectic drug therapy (fenfluramine and phentermine). This placebo-controlled, double-blind study lasted 104 weeks. We also determined concentrations of fasting insulin, triglycerides, total cholesterol, high-density lipoprotein cholesterol, apolipoprotein (apo) A-I, low-density lipoprotein cholesterol, and apo B. Results showed the following: a highly skewed, nongaussian distribution of serum Lp(a) values in the obese population, virtually identical to that reported for healthy adults; no clinically significant change in Lp(a) concentrations with weight loss; and further evidence of normalization of insulin, lipid, and lipoprotein concentrations with weight loss.     

Serum levels of lipids, lipoproteins and paraoxonase activity in pre-eclampsia

Serum paraoxonase 1 (PON1) activity and the oxidation of lipoproteins were investigated in 35 women with pre-eclampsia and in 35 healthy control women with normal pregnancies. Blood pressure, body mass index (BMI), serum levels of total cholesterol, triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB) and lipoprotein (a) (Lp[a]), and PON1 activity were assessed. There were no significant between-group differences in subject age, gestational age at diagnosis of pre-eclampsia, BMI, serum total cholesterol, triglycerides, LDL and ApoB levels. Mean systolic and diastolic blood pressures and serum Lp(a) were significantly higher in subjects with pre-eclampsia than in controls. Mean serum HDL, ApoA1 and PON1 activity were significantly lower in subjects with pre-eclampsia compared with controls. In conclusion, lipids and oxidized lipoproteins may play important roles in the pathogenesis of pre-eclampsia.     

Epigallocatechin gallate improves serum lipid profile and erythrocyte and cardiac tissue antioxidant parameters in Wistar rats fed an atherogenic diet

Oxidative stress is believed to contribute to the pathogenesis of hypercholesterolaemic atherosclerosis; hence, various antioxidant compounds are being evaluated for potential anti-atherogenic effects. The present study assessed the efficacy of epigallocatechin gallate (EGCG), an antioxidant component of the plant Camellia sinensis , in improving serum lipid profile and antioxidant parameters in erythrocytes and cardiac tissue in rats fed an atherogenic diet. In male albino Wistar rats fed an atherogenic diet for 30 days, significantly increased serum levels of total cholesterol, triglycerides and lipoprotein cholesterol fractions and cardiac risk ratio were noted, compared with levels in rats fed a normal diet. Intraperitoneal administration of EGCG (100 mg/kg) for 7 or 15 days to the atherogenic diet-fed rats resulted in significantly lower serum levels of total cholesterol, triglycerides, low-density and very low density lipoprotein cholesterol fractions and a significantly higher serum level of high-density lipoprotein cholesterol compared with levels in atherogenic diet-fed, saline-treated rats. Significantly higher mean malondialdehyde levels and significantly lower mean activities of antioxidant enzymes and mean levels of non-enzymatic antioxidants occurred in atherogenic diet-fed rats compared with those fed a normal diet. When atherogenic diet-fed rats received EGCG treatment for 7 or 15 days, significantly lower mean levels of MDA, higher mean levels of non-enzymatic antioxidants and higher mean activities of enzymatic antioxidants occurred, compared with those in saline-treated rats. Thus, EGCG appears to ameliorate disruptions of serum lipid profile and of antioxidant parameters in erythrocyte and cardiac tissue of Wistar rats fed an atherogenic diet; these results may be relevant to treating human atherosclerosis.     

Effects of pindolol on serum lipids, apolipoproteins, and lipoproteins in patients with mild to moderate essential hypertension

The effects of 12 weeks' administration of the beta-blocker pindolol (5 mg twice daily) on serum lipids, apolipoproteins (apo), and lipoproteins were studied in 20 normolipidemic patients with mild to moderate essential hypertension (WHO I-II). Pindolol significantly increased both high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), while very-low-density lipoprotein cholesterol (VLDL-C) was significantly decreased. Apo A-II levels were increased significantly and the apo B/apo A-I ratio, which is one of the atherogenic indexes, was decreased significantly after pindolol therapy. Total cholesterol, HDL subfraction cholesterols, the LDL-C/HDL-C ratio, triglycerides, apo A-I, apo B, apo C-II, apo C-III, and apo E did not change significantly.     

Influence of physicochemical properties on the patterns of association of a series of aliphatic esters of halofantrine with plasma lipoproteins.

Although the association of lipophilic drugs with plasma lipoproteins has not been fully characterized, there are several reports of lipoprotein association being influential in pharmacokinetic and pharmacodynamic profiles of important therapeutic agents. The current studies utilized a series of aliphatic esters of halofantrine to evaluate the role of several physicochemical properties on the interaction of the different compounds with plasma lipoproteins. Density gradient ultracentrifugation techniques were employed to determine drug association in triglyceride rich (TRL), low-density (LDL) and high-density lipoproteins (HDL), under both fasted and post-prandial conditions. Compound solubility in medium or long chain triglycerides was a useful indicator of the extent of drug-lipoprotein association, particularly for the triglyceride rich lipoproteins (chylomicrons and very low-density lipoproteins). This is likely a function of the compounds being solubilized within the apolar (triglyceride and cholesterol ester) lipid core. However, molecular size also played an important role in determining lipoprotein distribution, particularly for association with the more protein abundant lipoproteins, such as HDL. Lipoprotein association of Hf analogues containing longer unsaturated esters was best correlated with total lipoprotein surface area rather than with lipoprotein core lipid volumes.     

Preventing, stopping, or reversing coronary artery disease--triglyceride-rich lipoproteins and associated lipoprotein and metabolic abnormalities: the need for recognition and treatment

A substantial number of treated patients with or at high risk for coronary artery disease continue to have fatal and nonfatal coronary artery events in spite of significant reduction of elevated levels of low-density lipoprotein cholesterol. Other lipoprotein abnormalities besides an elevated level of low-density lipoprotein cholesterol contribute to risk of coronary artery disease and coronary artery events, and the predominant abnormalities that appear to explain much of this continued risk are an elevated serum triglyceride level and a low level of high-density lipoprotein cholesterol. Most patients with coronary artery disease have a mixed dyslipidemia with hypertriglyceridemia, which is associated and metabolically intertwined with other atherogenic risk factors, including the presence of triglyceride-rich lipoprotein remnants, low levels of high-density lipoprotein cholesterol, small, dense, low-density lipoprotein particles, postprandial hyperlipidemia, and a prothrombotic state. Aggressive treatment of these patients needs to focus on these other lipoprotein abnormalities as much as on low-density lipoprotein cholesterol. Combination drug therapy will usually be required. Reliable assessment of risk of coronary artery disease from lipoprotein measurements and response to therapy requires inclusion of all atherogenic lipoproteins in laboratory measurements and treatment protocols. At present this may be best accomplished by use of non-high-density lipoprotein cholesterol (total cholesterol minus high-density lipoprotein cholesterol) calculated from standard laboratory lipoprotein values. Ultimately, a more comprehensive assessment of coronary artery disease risk and appropriate therapy may include measurement of lipoprotein subclass distribution including determination of low-density lipoprotein particle concentration and sizes of the various lipoprotein particles.     

Comparison of the lipid profile and lipoprotein(a) between sedentary and highly trained subjects.

BACKGROUND: There is consolidated evidence that physical activity exerts beneficial effects on several chronic conditions and longevity, on the basis of its proposed biological effects, especially on lipid profiles. However, debate continues regarding the intensity of activity required for good health, as vigorous physical activity might overwhelm advantageous changes. In addition, little is known so far on the effect of a vigorous and regular aerobic training regimen on emerging markers of cardiovascular risk, such as lipoprotein(a), total/high-density lipoprotein cholesterol ratio and the atherogenic index of plasma. METHODS: To further investigate this topic, an extensive lipid profile, in accordance with the most recent guidelines issued by the American Heart Association (AHA)/American College of Cardiology (ACC) and the National Cholesterol Education Program (NCEP), was evaluated in 60 healthy male sedentary controls and in a wide population of professional endurance athletes, including 40 male professional cross-country skiers and 102 male professional road cyclists. RESULTS: Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), triglycerides, TC low-density lipoprotein cholesterol (LDL-C) ratio and the atherogenic index of plasma were significantly lower in both categories of professional athletes, whereas the mean HDL-C concentration was significantly higher. The concentration of lipoprotein(a) did not differ significantly between the groups. When compared to current NCEP or AHA/ACC goals, the percentage of patients with undesirable values was statistically different for all parameters tested, apart from lipoprotein(a). According to multiple stepwise logistic regression analysis, lower TC/HDL-C ratio in professional skiers and lower TC/HDL-C ratio and TC in professional cyclists were significantly associated with increased aerobic physical activity. CONCLUSIONS: Results of this case-control study confirm that elevated aerobic energy expenditure might be associated with a highly favorable stabilization of most traditional and emerging cardiovascular risk predictors. Therefore, a substantial increase in aerobic physical activity within the population might be recommended to reverse adverse lipid abnormalities, especially in subjects with a higher cardiovascular risk.     

Treatment of hypertension with dyslipidemia

Lifestyle modifications are the first approach to the treatment of dyslipidemia and hypertension, that is, control of overweight; reduced intake of saturated fat, cholesterol, sodium chloride, and alcohol; and increased physical activity. In high doses, thiazide diuretics and loop diuretics can induce at least short-term increases in levels of total plasma cholesterol, triglycerides, and low-density lipoprotein cholesterol. Low-dose thiazide diuretics do not produce these effects. beta-blockers may increase levels of plasma triglycerides transiently and reduce levels of high-density lipoprotein cholesterol. alpha-blockers may decrease serum cholesterol concentration to a modest degree and increase high-density lipoprotein cholesterol. Angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, calcium antagonists, and central adrenergic agonists have clinically neutral effects on levels of serum lipids and lipoproteins.     

Hormone replacement therapy in postmenopausal women and its effects on plasma lipid levels.

Postmenopausal women run the same risks of coronary heart disease as men. The lipid alterations observed at this time reflect increased blood levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C) and lipoprotein (a), and reduced high-density lipoprotein cholesterol (HDL-C) levels. These changes lead to a higher risk of coronary artery disease, and hormonal therapy has a favorable effect on lipid metabolism. In this paper we review the literature on hormone replacement therapy (HRT) in postmenopausal women with the emphasis on the role of lipids in the pathogenesis of coronary heart disease, and on the action of estrogens and their correlation with progestogens, as well as routes of HRT administration. We conclude that the HRT changes the lipid profile in a potentially anti-atherogenic direction, usually reducing LDL-C and increasing HDL-C and triglycerides. Otherwise, for postmenopausal women with established coronary disease HRT is not recommended.     

Alterations of serum resistin in normal pregnancy and pre-eclampsia

Resistin is expressed in human placenta and has been postulated to play a role in regulating energy metabolism in pregnancy. However, changes in serum resistin levels in normal pregnancy and in the setting of pre-eclampsia are far from understood. The purpose of the present study was to clarify the alterations in serum resistin level in normal pregnancy and pre-eclampsia. Blood samples were taken from 28 healthy non-pregnant women, 27 women in the first, 26 in the second and 26 in the third trimesters of normal pregnancy and 25 women with pre-eclampsia. Serum resistin concentrations were determined by using an ELISA, and mean serum resistin levels were compared with one-way ANOVA. Serum resistin levels were not significantly different among non-pregnant women and women in the first and second trimesters of pregnancy (P>0.05 for all). Serum resistin was significantly elevated in the third trimester of normal pregnancy compared with non-pregnant women (P<0.01) and women in the first (P<0.001) and second (P<0.001) trimesters of pregnancy. Serum resistin level was significantly lower in women with pre-eclampsia than women in the third trimester of normal pregnancy (P<0.001), but was comparable with those of non-pregnant women and women in the first and second trimesters of pregnancy (P>0.05 for all). In conclusion, we found an increase in serum resistin in the third trimester of normal pregnancy, but this increase was not present in pre-eclampsia. We postulate that these associations may offer insight into the mechanisms of maternal adaptation to pregnancy and the pathogenesis of pre-eclampsia.