Goretta Baldo-Enzi

Cardiovascular Effects of Anabolic Steroids in Weight‐Trained Subjects

The effects of large doses of anabolic steroids on 24‐hour blood pressure, cardiac structure and function, and lipid profiles were studied in 10 body builders using anabolic steroids and 14 body builders who did not use steroids (control subjects). All subjects underwent noninvasive 24‐hour blood pressure monitoring, echocardiography, Doppler analysis of transmitral flow, and analysis for lipoprotein and gonadotropin levels. Anabolic steroid users were studied at the end of a steroid cycle and after a period of withdrawal. Average 24‐hour blood pressure was similar in the two groups, but anabolic steroid users exhibited a smaller pressure reduction during sleep than did nonusers. This finding was present both at the end of treatment and after the period of withdrawal. Echocardiographic dimensional and functional indexes did not differ substantially between anabolic steroid users and the nonusers, and were similar in anabolic steroid users during use and after withdrawal. Anabolic steroid users also had higher LDL and lower HDL cholesterol levels than nonusers; Lp(a) was higher in nonusers, although this difference did not attain the level of statistical significance. These differences were more striking at the end of the treatment period. The results of this study show that chronic anabolic steroid intake causes an abnormal 24‐hour blood pressure pattern, characterized by a flattening of the diurnal curve, and minor changes of the dimensional echocardiographic parameters.

Lipid and apoprotein modifications in body builders during and after self-administration of anabolic steroids

To determine the effects of anabolic steroids on serum lipid and apoprotein levels, 14 white male body builders who self-administered steroids for 2 to 3 months (steroid users) were studied; 10 agreed to screening while they were taking the drugs (ON treatment) and also at about 3 months following their suspension (OFF treatment). Controls consisted of 17 body builders who had never taken steroids (nonusers), and a group of 18 healthy sedentary subjects (controls). During the period of steroid administration, there was a slight reduction in total serum cholesterol, with a marked cholesterol decrease in the high-density lipoprotein (HDL) subfractions HDL2 and HDL3, and a significant reduction in the HDL2 cholesterol/HDL3 cholesterol ratio; the percentage of serum cholesterol transported by low-density lipoproteins (LDL) increased significantly. In addition, a marked apoprotein (apo) A-I reduction in the HDL2 and HDL3 subfractions was observed, as well as an apo A-II decrease that was significant only in the HDL3 subfraction, with an A-I/A-II ratio significantly reduced in both subfractions. Serum apo B was only slightly increased, with a very high B/A-I ratio. Apolipoprotein C-II and E levels showed no modifications, while apo C-III reduced significantly. Lipid and apoprotein values returned to almost normal levels in the OFF treatment period. Findings in the group of nonusers were similar to those in sedentary subjects. These results indicate that anabolic steroids profoundly alter the serum lipid-protein profile, and the changes may be caused in part by the significant differences observed in apoprotein levels.

Effect of age on the response of blood lipids, body composition, and aerobic power to physical conditioning and deconditioning

The influence of age on the response of plasma lipids, body composition, and cardiovascular performance to physical training and detraining was studied in 12 older and 12 young adult male cyclists. The athletes were first examined at the peak of their seasonal preparation and then again 2 months after its suspension. Sedentary males matched for age, weight, and height comprised the respective control groups. During training, body fat mass (BFM) was significantly lower and maximum oxygen consumption (VO2max) higher in both groups of cyclists as compared with controls. No differences in serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein (apo) B, apo A-II, and fibrinogen were found. During the same phase, triglycerides (TG) and the LDL-C to high-density lipoprotein cholesterol (HDL-C) ratio were significantly lower and apo A-I, HDL-C, HDL3-C, and the apo A-I/apo B ratio were significantly higher in the athletes than in their corresponding sedentary controls. After physical deconditioning, BFM increased and VO2max decreased significantly in both groups of athletes. TG, very-low-density lipoprotein cholesterol (VLDL-C), and fibrinogen increased in young athletes while the LDL-C/HDL-C ratio increased, and apo A-I, HDL-C, HDL2-C, and HDL3-C decreased significantly in both young and older athletes. Thus, an aerobic training program induced an antiatherogenic lipoprotein profile and beneficial modifications in body composition and aerobic power in both older and younger subjects; a 2-month interruption in the program changed these parameters unfavorably in both groups. Age does not seem to influence significantly the plasma lipid response to physical deconditioning.

Analbuminaemia: a natural model of metabolic compensatory systems

SummaryImportant clinical signs are usually not present in analbuminaemia, a congenital condition inherited as an autosomal recessive trait, but several biochemical alterations in proteins, cholesterol, phospholipids and plasma beta lipoproteins have been observed.We studied two sibs, R.U. and R.R., with this disease and observed a striking increase in the variables mentioned above as well as a high LDL fraction with concomitant increase in apo B; increases in HDL3 and apo A-I and A-II levels were also observed. The lipoproteins, however, were not altered in morphology but showed a slight increase in lipid/protein ratio. Post-heparin lipolytic activity was normal in the male patient and reduced in the female while LCAT enzyme activity instead was increased in both. Fatty acids bound to phospholipids and serum cholesterol were mostly monounsaturated. Free fatty acid concentration was normal and they appeared mostly bound to the LDL and HDL3 fractions, which are increased in this disease and appear to replace albumin in one of its main carrier functions.

The renin-angiotensin-aldosterone system and carotid artery disease in mild-to-moderate primary hypertension.

Background The evidence linking activation of the renin— angiotensin system with accelerated cerebro-vascular atherosclerosis remains controversial. We therefore prospectively investigated the relationships of plasma renin activity and aldosterone levels with carotid artery lesions (CAL) in essential hypertension. Methods We evaluated the prevalence and severity of CAL and the intimal—medial thickness (IMT) with a high-resolution echo-Doppler technique in 107 cerebrovascularly asymptomatic consecutive primary hypertensives (55 male, 52 female) and in 70 (42 male, 28 female) normotensive controls. We also measured supine plasma renin activity (PRA) and aldosterone before and 45 min after captopril administration, while daily urinary excretion of sodium was measured. Results Both the prevalence (59.4 versus 26.2%) and severity of sex- and age-adjusted and unadjusted CAL and IMT were significantly higher in hypertensives than in controls. Regression analysis showed different predictors of IMT (age and captopril-stimulated-PRA, R2 = 0.27, P < 0.0001), score of CAL (mean blood pressure, R2 = 0.15, F = 12.73, P < 0.0001) and maximal stenosis (pulse pressure and known duration of hypertension R2 = 0.29, F = 14.58, P < 0.0001). Sex- and age-adjusted IMT did not differ between quartiles of renin-sodium profile. However, patients in the quartile with the highest PRA had the lowest score of CAL and an inverse relationship between age-adjusted PRA and IMT and CAL was found. Conclusions These results, besides confirming an association of both IMT and CAL with primary hypertension and ageing, demonstrate that CAL and IMT have different correlates. However, they do not support the contention that a high renin-sodium profile carries an excess risk of CAL in primary hypertensives with no clinical evidence of cerebro-vascular disease.

Pravastatin treatment in combined hyperlipidaemia

Combined hyperlipidaemia and the presence of small and dense LDL particles in the circulation are associated with an increased risk of myocardial infarction.The effect of pravastatin on plasma lipoproteins and on LDL size has been evaluated in a single-blind, randomised, placebo-controlled study in 24 patients with combined hyperlipidaemia; 12 patients on pravastatin and 12 on placebo.After 16 weeks on pravastatin, plasma total (−15%) and LDL (−23%) cholesterol and apo B (−13%) levels were significantly reduced and apo AI (+6%) had increased. LDL size (measured by gradient gel electrophoresis) had not changed. No adverse effect was observed.The study suggests that, in combined hyperlipidaemia, LDL size is not affected by variation in LDL receptor activity.

Relationship of Early Carotid Artery Disease With Lipoprotein (a), Apolipoprotein B, and Fibrinogen in Asymptomatic Essential Hypertensive Patients and Normotensive Subjects

Abstract Background We investigated the relationships between plasma lipids and lipoprotein fractions and carotid artery lesions (CAL) in 177 cerebro-vascularly asymptomatic subjects, of whom 107 were primary hypertensive patients and 70 normotensive controls. Methods The prevalence and severity of CAL, as assessed by calculating a score of severity (score of CAL) and the maximal stenosis of both sides, as well as the intimal-medial thickness (IMT) were evaluated with a high-resolution echo-Doppler technique. We measured total serum cholesterol, triglycerides, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, lipoprotein (a) [Lp(a)], Apo (apolipoprotein)AI, ApoAII, ApoB, and fibrinogen. Results Both the prevalence (59.4% vs 26.2%) and severity of sex- and age-adjusted and unadjusted CAL and IMT were significantly higher in hypertensive patients than in controls. Regression analysis showed different predictors of IMT and maximal stenosis. The variables that remained in the model were age, mean blood pressure (BP), and smoking for IMT; pulse pressure, known duration of hypertension (HT), fibrinogen, and ApoB for the score of CAL; and the last four variables along with age and mean BP for maximal stenosis. Furthermore, we identified a link between the atherogenic lipoprotein fractions Lp(a) and ApoB, fibrinogen and early carotid artery atherosclerotic changes. Conclusions The different correlates of IMT, CAL, and maximal degree of stenosis suggest that they reflect different events occurring in the arterial wall in response to aging, HT, and other risk factors, rather than simply different stages of the same atherosclerotic process.

Lipoprotein pattern and plasma lipoprotein lipase activities in patients with primary biliary cirrhosis

Plasma lipids, apoprotein A-I and B in serum and in lipoprotein fractions (VLDL + LDL, HDL2, and HDL3) obtained by preparative ultracentrifugation, as well as postheparin lipoprotein lipase activity (H-TGL and LPL) were evaluated in 17 subjects with primary biliary cirrhosis (stage II and III) subdivided into two groups according to the presence or absence of lipoprotein X (Lp-X). A reduction in total lipoprotein lipase activity was observed in both patient groups, compared to controls (P<0.01); the hepatic lipoprotein lipase was significantly reduced (P<0.01) only in the Lp-X-positive group. The lipid (477.8+154.3 vs 239.6±51.1; P<0.01) and protein (147.4±37.1 vs 83.3±19.7; P< 0.01) masses in the VLDL + LDL fraction of the Lp-X-positive group were increased compared to controls. In the same group, the HDL2 fraction also showed an increase in lipid (186.6±80.0 vs 77.9±21.6; P<0.01) and protein (133.9±60.0 vs 67.9±16.5; P <0.01) masses; in addition, the HDL2 percent lipid composition was different in the two patient groups, showing a decrease in esterified cholesterol (20.4±3.6 vs 25.7±2.2; P <0.01) and an increase in phospholipids (59.2±2.9 vs 54.8±2.6; p<0.01) in the Lp-X-positive group. Apo B was also increased in Lp-X-positive patients both in the serum (134.0±27.6 vs 90.9±7.3; P<0.01) and in the VLDL + LDL fraction (134.0±22.2 vs 72.5±16.5; P<0.01). The differences seen in lipoprotein concentration and composition in the two patient groups seem related, in part, to the presence of Lp-X or, better, to the stage of the disease. The reduction in hepatic lipase may play an important role in determining the increase and altered composition of the HDL2 subfraction.

Comparison of lipoprotein(a) assay methods in serum and in a plasminogen-free fraction

We compared five immunoassays for lipoprotein(a) (Lp(a)) determination (end-point immunonephelometry, two-site IRMA and three different ELISA methods) in order to verify their agreement. Since it has been demonstrated that human apo(a) structure is closely similar to that of plasminogen, cross-reactivity of apo(a) antibodies with plasminogen represents an important technical problem in serum Lp(a) quantification. On this account we used a plasminogen-free fraction obtained by one-step ultracentrifugation at a density of 1.125 g/ml, in which no plasminogen activity was found. A satisfactory correlation between serum and plasminogen-free fraction Lp(a) values was found for all the methods; the limits of agreement were too high, however, to use serum and fraction interchangeably. Furthermore, it emerged that the different assays were more comparable and individual Lp(a) differences between methods were less spread when plasminogen-free fraction was used instead of serum.

Serum Lipids, Lipoprotein Analysis and Apoprotein A-I, A-II and B Levels in Friedreich’s Ataxia

Serum lipid, lipoprotein and apoprotein parameters were evaluated in 15 patients (7 males and 8 females) with Friedreichs ataxia. Serum lipid levels in patients showed no significant differences compared to controls. Small reduction in serum phospholipid and in total HDL and HDL3 cholesterol levels were observed, and the female patients presented a slight reduced total cholesterol level; among the serum apoproteins, apo B was reduced only in the males. The most interesting findings concerned the lipoproteins, since both lipid and protein masses of the VLDL, LDL and HDL2 fractions were reduced. In reference to lipoprotein composition, however, HDL2 was the most modified fraction, showing an important protein reduction. From this point of view, this lipoprotein seems the most responsible for the changes observed in our patients. The meaning of this modified lipoprotein pattern in the pathophysiology of Friedreichs ataxia is not clear.