Factores cardiometabólicos asociados y prevalencia de concentraciones bajas de colesterol HDL y de dislipidemia aterogénica. Estudio SIMETAP-DA / Related cardiometabolic factors and prevalence of low HDL-cholesterol levels and atherogenic dyslipidemia. SIMETAP-AD study

OBJETIVO: Determinar las prevalencias ajustadas por edad y sexo de concentraciones bajas de colesterol HDL (cHDL-bajo) y de dislipidemia aterogénica (DA), y valorar sus asociaciones con factores de riesgo cardiovascular, enfermedad renal crónica, enfermedades cardiovasculares y cardiometabólicas. MÉTODOS: Estudio observacional transversal de base poblacional realizado en atención primaria, con sujetos adultos seleccionados aleatoriamente. Se consideró DA si los pacientes tenían hipertrigliceridemia (triglicéridos≥150mg/dL) y cHDL-bajo (<40mg/dL [hombres],<50mg/dL [mujeres]). Se determinaron las tasas de prevalencia crudas y ajustadas por edad y sexo, y se realizó análisis univariado y multivariante para evaluar los factores cardiometabólicos relacionados. RESULTADOS: Población de estudio con 6.588 adultos (55,9% mujeres) con edad media de 55,1 (±17,5) años. Las medias de cHDL fueron 49,2 (±12,6) mg/dL en hombres y 59,2 (±14,7) mg/dL en mujeres. Las prevalencias crudas de cHDL-bajo y de DA fueron 30,8% (IC95%: 29,7-31,9), y 14,3% (IC95%: 13,5-15,2), respectivamente. Las prevalencias ajustadas de cHDL-bajo fueron 28% en hombres y 31% en mujeres, y de DA fueron 16,4% en hombres y 10,6% en mujeres. El 73% de la población con DA tenía riesgo cardiovascular alto o muy alto. Los factores independientes asociados con cHDL-bajo o con DA fueron diabetes, tabaquismo, obesidad abdominal y obesidad. Los principales factores asociados con cHDL-bajo y con DA fueron hipertrigliceridemia y diabetes, respectivamente. CONCLUSIONES: Casi un tercio de la población adulta presentaba cHDL-bajo y la mitad de ellos cumplía criterios de DA. Los factores cardiometabólicos se asociaban con cHDL-bajo y DA, destacando la hipertrigliceridemia con el cHDL-bajo, y la DM con la DA

AIM: To determine the crude and sex- and age-adjusted prevalence rates of atherogenic dyslipidemia (AD) and low HDL-cholesterol levels (low-HDLc), and to assess their associations with cardiovascular risk factors, chronic kidney disease, cardiovascular and cardiometabolic diseases. METHODS: Population-based cross-sectional study conducted in Primary Care, with randomly selected adult subjects. The AD was considered if the patients had hypertriglyceridemia (triglycerides≥150mg/dL) and low-HDLc (<40mg/dL [men];<50mg/dL [women]). Crude and sex- and age-adjusted prevalence rates were determined, and univariate and multivariate analysis were performed to assess related cardiometabolic factors. RESULTS: Study population with 6,588 adults (55.9% women) with mean age 55.1 (±17.5) years. The mean HDLc levels were 49.2 (±12.6) mg/dL in men and 59.2 (±14.7) mg/dL in women. The crude prevalence rates of low-HDLc and AD were 30.8% (95%CI: 29.7-31.9), and 14.3% (95%CI: 13.5-15.2), respectively. The adjusted prevalence rates of low-HDLc were 28.0% in men and 31.0% in women, and AD were 16.4% in men and 10.6% in women. Seventy-three percent of the population with AD had high or very high cardiovascular risk. The independent factors associated with low HDLc or with AD were diabetes, smoking, abdominal obesity, and obesity. The major factors associated with low HDLc and AD were hypertriglyceridemia and diabetes, respectively. CONCLUSIONS: Almost a third of the adult population had low HDL-C and half of them met AD criteria. Cardiometabolic factors were associated with low HDL-C and AD, highlighting hypertriglyceridemia with low HDLc, and DM with AD

Exploring the effects of the atherosclerosis progression and the choice of affected arteries in the design of experiments with Apolipoprotein E-deficient mice / La exploración de los efectos de la progresión de la aterosclerosis y la elección de las arterias afectadas en el diseño de experimentos con ratones deficientes en apolipoproteína E

The objective of this study is to explore the longitudinal progression of atherosclerosis and the correlation between methods to measure the lesion in apolipoprotein E-deficient mice. Atherosclerosis progression was assessed by measurements of foam cell-rich depositions in their proximal aortas, and/or in surgically excised arteries, to assess the histological luminal narrowing. A longitudinal study was performed by comparing the values for carotid, aorta, and femoral and iliac arteries using common histological techniques. There were no significant differences in progression between different arteries, but correlation with the classical measurement of atherosclerosis in the aortic root was poor. Each laboratory requires specific standardization. Carotid arteries were sensitive to atherosclerosis in these mice, and progression was exponential. In conclusion, morphometric data show the importance of the choice of the duration of treatment, the appropriate controls, and the age at which to begin the experiments

El objetivo de este estudio es explorar la progresión longitudinal de la aterosclerosis y la correlación entre los métodos para medir la lesión en los ratones deficientes en apolipoproteína E. La progresión de la aterosclerosis se evaluó mediante mediciones de deposiciones ricas en células espumosas en las aortas proximales y/o en las arterias extirpadas quirúrgicamente para evaluar histológicamente el estrechamiento luminal. Se realizó un estudio longitudinal, y los valores para la carótida, la aorta, las arterias femorales e ilíacas se compararon mediante técnicas histológicas comunes. No hubo diferencias significativas en la progresión entre las diferentes arterias, pero la correlación con la medición clásica de la aterosclerosis en la raíz aórtica era pobre. Cada laboratorio requiere su normalización específica. Las arterias carótidas fueron sensibles a la aterosclerosis en estos ratones y la progresión fue exponencial. En conclusión, los datos morfométricos muestran la importancia en la elección de la duración del tratamiento, los controles apropiados y la edad a la cual comenzar los experimentos

A comparison of the efficacy of combined ezetimibe and statin therapy with doubling of statin dose in patients with remnant lipoproteinemia on previous statin therapy.

BACKGROUND AND PURPOSE: It remains undetermined whether the addition of ezetimibe to ongoing statin therapy is more effective than increasing the dose of statin for reducing remnant lipoprotein levels in patients with remnant lipoproteinemia on previous statin treatment. This study examined whether combined ezetimibe and statin therapy resulted in a greater improvement in remnant lipoprotein levels and endothelial function than with the dose of statin in patients with remnant lipoproteinemia on previous statin treatment. METHODS AND RESULTS: A total of 63 patients with stable coronary artery disease and high levels of remnant-like lipoprotein particle cholesterol (RLP-C) (≥5.0 mg/dL) on statin treatment were assigned randomly to two groups and treated with either addition of ezetimibe (10mg/day, n=32) or doubling of statin dose (n=31). The lipid profiles and flow-mediated dilation (FMD) of the brachial artery were measured at enrollment and after 6 months of treatment. Statin and ezetimibe combined therapy reduced RLP-C and improved FMD to a greater extent than doubling the statin dose (% reduction in RLP-C, 48 ± 18% vs. 33 ± 24%, respectively, p=0.01; % improvement in FMD, 47 ± 48% vs. 24 ± 23%, respectively, p=0.02). CONCLUSIONS: The addition of ezetimibe to ongoing statin treatment reduced RLP-C levels and improved endothelial dysfunction to a greater extent than doubling the statin dose in patients with high RLP-C levels on previous statin treatment. The present results are preliminary and should be confirmed by further studies on a larger number of study patients.

[Primary and secondary hypocholesterolemia].

Hypocholesterolemia is characterized by serum total cholesterol that is lower than the 5th percentile for age and sex, or the cut-off value which predicts the adverse prognosis by epidemiological study. Unlike hypercholesterolemia, physicians pay less attention to the morbidity, causes and consequences of hypocholesterolemia in clinical practice. In fact, hypocholesterolemia is a common dislipidemia, and mainly results from secondary factors. The causes of primary hypocholesterolemia are some disorders owing to genetic mutation in the pathway of cholesterol absorption, biosynthesis or metabolism, including abetalipoproteinemia, hypobetalipoproteinemia, Tangier disease, chylomicron retention disease and inherited disorders of cholesterol biosynthesis. The causes of secondary hypocholesterolemia comprise anemia, hyperthyroidism, malignancy, live disease, critical illness, serious stress, malabsorption or malnutrition, acute or chronic infection, chronic inflammation, and use of some drugs. In addition, what's more important is that hypocholesterolemia can result in some adverse events, such as increased mortality, intracerebral hemorrhage, cancer, infection, adrenal failure, suicide and mental disorder. Therefore, with the practice of intensive lipid-lowering treatment and the tendency to the increased indications of statins, it's high time that physicians attached more importance to hypocholesterolemia.

Effects of dietary sodium on reactive oxygen species formation and endothelial dysfunction in low-density lipoprotein receptor-deficient mice on high-fat diet.

Hypertension and high serum cholesterol level are important risk factors for atherosclerosis and coronary heart disease. In the present study we tested the hypothesis whether high sodium intake, when given in combination with Western type high-fat diet, induces endothelial dysfunction and promotes atherosclerosis. Furthermore, the role and enzyme sources of increased oxidative stress were examined. Low-density lipoprotein receptor-deficient mice (LDLR(-/-)) and control C57Bl/6 mice received either high-fat, normal-sodium diet (fat 18% and cholesterol 0.5%; NaCl 0.7%; w/w) or high-fat, high-sodium diet (7% NaCl w/w) for 12 weeks. Superoxide formation was assessed by lucigenin enhanced chemiluminescence, endothelial functions were examined ex vivo, and atherosclerotic lesions from the aorta were assessed by light microscopy. High-fat, high-sodium diet increased systolic blood pressure in LDLR(-/-) mice but not in C57Bl/6 mice, whereas it induced cardiac hypertrophy in both mouse strains. Dietary combination of fat and sodium induced endothelial dysfunction in LDLR(-/-) mice. Preincubation with a superoxide scavenger Tiron normalized endothelial dysfunction, whereas the hydrogen peroxide scavenger catalase did not alter endothelial function. High sodium intake induced superoxide formation in LDLR(-/-) mice on high-fat diet. Stimulation of muscarinic receptors in the endothelial cells by acetylcholine increased superoxide generation, whereas preincubation with the nitric oxide synthase (NOS) inhibitor L-arginine methyl ester or endothelium removal reduced superoxide production. Inhibition of nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase by apocynin decreased vascular superoxide formation whereas the xanthine oxidase inhibitor oxypurinol did not significantly affect oxidative stress in LDLR(-/-) mice. In conclusion, the detrimental effects of dietary sodium on endothelial function and progression of atherosclerosis in LDLR(-/-) mice on high-fat diet are mediated by increased ROS formation mainly through uncoupled NOS and NADPH oxidase. The present study also underscores the importance of superoxide and endothelial NOS uncoupling in the pathogenesis of endothelial dysfunction.

Acute exercise-induced changes in basal VLDL-triglyceride kinetics leading to hypotriglyceridemia manifest more readily after resistance than endurance exercise.

Resistance training is considered less effective than endurance training in lowering plasma triglyceride (TG) concentrations. Acutely, however, a single bout of strenuous exercise, whether endurance or resistance, increases the efficiency of very low-density lipoprotein (VLDL)-TG removal from the circulation and leads to hypotriglyceridemia. The comparative effects of these two types of exercise on VLDL-TG metabolism are not known. We therefore examined basal VLDL-TG kinetics by using stable isotope-labeled tracers in seven healthy, nonobese, untrained young men in the postabsorptive state, the morning after a single 90-min bout of either low-intensity endurance exercise (approximately 30% of peak oxygen consumption) or high-intensity resistance exercise (3 sets of 10 repetitions for 12 exercises at 80% of peak torque production), matched for total energy expenditure (approximately 400 kcal), or an equivalent period of rest on the preceding afternoon. Compared with rest, resistance exercise lowered fasting plasma VLDL-TG concentration by -28 +/- 10% (P = 0.034), increased VLDL-TG plasma clearance rate by 30 +/- 8% (P = 0.003), and shortened the mean residence time (MRT) of VLDL-TG in the circulation by -36 +/- 11 min (P = 0.016), whereas endurance exercise had no effect (all P > 0.05). Basal VLDL-TG plasma clearance rate was greater (P = 0.003) and VLDL-TG MRT was shorter (P = 0.012) the morning after resistance than endurance exercise. We conclude that, for the same total energy expenditure, resistance exercise is more potent than endurance exercise in eliciting changes in VLDL-TG metabolism that have been linked with hypotriglyceridemia, and it should thus be considered as an alternative to or in addition to endurance exercise for the control of plasma TG concentrations.

Growth hormone receptor deficiency results in blunted ghrelin feeding response, obesity, and hypolipidemia in mice.

We have previously shown that growth hormone (GH) overexpression in the brain increased food intake, accompanied with increased hypothalamic agouti-related protein (AgRP) expression. Ghrelin, which stimulates both appetite and GH secretion, was injected intracerebroventricularly to GHR-/- and littermate control (+/+) mice to determine whether ghrelin's acute effects on appetite are dependent on GHR signaling. GHR-/- mice were also analyzed with respect to serum levels of lipoproteins, apolipoprotein (apo)B, leptin, glucose, and insulin as well as body composition. Central injection of ghrelin into the third dorsal ventricle increased food consumption in +/+ mice, whereas no change was observed in GHR-/- mice. After ghrelin injection, AgRP mRNA expression in the hypothalamus was higher in +/+ littermates than in GHR-/- mice, indicating a possible importance of AgRP in the GHR-mediated effect of ghrelin. Compared with controls, GHR-/- mice had increased food intake, leptin levels, and total and intra-abdominal fat mass per body weight and deceased lean mass. Moreover, serum levels of triglycerides, LDL and HDL cholesterol, and apoB, as well as glucose and insulin levels were lower in the GHR-/- mice. In summary, ghrelin's acute central action to increase food intake requires functionally intact GHR signaling. Long-term GHR deficiency in mice is associated with high plasma leptin levels, obesity, and increased food intake but a marked decrease in all lipoprotein fractions.

Effects of cholesterol and apolipoprotein E on retinal abnormalities in ApoE-deficient mice.

PURPOSE: To examine the pathologic changes in the retina of apolipoprotein E (apoE)-deficient mice fed a high-cholesterol diet. METHODS: ApoE-deficient mice (ApoE) were maintained on either regular mouse chow (ApoE-R) or a high-cholesterol diet (ApoE-C) for 25 weeks. Age-matched control C57BL/6J mice (C57) were also maintained on either regular mouse chow (C57-R) or a cholesterol-containing diet (C57-C). Retinal function was assessed by dark-adapted electroretinography (ERG). The eyes were embedded, sectioned, and analyzed by histologic and immunohistochemical methods, as well as by light and transmission electron microscopy. RESULTS: After the 25-week feeding period, ERG tracings of ApoE-C mice revealed significant increases of a- and b-wave implicit times when compared with the C57-R group of mice. In addition, there were reductions in oscillatory potential (OP) amplitudes in the ApoE-C group. However, a- and b-wave amplitudes appeared to be unchanged among the four groups of mice. Light microscopic examination of the retinas showed that compared with control C57-R mice, ApoE-C mice had significantly lower cell numbers in the inner and outer nuclear layers (85.1% +/- 4.6%, P < 0.05 and 81.4% +/- 3.7%, P < 0.01 of C57-R controls, respectively). Transmission electron microscopy of apoE-deficient mice revealed cells of the inner nuclear layer with condensation of nuclear chromatin and perinuclear vacuolization in focal areas. Bruch's membrane was also found to be thicker, and its elastic lamina appeared disorganized and discontinuous. Immunohistochemistry demonstrated diminished or no immunoreactivity for carbonic anhydrase II and calretinin in the retinal layers of apoE-deficient mice. CONCLUSIONS: Overall, there were increasing abnormalities of retinal function and cellular morphology among the four groups of mice in the order of C57-R < C57-C < ApoE-R < ApoE-C. These findings suggest that apoE and/or cholesterol play an important role in retinal function.

Hyperinsulinemic hypoalphalipoproteinemia as a new indicator for coronary heart disease.

OBJECTIVES: The purpose of this study was to investigate the association among insulin resistance, high density lipoprotein cholesterol (HDL-C) and coronary heart disease (CHD), and to test the hypothesis that HDL-C may ameliorate the adverse effects of insulin. BACKGROUND: Serum low HDL-C (hypoalphalipoproteinemia) and hyperinsulinemia are independent predictors for CHD, but a strong negative correlation exists between them, as in patients with syndrome X. METHODS: Fifty-four pairs of cases (M/F: 49/5), defined as patients with angiographically proved CHD, and control subjects (M/F: 49/5) matched with cases with regard to gender and age were included. Insulin resistance was assessed by the homeostasis model assessment (HOMA). RESULTS: Cases had increased HOMA insulin resistance and lower serum levels of HDL-C than controls. A receiver operating characteristic (ROC) curve analysis indicated that HDL-C and insulin resistance were significant discriminators of CHD (area under ROC curve: 0.72 and 0.69, respectively). The interaction between HDL-C and the association of insulin resistance with CHD was significant: subjects with hyperinsulinemia and high HDL-C had no increased risk of CHD. Multivariate conditional logistic regression analysis showed that hyperinsulinemic hypoalphalipoproteinemia was a stronger indicator for CHD than either HDL-C or insulin resistance alone (-2 log likelihood: 19.0 vs. 12.6 or 15.7). CONCLUSIONS: Hyperinsulinemic hypoalphalipoproteinemia was a more potent indicator for CHD than either insulin resistance or low serum HDL-C levels alone, and the adverse effects of hyperinsulinemia seem to be ameliorated by high HDL-C levels.

Fibrinolytic response in subjects with hypertriglyceridemia and low HDL cholesterol.

The combination of hypertriglyceridemia and low high-density lipoprotein cholesterol (HDL-C) appears to be an excessively high risk factor for coronary artery disease (CAD). In the Helsinki study, both coronary events and mortality were decreased by gemfibrozil, especially in subjects with low HDL-C and high triglycerides (TG). On the other hand, it is known that high levels of TG can be associated with high levels of circulating plasminogen activator inhibitor (PAI), which is also a possible risk factor for CAD. The aim of the present study was to see: 1) whether the combination of low HDL-C and high TG is associated with a more impaired fibrinolytic response than in either isolated condition, and 2) whether gemfibrozil administration can improve fibrinolysis in patients with both high TG and low HDL-C. Twelve non-obese, non-diabetic subjects (eight men, four women; mean age 55 +/- 13 yrs) with low HDL-C (< 35 mg/dL men; < 45 mg/dL women) and high TG (mean 253.6 +/- 42.6 mg/dL) entered the study (Group A). Additionally fourteen comparable subjects with normal HDL-C were also investigated (Group B), plus 12 comparable subjects with isolated low HDL-C (Group C). Ten healthy people served as the control group. The following plasma fibrinolytic parameters were measured: tissue plasminogen activator antigen, PAI antigen and activity, euglobulin fibrinolytic activity (EFA) on fibrin plates, plasminogen and alpha-2-antiplasmin activities. All except the latter two values were also measured after venous occlusion (vo). In baseline conditions, patients in Groups A and B had higher EFA values before vo and higher PAI-1 antigen and alpha-2-antiplasmin levels after vo than those of controls or the subjects in Group C. The relationship between PAI antigen and PAI activity and TG was not confirmed in our population (n = 48). We also saw no interference due to HDL-C, while there was a significant relationship between EFA before vo and both TG and cholesterol. After gemfibrozil treatment (600 mg bid for 12 weeks), the lipid profiles of subjects with high TG and low HDL-C were significantly improved. There was also a slight reduction of PAI activity after vo, while the PAI-1 antigen had decreased significantly from baseline after vo (56.3 +/- 13 ng/mL before vo; 48.4 +/- 21 ng/mL after vo; P = 0.04). The higher risk of CAD in patients with low HDL-C and high TG might be in part related to impairment of fibrinolysis, which occurs in patients with isolated high TG. The close relationship existing between both TG and cholesterol levels and fibrinolytic activity confirm the key role of this latter process in the development of CAD.

Hypolipidaemic effect of fruit juice of Emblica officinalis in cholesterol-fed rabbits.

The lipid lowering and antiatherosclerotic effects of Emblica officinalis (Amla) fresh juice were evaluated in cholesterol-fed rabbits (rendered hyperlipidaemic by atherogenic diet and cholesterol feeding). E. officinalis fresh juice was administered at a dose of 5 ml/kg body weight per rabbit per day for 60 days. Serum cholesterol, TG, phospholipid and LDL levels were lowered by 82%, 66%, 77% and 90%, respectively. Similarly, the tissue lipid levels showed a significant reduction following E. officinalis juice administration. Aortic plaques were regressed. E. officinalis juice treated rabbits excreted more cholesterol and phospholipids, suggesting that the mode of absorption was affected. E. officinalis juice is an effective hypolipidaemic agent and can be used as a pharmaceutical tool in hyperlipidaemic subjects.

Recent concepts of lipoprotein pathophysiology.

Molecular genetic approaches have added greatly to the understanding of the human hyperlipoproteinemias. Studies in mice have added interesting new information. Transgenic mice over-expressing or deficient in various individual proteins important in lipoprotein metabolism have reproduced some dyslipidemias and permitted further pinpointing of the functions of apolipoproteins, lipoprotein receptors, lipid transfer proteins and enzymes. Cross-breeding of mice with single defects has reproduced certain dyslipidemia syndromes and permits examination of the combined etiologic effects of more than one gene.

Low levels of high-density lipoprotein cholesterol (hypoalphalipoproteinemia). An approach to management.

Clinical management of dyslipidemias has focused primarily on the low-density lipoprotein cholesterol (LDL-C) fraction; however, lipid disorders accompanied by low levels of high-density lipoprotein cholesterol (HDL-C) (hypoalphalipoproteinemia) are common, particularly among subjects with the diagnosis of coronary artery disease prior to age 55 years. The therapeutic objectives for high-risk subjects with dyslipidemias is directed initially toward reduction of the LDL-C fraction; thereafter, aggressive efforts aimed at raising the HDL-C fraction may be warranted. Strategies for raising the HDL-C fraction start with hygienic measures that include aerobic exercise, weight loss, smoking cessation, withdrawal of agents secondarily lowering HDL-C, and estrogen replacement. Pharmacotherapy selected according to the dyslipidemia that accompanies the HDL-C disorder is indicated for subjects who manifest premature coronary artery disease or who have a familial history of coronary artery disease and hypoalphalipoproteinemia.

Lipemia postprandial en sujetos con hipoalfalipoproteinemia primaria e hipoalfalipoproteinemia asociada a diabetes / Postprandial lipids and lipoproteins in primary hypoalphalipoproteinemia and hypoalphalipoproteinemia associated with diabetes

El acúmulo durante el postprandio (PP) de lipoproteínas de muy baja densidad y sus remanentes, se considera potencialmente aterogénico. El objetivo del presente estudio fue comparar la lipemia PP en pacientes con hipoalfalipoproteinemia asociada a DMNID (HADM) y pacientes con HA primaria (HAP). Se incluyeron ocho pacientes del sexo masculino en cada grupo con edad (media ñ DE) de 54 ñ 10 años, lípidos basales de CT 199 ñ 22 vs 160 ñ 33, C-LDL 117 ñ 27 vs 113 ñ 24, TG 250 ñ 146 vs 102 ñ 24 y C-HDL 29 ñ 3 vs 25 ñ 1 mg/dL. Después de un ayuno de 12 horas, se administró una carga oral de 65 g de grasa/m* de superficie corporal. Durante las siguientes 12 horas se efectuaron mediciones horarias de CT, TG y glucemia. Cada tres horas se practicó ultracentrifugación del plasma para determinación del colesterol de las lipoproteínas de alta densidad y se determinaron el colesterol y los triglicéridos en cada una de las distintas fracciones lipoproteicas. Los resultados mostraron que la magnitud de la trigliceridemia PP es significativamente mayor en los pacientes con HA-DM y está condicionada predominantemente por la trigliceridemia de ayunas. El tipo de respuesta de la lipemia PP (porciento delta) fue similar en ambos grupos de pacientes. Los máximos incrementos sobre el valor basal se observaron en los triglicéridos totales (150 vs 140 porciento HA-DM vs HAP) y TG de las LRT (188 vs 197 porciento), con mínimos decrementos en el C-HDL (-11 vs 13 porciento) y oscilaciones en uno y otro sentido, practicamente sin modificaciones, del C-LDL. La duración de la lipemia se prolongó discretamente en los pacientes con HA primaria, aunque las características de la lipemia fueron muy similares en pacientes con DM que tuvieron cifras menores de triglicéridos de ayuno. En la HA primaria pudiera coexistir un trastorno en el metabolismo de las lipoproteínas ricas en triglicéridos que se manifieste por una depuración más lenta de las mismas durante el postprandio. El C-HDL de ayunas en pacientes con HA no es un marcador que permita inferir el tipo de excursión postprandial de los triglicéridos.

[The effect of lipomodulators on the antigen-specific reactivity of the respiratory pathways]. / Vliianie lipomoduliatorov na antigenspetsificheskuiu reaktivnost' dykhatel'nykh putei.

Studies of guinea pigs subjected to intragastric administration of lipomodulators within the period of inductive phase sensibilization development have revealed that intensity of the contractile reaction of isolated tracheal rings depends on the specific allergen. Cholesterol promoted an increase in the contractile activity of tracheal rings. The administration of clofibrate blocked the formation of antigen-specific tracheal reactivity in the sensibilized animals.