Patterns of serum lipids derangements and cardiovascular risk assessment in patients with primary biliary cholangitis.

INTRODUCTION AND OBJECTIVES: Primary biliary cholangitis (PBC) is a chronic cholestatic autoimmune disease that disrupts the cholesterol metabolism. Our aim was to investigate the frequency of dyslipidemias and to evaluate the risk of cardiovascular events in a historic cohort of patients with PBC. PATIENTS: All patients attended from 2000 to 2009 with histological diagnosis of PBC were included and were compared with healthy controls. The 10-year cardiovascular risk was estimated by the Framingham risk score. RESULTS: Fifty four patients with PBC were included and compared to 106 controls. Differences in total cholesterol (263.8±123.9mg/dl vs. 199.6±40, p=0.0001), LDL-cholesterol (179.3±114.8 vs. 126.8±34.7, p=0.0001), HDL-cholesterol (62.4±36.2mg/dl vs. 47.3±12.3, p=0.0001) and triglycerides (149.1±59.1mg/dl vs. 126.4±55.4, p=0.001) were found. Hypercholesterolemia (>240mg/dl) was found in 52.4% of the patients with PBC vs. 11% in the control group, high LDL-cholesterol (160-189mg/dl) in 45.2% of the patients with PBC vs. 10% in controls and hyperalphalipoproteinemia (HDL-cholesterol >60mg/dl) in 45.2% of the patients with PBC vs. 16% in controls. The 10-year cardiovascular risk was 5.3%±5.9 in the patients with PBC and 4.1%±5.7 in the control group (p=0.723, IC 95%=0.637-1.104). Only one cardiovascular event (stroke) in a patient with PBC was registered in a mean follow up time of 57.9±36.5 months. CONCLUSIONS: Marked derangements in serum lipids and a high frequency of dyslipidemias are found in patients with PBC, however, these do not increase the risk of cardiovascular events.

Persistent High Non-High-Density Lipoprotein Cholesterol in Early Childhood: A Latent Class Growth Model Analysis.

OBJECTIVES: To examine patterns of non-high-density lipoprotein (HDL) cholesterol in early childhood and identify factors associated with persistent high non-HDL cholesterol in healthy urban children. STUDY DESIGN: We identified all children enrolled in a primary care practice-based research network called TARGet Kids! (The Applied Research Group for Kids) with ≥3 laboratory measurements of non-HDL cholesterol. Latent class growth model analysis was performed to identify distinct trajectory groups for non-HDL cholesterol. Trajectory groups were then categorized into "normal" vs "persistent-high" non-HDL cholesterol based on guideline cut-off values and logistic regression was completed to examine the association between trajectory group and the presence of anthropometric and cardiometabolic risk factors. RESULTS: A total of 608 children met inclusion criteria for the trajectory analysis (median age at enrolment = 18.3, IQR = 27.9 months). Four trajectory groups were identified with 2 groups (n = 451) categorized as normal non-HDL cholesterol and 2 groups (n = 157) as persistent high non-HDL cholesterol. Family history of high cholesterol (OR 2.04, 95% CI 1.27-3.28) was associated significantly with persistent high non-HDL cholesterol, whereas East/Southeast Asian vs European ethnicity (OR 0.33, 95% CI 0.14-0.78), longer breastfeeding duration (OR 0.96, 95% CI 0.93-1.00), and greater birth weight (OR 0.69, 95% CI 0.48-1.00) were associated with lower odds of persistent high non-HDL cholesterol. CONCLUSIONS: Patterns of non-HDL cholesterol are identified during early childhood, and family history of high cholesterol was associated most strongly with persistent high non-HDL cholesterol. Future research should inform the development of a clinical prediction tool for lipids in early childhood to identify children who may benefit from interventions to promote cardiovascular health.

Asymptomatic individuals with high HDL-C levels overexpress ABCA1 and ABCG1 and present miR-33a dysregulation in peripheral blood mononuclear cells.

Considering the growing knowledge and perspectives on microRNAs (miRNAs) that control high-density lipoprotein cholesterol (HDL-C) levels and metabolism, this study aimed at evaluating whether hsa-miR-33a and hsa-miR-128a are differentially expressed in peripheral blood mononuclear cells from asymptomatic individuals with low and high HDL-C, as well as at investigating the potential relationships with ATP binding cassete transporter A1 (ABCA1) expression, cholesterol efflux capacity and other parameters related with reverse cholesterol transport. In addition, the associations with cardiovascular risk were investigated by carotid-intima media thickness (cIMT). Asymptomatic volunteers of both genders (n=51) were classified according to HDL-C (mg/dL) in hypoalphalipoproteinemics (hypo, HDL-C ≤3 9), hyperalphalipoproteinemics (hyper, HDL-C ≥ 68) and controls (CTL, HDL-C ≥ 40<68). cIMT, lipids, lipoproteins, HDL size and volume, C reactive protein and insulin were determined, as well as the activities of several proteins and enzymes related to HDL metabolism. In a subgroup of 19 volunteers the cellular cholesterol efflux and HDL composition were determined. Total RNA was extracted from peripheral blood mononuclear cells for relative quantification experiments. Hypo volunteers presented significantly higher levels of triglycerides, VLDL-C and insulin; in addition, HDL size and volume decreased when compared with CTL and hyper. Regarding gene expression analysis, the hyper group presented a decrease of 72% in hsa-miR-33a and higher mRNA expression of ABCA1 and ABCG1 when compared with CTL. No significant differences in hsa-miR-128a expression, cholesterol efflux, cIMT or plaques were found. Further studies are necessary to elucidate the mechanisms underlying the complex miRNA network, regulating cellular cholesterol homeostasis in humans and its clinical repercussions.

Low birthweight and elevated levels of lipoprotein(a) in prepubertal children.

AIM: To evaluate whether healthy prepubertal children with low birthweight (LBW) exhibited higher serum levels of lipoprotein(a) (Lp(a)) than did those with normal birthweight (NBW). METHODS: A total of 350 healthy children aged 6 to 9 years and in Tanner stage 1 were enrolled in a community-based cross-sectional study. Family history of hypertension, diabetes or cardiovascular disease (CVD) in parents and grandparents; active smoking; a diagnosis of acute or chronic illness; and intake of vitamins or nutritional supplements were exclusion criteria. The cut-off point for Lp(a) was 0.79 µmol/L. RESULTS: LBW was identified in 51 (14.6%) children. In total, 42 (12.0%) children had elevated Lp(a) levels, with 25 (49.0%) and 17 (5.7%) in the LBW and NBW groups, respectively (P < 0.0005). None of the children had adverse cardiovascular outcomes. Average body mass index (BMI) (17.1 ± 3.3 and 18.8 ± 3.9, P = 0.001), glucose levels (4.5 ± 0.5 and 4.8 ± 0.4 mmol/L, P = 0.007), insulin levels (67.4 ± 45.1 and 86.1 ± 54.9 pmol/L, P = 0.02), and Lp(a) levels (0.52 ± 0.21 and 1.40 ± 0.49 µmol/L, P < 0.0005) were higher in the children with LBW than in the children with NBW. A multivariate analysis adjusted by age, sex, raw BMI, BMI standard deviation score and insulin level showed a significant association between LBW and elevated levels of Lp(a) (odds ratio 8.02, 95% confidence interval 7.3-21.3; P < 0.0005). CONCLUSIONS: LBW was shown to be strongly associated with elevated serum levels of Lp(a).

Protective modulation of carotid atherosclerosis in hyperalphalipoproteinemic individuals.

To determine whether hyperalphalipoproteinemia modifies carotid intima-media thickness (cIMT) and/or influences the relationship of clinical and biochemical parameters with cIMT. This study was conducted on 169 asymptomatic individuals, classified as hyperalphalipoproteinemic (Hyper-A) (Hyper-A, n = 71, HDL-C > or =68 mg/dL) and controls (CTL) (CTL, n = 98, HDL-C >32 and <68 mg/dL). Enzymatic, nephelometric and ultracentrifugation methods were used for biochemical determinations. Hepatic lipase (HL), lipoprotein lipase (LPL), cholesteryl ester transfer protein (CETP) and phospholipids transfer protein (PLTP) activities were measured by radiometric exogenous methods. The prevalence of dyslipidemia, hypertension, smoking, sedentariness, postmenopausal women, coronary artery disease (CAD) and familial history of CAD were determined. High resolution beta-mode carotid ultrassonography was performed. The Hyper-A group was older and had higher frequencies of hypercholesterolemia (40%), hypertension (31%), sedentariness (37%) and postmenopausal women (1%). In Hyper-A individuals, the mean cIMT after adjustment for age and gender was similar between the groups (0.85 +/- 0.24 mm Hyper-A versus 0.69 +/- 0.17 mm CTL). In multivariate models, age was a significant predictor of cIMT in Hyper-A (R (2) = 0.04, p < or = 0.001), independently of other clinical or biochemical factors. In contrast to CTL, where age (R (2) = 0.63 p < or = 0.001), male sex (R (2) = 0.03, p < or = 0.001), blood pressure (R (2) = 0.006, p < or = 0.001) and HDL-C (R (2) = 0.02, p < 0.022) accounted for the cIMT variations. Despite an increased prevalence of cardiovascular risk factors in Hyper-A and resistance of carotid thickness to modulation by metabolic and anthropometric factors (except age), the similarity in cIMT between Hyper-A and healthy individuals emphasizes the atheroprotective effects of HDL.

Lipemia retinalis in a 35-day-old infant with hyperlipoproteinemia: case report.

A rare case of hyperlipropoteinemia in a 35-day-old infant who presented not only high blood levels of cholesterol and triglycerides but also an ocular manifestation described as lipemia retinalis. The fundoscopic abnormality cleared as the levels of chilomicrons in plasma dropped. Lipemia retinalis is an important and reliable parameter of high levels of chilomicrons and triglycerides and should be considered as a significant clue while diagnosing.

Lipemia retinalis in a 35-day-old infant with hyperlipoproteinemia: case report / Lipemia retinalis em recém-nascido com 35 dias: relato de caso

A rare case of hyperlipropoteinemia in a 35-day-old infant who presented not only high blood levels of cholesterol and triglycerides but also an ocular manifestation described as lipemia retinalis. The fundoscopic abnormality cleared as the levels of chilomicrons in plasma dropped. Lipemia retinalis is an important and reliable parameter of high levels of chilomicrons and triglycerides and should be considered as a significant clue while diagnosing.

Caso raro de hiperlipoproteinemia em recém-nascido com 35 dias de idade. Identificados altos níveis de colesterol e triglicérides associados a manifestãção ocular descrita como lipemia retinalis. As alterações oculares mostraram melhora uma vez que os níveis séricos foram controlados. Lipemia retinalis é parâmetro confiável e importante a ser considerado como suspeita de alterações de colesterol e triglicérides em crianças e em adultos.

Diminished macrophage cholesterol removal rate by the altered HDL metabolism in the Nagase analbuminemic rat.

Dyslipoproteinemia of the Nagase analbuminemic rat (NAR) is characterized by elevated concentrations of VLDL and LDL attributed to increased rates of liver lipoprotein synthesis. Increased lysophosphatidylcholine (LPC) in NAR HDL has been attributed to high plasma LCAT activity. We show here that, as compared with Sprague-Dawley rats (SDR), NAR plasma triacylglycerol (TAG), total cholesterol (TC), HDL TAG, protein, total phospholipids (PL), LPC, and PS are increased. These alterations rendered the NAR HDL particle more susceptible to the activity of the enzyme hepatic lipoprotein lipase (HL), which otherwise was unaltered in our study. Fractional catabolic rates in blood of the autologous 125I-apoHDL (median and lower quartile values), were, respectively, 0.231 and 1.645 (n = 10) in NAR as compared with 0.140 and 0.109 (n = 10) in SDR (P = 0.012), corresponding to synthesis rates of HDL protein of 89.8 +/- 33.7 mg/d in NAR and 17.4 +/- 6.5 mg/d in SDR (P = 0.0122). Furthermore, Swiss mouse macrophage free-cholesterol (FC) efflux rates, measured as the percent [14C]-cholesterol efflux/6 h, were 8.2 +/- 2.3 (n = 9) in NAR HDL and 11.2 +/- 3.2 (n = 10) in SDR HDL (P = 0.03). Therefore, in NAR the modification of the HDL composition slows down the cell FC efflux rate, and together with the increased rate of plasma HDL metabolism influences the reverse cholesterol transport system.

Locus on chromosome 6p linked to elevated HDL cholesterol serum levels and to protection against premature atherosclerosis in a kindred with familial hypercholesterolemia.

Heterozygous familial hypercholesterolemia (FH) is a highly atherogenic genetic disorder leading to premature coronary heart disease (CHD), usually before 60 years of age. We studied an extended multigenerational kindred with FH linked to chromosome 1p32 in which atherosclerotic complications were either delayed or prevented in individuals with elevated HDL cholesterol (HDL-C) levels or hyperalphalipoproteinemia (HA). Premature CHD was observed in FH individuals without HA. The study of this family established that the HA trait in the family also followed an autosomal dominant mode of inheritance with a pattern of segregation independent from FH. We identified a locus on chromosome 6 linked to elevated HDL-C levels (HA) in this family. Haplotype analysis refined the localization to a 7.32-cM interval (73 to 80 cM from pter) flanked by markers D6S1280 and D6S1275. Parametric 2-point and multipoint analyses yielded maximum LOD scores of 3.05 and 3.17, respectively. This finding was confirmed with a nonparametric multipoint score of 3.78 (P=0.0009). We propose that this locus, linked to elevated HDL-C levels, confers protection against premature CHD within an FH context.

Screening of preformed oxidised low density lipoprotein isolated by a polyanion precipitation method. Its correlation with serum triglyceride levels.

For clinical and epidemiological screening a simple and sensitive methodology was developed for detection of preformed lipid peroxides (LPO) in low density lipoprotein (LDL). For this purpose, the iodometric assay of El-Saadani et al. (J Lipid Res 1989;30:627-30) was adapted to the fraction containing LDL isolated by polyanion precipitation avoiding ultracentrifugation. This fraction also includes intermediate density lipoprotein. Stratifying 53 individuals by their serum triglyceride levels (TG) the highest quartile showed a highly significant elevation of LDL-LPO compared with the lowest one (69.2 +/- 41.2 vs 22.9 +/- 10.0 nmol mg-1 LDL-apo B, P < 0.001). LDL-LPO concentration also showed a strong correlation with TG (r = 0.73, P < 0.00001) and significant inverse correlations with high density lipoprotein cholesterol (HDL-C) and HDL3-C subfraction (r = -0.37, P < 0.01 and r = -0.38, P = 0.01, respectively). The TG/HDL-C ratio, which is closely associated with insulin resistance, was strongly correlated with LDL-LPO (r = 0.83, P < 0.00001). Significant elevations of LPO were observed in phenotypic hyperlipoproteinemias (HLP) IIb and IV (P < 0.01 and P < 0.02, respectively) and when expressing LPO in mol/mol of LDL-apo B, two- and 2.5-fold higher values were found in types IIb and IV HLP, respectively, compared with normolipidemic subjects, suggesting a more oxidative environment for apo B in both phenotypes. No variations in LPO were found in type IIa HLP. This simple assay for in vivo detection of LDL-LPO, emphasises the possible atherogenic effect of TG through their oxidative capacity and suggests the integration of LPO to the cluster of associated risk factors: high TG, low HDL-C and insulin resistance.

The mutation Ala677-->Val in the methylene tetrahydrofolate reductase gene: a risk factor for arterial disease and venous thrombosis.

Mild hyperhomocysteinemia has been identified as a risk factor for arterial disease and for venous thrombosis. Individuals homozygous for the thermolabile variant of the methylene tetrahydrofolate reductase gene (MTHFR) which results from a common mutation Ala677-->Val and is found in 5-15% of the general population, have significantly elevated plasma homocysteine levels and may account for one of the genetic risk factors in vascular disease. We have analyzed the prevalence of MTHFR-T homozygotes in patients with arterial disease or venous thrombosis. We studied 191 patients with arterial disease and 127 individuals with venous thrombosis and compared with 296 unmatched controls. The results showed that there was a high prevalence of homozygotes for the mutated MTHFR-T allele among a group of patients with arterial disease (19%) in the absence of hyperlipoproteinemia, hypertension, and diabetes mellitus when compared to controls (4%), odds ratio of 5.52 (95% C.I., 2.27 to 13.51). The prevalence of homozygotes among patients with venous thrombosis was 11%, odds ratio of 2l93 (95% C.I., 1.23 to 7.01). The risk of venous thrombosis remained high, odds ratio of 2.63, even after we excluded 27 patients with hereditary thrombophilia (e.g. factor V Leiden, dysfibrinogenemia, deficiency of protein C, protein S, antithrombin III, or factor XII) from the 127 overall cases with venous thrombosis. These data support the hypothesis that being a homozygote for the MTHFR-T is a risk factor for the development of arterial disease and also for venous thrombosis.

Electroforesis de lipoproteínas en gel de agarosa / Lipoproteins in agar gel electrophoresis

Los perfiles de los tipos clásicos mencionados pueden encontrarse en forma aislada o en diversas combinaciones. Muchas veces el perfil resulta limítrofe entre dos clasificaciones, siendo difícil incluirlo en uno de los dos tipos. Este problema se presenta en el 10%de las muestras

Electroforesis de lipoproteínas en gel de agarosa / Lipoproteins in agar gel electrophoresis

Los perfiles de los tipos clásicos mencionados pueden encontrarse en forma aislada o en diversas combinaciones. Muchas veces el perfil resulta limítrofe entre dos clasificaciones, siendo difícil incluirlo en uno de los dos tipos. Este problema se presenta en el 10%de las muestras

[Non-insulin-dependent diabetes mellitus and hyperlipoproteinemia in patients with ischemic cardiopathy]. / Diabetes mellitus no-insulino-dependiente e hiperlipoproteinemia en pacientes con cardiopatía isquémica.

Cardiovascular disease (CVD) constitutes the main cause of death in diabetes mellitus (DM): Previous studies at the "Instituto Nacional de Cardiología de México" have investigated the metabolic alterations of survivors of a myocardial infarction (MI), but none of them had focused on the metabolic profile of the diabetic patient. We compared two groups of patients with ischemic heart disease (IHD), one with (DMG) and one without (NDMG) Diabetes Mellitus, to investigate differences in the prevalence and nature of hyperlipoproteinemias (HLP) and other risk factors of atherosclerosis. DMG consisted of 117 patients (75 male, 42 female) and NDMG consisted of 119 patients (91 male y 28 female). (Female NDMG vs female DMG p less than 0.05). The presence of risks factors of atherosclerosis was investigated in all patients, and total cholesterol (chol) triglycerides (TG) and glucose were measured in post-absorptive phase. There were no differences regarding mean age (DMG: 60 +/- 8 years, NDM: 60 +/- 11 years), Quetelet Index (Kg./mt2: DMG: 26.5 +/- 3, NDMG: 26.7 +/- 3), TG: (DMG: 246.2 +/- 125, NDMG: 223.5 +/- 129) or Chol (DMG: 216 +/- 42 mg/dl, NDMG: 225 +/- 45 mg/dl). Hypertriglyceridemia was significantly higher in patients with DM, as a whole and when both sexes were studied separately (p less than 0.05). Hypercholesterolemia was significantly higher in NDMG (p less than 0.05) and without significance, in diabetic women. (p less than 0.05). Type IV phenotype was higher in DMG (p less than 0.05) whereas phenotypes IIa and IIa + IIb were more prevalent among non-diabetics (p less than 0.001, p less than 0.0001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

[Metabolic disorders in survivors of myocardial infarct]. / Alteraciones metabólicas en sobrevivientes de infarto miocárdico.

Several lines of evidence have clearly established the role of lipoproteins as risk factors for the development of atherosclerosis. Epidemiologic studies from different countries have found that about one third of myocardial infarction survivors under 60 years of age are hyperlipidemic. The acute stress reaction occurring in the first hours following an acute myocardial infarction causes distinct changes in the patient's metabolic profile, these changes include a significant reduction of total cholesterol and cholesterol associated with low density lipoproteins and a usually mild elevation of blood glucose. With the purpose of establishing the prevalence and severity of lipoprotein disorders found in myocardial infarction survivors living in Mexico city we conducted a prospective study of 106 consecutive admissions to the coronary care unit at the National Institute of Cardiology with the fully proven diagnosis of acute myocardial infarction, we included only patients younger than 60 years of age that could be sampled within the first 72 hours of the appearance of typical symptoms, at this time the coronary risk factor profile was assessed and blood samples were drawn (acute sample). After three months of the diagnosis we sampled 81 of the original 106 patients (chronic sample). The comparison of these 81 patients showed remarkable differences in the lipid values obtained on each sample. The mean value for total cholesterol in the acute sample was 225 mg/dl whereas the corresponding value for the chronic sample was 240.5 mg/dl (p less than 0.005). This difference was also highly significant for the low density fraction. On the basis of the chronic sample analysis we estimated a prevalence of hyperlipoproteinemia of 35.8%. (II: 18.5%, III: 2.5%, IV: 14.8%), an additional subgroup of 10 patients (12.3%) had the hypo-HDL phenotype raising the number of subjects at risk for atherosclerosis to as high as 48.1% considering only the lipoproteins. The prevalence figures for the rest of the risk factors were as follows: 70.3% for tobacco smoking, 35.8% for Systemic Arterial Hypertension, 33.4% for Obesity and 30.8% for Diabetes Mellitus. Among the group of 81 patients, 17 were known diabetics, eight additional cases of Diabetes Mellitus were diagnosed at the chronic phase (two with fasting hyperglycemia and six with diagnostic oral glucose tolerance tests). The "acute plase" glycemia for these eight subjects was significantly higher (mean: 98.4 mg/dl) than the corresponding value for the non diabetic patients (mean: 83.4 mg/dl p less than 0.002), the seventeen known diabetics had a mean glycemia of 150.6 mg/dl in the acute sample.(ABSTRACT TRUNCATED AT 400 WORDS)

Efectos del aceite de hígado de bacalao como fuente de ácidos grasos n-3 sobre las lipoproteínas y la viscosidad sanguínea en pacientes con hiperlipoproteinemias primarias / Effects of cod liver oil as a source of fatty acids n-3 on lipoproteins and blood viscosity in patients with primary hyperlipoproteinemia

Las dietas ricas en AG-n-3 se consideran antiaterogénicas. El aceite de hígado de bacalao (AHB) contine 19 g/dl de AG-n-3 y 850 mg de colesterol, por lo cual estudiamos su efecto sobre las lipoproteínas plasmáticas y la viscosidad sanguínea en pacientes con hiperlipoproteinemias primas (clasificados según la OMS) y/o B-VLDL elevada, que se definió por la relación col-VLDL/TG > 0,35, beta ancha en el lipidograma electroforético y test de precipitación con heparina-MgCl2-NaCl. El grupo A, compuesto por pacientes de tipos IIa (n = 4), IIb (4), IV (2) y B-VLDL elevada, 1) recibió 50 ml/día de AHB. El grupo B, compuesto por pacientes por tipo IIa (4), IIb (9), IV (4), B-VLDL elevada (5) y V (2) recibió 25 ml/día. Un mes antes del tratameitno y durante éste dieta de los pacientes era baja en hidratos de carbono refinados, con menos de 300 mg de colesterol al día y supresión de etanol. en las muestras basales y a los 21 días de tratamiento se midieron TG, Col-en VLDL, LDL, HDL2 y HDL3, apo A1 y apo B, viscosidades sanguíneas, sérica y plasmática. En el grupo A disminuyeron TG (p < 0,05), pero col-VLDL/TG aumentó (p < 0,01) y apreció B-VLDL en 6 de 11 pacientes. En el grupo B, bajaron TG y col-VLDL (p < 0,02 y p < 0,05, respectivamente) pero los 5 pacientes con B-VLDL basal no mejoraron. Apo A1 aumentó (p < 0,05). El col-LDL no disminuyó en níngún grupo. El AHB no tiene efecto en pacientes con B-VLDL basal o hiperlipémicos de tipos IIa o IIb, en cambio los pacientes de tipo IV mejoraran. El AHB disminuye la viscosidad sanguínea (p < 0,05) pero no afecta la plasmática

Efectos del aceite de hígado de bacalao como fuente de ácidos grasos n-3 sobre las lipoproteínas y la viscosidad sanguínea en pacientes con hiperlipoproteinemias primarias / Effects of cod liver oil as a source of fatty acids n-3 on lipoproteins and blood viscosity in patients with primary hyperlipoproteinemia

Las dietas ricas en AG-n-3 se consideran antiaterogénicas. El aceite de hígado de bacalao (AHB) contine 19 g/dl de AG-n-3 y 850 mg de colesterol, por lo cual estudiamos su efecto sobre las lipoproteínas plasmáticas y la viscosidad sanguínea en pacientes con hiperlipoproteinemias primas (clasificados según la OMS) y/o B-VLDL elevada, que se definió por la relación col-VLDL/TG > 0,35, beta ancha en el lipidograma electroforético y test de precipitación con heparina-MgCl2-NaCl. El grupo A, compuesto por pacientes de tipos IIa (n = 4), IIb (4), IV (2) y B-VLDL elevada, 1) recibió 50 ml/día de AHB. El grupo B, compuesto por pacientes por tipo IIa (4), IIb (9), IV (4), B-VLDL elevada (5) y V (2) recibió 25 ml/día. Un mes antes del tratameitno y durante éste dieta de los pacientes era baja en hidratos de carbono refinados, con menos de 300 mg de colesterol al día y supresión de etanol. en las muestras basales y a los 21 días de tratamiento se midieron TG, Col-en VLDL, LDL, HDL2 y HDL3, apo A1 y apo B, viscosidades sanguíneas, sérica y plasmática. En el grupo A disminuyeron TG (p < 0,05), pero col-VLDL/TG aumentó (p < 0,01) y apreció B-VLDL en 6 de 11 pacientes. En el grupo B, bajaron TG y col-VLDL (p < 0,02 y p < 0,05, respectivamente) pero los 5 pacientes con B-VLDL basal no mejoraron. Apo A1 aumentó (p < 0,05). El col-LDL no disminuyó en níngún grupo. El AHB no tiene efecto en pacientes con B-VLDL basal o hiperlipémicos de tipos IIa o IIb, en cambio los pacientes de tipo IV mejoraran. El AHB disminuye la viscosidad sanguínea (p < 0,05) pero no afecta la plasmática (AU)