Highly sensitive detection and discrimination of LR and YR microcystins based on protein phosphatases and an artificial neural network.

The inhibition characteristics of three different protein phosphatases by three microcystin (MC) variants--LR, YR, and RR--were studied. The corresponding K (I) for each enzyme-MC couple was calculated. The toxicity of MC varies in the following order: MC-LR > MC-YR > MC-RR. The sensitivity of the enzymes increased in the following order: mutant PP2A < mutant PP1 < natural PP2A. The best limit of detection obtained was 21.2 pM MC-LR using the most sensible enzyme. Methanol, ethanol, and acetonitrile up to 2 % (v/v) may be used in inhibition measurements. An artificial neural network (ANN) was used to discriminate two MC variants--LR and YR--using the differences in inhibition percentages measured with mutant PP1 and natural PP2A. The ANN is able to analyze mixtures with concentrations ranging from 8 to 98 pM MC-LR and 31 to 373 pM MC-YR.

LDL from obese patients with the metabolic syndrome show increased lipid peroxidation and activate platelets.

AIMS/HYPOTHESIS: This study assessed oxidative stress in LDL from obese patients with the metabolic syndrome and compared it with that in LDL from type 2 diabetic patients or control volunteers. It also determined the effect on platelets of LDL from the three groups. METHODS: The profiles of lipids, fatty acids and fatty acid oxidation products were determined in LDL isolated from plasma of patients with the metabolic syndrome, patients with type 2 diabetes and volunteers (n = 10 per group). The effects of LDL from the participant groups on the platelet arachidonic acid signalling cascade and aggregation were investigated. RESULTS: Compared with LDL from control volunteers, LDL from obese metabolic syndrome and type 2 diabetic patients had lower cholesteryl ester, higher triacylglycerol and lower ethanolamine plasmalogen levels. Proportions of linoleic acid were decreased in phosphatidylcholine and cholesteryl esters in LDL from both patient groups. Among the markers of lipid peroxidation, oxidation products of linoleic acid (hydroxy-octadecadienoic acids) and malondialdehyde were increased by 59% and twofold, respectively in LDL from metabolic syndrome and type 2 diabetic patients. LDL from metabolic syndrome and type 2 diabetic patients were equally potent in activating the platelet arachidonic acid signalling cascade through increased phosphorylation of p38 mitogen-activated protein kinase and cytosolic phospholipase A(2), and through increased thromboxane B(2) formation. LDL from patients with the metabolic syndrome and type 2 diabetes potentiated platelet aggregation by threefold and 3.5-fold respectively, whereas control LDL had no activating effects on platelets. CONCLUSIONS/INTERPRETATION: The metabolic syndrome in obese patients, without or with diabetes, is associated with increased oxidative stress in LDL, which triggers platelet activation.

The first results demonstrating efficiency and safety of a double-column whole blood method of LDL-apheresis.

LDL-apheresis is a treatment for familial hypercholesterolemia in addition to diet and drug therapy. In the past, LDL-apheresis techniques consisted in separating plasma from blood and adsorbing plasma LDL-C whereas recent methods remove LDL-C directly from whole blood. The whole blood system developed by Kaneka consists of a single-column (Liposorber DL-75) treatment (SCWB) but a double-column whole blood (DCWB) method has recently been developed (Liposorber DL-50 x 2). When 1.6 blood volumes (plus 1l) were processed, acute reductions of total cholesterol and LDL-C were 67.9+/-6% and 80.2+/-4.5%, respectively. The performances of the DCWB method were compared to other LDL-apheresis methods. Assessed in 10 patients, the DCWB method is more efficient than the SCWB method with higher reduction rates of LDL-C (79.7+/-4.9 vs. 68.2+/-5.0% p<0.0001) and apolipoprotein-B (79.5+/-5.4 vs. 67.4+/-5.4% p<0.0001). In a sub group of five patients having the highest LDL-C baseline levels, the LDL-C reduction rates obtained by the DCWB method are equivalent to those obtained by the conventional LDL-apheresis method consisting of preliminary plasma separation followed by plasma LDL-C adsorption and used as first line apheresis therapy (80.5+/-4.5 vs. 79.0+/-5.9%). The safety of DCWB was demonstrated in 12 patients with only a low frequency of mild and transient adverse effects (4%). In conclusion, the DCWB LDL-apheresis method provides efficient removal of LDL-C, a low level of adverse effects, and a shortened duration of the procedure.

Modulation of phenotypic expression of APOA5 Q97X and L242P mutations.

OBJECTIVE: To provide phenotypic and functional data in new patients with APOA5 mutations and to identify genetic and metabolic factors influencing their phenotypic expression. METHODS AND RESULTS: By sequencing APOA5 gene in a cohort of 286 hyperchylomicronemic subjects, free of LPL or APOC2 mutations, we identified 4 unrelated carriers of the Q97X mutation (3 heterozygotes and 1 homozygote) and one heterozygote with a new L242P mutation. Postheparin LPL activity level was reduced by about 50% in Q97X heterozygotes and more than 90% in the Q97X homozygote, but was normal in the L242P patient after resolution of hyperchylomicronemia. Plasma apoAV was undetectable in the Q97X homozygote and in the normal range in the L242P and Q97X heterozygous carriers. In Western blot studies, the association of apoAV with plasma lipoproteins was altered in Q97X heterozygous carriers but not in the L242P carrier. Hyperchylomicronemic heterozygotes for both mutations carried an additional APOA5 variant haplotype and/or APOE variant (E2 or E4). Type 2 diabetes or metabolic syndrome were not a major phenotypic determinant. CONCLUSIONS: The L242P mutation was present in a hyperchylomicronemic proband but its causal involvement remains to be established. The Q97X mutation was clearly involved in hyperchylomicronemia with evidence of concomitant altered intravascular lipolysis, and a complete apoAV deficiency in the homozygote. The phenotypic expression variability of APOA5 mutations was mostly influenced by compound heterozygosity with APOA5 variant haplotypes plus additional genetic factors, and in a lesser extent by the metabolic environment.

[Is there an interaction between sleep-disordered breathing, depression and apolipoprotein E phenotype?]. / Existe-t-il une relation entre syndrome d'apnées du sommeil, dépression et phénotype de l'apolipoprotéine E?

Sleep-disordered breathing (SDB) is widely underdiagnosed among adults. However, SDB may be considered as a public health problem because of clinical consequences for the patient: impaired awake performance, increased risk factor for cardiovascular diseases and increased prevalence of depression. Apolipoprotein E (apoE), a protein involved in lipid metabolism, has 3 major alleles e2, e3 and e4. Recently, it has been shown that apoE e4 allele, a well-known risk factor for cardiovascular diseases, was also associated with SDB. In this study, we assessed a potential interaction between SDB, depression and apoE phenotype. 92 male patients (36-79 years old, mean age 58.0 11.2) consulting in hospital for SDB were enrolled in the study. Each patient had the following exams: 1) overnight polysomnography to determine apnea/hypopnea index (AHI=average number of respiratory events 10 seconds with no breathing per hour). A moderate-to-severe SDB was defined with AHI 15. 2) a psychiatric examination to look for previous or present symptoms of depressive illness. 3) blood sampling to determine apoE genotype (using PCR-RFLP method). In our study, allele frequencies for apoE e2, e3 and e4 were similar to those reported in general population. Among 92 patients, 68 (74%) presented moderate-to-severe SDB and 28 (30%) previous or present symptoms of depressive illness. Our results indicate that: 1) apoE e4 was significantly associated with moderate-to-severe SDB (n=92, p=0.03), 2) scores of apnea-hypopnea index were significantly higher in e4-positive versus e4-negative participants (n=57, p=0,05) and 3) ApoE and depression were not linked. This study confirms a potential interaction between SDB and apoE phenotype, as recently reported. This suggests that e4 allele might be a genetic risk factor for SDB (e4 allele frequency higher in patients with moderate-to-severe SDB versus general population) and/or consequently a deleterious factor for this pathology (increased AHI in e4-positive versus e4-negative patients). Depression might be only one of clinical consequences of SDB. Thus, SDB leads to repeated hypoxemia and numerous awakenings resulting in fatigue and decreased cognitive abilities suitable to the onset of depressive illness in vulnerable persons.

[Should blood samples be drawn on heparin-anticoagulant for lipid analysis?]. / Peut-on prélever le bilan lipidique sur héparine?

Lipid profile is often performed on heparinized-plasma because nothing in particular is explained in the technical data sheet about anticoagulant and because few data (mainly with EDTA anticoagulant) are available in literature. In order to evaluate heparinized-plasma vs serum differences, 50 normo- or hyperlipidemic samples were collected and assayed in 3 clinical laboratories in Lyon on Hitachi analysers with Roche Diagnostic reagents. Lipid values are lower in plasma than in serum; the average negative bias for cholesterol levels is 2 to 4,5% and for triglycerides about 3%, depending on the laboratory; the effect on HDL-cholesterol values is not significant. These results were confirmed by manual procedure on 28 samples with Roche Diagnostic reagent and two similar other reagents (Biomerieux and Randox). A negative bias of 4% on total cholesterol and triglycerides levels is not very important for clinical diagnosis but it is more serious for LDL-cholesterol estimated with Friedewald equation; LDL-cholesterol value needs accuracy because it is a therapeutic goal with statin therapy and an high negative bias (until 0,70 g/L in our results) is unacceptable; moreover, there is a real risk of providing false total cholesterol results. Therefore it is essential to collect blood for lipid profile without any anticoagulant.

Apolipoprotein B48 glycosylation in abetalipoproteinemia and Anderson's disease.

BACKGROUND & AIMS: Abetalipoproteinemia and Anderson's disease are hereditary lipid malabsorption syndromes. In abetalipoproteinemia, lipoprotein assembly is defective because of mutations in the microsomal triglyceride transfer protein. Here, we evaluated the intracellular transport of apolipoprotein B48 to localize the defect in Anderson's disease. METHODS: Asparagine-linked oligosaccharide processing of apolipoprotein B48 in normal and affected individuals was determined by the endoglycosidase H and F sensitivities of the protein after metabolic labeling of intestinal explants in organ culture. Cell ultrastructure was evaluated with electron microscopy. RESULTS: In Anderson's disease as in normal individuals, there was a time-dependent transformation of high mannose endoglycosidase H-sensitive oligosaccharides, of endoplasmic reticulum origin, to complex endoglycosidase H-resistant oligosaccharides, added in the Golgi network. In contrast, despite the translocation of apolipoprotein B48 into the endoplasmic reticulum in patients with abetalipoproteinemia and in biopsies treated with Brefeldin A, which blocks anterograde transport between the endoplasmic reticulum and the Golgi network, there was no transformation of endoglycosidase H-sensitive oligosaccharides. CONCLUSIONS: In abetalipoproteinemia and Anderson's disease, apolipoprotein B48 is completely translocated into the endoplasmic reticulum, but only in Anderson's disease is the protein transported to the Golgi apparatus. This suggests that Anderson's disease is caused by a post-Golgi cargo-specific secretion defect.

[Variation in cholesterol, lipoproteins and triglycerides after heart transplantation in children]. / Variations du cholestérol, des lipoprotéines et des triglycérides après transplantation cardiaque chez l'enfant.

Total cholesterol, HDL and LDL-cholesterol and triglyceride levels may contribute to the development or progression of coronary artery disease of the transplanted heart. The aim of this retrospective study was to determine the short and long-term lipid profiles of transplanted children and to identify factors influencing these dyslipidemias. Twenty-three patients aged 9.5 +/- 5.9 years at cardiac transplantation were followed up for 5.8 +/- 3.1 years. All were on triple therapy with normal diets. The total cholesterol increased by 17% during the first year (4.47 +/- 1.01 mMol/l to 5.25 +/- 1.22 mMol/l at 1 year: p < 0.05) with a peak at 3 months of 5.31 +/- 1.28 mMol/l correlating with the dosage of prescribed corticosteroids. LDL-cholesterol levels increased by 20% during the first year (2.26 +/- 0.67 mMol/l to 3.29 +/- 0.99 mMol/l at 1 year: p = 0.018). HDL-cholesterol levels increased from 1.02 +/- 0.27 mMol/l to a maximum of 1.55 +/- 0.4 mMol/l at 1 year, p < 0.05. Lipoprotein A1, a protecting sub-fraction of HDL, did not change significantly. Changes in triglyceride levels were not significant despite a tendency to hypertriglyceridaemia in the early phases. After one year, serum cholesterol and lipoprotein levels remained higher than the initial values. These results show that cardiac transplant children are exposed to the risk of atherogenic hyperlipidaemia and require systematic lipid profile monitoring, dietary advice and lipid lowering drugs.

Excessive body weight as a new independent risk factor for clinical and pathological progression in primary IgA nephritis.

Experimental evidence suggests a role for obesity in the formation and progression of some glomerular lesions, but data for human glomerulonephritis are lacking. In a cohort of 162 incident patients with biopsy-proven immunoglobulin A (IgA) nephropathy, we assessed whether the presence of an elevated body mass index (BMI >/= 25 kg/m(2)) at the time of the first renal biopsy (RB1) correlated with clinical data at RB1 (24-hour proteinuria, arterial hypertension, and renal function), pathological data (global optical score [GOS] with detailed pathological indices), and clinical progression to both arterial hypertension and chronic renal failure (CRF). In both univariate and multivariate analyses, the presence of an elevated BMI at RB1 was significantly associated with the severity of pathological renal lesions (GOS and vascular, tubular, and interstitial indices). Hypertension-free survival was significantly less in overweight patients (P: < 0.0001) compared with those with normal weight. In a Cox regression analysis for hypertension-free survival including 24-hour proteinuria greater than 1 g, GOS, and metabolic parameters, only elevated BMI and GOS were independent factors for the development of arterial hypertension. CRF-free survival was also significantly less in patients with an excessive BMI. In a multivariate Cox regression analysis for CRF-free survival, hypertension, GOS, and BMI at RB1 were independent risk factors for CRF. In IgA nephropathy, excessive body weight and/or BMI are underestimated predictive factors for the development of arterial hypertension and, ultimately, CRF.

[Hypocholesterolemias: causes and diagnosis]. / Les hypocholestérolémies: causes et diagnostic.

Most of the hypocholesterolemias in adults and children are presented and the non-cardiovascular risk of low serum cholesterol (cancer, depressive illness.) is discussed. A good assessment of hypocholesterolemia is provided by usual laboratory lipid tests (total, HDL- and LDL-cholesterol, apolipoproteins B and A1) and completed by lipid assays of parents in case of familial diseases. The diagnosis of secondary hypocholesterolemias is easy in well-known causes (liver diseases, hyperthyroidism, digestive malabsorption) but less obvious in other cases (fever, traumatism, inflammatory disease); nevertheless, it is necessary to avoid expensive laboratory investigations which will be reserved for severe familial hypocholesterolemias (in order to improve the treatment and the knowledge of these rare diseases); however diagnosis fails in some well-tolerated familial cases.

Decrease in carotid intima-media thickness after one year growth hormone (GH) treatment in adults with GH deficiency.

An increased carotid arterial intima-media thickness (IMT) has been reported in hypopituitary adults untreated for GH deficiency. In the present study, the effect of GH replacement on IMT and cardiovascular risk factors was prospectively investigated, in GH deficiency patients treated at a mean dose of 1 UI/day during 1 yr (n = 22) and 2 yr (n = 11). The IMT measurements were performed by the same experienced physician, and the coefficient of variation (calculated in two control groups) was below 6.5%. IMT at baseline was related to conventional risk factors. After 1 yr GH treatment, IMT decreased from 0.78 +/- 0.03 mm to 0.70 +/- 0.03 mm (P < 0.001). The decrement was observed in 21 of 22 patients. After 2 yr GH treatment, IMT had stabilized at 0.70 +/- 0.04 mm and remained significantly different from baseline values (P < 0.003). GH treatment resulted in a moderate decrease in waist circumference and body fat mass and an increase in VO2 max. Conventional cardiovascular risk factors were unmodified except for a transient 10% decrease in low-density lipoprotein cholesterol at 6 months. The contrast between the limited metabolic effect of treatment and the importance and precocity of the changes in IMT suggests that the decrease in IMT was not exclusively attributable to a reversal in the atherosclerotic process. A direct parietal effect of GH replacement on the arterial wall might also be involved. The consequences, in terms of cardiovascular risk, should be established by randomized prospective trials.

[Early manifestations of Tangier disease]. / Les manifestations précoces de la maladie de Tangier.

BACKGROUND: The diagnosis of Tangier disease in childhood is based on the specific aspect of tonsils or by screening relatives of affected subjects. CASE REPORT: A moderately enlarged liver associated with splenomegaly was found upon routine physical examination of a 3 month-old breast-fed boy, born in Turkey from consanguineous parents. Laboratory studies disclosed moderate increase in serum alanine aminotransferase activity (ALAT 52 UI/l, N < 30). The diagnosis of Tangier disease was confirmed by studies of plasma cholesterol and apolipoprotein A. By 8 months of age, the patient had enlarged orange tonsils. Small cervical, axillary and inguinal lymphadenopathies were present. The tonsilar and adenoidal tissues were removed at 18 months of age because the patient suffered from chronic airway obstruction. Colonoscopic examination revealed tiny flat orange spots, 1 to 2 mm in diameter, scattered throughout the rectosigmoidal and colonic mucosa. Survey of the family led to the discovery of one sister, with asymptomatic apolipoprotein Al deficiency and a normal sister, while the parents were heterozygotes for Tangier disease. CONCLUSION: Enlarged liver associated with a moderate level in serum aminotransferase may be an early manifestation of Tangier disease in infants. Rectosigmoidal and colonic lesions may be convenient for biopsy when tonsillectomy is not indicated.

High blood pressure and metabolic disorders are associated in the Lyon hypertensive rat.

OBJECTIVE: A large population of F2 rats, obtained from a cross between male Lyon hypertensive (LH) rats and female Lyon normotensive (LN) rats, was studied in order to assess the relationship between increased body weight, hyperlipidaemia and high blood pressure which characterize LH rats. METHODS: Mean arterial pressure (MAP) was recorded in male, conscious, freely moving LH, LN, F1 and F2 rats aged 30 weeks. Plasma total cholesterol, high-density lipoprotein-, low-density lipoprotein- and very low-density lipoprotein-cholesterol, phospholipids, triglycerides, insulin and glucose were measured. RESULTS: In the F2 cohort it was observed that high MAP was a recessive trait that depends on several genes and was unrelated to body weight. The left ventricular weight, corrected for tibia length, was correlated with MAP. Plasma total and high-density lipoprotein-cholesterol and phospholipids concentrations were lower in the F1 rats than in the LN rats, suggesting an overdominance of the LN alleles. In the F2 rats MAP was related to total, high-density lipoprotein- and low-density lipoprotein-cholesterol. Plasma triglycerides, insulin and the insulin:glucose ratio, which were higher in the LH rats than in the LN rats, were also correlated with MAP in the F2 cohort. Using stepwise multiple regression analysis, MAP remained correlated with plasma total cholesterol, insulin and the insulin:glucose ratio, but not with triglycerides. CONCLUSIONS: Hypertension in LH rats is a recessive trait that is independent of body weight. In addition, the cosegregation of blood pressure with plasma cholesterol and, to a lesser degree, with insulin levels, which was observed in the present study provides the first direct evidence that these phenotypes are associated and are not due simply to genetic drift in the Lyon model.

Apolipoprotein E phenotyping by isoelectric focusing in immobilized pH gradients and silver staining.

A simple and high resolution procedure of apoprotein E (apo E) phenotyping by isoelectric focusing with immobilized pH gradients and silver staining is described. This method needs delipidated very low density lipoproteins (isolated from 1 mL of serum) but obviates immunoblotting as well as neuraminidase treatment in routine applications because the sialylated forms are clearly separated. Immunoblotting (with polyclonal and monoclonal anti-apo E antiserum), cysteamine and neuraminidase treatment, and pI markers allowed the localization of three main alleles, xi 2, xi 3, xi 4 and the detection of variants or rare alleles (6/450 determinations). The serum amyloid A (SAA) apolipoproteins (SAA1,SAA2) could be characterized unequivocally (especially with E3 and E4). Silver staining proved more sensitive than Coomassie Brilliant Blue and needs only 5 micrograms of protein in the sample. The results of 403 normo-or hyperlipidemic patients are shown. In the group of 191 normolipidemic patients (cholesterol less than 6.40 mmol/L triglycerides less than 2 mmol/L), the relative frequency of the xi 3 allele (0.83) is higher than in other reports on Caucasians (about 0.77) whereas the xi 4 allele is lower. As previously described, we find a high frequency of the 4/3 phenotype in hypercholesterolemia and 3/2 in hypertriglyceridemia. The high frequency of the E2/E2 phenotype, usually associated with hyperlipidemia, and variants in complex hypertriglyceridemia makes the apo E phenotyping necessary in many cases of dyslipidemias.

[Relation of alcohol consumption and blood lipids and apolipoproteins--a study of a population of 3,897 wage-earners from the Lyon region]. / Relations entre consommation d'alcool, et lipides et apolipoprotéines sériques--étude dans une population de 3,897 salariés de la région lyonnaise.

Between June 1982, and September 1984, a survey was conducted among 3,897 employees in the Region of Lyon to study the relationship between alcohol consumption and serum concentrations of total cholesterol and triglycerides. In 400 randomly selected men, the following data were also obtained: concentrations of the cholesterol of the high density lipoproteins (HDL) and of their subfractions, and concentrations of the apoproteins A-I, A-II and B. All these biochemical concentrations increased, more or less, with alcohol consumption. Relative to non drinkers, the concentrations increased among males who declared drinking more than 80 grams of alcohol per day: for total cholesterol, by 10.0%; for triglycerides, by 24.7%; for HDL-cholesterol, by 26.7%; for HDL2-cholesterol, by 76.0%; for HDL3-cholesterol, by 15.0%; for apoprotein A-I, by 30.0%; for apoprotein A-II, by 52.2%; for apoprotein B, by 5.1%. These results, with the limitations inherent in a cross-sectional study, suggest that regular consumption of alcohol raises the concentrations of blood lipid components, both atherogenic and non-atherogenic.

[Lecithin cholesterol acyltransferase (LCAT) and lipid cardiovascular risk factors in hemodialysis patients]. / Lécithine cholestérol acyltransférase (LCAT) et facteurs lipidiques de risque cardiovasculaire chez les hémodialysés.

In order to study the reliability of plasma LCAT activity as a marker of cardiovascular risk, we compared 66 chronic hemodialysis patients with a control group (n = 72) and a coronary artery disease (CAD) patients group (n = 46). The decrease of LCAT activity (measured by the Nagasaki method) did not appear as a marker of CAD risk; if this activity was effectively lower in 51 of the hemodialysis patients (p less than 0.001) than in the patients of the control group, it was higher in CAD patients (p less than 0.001). In the remaining 15 hemodialysis patients, we found an almost undetectable LCAT activity, not accompanied by a change in esterification percentage when compared with the other hemodialysis patients; the mixing of these serums with control group restored an enzymatic activity and excludes the presence of an inhibitor. The only risk factors common to hemodialysis and CAD patients was the decrease of HDL cholesterol and the high frequency of combined hyperlipoproteinemia.

Swim training in genetically hypertensive rats of the Lyon strain: effects on plasma lipids and lipoproteins.

We studied the effects of training by forced swimming on plasma lipid and lipoprotein concentrations in the Lyon genetically hypertensive rats (LH), its normotensive (LN) and low blood pressure (LL) controls. Training was carried out 5 days a week for 5 weeks. The duration of daily training sessions was increased 15 min per day, from 2 to 6 h/day. Following training low density lipoprotein-cholesterol (LDL-C) was significantly lower (P less than 0.01) in LL, and the very low density lipoprotein (VLDL-C) was also lower in LN (P less than 0.01) and LH (P less than 0.05) rats compared with their sedentary controls. High density lipoprotein-cholesterol (HDL-C) was not significantly increased after training in all strains. Compared with controls, plasma total cholesterol, plasma triglycerides and phospholipids were not modified by training. The reduction of LDL-C, VLDL-C as well as the increase of the HDL-C:VLDL-C ratio suggest a beneficial effect of training on atherosclerosis and perhaps coronary heart disease risk.

Plasma lipoproteins and fatty acid composition after "minipill".

A study of the effect of a low-dose oral contraceptive, Adepal (ethinyl estradiol and levonorgestrel, 30 and 150 micrograms on the 5th to 12th, 40 and 200 micrograms on the 13th to 28th, respectively) on the blood lipids, lipoproteins and fatty acid composition has been conducted on 13 young women before and after six months of treatment. All together, total cholesterol concentration did not vary; however, the high cholesterol values decreased whereas the low cholesterol values increased with the pill. Triglyceride levels increased significantly (p less than 0.001). High density lipoprotein (HDL)-cholesterol decreased clearly (p less than 0.001) regardless of the cholesterol value at the beginning; low and very low density lipoprotein (LDL + VLDL)-cholesterol increased slightly, as well as the apoprotein B (Apo B) concentration (p less than 0.05). The lipoprotein electrophoresis showed intermediate bands (IDL) in 5/12 of the women after treatment. The three major classes of lipoprotein showed some variations in the fatty acid composition after the oral contraceptive; in any lipid class from any lipoprotein, the linoleic (18: 1 omega 6), arachidonic (20: 4 omega 6) and eicosapentaenoic (20: 5 omega 3) acids decreased whereas the palmitic (16: 0) and oleic (18: 1 omega 9) acids increased. Our results suggest that a low-dose contraceptive like Adepal produces, nevertheless, some significative modifications of plasma lipids and lipoproteins.

PIP: A study of the effect of a low-dose oral contraceptive (OC; Adepal--ethinyl estradiol and levonorgestrel), given in doses of 30 and 150 mcg on days 5-12, 40 and 200 mcg on days 13-28, on blood lipids, lipoproteins, and fatty acid composition has been conducted on 13 young women before and after 6 months of treatment. All together, total cholesterol concentration did not vary; however, the high cholesterol values decreased whereas the low cholesterol values increased with the pill. Triglyceride levels increased significantly (p0.001). High density lipoprotein-cholesterol decreased clearly (p0.001), regardless of the cholesterol value at the beginning; low and very low density lipoprotein-cholesterol increased slightly, as well as the apoprotein B concentration (p0.05). The lipoprotein electrophoresis showed intermediate bands in 5/12 of the women after treatment. The 3 major classes of lipoprotein showed some variations in the fatty acid composition after the OC; in any lipid class from any lipoprotein, the linoleic acid (18: 1 omega 6), arachidonic (20: 4 omega 6), and eicosapentaenoic (20: 5 omega 3) acids decreased whereas the palmitic (16: 0) and oleic (18: 1 omega 9) acids increased. Results suggest that a low-dose contraceptive like Adepal produces, nevertheless, some significant modifications in plasma lipids and lipoproteins.