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Search Results: 1 - 10 of 191286 matches for " Genovefa D. Kolovou "
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Platelet activating factor levels and metabolism in tangier disease: a case study
Vana Kolovou, Vasiliki D Papakonstantinou, George Stamatakis, Sophia N Verouti, Marianna N Xanthopoulou, Genovefa Kolovou, Constantinos A Demopoulos
Lipids in Health and Disease , 2012, DOI: 10.1186/1476-511x-11-89
Abstract: The EC50 value of PRP was measured by an aggregometer. The determination of the specific activity of PAF-CPT and Lyso-PAF-AT was made after in vitro enzymatic assay, chromatographic separation and measurement of the produced PAF in a biological assay with washed rabbit platelets. The determination of PAF-AH and Lp-PLA2 was made after an in vitro enzymatic assay from the decay of radioactive PAF.The TD patient had lower bound-PAF values in blood, decreased specific activity of PAF-CPT and Lyso-PAF-AT, increased specific activity of PAF-AH in platelets and leukocytes and Lp-PLA2 activity in plasma compared to healthy women. The EC50 of PAF and Thrombin were higher compared to healthy women.The increased Lp-PLA2 activity, as well as, the decreased activities of PAF-CPT and Lyso-PAF-AT, explain the decreased bound-PAF level in TD patient and the EC50 of PAF. However, total PAF is in a normal range and this probably can explain one of the reasons this TD patient has no CAD.
Severe/Extreme Hypertriglyceridemia and LDL Apheretic Treatment: Review of the Literature, Original Findings
Olga Diakoumakou,Georgios Hatzigeorgiou,Nikos Gontoras,Maria Boutsikou,Vana Kolovou,Sophie Mavrogeni,Vassiliki Giannakopoulou,Genovefa D. Kolovou
Cholesterol , 2014, DOI: 10.1155/2014/109263
Abstract: Hypertriglyceridemia (HTG) is a feature of numerous metabolic disorders including dyslipidemias, metabolic syndrome, and diabetes mellitus type 2 and can increase the risk of premature coronary artery disease. HTG may also be due to genetic factors (called primary HTG) and particularly the severe/extreme HTG (SEHTG), which is a usually rare genetic disorder. Even rarer are secondary cases of SEHTG caused by autoimmune disease. This review considers the causes of SEHTG, and their management including treatment with low density lipoprotein apheresis and analyzes the original findings. 1. Introduction A positive correlation between high triglycerides (TGs) concentration and coronary heart disease (CHD) has been established in numerous studies [1–11]. Hypertriglyceridemia (HTG) is prevalent in 18.6% of men and 4.2% of women between 16 and 65 years of age. The Adult Treatment Panel (ATP) III guidelines, published 13 years ago [12], described normal TGs concentration <150?mg/dL (<1.6?mmol/L), borderline-high TGs as 150 to 199?mg/dL (1.6–2.2?mmol/L), high TGs as 200 to 499?mg/dL (2.2–5.6?mmol/L), and very high TGs as >500?mg/dL (>5.6?mmol/L). However, severe/extreme hypertriglyceridemia (SEHTG) should be considered when values are greater than 1,000?mg/dL (11.2?mmol/L) because this places individuals at significant increased risk of pancreatitis. With TG values less than 1,000?mg/dL (5.6?mmol/L) one should be focused on the risk of premature CHD [13]. HTG is a feature of numerous metabolic disorders including dyslipidemias, metabolic syndrome, and diabetes mellitus type 2 (DMT2) and can increase the risk of premature CHD [14, 15]. These metabolic disorders may be caused by interactions between genetic and nongenetic factors since those subjects present usually similar clinical features (android type of obesity, ectopic fat deposition, thin arms and legs, increased waist circumference, upper body obesity, and in case of SEHTG eruptive xanthomas) [16, 17]. Visceral fat is considered to behave as ectopic fat deposition. It accumulates TGs in cases when body fat storage exceeds the capacity of fat stores. Furthermore, subjects with HTG usually present insulin resistance, hepatic steatosis, and DMT2. Thus, all the above can be called “hypertriglyceridemic phenotype.” Additionally, several studies (including ours) showed that postprandial HTG is manifested in subjects with hypertriglyceridemic phenotype [18]. HTG may also be due to genetic factors (called primary HTG) and particularly the SEHTG, which is a usually rare genetic disorder. Even rarer are secondary
Low fasting low high-density lipoprotein and postprandial lipemia
Genovefa D Kolovou, Katherine K Anagnostopoulou, Nektarios Pilatis, Nikolaos Kafaltis, Konstandina Sorodila, Eleftherios Psarros, Dennis V Cokkinos
Lipids in Health and Disease , 2004, DOI: 10.1186/1476-511x-3-18
Abstract: Fifty two Greek men were divided into 2 main groups: a) the low HDL group (HDL < 40 mg/dl), and b) the control group. Both groups were further matched according to fasting TG (matched-low HDL, and matched-control groups). The fasting TG concentrations were higher in the low HDL group compared to controls (p = 0.002). The low HDL group had significantly higher TG at 4, 6 and 8 h postprandially compared to the controls (p = 0.006, p = 0.002, and p < 0.001, respectively). The matched-low HDL group revealed higher TG only at 8 h postprandially (p = 0.017) compared to the matched-control group. ROC analysis showed that fasting TG ≥ 121 mg/dl have 100% sensitivity and 81% specificity for an abnormal TG response (auc = 0.962, p < 0.001).The delayed TG clearance postprandially seems to result in low HDL cholesterol even in subjects with low fasting TG. The fasting TG > 121 mg/dl are predictable for abnormal response to fatty meal.The hypothesis that low levels of high density lipoprotein (HDL) cholesterol is associated with coronary heart disease (CHD), raised since the 1950s [1]. Fifty years later, it was well-established [2,3] as it has been excellently proved after a number of large prospective studies [4,5]. In the PROCAM Study [6] 45% of men and women who developed CHD had an HDL cholesterol lower than 35 mg/dl. In the Framingham Heart Study, total cholesterol levels did not provide a predictive value in identifying people at risk for CHD compared to cholesterol/HDL ratio [7]. Furthermore, a change in ratio is better predictor for successful CHD risk reduction than changes in total cholesterol levels. There is no longer any doubt that HDL cholesterol is a powerful independent inverse predictor of CHD. On the other hand, the long duration of the postprandial lipemia and repetition of meals during the daytime leads to important changes of lipoproteins postprandially. Studies have shown that disturbed postprandial lipemia is found in patients with CHD [8,9] and other cond
Postprandial lipemia in men with metabolic syndrome, hypertensives and healthy subjects
Genovefa D Kolovou, Katherine K Anagnostopoulou, Antonis N Pavlidis, Klelia D Salpea, Stella A Iraklianou, Konstantinos Tsarpalis, Dimitris S Damaskos, Athanasios Manolis, Dennis V Cokkinos
Lipids in Health and Disease , 2005, DOI: 10.1186/1476-511x-4-21
Abstract: OFTT was given to 33 men with MetS (defined by the Adult Treatment Panel III), 17 HTN and 14 healthy men. The MetS group was further divided according to fasting triglycerides (TG) into TG ≥ 150 [MetS+TG, (n = 22)] or <150 mg/dl [MetS-TG (n = 11)], and into those with or without hypertension [MetS+HTN (n = 24), MetS-HTN (n = 9), respectively]. TG concentrations were measured before and at 4, 6 and 8 h after OFTT and the postprandial response was quantified using the area under the curve (AUC) for TG.The postprandial response was significantly higher in MetS compared to HTN and healthy men [AUC (SD) in mg/dl/h; 2534 ± 1016 vs. 1620 ± 494 and 1019 ± 280, respectively, p ≤ 0.001]. The TG levels were increased significantly in MetS+TG compared to MetS-TG subjects at 4 (p = 0.022), 6 (p < 0.001) and 8 hours (p < 0.001). The TG were increased significantly in MetS-TG compared to healthy subjects at 4 (p = 0.011), 6 (p = 0.001) and 8 hours (p = 0.015). In linear regression analysis only fasting TG levels were a significant predictor of the AUC (Coefficient B = 8.462, p < 0.001).Fasting TG concentration is the main determinant of postprandial lipemia. However, an exaggeration of TG postprandialy was found in normotriglyceridemic MetS and HTN compared to healthy subjects. This suggests that intervention to lower fasting TG levels should be recommended in MetS subjects.In 1988, Reaven et al. proposed insulin resistance as the underlying metabolic aberration linking essential hypertension (HTN), dyslipidemia, type 2 diabetes and other abnormalities associated with an increased risk of atherosclerotic cardiovascular disease in adults [1]. This constellation is now designated as the metabolic syndrome (Mets). Since then, many epidemiological studies have shown that MetS is associated with an increased incidence of coronary heart disease (CHD) [2,3]. MetS is clinically characterized by the presence of abnormal fasting triglyceride (TG) levels, low high-density lipoprotein (HDL) c
Sex-associated effect of CETP and LPL polymorphisms on postprandial lipids in familial hypercholesterolaemia
Katherine K Anagnostopoulou, Genovefa D Kolovou, Peggy M Kostakou, Constantinos Mihas, Georgios Hatzigeorgiou, Christina Marvaki, Dimitrios Degiannis, Dimitri P Mikhailidis, Dennis V Cokkinos
Lipids in Health and Disease , 2009, DOI: 10.1186/1476-511x-8-24
Abstract: We selected and genotyped 80 men and postmenopausal women heterozygous for familial hypercholesterolaemia (main group) as well as 11 healthy control subjects. Patients were subgrouped based on their response to oral fat tolerance test. The oral fat tolerance test was defined as pathological when postprandial triglyceride concentration was higher than the highest triglyceride concentration observed in healthy subjects (220 mg/dl) at any time (2, 4, 6 or 8 h).In the pathological subgroup, men had significantly higher incremental area under the curve after oral fat tolerance test than postmenopausal women. Furthermore, multivariate analysis revealed a gender association of TaqIB and I405V influence on postprandial lipaemia in this subgroup.In conclusion, it seems that gender and TaqIB polymorphism of the cholesteryl ester transfer protein gene were both associated with the distribution of triglyceride values after oral fat tolerance test, only in subjects with a pathological response to oral fat tolerance test. Specifically, men carrying the B2 allele of the TaqIB polymorphism showed a higher postprandial triglyceride peak and a delayed return to basal values compared with women carrying B2. However, further investigations in larger populations are required to replicate and confirm these findings.The mechanisms that control the cholesteryl ester transfer protein (CETP) have attracted attention, since plasma CETP concentration is associated with increased risk for premature atherosclerosis [1]. The CETP concentration and activity in plasma is dependent on several factors such as environmental components including dietary cholesterol [2], alcohol [3], smoking and obesity [4], gender [5], and genetic influence (e.g. polymorphism of CETP gene) [6-8]. CETP plays a major role in the remodeling of lipoprotein particles by mediating the transfer of high density lipoprotein (HDL) cholesteryl esters. When the level of triglyceride (TG)-rich lipoproteins is normal, CETP transfers
Association of gender, ABCA1 gene polymorphisms and lipid profile in Greek young nurses
Vana Kolovou, Apostolia Marvaki, Agathi Karakosta, Georgios Vasilopoulos, Antonia Kalogiani, Sophie Mavrogeni, Dimitrios Degiannis, Christina Marvaki, Genovefa Kolovou
Lipids in Health and Disease , 2012, DOI: 10.1186/1476-511x-11-62
Abstract: The study population consisted of 447 (87 men) unrelated nurses who were genotyped for ABCA1 gene polymorphisms. Additionally, lipid profile [total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol (LDL-C) and apolipoprotein A1] was evaluated.The distribution of all three studied ABCA1 gene polymorphisms did not differ according to gender. However, only R219K genotype distribution bared borderline statistical significance (p?=?0.08) between the two studied groups. Moreover, allele frequencies of R219K, R1587K and I88M polymorphisms did not differ according to gender. In general, blood lipid levels did not seem to vary according to ABCA1 gene polymorphisms, when testing all subjects or when testing only men or only women. However, a significant difference of LDL-C distribution was detected in all subjects according to R1587K genotype, indicating lower LDL-C levels with KK polymorphism (p?=?0.0025). The above difference was solely detected on female population (p?=?0.0053).The ABCA1 gene polymorphisms frequency, distribution and lipid profile did not differ according to gender. However, in the female population the KK genotype of R1587K gene indicated lower LDL-C levels. Further studies, involving a higher number of individuals, are required to clarify genes and gender contribution.ATP-binding cassette transporter A1 (ABCA1) mediates the transport of cholesterol and phospholipids from cells to lipid-poor apolipoproteins. Animals and human studies documented that defects in the ABCA1 pathway are significant determinants of coronary artery disease (CAD) [1]. Inactivation of ABCA1 gene in macrophages increases atherosclerotic lesions in hyperlipidemic mice [2,3], and overexpressing human ABCA1 in transgenic mice retards atherogenesis [4,5]. The ABCA1 gene is located on the chromosome 9 in the area 9q31.1 and encodes ABCA1 protein. ABCA1 protein is expressed in liver, macrophages, intestines, lungs etc. Several ABCA1 gen
ATP-binding cassette transporter A1 gene polymorphisms and serum lipid levels in young Greek nurses
Vana Kolovou, Genovefa Kolovou, Apostolia Marvaki, Agathi Karakosta, Georgios Vasilopoulos, Antonia Kalogiani, Dimitrios Degiannis, Christina Marvaki, Constantinos A Demopoulos
Lipids in Health and Disease , 2011, DOI: 10.1186/1476-511x-10-56
Abstract: The study population consisted of 308 unrelated nurses who were genotyped and the ABCA1 polymorphisms were detected. Additionally, lipid profile [total cholesterol (TC), triglycerides (TGs), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and apolipoprotein (apo) A] was evaluated.There was no difference in the genotypic and allelic frequencies of the R219K polymorphism according to lipid profile. The R1587K genotypes differed significantly according to TC, LDL-C and TGs concentration (p = 0.023, p = 0.014 and p = 0.047, respectively). Particularly, significant difference in TC, LDL-C and TGs concentration was detected between RK and RR genotypes (p = 0.006, p = 0.004, p = 0.014, respectively). Women with RK genotype compared to RR genotype had higher concentration of TGs (134.25 mg/dl vs 108.89 mg/dl, p = 0.014, respectively), total cholesterol (207.41 mg/dl vs 187.69 mg/dl, p = 0.006, respectively), and LDL-C (110.6 mg/dl vs 96.9 mg/dl, p = 0.004, respectively).These findings suggest that the R1587K polymorphism of ABCA1 gene was associated with lipid profile of Greek nurses. Women with RK genotype had higher TGs, total and LDL-C concentration compared to RR genotype. These observations may be significant in assessing the risk of CAD since a 1% change in LDL-C is associated with a 1% change of cardiovascular events. Also, TGs concentration were documented to play a significant role in women. However, this needs to be confirmed by larger studies.The ATP-binding cassette transporter A1 (ABCA1) acts as a vehicle for cellular cholesterol which after crossing cell membrane bounds to acceptor molecule such as apolipoprotein (apo) A [1-3]. Thus, ABCA1 influences the initial steps in high density lipoprotein (HDL) formation and in reverse cholesterol transport. The ABCA1 protein belongs to ABC proteins family, which are ingredients of biological membranes and use ATP to transfer various particles such as lipids [1]. The ABCA1 prote
The role of common variants of the cholesteryl ester transfer protein gene in left main coronary artery disease
Genovefa Kolovou, Ioannis Vasiliadis, Vana Kolovou, Agathi Karakosta, Sophie Mavrogeni, Evaggelia Papadopoulou, Spiridon Papamentzelopoulos, Vasiliki Giannakopoulou, Apostolia Marvaki, Dimitrios Degiannis, Helen Bilianou
Lipids in Health and Disease , 2011, DOI: 10.1186/1476-511x-10-156
Abstract: The DNA of 471 subjects [133 subjects with angiographically documented left main coronary artery disease (LMCAD), 241 subjects with more peripheral coronary artery disease (MPCAD) and 97 subjects self reported healthy (Controls)] was analyzed for the frequency of TaqIB and I405V polymorphisms in the gene coding CETP.There is no significant difference in CETP allele frequency or genotype distribution among LMCAD and MPCAD patients although there is statistical difference between LMCAD and Controls (p = 0.001). Specifically, patients with LMCAD and B1B1 genotype of TaqIB polymorphism were more frequent present compared to Controls (33.8% vs 22.9%, respectively). The frequency of B2B2 genotype was 3 times lower in the LMCAD group compared to Controls (10.5% vs 30.2%, respectively). In the LMCAD group the frequency of B1 allele compared to Controls was higher (62% vs 46%, respectively, p = 0.001). The relationship between TaqIB gene polymorphism and the LMCAD was independent of lipid profile, with the exception of apolipoprotein A.These findings indicate that the TaqIB polymorphism may have potential importance in screening individuals at high risk for developing CAD. However, this polymorphism cannot distinguish between LMCAD and MPCAD. Further prospective investigations in larger populations are required to confirm these findings.The evolution of coronary artery disease (CAD) is influenced by various genetic and environmental factors. The genetic contribution is documented by a positive family history for myocardial infarction and is considered to be a strong cardiovascular risk factor [1,2]. This has been supported even after adjustment for classical risk factors such as diabetes mellitus, dyslipidemia, hypertension and others [3-5]. Furthermore, the level of high density lipoprotein cholesterol (HDL-C) in plasma is a major determinant of susceptibility to coronary atherosclerosis [6-8]. Genetic studies have recognized the impact of genetic mutations on plasma HDL-C
Changes in Lipids and Lipoproteins after Selective LDL Apheresis (7-Year Experience)
Genovefa Kolovou,Georgios Hatzigeorgiou,Constantinos Mihas,Nikos Gontoras,Panagiotis Litras,Dimitris Devekousos,Panagiota Kontodima,Constantina Sorontila,Helen Bilianou,Sophie Mavrogeni
Cholesterol , 2012, DOI: 10.1155/2012/976578
Abstract: Background. The aim of the study was to investigate the changes in plasma lipids and lipoproteins and the cardiovascular events after selective LDL apheresis. Methods and Results. Two pediatric patients with familial hypercholesterolemia aged 11 and 13 years and 19 dyslipidemic adults aged 41 ± 14 years underwent direct adsorption of lipoproteins (DALI) sessions. The mean follow-up period was 47 ± 23 months. The total cholesterol (TC) values before and after treatment were 8.2 ± 2.2 and 3.1 ± 1.6 mmol/l (318 ± 86 and 122 ± 62 mg/dL), respectively. The interval mean of TC was 6.9 ± 1.9 mmol/l (268 ± 75 mg/dL). The LDL cholesterol concentrations before and after treatment were 6.6 ± 2.1 and 1.7 ± 1.1 mmol/l, (256 ± 82 mg/dL and 65 ± 41 mg/dL), respectively. The percentage of acute LDL cholesterol reduction was 75 ± 11%. Cardiovascular events were observed in seven patients. The average annual event rate was 5.51%. Conclusion. LDL apheresis is a very important therapeutic tool in managing patients at high risk for premature CAD or with aggressive CAD, despite adequate medical treatment.
Changes in Lipids and Lipoproteins after Selective LDL Apheresis (7-Year Experience)
Genovefa Kolovou,Georgios Hatzigeorgiou,Constantinos Mihas,Nikos Gontoras,Panagiotis Litras,Dimitris Devekousos,Panagiota Kontodima,Constantina Sorontila,Helen Bilianou,Sophie Mavrogeni
Cholesterol , 2012, DOI: 10.1155/2012/976578
Abstract: Background. The aim of the study was to investigate the changes in plasma lipids and lipoproteins and the cardiovascular events after selective LDL apheresis. Methods and Results. Two pediatric patients with familial hypercholesterolemia aged 11 and 13 years and 19 dyslipidemic adults aged 41?±?14 years underwent direct adsorption of lipoproteins (DALI) sessions. The mean follow-up period was 47?±?23 months. The total cholesterol (TC) values before and after treatment were 8.2?±?2.2 and 3.1?±?1.6?mmol/l (318?±?86 and 122?±?62?mg/dL), respectively. The interval mean of TC was 6.9?±?1.9?mmol/l (268?±?75?mg/dL). The LDL cholesterol concentrations before and after treatment were 6.6?±?2.1 and 1.7?±?1.1?mmol/l, (256?±?82?mg/dL and 65?±?41?mg/dL), respectively. The percentage of acute LDL cholesterol reduction was 75?±?11%. Cardiovascular events were observed in seven patients. The average annual event rate was 5.51%. Conclusion. LDL apheresis is a very important therapeutic tool in managing patients at high risk for premature CAD or with aggressive CAD, despite adequate medical treatment. 1. Introduction The relationship between serum cholesterol and the risk of cardiovascular disease has been firmly established. For more than 2 decades, multiple clinical trials have documented the cardiovascular benefit of lowering low-density lipoprotein (LDL) cholesterol. Familial hypercholesterolemia (FH) is one of the most common genetic disorders, characterized by increased levels of LDL cholesterol, tendons’ xanthomas, and premature atherosclerosis [1]. The frequency of heterozygous (hFH) in most populations is 1 in 500 births with exceptions in Christian Lebanese, where is 1 in 170 births, Afrikaner 1 in 70–100 births, and French Canadian ancestries 1 in 200 births [1, 2]. The homozygous (HFH) is very rare (1 in 1000000 births) with symptoms presenting during childhood and early death due to coronary artery disease (CAD). Approximately 22000 individuals in Greece are assumed to be hFH, with the majority of them being undiagnosed. FH can be caused by mutations in LDL receptor gene (LDLR), the apolipoprotein B-100 gene (APOB), and the protein convertase subtilisin/kexin type 9 (PCSK9) [3, 4]. Worldwide, more than 1200 mutations of LDLR gene have been reported [5]. The clinical diagnosis of FH is based on various diagnostic criteria such as Simon Broome, Dutch, and Great Britain [6, 7]. The identification and treatment of affected individuals is very important matter, since it has been documented that there is a significant reduction of morbidity and mortality with the
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