Biomedical subjects

Evelin Katona

Publications and source records attributed to Evelin Katona.

9 recordsLinked to original sources

PubMed2006

Orlistat increases serum paraoxonase activity in obese patients.

BACKGROUND AND AIM: Previous studies have demonstrated that oxidative stress is increased in obese patients. The high-density lipoprotein (HDL) associated human paraoxonase 1 (PON1) can inhibit low-density lipoprotein oxidation and has an antiatherogenic effect. Our objective was to assess the effects of orlistat therapy combined with diet on body mass index (BMI), waist circumference, lipid parameters, blood pressure, serum glucose level and PON1 activity. METHODS AND RESULTS: A longitudinal, multicenter, randomized study with and without orlistat treatment was performed. One hundred thirty nine otherwise healthy, obese subjects were divided in to two groups: 78 persons received orlistat (120 mg three times a day) combined with diet while 61 persons were kept on diet only. Anthropometrical parameters, serum lipid levels and PON1 activity were measured at baseline and after 6 months of treatment. BMI and waist circumference were reduced more pronouncedly in the orlistat group than in the control group. Patients receiving orlistat also had significantly greater improvements in fasting blood glucose levels and blood pressure. The orlistat-treated group showed a greater reduction in total cholesterol and triglyceride levels. In addition, the serum PON1 activity in these patients was significantly increased compared to the diet-only group. CONCLUSIONS: The 6-month treatment with orlistat had a beneficial effect on the lipid profile and improved the antioxidant status by increasing serum PON1 activity. However, because of the limited therapeutic effectiveness, obese patients with hypercholesterolemia should receive additional lipid lowering medications.

Adult↗

PubMed2006

[A practicing physician's view on obesity].

Overweight and obesity are worldwide problems, its health and psychosocial burden on the individual and on society are tremendous. Diagnosing obesity is rather easy, and is based on simple anthropometric measurements, such as body weight, height and waist circumference. The different classes of obesity are determined by body mass index, which, together with waist circumference and comorbid conditions and other risk factors determine the individual risk for mortality and morbidity. Obesity is due to genetic and environmental factors, mainly is the consequence of excess calorie intake and sedentary lifestyle. The fat mass of the body is under neuroendocrine control, the central controller is the hypothalamus. Leptin, produced by adipocytes in proportion to fat mass, is the afferent signal to the hypothalamus. Decreasing or increasing levels of leptin result in orexigen and anorexigen neurotransmission, which mediate efferent activation towards food consumption and energy storage, or towards food restriction and energy expenditure, respectively. The balance of these events and/or the ,set point" of the controller--if leptin resistance is present--is shifted towards higher body/fat mass in obesity. Management of obesity is complex, however, in all stages of obesity lifestyle changes are mandatory--including diet, exercise and behavior modification. Pharmacotherapy might be needed if lifestyle changes alone do not result an acceptable weight loss. For the long-term treatment of obesity sibutramin and orlistat are the available approved drugs. In case of morbid obesity (body mass index > 40 kg/m2, or > 35 kg/m2 plus comorbid conditions and other risk factors) surgery might be the treatment of choice. There are different surgical methods, among those a widely used method nowadays is the laparoscopic adjustable gastric banding procedure.

Algorithms↗

PubMed2005

Identification of a novel deletion in the ABCC6 gene leading to Pseudoxanthoma elasticum.

BACKGROUND: Pseudoxanthoma elasticum (PXE) is an inherited systemic disorder, characterized by dermal, ocular and cardiovascular lesions. Genetic defects of the ABCC6 (MRP6) transporter are known to cause PXE. OBJECTIVES: The purpose of this study was to identify the genetic background of a PXE patient with a very early onset of the disease and severe systemic involvement. METHODS: Direct sequencing of genomic DNA obtained from peripheral whole blood. RESULTS: Our patient was found to be compound heterozygous with both ABCC6 alleles having genomic deletions. A novel exon 24-25 deletion was identified on one allele, while the frequently observed exon 23-29 deletion was found on the other allele. The novel deletion is 4.68 kb long and was shown to extend from intron 23 to 25. DNA-sequencing of a 2.03 kb fusion fragment revealed the deletion breakpoints within introns 23 and 25 originating in the middle of two Alu-repeats. CONCLUSION: In a patient with severe clinical symptoms, we found two genomic deletions in regions that might be important for function of the ABCC6 transporter. Genomic deletions in ABCC6 may occur more frequently in PXE patients than previously expected and future genetic analysis should focus on these mutations as well.

Adult↗

PubMed2005

Effect of hyperlipidemia on QT dispersion in patients without ischemic heart disease.

BACKGROUND: Lipoproteins are known to exert direct and indirect effects on cardiovascular function, but their effects on ventricular repolarization have not yet been clearly elucidated. OBJECTIVES: To assess the effect of hyperlipidemia on the longest QT interval (QTmax) of the 12-lead surface electrocardiogram (ECG) and on QT dispersion (QTd) in type IIb hyperlipidemic patients without myocardial ischemia, and to compare these patients with healthy control subjects. METHODS: Ninety-six hyperlipidemic patients (44 men and 52 women; mean age 53+/-13 years) and 101 healthy control subjects (43 men and 58 women; mean age 46+/-16 years) were examined. Total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol (LDL-C), triglyceride, apolipoprotein (apo) A1, apo B, lipoprotein(a), QTmax and QTd were measured. According to heart rate, corrected QTmax and corrected QTd were also determined. RESULTS: A significant difference was observed between the two groups of subjects with respect to serum cholesterol, LDL-C, triglyceride, apo B, QTmax, corrected QTmax, QTd and corrected QTd. A positive significant correlation was found between cholesterol, triglyceride, LDL-C and all of the studied ECG parameters, between high density lipoprotein cholesterol and QTmax, apo B and QTd, and between body mass index and all of the studied ECG markers. CONCLUSIONS: Hyperlipidemia may have a direct effect on the studied ECG markers.

Adult↗

PubMed2004

[The non-lipid effects of statins].

In the past 15 years statins have gained recognition as one of the successful drugs in cardiovascular therapy and are now regarded as important as the beta blocking agents and ACE inhibitors. Since the publication of the Scandinavian Simvastatin Survival Study in 1994, the clinical application of statins has become increasingly widespread. Numerous large-scale clinical end-point trials have demonstrated that statin therapy reduces cardiovascular morbidity and mortality. Their beneficial therapeutic effects, besides their lipid lowering role, have been attributed to their non-lipid modifying ability, called the pleiotropic effect. The clinical consequences of the latter are not well understood, simply because differentiating between their lipid modifying and pleiotropic effects is not possible in vivo. In this article the authors summarize the evidence of the pleiotropic effects based on results of the latest in vitro experiments. They describe the influence of statins on endothelial dysfunction and thrombus formation, their anti-inflammatory, plaque-stabilizing and antioxidant effects, as well as their CRP and angiogenesis modifying non-lipid effects. The authors further discuss the effects of these drugs on tumors, osteoporosis and dementia. Although all members of the statin family inhibit the same enzyme in the cholesterol synthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase), their various pharmacokinetic properties, and tissue selectivity (lipophilicity and hydrophilicity) are responsible for their different pleiotropic effects.

Aged↗

PubMed2004

Serum cholesterols have a more important role than triglycerides in determining intima-media thickness of the common carotid artery in subjects younger than 55 years of age.

OBJECTIVE: The role of serum cholesterol and triglycerides in carotid artery atherosclerosis is controversial. We measured carotid artery intima-media thickness (IMT), a marker of atherosclerosis in subjects younger than 55 years of age with a 6-fold range of serum cholesterol levels (3.93-25.03 mmol/L) and a 200-fold range of triglyceride levels (0.36-75.97 mmol/L). METHODS: Eighty-six patients with increased serum lipid values and 30 subjects with normal lipid values were included. Serum lipids were measured after an overnight fast. High-resolution sonographic investigations of the carotid arteries of all patients were videotaped. Intima-media thickness was measured offline at 1-mm increments in the distal 10-mm segments of both common carotid arteries by a reader blinded to patient characteristics. First, IMT was compared among groups defined by their cholesterol and triglyceride levels with the use of traditional cutoff values. Next, all subjects were pooled, and general regression analysis was performed to identify significant predictors of IMT with age, body mass index, lipid values, sex, diabetes, hypertension, and smoking status as independent variables. RESULTS: Intima-media thickness was larger in patient groups with high cholesterol levels (ie, the hypercholesterolemic and combined hyperlipidemic groups) than in the control, borderline, and isolated hypertriglyceridemic groups (P < .01). In the general multiple regression model, IMT correlated positively with total cholesterol level (beta = 0.343; P = .002) and age (beta = 0.3; P = .006) but not with triglyceride level. CONCLUSIONS: Both the group comparisons and the general regression analysis of the pooled data suggest that hypercholesterolemia has an important role in early onset IMT changes in the common carotid artery, whereas hypertriglyceridemia does not have an appreciable role.

Adult↗

PubMed2002

[Frequency of hyperhomocysteinemia in hemodialysis patients with folic acid supplementation].

BACKGROUND: It is known that hyperhomocystinemia is an independent risk factor for development of atherosclerosis. In end stage renal disease the frequency of hyperhomocystinemia is much greater than in normal populations. AIM: In this study homocystein (Hcy), folic acid and vitamin B12 concentrations were determined in 125 chronic renal failure patients being on folic acid supplementation (3 mg/day). In 107 patients the frequency of C667T polymorphism of methylene tetrahyrofolate reductase (MTHFR) was also determined. The relationships between these parameters were also studied. RESULTS: It was found that in these patients who are under continuous folic acid supplementation the mean level of homocysteine was 16.8 +/- 7.2 mumol/L, a value considerably lower than the homocysteine concentration reported for non-supplemented patients. The elevation of homocysteine concentrations was independent of gender, time spent in renal replacement therapy, and the type of renal replacement therapy (hemodialysis: 17.6 +/- 12.6; hemodiafiltration: 16.6 +/- 12.9 mumol/L). Data showed an inverse relation between plasma homocysteine concentrations and the concentrations of folic acid and vitamin B12. Moderately severe hyperhomocystinemia (Hcy > 20 mumol/L) was found in about 30% of patients. In those the frequency of patients for homozygous T677 allele of MTHFR was about 25-30%. However, in all ESRD patients the frequency of the homozygotes was the same then in the normal population. Homocysteine plasma levels correlated with MTHFR polymorphism: in the wild type group Hcy was 14 +/- 7 mumol/L, in the heterozygous group was 17.2 +/- 6.2 mumol/L, and in the homozygous group was 21 +/- 19 mumol/L. CONCLUSIONS: Long-term folic acid supplementation decreased the homocysteine level in end stage renal disease patients. However, in folic acid resistant group, who were in 30% homozygotes for C667T of MTHFR (suggesting that homocysteine-methionine remethylation cycle is disturbed), instead of the administration of folic acid, methylene tetrahydrofolate supplementation might be considered.

Adult↗

PubMed2002

Determination of DNA damage induced by oxidative stress in hyperlipidemic patients.

In the present paper, we report data on the genotoxic properties of hydrogen peroxide in polymorphonuclear neutrophils (PMNLs) separated from normolipidemic and type II/a hyperlipidemic patients. In all, 15 hyperlipidemic patients (11 female, 4 male, mean age 54.6+/-10.25 years) were involved in the study, and 7 normolipidemic patients (5 female, 2 male, mean age 53.4+/-8.07 years) served as controls. Using the comet assay, there was a significant difference in the degree of DNA damage between the two groups. The visual score characteristic of the degree of DNA damage was 350.97+/-31.31 in the hyperlipidemic group, while it was 289.5+/-29.49 in the control group (P<0.001). In the hyperlipidemic patients, a positive correlation was found between the degree of DNA damage and the basic oxidation of PMNLs (r=0.517), and the superoxide anion production of the cells stimulated with phorbolmiristate acetate (PMA) (r=0.326) and formyl-Met-Leu-Phe (FMLP) (r=0.525) as well. There was a negative correlation between DNA damage and HDL-associated antioxidant paraoxonase (PON) activity (r=-0.469), and the PON/HDL ratio (r=-0.631). No correlation was found between the degree of DNA damage and the plasma concentration of nitric oxide (NO) (r=0.098) and thiobarbituric acid-reactive substances (TBARS) (r=0.061) in hyperlipidemic patients. Our results show that in hyperlipidemic patients there is an increase in lymphocyte DNA damage caused by oxidative stress when compared to normolipidemic individuals as demonstrated by comet assay. Decreased antioxidant capacity in hyperlipidemic patients may play a significant role in this process.

Adult↗

PubMed2002

Serum paraoxonase activity changes in patients with Alzheimer's disease and vascular dementia.

The prevalence of Alzheimer's disease (AD) and vascular dementia (VAD) increases with aging of the population. The role of lipoproteins in the pathogenesis of AD is unclear: apoE(2) offers protection and apoE(3) is neutral, while apoE(4) promotes the development of the disease. Recently, several studies have confirmed the role of oxidative stress in the pathogenesis of AD and VAD. HDL-associated paraoxonase is one of the antioxidative enzymes that may reduce LDL oxidation. In our study, we investigated the lipid parameters of the sera and the serum paraoxonase activity in patients with AD and VAD. Lipid parameters were determined by an autoanalyzer in 30 AD patients, 40 VAD patients and 40 healthy, age-matched control (C) subjects. Paraoxonase activity was measured spectrophotometrically using paraoxon as the substrate. The phenotypic distribution of paraoxonase was determined by the dual substrate method, using paraoxon and phenylacetate as substrates. In our results, we found that most of the patients with AD had the apoE(4) isoform, consistent with other studies. In the VAD and AD patients we found significantly higher total-cholesterol compared to the control group (C: 4.71 +/- 0.89, VAD: 6.3 +/- 0.8, AD: 6.52 +/- 0.7 mmol/l; p < 0.01) and LDL-cholesterol levels (C: 2.6 +/- 0.6, VAD: 3.96 +/- 0.8, AD: 3.84 +/- 0.6 mmol/l; p < 0.001). The HDL-associated antioxidant, paraoxonase activity did not differ significantly in the patient groups, but compared to the healthy control subjects, paraoxonase activity was significantly lower in both of the patient groups (C: 188 +/- 55 U/l; AD: 131 +/- 37, VAD: 151 +/- 50 l; p < 0.05). Our results suggest that the defect in HDL-associated antioxidant capacity plays a role in the pathogenesis of Alzheimer's disease and vascular dementia.

Alzheimer Disease↗