Search PubMed⌕ Search

Biomedical subjects

R Ceska

Publications and source records attributed to R Ceska.

At least 55 records · Page 3Linked to original sources

[Frequency of occurrence of apolipoprotein E isoforms in patients with various types of hyperlipoproteinemias].

BACKGROUND: Apolipoprotein E is a polymorphic protein playing a crucial role in the metabolism of plasma lipoproteins. Three alleles referred to as epsilon 2, epsilon 3 and epsilon 4 code for three common isoforms of apoE. The most frequent allele in the population at large is epsilon 3 allele. epsilon 2 and epsilon 4 alleles are connected with lipoprotein disorders as well as with other diseases. The aim of our study was to establish frequencies of apoE coding alleles in patients with different types of hyperlipidaemia (HLP) and to reveal differences in their distribution in comparison with the general population. METHODS AND RESULTS: Therefore apoE genotype was assayed in 752 patients with primary HLP and 291 subjects randomly selected from the general Czech population. Allele frequencies were determined separately in a group of patients with familial hypercholesterolaemia (FH), polygenic hypercholesterolaemia (PHC), familial combined hyperlipidaemia (FCH) and in patients with type III. hyperlipidaemia (III). In patients with HLP a significantly higher frequency of epsilon 4 allele than in control subjects was found. In the group of FH patients frequency of the epsilon 2 allele was higher than in control subjects. In patients with PHC a significantly higher frequency of the epsilon 4 allele and lower frequency of the epsilon 2 allele were observed. In the group of FCH patients distribution of epsilon alleles did not differ from the control group. Frequency of the epsilon 2 allele in patients with type III. hyperlipidaemia was significantly higher than in controls. CONCLUSIONS: We conclude that there exist significant differences in frequencies of apoE coding alleles between patients with primary hyperlipidaemia and a randomly selected population sample. The revealed differences in allelic distribution suggest that the impact of apoE polymorphism is not uniform in all types of hyperlipidaemia.

Alleles↗

[Negative aspects of the Western life style and possibilities of intervention in patients with familial combined hyperlipidemia].

BACKGROUND: Evaluation of the effect of intervention on changes in the lifestyle of patients with combined familial hyperlipidaemia (CFH). METHODS AND RESULTS: The group comprised 154 patients with CFH where changes in the lipid profile, diet, basic anthropometric data and smoking were recorded 3-6 months following intervention. In addition to little willingness to have a check-up examination the authors recorded significant shortcomings in the lifestyle of these patients with a high cardiovascular risk: a large number of smokers (51%), serious shortcomings in the composition of the diet (excessive intake of animal fats a proteins, inadequate intake of vegetable proteins, dietary fibre and vitamins, in particular E and C), overweight and a high percentage of body fat. CONCLUSIONS: While the attention devote to pharmacotherapy with hypolipidaemic agents is justified we should not forget systematic intervention as regards changes in lifestyle. This appeal is even more urgent in conjunction with the low motivation and willingness of patients to change their lifestyle. Special attention should be focused on smokers (in addition to effect on lipids also greater cumulation of risk factors).

Female↗

[Genetic predisposition for the multiple metabolic syndrome. Part 4. Apolipoprotein E and lipoprotein (a)].

Apolipoprotein E (apo E) is a genetically polymorphous glykoprotein made up of 299 amino acids. It is an important part of triacylglycerol rich lipoproteins [chylomicrons, lipoproteins with a very low density (VLDL) and their "residues"]. Apo E is a ligand of apo B, E receptors and thus regulates in a marked way the homeostasis of lipids and lipoproteins in plasma. The genetic polymorphism of apo E is controlled by three alleles epsilon 2, epsilon 3, epsilon 4 which influence individual plasma cholesterol levels and thus the process of atherogenesis. Lipoprotein (a) [Lp(a)] is a plasma lipoprotein which is another independent, genetically determined risk factor in the process of atherogenesis. The basis of its structure is a micelle of LDL which is linked by a disulphidic covalent with the glycoprotein of the apolipoprotein (a). Lp (a) was detected in atherosclerotic plaques and it is assumed that it participates in the penetration of lipids into the vascular wall. Its thrombogenic properties were also detected due to its structural relationship with plasminogen to which it is linked and inhibits competitively the transformation of plasminogen to plasmin.

Alzheimer Disease↗

[Genetic predisposition in multiple metabolic syndrome. Part 3. Metabolism of lipids, lipoproteins and apolipoproteins].

The author discusses metabolic processes during exogenous and endogenous lipid transport and deviations in the metabolism of lipids, lipoproteins and apolipoproteins in multiple metabolic syndrome and in so-called diabetic dyslipidaemia. Specific phenotypic manifestations of diabetic dyslipidaemia include hypertriacylglycerolaemia, hypercholesterolaemia, elevated plasma levels of LDL-cholesterol and apolipoprotein B and reduced levels of HDL-cholesterol and apolipoprotein B and reduced levels of HDL-cholesterol and apolipoprotein A-I. Other recent findings relating to this syndrome include evidence of elevated concentrations of small and dense LDL micelles (< 25 nm), so-called LDL phenotype B, which are easily modified (e.g. by oxidation, glycation etc.), and subsequent uptake by "scavenger" receptors into macrophages which after filling become foam cells and penetrate into the vascular wall. Elevated levels of small and dense LDL micelles, the accelerating process of atherogenesis, were proved in all multiple metabolic syndrome carriers. The atherogenic lipoprotein phenotype hastens markedly atherogenesis and subsequent manifestation of cardiovascular diseases.

Apolipoproteins↗

[Genetic predisposition in multiple metabolic syndrome. Part 2. Candidate genes in type II diabetes mellitus].

The author presents a review on candidate genes of proteins involved in the metabolism of glucose, lipids and other metabolites (glucose carriers, insulin receptors, proinsulin, glucokinase, amyline, glycogen synthase). One of the main causes of enhanced atherogenesis in patients with type II diabetes (NIDDM) are marked genetically conditioned deviations of the lipid, lipoprotein and apolipoprotein metabolism. In the metabolic dyshomeostasis of multiple metabolic syndrome participate in the process of atherogenesis also: isoforms of apolipoprotein E4, isoforms of apolipoprotein A-IV-1/1, hyperuricaemia, raised levels of the plasminogen activator inhibitor 1 (PAI-1), hyperfibrinogenaemia, hyperhomocysteinaemia and other metabolites (cytokines, endothelin etc.). Patients with a greated genetic sensitivity manifest diabetes sooner and more intensely and die at a younger age in particular from cardiovascular disease, but also on account of a higher incidence of tumours diseases.

Arteriosclerosis↗

Diet, smoking, and blood lipids in patients with combined familial hyperlipidaemia.

This study analysed the diet (based on a 7-day-record), smoking habits and basic anthropometric parameters of patients with familial combined hyperlipidaemia (N = 154, 52% men, 48% women, mean age 55.73 +/- 12.95). These data were correlated with blood lipids and lipoproteins. In high-risk patients' diets we found not quantitative, but mostly qualitative shortcomings: the average energy intake was 104% of the recommended daily intake (RDI), but 34% of the energy was derived from fats. The daily fat intake represented 137% of RDI, and 60 g were of animal and 24 g of vegetable origine. The protein intake was 120% of RDI (155% animal, 75% vegetable protein), the carbohydrate intake was only 86% and the fibre intake 71% of RDI. A very high intake both of cholesterol--139% of RDI and NaCl 151% of RDI--was recorded, while the intake of antioxidant vitamins C and E was only 82% and 35% of RDI, respectively. Current smoking was recorded in 51% of patients. Smokers had also a poorer diet: higher animal fat and protein, as well as a higher cholesterol intake, lower vegetable fat, protein, fibre and vitamin E intake. Surprisingly smokers were found to ingest more vitamin C than non-smokers. As to blood lipids: smokers vs. non-smokers had the following values in mmol/l (SD): total cholesterol 7.8 (+/- 1.3) vs. 7.7 (+/- 1.82), triacylglycerols 3.27 (+/- 2.13) vs. 3.2 (+/- 3.11), HDL-cholesterol 1.25 (+/- 0.39) vs. 1.36 (+/- 0.43), LDL-cholesterol 5.11 (+/- 1.39) vs. 4.95 (+/- 1.51), and, in g/l, apolipoprotein A1 1.8 (+/- 0.30) vs. 1.66 (+/- 0.35), apolipoprotein B 1.66 (+/- 0.35) vs. 1.52 (+/- 0.44), lipoprotein (a) 0.36 (+/- 0.27) vs. 0.43 (+/- 0.50), all without statistical significance. For smokers vs. non-smokers anthropometric data were as follows (mean, SD): body mass index (BMI) 27.74 (+/- 3.77) vs. 27.02 (+/- 3.30), waist/hip ratio (WHR) 0.895 (+/- 0.086) vs. 0.911 (+/- 0.093), and % of body fat 29.6 (+/- 7.4) vs. 27.9 (+/- 7.9). Our conclusions suggest, that lifestyle choice are of great importance for patients with this serious genetic lipid metabolism disorder and that it is important to recognise the danger of risk factor cumulation in connection with cardiovascular diseases.

Body Constitution↗

Serum leptin concentrations in patients with combined hyperlipidemia: relationship to serum lipids and lipoproteins.

Leptin is a protein hormone produced predominantly by adipocytes. Serum leptin concentrations in healthy individuals positively correlate with the body fat content and body mass index, i.e. they are higher in obese than in lean subjects. The relations between serum leptin concentration and serum lipids and lipoproteins is not yet clear. The aim of our study was to compare serum leptin concentrations in 22 randomly selected patients with untreated combined hyperlipidemia and 19 healthy control subjects matched for age and the body mass index. The relationship was studied between serum leptin concentrations and serum lipids (total, HDL, LDL cholesterol and triglycerides) and lipoproteins (lipoprotein (a), apolipoprotein B). It was found that serum leptin levels in patients with combined hyperlipidemia did not significantly differ from those of control subjects (6.69+/-4.3 vs 5.78+/-3.2 ng.ml(-1)). Serum leptin concentrations in both groups correlated positively with the body mass index. The relationship between leptin concentrations and lipid or lipoprotein levels found in any of the studied groups was not statistically significant. We conclude that serum leptin concentrations in patients with combined hyperlipidemia as well as in healthy control subjects reflect the body fat content and have no significant relation to serum lipids or lipoproteins.

Adult↗

The effect of four-year hypolipidaemic treatment on the intimal thickness of the common carotid artery in patients with familiar hyperlipidaemia.

BACKGROUND: Cholesterol lowering in patients with above-average cholesterol levels has been shown to reduce the progression of atherosclerosis. We assess the effects of lipid lowering therapy on the progression of early, preintrusive carotid arterial atherosclerosis in high risk patients with familial hyperlipidaemia free of symptomatic cardiovascular disease. METHODS: Fifty-two patients with familial hyperlipidaemia by were treated by diet and various hypolipidaemic drugs. Eighteen individuals were not taking hypolipidaemic drugs. In a prospective study by B-mode ultrasound we assessed the intima-media thickness of the distal common carotid arterial (CCA) far wall at baseline and after 4 years. RESULTS: In a subgroup of 25 patients with familial hypercholesterolaemia there was a significant decrease in total and LDL cholesterol and reduction in the intima-media thickness (IMT) of the common carotid artery from 0.78+/-0.22 mm to 0.69+/-0.17 mm (p=0.004). In a subgroup of 27 patients with familial combined hyperlipidaemia significant decreases in total and LDL cholesterol and triglycerides were associated with a decrease in the IMT of common carotid. artery from 0.72+/-0.22 mm to 0.67+/-0.15 mm (p=0.044). In 18 individuals, who were not taking hypolipidaemic drugs, there were no significant changes in the levels of cholesterol and triglycerides and in the IMT of the common carotid artery (increase from 0.58+/-0.18 mm to 0.62+/-0.13 mm, p>0.05). CONCLUSIONS: Lipid-lowering therapy in patients with familial hyperlipidaemia free of symptomatic cardiovascular disease reverses the progression of early, preintrusive atherosclerosis of the carotid artery. It is a beneficial sign indicating the possibility for atherosclerosis regression.

Carotid Artery, Common↗

[What was not included in the recommendations for the diagnosis and therapy of hyperlipoproteinemia in childhood].

Screening and treatment of hyperlipidaemia should be the concern of paediatricians. This is suggested by the finding of fatty streaks and other atheromatic changes in children. The authors prefer selective to nationwide screening in children who have close relatives with coronary heart disease or cerebral haemorrhage before the age of 55 years in men and 65 years in women or elevated total cholesterol levels. In case of repeated total cholesterol levels of 4.4-5.2 mmol/l the authors recommend annual, in case of levels above 5.2 mmol/l 3-6 month intervals between examinations. The authors found values above 5.2 mmol/l in one quarter of otherwise healthy children. In addition to the hyperlipidaemic theory there is the infectious theory of development of atherosclerosis and the theory of programming of coronary heart disease during pregnancy. By dietary and lifestyle provisions it is possible to reduce hyperlipidaemia in the great majority of children. In boys above 10 years and girls above 20 years resins are indicated if the total cholesterol level is above 8 mmol/l.

Adolescent↗

[Favorable effect of treatment with statins on the intima of the common carotid artery in patients with familial hyperlipoproteinemia].

BACKGROUND: In recent years evidence was provided that by measuring the width of the intima of the carotid artery, evaluated by sonography, it is possible to assess the development of arteriosclerosis. The authors used this method to evaluate hypolipidaemic treatment. METHODS AND RESULTS: The authors followed-up by clinical and laboratory methods and treated for a period of 47 months 63 patients with familial hyperlipoproteinaemia. At the beginning and at the end of the follow-up period they made sonographic examinations of the common carotid artery. In 31 patients treated by statins they observed statistically significant changes: cholesterol declined by 23%, LDL cholesterol by 25.3%. The maximal rate in the common carotid artery (ACC) declined from 93 +/- 22 to 73 +/- 13 cm/s. The diameters of the ACC increased from 6.0 +/- 0.8 to 6.5 +/- 0.8 mm. The intima of the ACC diminished from 0.84 +/- 0.26 to 0.75 +/- 0.20 mm. In 22 patients treated with fibrates the anticipated lipid changes occurred. The diameter of ACC did not change, the decline in the width of the intima of the ACC was not statistically significant. In 10 patients who decided that they wanted only dietary treatment the changes in the investigated parameters were small. CONCLUSIONS: In patients with familial hyperlipidaemia who were treated with statins for almost four years the authors observed a diminution of the width of the intima of the common carotid artery which is considered a sign of regressing atherosclerosis.

Anticholesteremic Agents↗

[Familial hypobetalipoproteinemia].

BACKGROUND: Familial hypobetalipoproteinaemia (FHBL) is a relatively rare inborn error of metabolism which must be considered in the differential diagnosis of hypocholesterolaemia which cannot be explained by secondary causes (severe malnutrition, generalization of neoplastic disease etc.). METHODS AND RESULTS: In the submitted paper the authors present the results assembled in a family with four heterozygotes with FHBL. The proband is a 27-year-old woman (total cholesterol (TCh) 1.70, triacylglycerols (TG) 0.20, HDL-cholesterol (HDL-ch.) 1.38, LDL-cholesterol (LDL-ch.) 0.34 all in mmol/l, apolipoprotein B (apo B) 0.25, lipoprotein(a)(Lp(a) 0.09 all in g/l, isoforms of apolipoprotein E/E3 (iso apo E). Mother (age 53 years) of the proband (TCh 3.06, TG 0.37, HDL-ch. 1.99, LDL-ch. 0.90 all in mmol/l, Apo B 0.37, Lp(a) 0.14 all in g/l, iso apo E3/E3)). Two of the proband's sisters (23 and 20 years) (TCh 3.92 and 2.55 resp., TG 0.57 and 0.23 resp. HDL-ch. 1.86 and 1.63 resp., LDL-ch. 1.80 and 0.82 resp. all in mmol/l, Apo B 0.73 and 0.37 resp., Lp(a) 0.47 and 0.63 resp. all in g/l, iso apo E2/E3 and E2/E3 resp.). The diagnosis confirms the autosomal dominant transmission. During the proband's pregnancy (during the 38th week), contrary to normocholesterolaemic women the TCh did not rise (1.43 mmol/l, the TG level (0.62 mmol/l), Apo B (0.43 and Lp(a) 0.18 all in g/l rose. CONCLUSIONS: According to the available literature this is the first description of FHBL in our literature and a priority investigation of plasma lipid concentrations, lipoproteins and apolipoproteins in a women with a heterozygous form of FHBL during pregnancy.

Adult↗

Decreasing common carotid artery intimal thickness during hypolipidemic therapy.

It has been demonstrated in recent years that ultrasound can be used to measure common carotid artery intimal thickness; an increase in intimal thickness is regarded as an early stage of atherosclerosis. This study was designed to establish whether or not intimal thickness can be modulated by therapy. Twenty-nine patients with familial hyperlipoproteinemias had follow-up ultrasound of the common carotid artery after twenty-nine months of comprehensive therapy. In 21 patients with familial hypercholesterolemia, intimal thickness decreased from 0.83 to 0.68 mm (P < 0.01), in 9 with familial combined hyperlipoproteinemia, the decrease was from 0.77 to 0.74 mm (a decrease was seen in only 50% of patients). With the group taken as a whole, the larger decrease was observed in patients treated with statins while the reduction was less marked in those administered fibrates. The authors found a decrease in common carotid artery intimal thickness following hypolipidemic therapy in patients with hyperlipoproteinemias. Their impression is that this was a manifestation of atherosclerosis regression.

Adult↗

[The effect of 4 years' of hypolipemic treatment on the width of the common carotid artery intima in patients with familial hyperlipidemias].

Sixty-four patients with familial hyperlipoproteinaemia were treated for almost four years by dietetic treatment and various hypolipidaemic drugs. In 25 patients with familial hypercholesterolaemia who had clinical signs of ischaemic heart disease total and LDL-cholesterol declined and the width of the intima of the common carotid artery diminished from 0.78 mm to 0.69 mm (p = 0.004). In the above artery the maximal flow rate of blood declined. The increase was, however, not statistically significant. In 12 patients with familial hypercholesterolaemia who suffered from ischaemic heart disease the width of the intima of the common carotid artery and maximum flow rate did not change, however, the diameter of the artery increased (from 6.3 to 6.6 mm, p = 0.034). In 27 patients with familial combined hyperlipidaemia during the drop of cholesterol, LDL-cholesterol and triacylglycerols the width of the intima of the common carotid artery diminished (from 0.72 to 0.67 mm, p = 0.044), the diameter of the artery increased (from 6.1 to 6.4 mm, p = 0.014). The authors assume that the reduction of the width of the intima during hypolipidaemic treatment reflected the decline of cholesterol in the arterial wall and is a favourable sign which indicates possible regression of atherosclerosis.

Carotid Artery, Common↗

[The effect of micronized fenofibrate on lipid parameters and fibrinogen in heterozygous familial hypercholesterolemia and familial combined hyperlipidemia].

BACKGROUND: The aim of the study was to approve the hypolipidemic potency of the new drug from the group of fibrate derivates Lipanthyl 200 M(R) (micronized fenofibrate, cps a 200 mg, Laboratoires Fournier, France) in patients with familial hyperlipoproteinemias. The drug has been administered in constant dose of 200 mg daily with the evening meal for three months. Clinical examinations and monitoring of safety laboratory have been performed in addition to complete analysis of lipids, lipoproteins and apolipoproteins during the study. METHODS AND RESULTS: The group of 30 patients consisted from 14 heterozygotes of familial hypercholesterolemia and 16 patients affected by familial combined hyperlipidemia. Levels of total, HDL- and LDL-cholesterol, triglycerides, apolipoproteins A-I and B and Lp(a) have been measured and concentrations of fibrinogen in plasma as well. Concentration of total cholesterol 8.29 +/- 1.3 mmol/l on the beginning of the study decreased after one and three months of the treatment to 6.94 +/- 1.19 resp. 6.98 +/- 1.21 mmol/l, concentration of triglycerides has been reduced from 2.86 +/- 1.29 mmol/l to 1.70 +/- 0.86 and 1.74 +/- 0.99 mmol/l respectively HDL-cholesterol raised from 1.14 +/- 0.32 mmol/l to 1.27 +/- 0.36 and to 1.34 +/- 0.37 mmol/l in contrast to decrease of LDL-cholesterol 5.88 +/- 1.53 mmol/l on the beginning of the study to 4.87 +/- 1.49 and 4.79 +/- 1.60. Apo B in plasma fall after three month period of the treatment from 1.83 +/- 0.43 g/l to 1.46 +/- 0.47 g/l. On the other hand the concentration of apolipoprotein apo A-I1.20 +/- 0.35 g/l increased to 1.40 +/- 0.32 g/l. Fibrinogen in plasma was reduced from 3.63 +/- 0.69 g/l to 2.77 +/- 0.50 g/l. Also this decrease was statistically significant. CONCLUSIONS: Micronized fenofibrate is a potent hypolipidemic drug with only rare side effects. It is very good tolerated by the patients. Micronized fenofibrate is particularly prescribed for combined hyperlipidemia, however we can use it also in some patients with familial hypercholesterolemia. For to the treatment very resistant hyperlipoproteinemias we should consider combined drug therapy.

Adult↗

[Analysis of nutritional habits in patients with familial combined hyperlipidemia].

BACKGROUND: Our objective was to analyze dietary habits of patients with the IIb phenotype of familial combined hyperlipidaemia. These patients were instructed on the proper composition of their diet and they thought that they adhered to these recommendations. METHODS AND RESULTS: The authors examined 41 patients with IIb phenotype of familial combined hyperlipidaemia. Based on their seven-day dietary records their daily intake was calculated and compared with recommended daily allowances as regards energy intake, intake of plant and animal proteins, fats, linoleic acid, carbohydrates, calcium, iron, potassium, fibre, vitamin A, thiamin, pyridoxine, vitamin C, E, cholesterol and NaCl (Progana programme). With the above results the total serum cholesterol, serum triglyceride, HDL and LDL serum cholesterol and nutritional status (body mass index, percentage of body fat and waist hip/ratio) were compared. When the energy intake was acceptable (99% of the recommended allowance), the fat intake was excessive (138%) as well as the intake of animal protein (148%), cholesterol (145%) and NaCl (159% of the recommended allowance), while the intake of plant proteins and fibre and some vitamins was inadequate. A statistically significant relationship was revealed only as regards the linoleic acid intake and total serum cholesterol (inverse relationship at the 95% probability level, r = 0.43), the other investigated relationships were insignificant. The body mass index values (in men and women 26) and the percentage of body fat (22% in men and 34% in women) are above the recommended range. CONCLUSIONS: Dietary errors in the investigated group thus did not pertain, to the quantity of the diet but its composition. From the results ensures that doctors should pay great attention to explaining dietary principles to their patients.

Adult↗