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Introduction: Glykogen Phosphorylase BB is considered a timely and specific marker of acute coronary syndrome. A kit for measuring Glykogen Phosphorylase BB in routine diagnosis has been released recently., Objective of the Study: To test the utilisation of Glykogen Phosphorylase BB measurement in the diagnosis of acute coronary syndrome., Method: 70 patients with suspected acute coronary syndrome were tested. A final diagnosis of acute coronary syndrome/non-coronary difficulties was made according to ESC/ACC/AHA criteria. Measurements of troponin I, myoglobin and GPBB in venous plasma (heparin-lithium) were taken for all probands on admission and two and six hours later., Results: Individuals with acute coronary syndrome (n = 52) had significantly higher levels of Glykogen Phosphorylase BB on admission and 2 hours after admission (21.9 vs 6.2; 18.7 vs 5.9 microg/l; p < 0.01). Levels of Glykogen Phosphorylase BB had a greater diagnostic effectiveness for the presence of acute coronary syndrome than levels of troponin I (threshold below ROC curve 0.89 vs. 0.78; 0.87 vs. 0.67). In the first two hours after admission, only levels of Glykogen Phosphorylase BB were included as independent variables in the regression model for the incidence of acute coronary syndrome (p < 0.05). When the group of patients with myocardial necrosis (n = 39; acute myocardial infarction without ST elevations on ECG; NSTEMI) is removed from the group with acute coronary syndrome, it was found that only GPBB and cTnl were independent variables in the regression model on initial testing and after two hours. After adjusting GPBB to cTnl, significantly higher levels of GPBB adjusted to troponin I were found in persons with NSTEMI (14.5 vs -48.0; p < 0.01)., Conclusion: Measurement of Glykogen Phosphorylase BB has excellent effectiveness independently of troponin in the first hours after the onset of acute coronary syndrome and should ensure the correct diagnosis of acute coronary syndrome in combination with troponin.

Assessment of carbohydrate-deficient serum transferrin CDT) is considered a very useful indicator of alcohol abuse. There is a number of methods for assessment of CDT. In clinical practice most frequently assessment of the percentage ratio of CDT in transferrin is used. In our hospital we assessed CDT by the method of homogeneous immunoanalysis (Boehringer Mannheim (CDT-BM). Because we obtained a relatively high percentage of false results and because we found in the literature reference to a new method of homogeneous immunoanalysis (The Sanqui BioTech-CD-SB) with a different cut-off, we decided to compare the results of the estimations by the two methods and assess the percentage of false results. We examined a group of 49 patients incl. 16 who admitted alcohol abuse (> 60 g alcohol more than four times per week). As anticipated, we found that the %CDT assessed by the CDT-BM method was significantly higher than the percentage CDT-SB. After classification of the group into sub-groups with regard to alcohol intake the two sub-groups differed significantly only in values of CDT-SB and CDT-BM. In the group of patients with alcohol abuse we found relations between CDT-MB and indicators of hepatic lesions. In CDT-SB we found only an association with AST. This finding could suggest a greater specificity of CDT-SB. We confirmed data in the literature that GMT is independent on CDT and the mean corpuscular volume is independent on CDT in subjects with alcohol abuse. In abstainers who negated alcohol intake we found also when assessing CDT-SB a significant gender differentiation which is described in the literature (the reason is probably the fact that the CDT-SB method analyzes, contrary to CDT-BM, only asialo,-monosialo and disialylic isoforms of transferrin and women have higher levels of monosialylic forms). In our group the examination of %CDT by the new method, the Sanqui Biotech for alcohol abuse, had an almost absolute specificity and sensitivity. Contrary to the older Boehringer-Mannheim method we did not record any false increase in any patient with signs of hepatopathy nor any false negative results). We assume that the described methodical innovation of the analysis could facilitate the differential diagnosis of various diseases in different medical disciplines (internal medicine, neurology, psychiatry, assessment of work capacity).

Unlabelled: During the last decade several papers were published where obesity in included among the building stones of the so-called metabolic cardiovascular syndrome (along with hypertension, dyslipidaemia, impaired glucose tolerance and hyperinsulinaemia). Several months ago it was also revealed that some patients with the metabolic syndrome suffer from hyperleptinaemia. Leptinaemia is considered by some authors as independent indicator of the risk of accelerated atherosclerosis. The cause of these hypothesis were (in addition to the known conclusions on the occurrence frequent incidence of leptin resistance and insulin resistance) in particular the results of experimental studies where evidence was provided that infusion induced hyperleptinaemia leads in animals to hypertension due to its direct effect on sympathicotonia and peripheral vascular resistance. The authors of these hypothesis assume that hyperleptinaemia (in particular in subjects with metabolic syndrome) in one of the basic causes of hypertension which is frequently encountered in these patients., Objective: To assess the relations between leptinaemia and the blood pressure reading (actual and mean values) and leptinaemia and the classification of hypertension according to WHO., Method: The authors examined 35 hypertensive subject and 10 subject with tetanies (without hypertension). The blood pressure was assessed under standard conditions (rest, semi-recumbent position, three readings). The mean blood pressure readings during the last three months were obtained from case records. Leptin was assessed by the ELISA method of Bio Vendor Co., Results: The group of hypertonic can be classified as subjects with mild obesity (BMI 30.1). The values of leptin were elevated but did not differ significantly from those of the normal population. No correlations were found between leptinaemia (incl. values calculated for BMI) and the actual and mean blood pressure readings. No correlations were found between leptinaemia (incl. BP calculated with regard to BMI) and the stage of hypertension according to WHO., Conclusion: Hypertonic subject do not differ significantly as to the serum leptin concentration from the general population. Leptinaemia does not correlate with the actual or mean blood pressure reading nor with stage of hypertension according to the WHO classification. Thus the authors did not confirm the hypothesis on the fundamental effect of leptinaemia on the genesis and development of hypertension. It is probable that leptin is only one of the many factors which have an impact on blood pressure.

Introduction: Leptin is a protein, determined by the ob-gene which influences in a fundamental way the energy metabolism of the organism. A significant effect of leptin on the haematopoietic, immunological and endocrinological system cannot be ruled out nor its effect on the course of pregnancy and maturation of the organism. In humans leptinaemia correlates with the amount of subcutaneous fat which is due to a receptor or post-receptor disorder, obese subjects suffer frequently from hyperleptinaemia., Objective: To assess the mean leptinaemia of the general population, seek relations between leptinaemia and anthropological indicators and age., Methods: Using the method of random sampling the authors examined a group of 538 probands (252 males, 286 females) incl. 12% healthy students of the Faculty of Physical Culture in Olomouc, 37% subjects without acute or chronic complications feeling in good health and 37% patients of the metabolic and diabetological ambulance of the hospital in Sternberk. In each patient a detailed case-history was recorded, an anthropological examination was made and a venous blood sample was taken for leptin analysis (serum, ELISA-sandwich method of BIOVENDOR Co.), Results: Spectrum of patients, whose condition and age distribution in our group corresponded to the general population of the Czech Republic. The mean age of the probands was 51 years (18 to 82 years), the examined group can be characterized as subjects lacking signs of obesity. Leptinaemia was on average about 10 ng/ml (minimum 0, maximum 97.9 ng/ml), whereby men had values round 6 and women round 14 ng/ml (women had also a greater adipose tissue mass). Non-obese subjects (BMI<26) had a mean leptinaemia of 5 (women cca 6, men cca 2 ng/ml), obese subjects (BMI>30) have a leptinaemia of cca 19 ng/ml (women about 26, men about 13 ng/ml). With advancing age the leptinaemia in adults rises up to the age of 70, in subjects above 70 years it does not change (in women it declines significantly). The dynamics of leptinaemia imitate the changes of BMI and percentage of adipose tissue (in men also a rise in WHR). Leptinaemia is associated with the BMI (correlation coefficient 0.55), with the percentage of body fat (correlation coefficient 0.75), and in men with the WHR (correlation coefficient 0.82). The association between ageand leptinaemia is only indicated (correlation coefficient 0.29) and is not very close. According to the authors results subcutaneous body fat is responsible for cca 60% of the variability of leptinaemia (in women as much as 74%), BMI for 23%, age and sex for cca 9% of the vriability of leptinaemia. In men the WHR is responsible for 66% of the variability of leptinaemia. With an increase of subcutaneous adipose tissue by 1% the leptinaemia increases by some 0.54 ng/ml (in men by 0.22 ng/ml, in women by 0.84 ng/ml), with increasing BMI leptinaemia rises by 0.44 ng/ml/u (in men by 1.3 ng/ml, in women by 1.72 ng/ml), with advancing age leptin rises by 0.24 ng/ml/year (in men by 0.16 ng/ml, in women by 0.28 ng/ml), changes of leptinaemia imitate changes of BMI and the percentage of body fat. With increasing WHR in men the leptinaemia rises by 2.6 ng/ml/0.1 WHR., Conclusion: Standards of leptinaemia for the general population of the Czech Republic were elaborated. Leptinaemia correlates most closely of all anthropometric indicators with subcutaneous fat and in men with the WHR index. With advancing age between 20 and 70 years leptunaemia rises and then decliunes insignificantly (in women the changes are however significant). The primary cause of the mentioned differencesare probably changes of the bodily constitution.

Leptin is a small protein produced mainly by adipocytes. Recently, its relationship to obesity has been studied extensively. It was proved that obese individuals have either relative or absolute leptin deficiency. Several years ago, leptin was found to be produced also by the placenta. This stimulated us to study relationship between leptinemia and placental hormones in 85 women in the second gravidity trimester. Within the prenatal screening, these pregnant women were subjected to analysis of AFP, hCG, SP-1 glycoprotein and leptin and the results obtained were processed statistically. The control group consisted of 20 nonpregnant women with tetany. Women in the second gravidity trimester were found to have a significantly higher leptinemia than nongravid women (even with respect to body weight). This may be due to a larger amount of adipose tissue during gravidity and also leptin-resistance. Moreover, we recorded a negative correlation between leptinemia related to body weight and concentration of SP-1 glycoprotein. This finding supports the presumption that mother's leptinemia correlated negatively in the second gravidity trimester with quality and quantity of the placental syncytiotrophoblast. Our findings can be explained as follows: the biological effect of leptin is metabolically unfavourable for the growth of the foetus and the placenta. An increased leptinemia with advancing gravidity can be caused by a larger fatty mass and an increased activity of adipocytes when leptin presence increases in system circulation but the organism begins to be leptin-resistant and an "unfavourable" metabolic effect fort the gravid woman and the foetus is not distinct. These findings thus support the hypothesis postulating the nonsignificance of leptin production in human placenta and on the contrary the necessity of leptin-resistance for foetus development from the metabolic point of view. Thus, a decreased leptinemia immediately before and after the delivery could be caused by the still unclear regulators of leptin sensitivity. This is again a metabolically highly favourable state (reduced appetite, decreased body weight, increased energy output and others).

Leptin is protein produced by mature adipocytes into the system circulation and gives information to hypothalamic centers about fat amount in the organism. Leptin is supposed to play a causal role in energy output of the organism and influences the appetite (antiobese effect). Obese individuals were proved to have frequently hyperleptinemia. This disease is caused by a postreceptor disorder (however, several obese families had also normoleptinemia or even hypoleptinemia which is caused by polymorphism of Ob-gene). It was also found that leptin administration in animals leads to reduced appetite and decreased body weight. Interpretation of leptinemia in human is very complicated because leptinemia is influenced by many independent regulations (hormones, stress, food intake, motor activity atc.). Obesity is often associated with hyperinsulinemia and insulin resistance (a frequent cause of human mortality) so that correlations between insulin and leptin are intensively studied. Experimental models and animal studies revealed the existence of adipoinsular axis and it was found that insulin and leptin are contrahormones. In human studies, the majority of authors did not find correlation between leptinemia and markers of insulin secretion. Similar conclusions were drawn out in our previous paper [118]. This may be due to complex regulations of leptinemia in the organism and the use of biochemical markers with limited validity (insulin, C-peptide in fasting state and after stimulation). Therefore we decided to study correlation between leptinemia and intact proinsulin in the serum which is now considered to be the most valid marker of insulin secretion and provides information about an average "daily" insulinemia. This study was stimulated by the fact that increased leptinemia is found also in persons with prolonged hyperinsulinemia (a short-term hyperinsulinemia does not affect leptin concentration so that no available marker of insulin secretion is valid). We examined the group of 31 probands, patients of the Metabolic and Diabetologic Center at the hospital in Sternberk. They were diabetic patients of type 2 who were treated by peroral antidiabetics and insulin and who met criteria of good compensation. However, no correlation between leptinemia and proinsulinemia was found. We suppose that this failure was due to complicated fine regulations affecting leptinemia and also to the fact that intact proinsulin is not an "ideal" marker of a long-term hyperinsulinemia (correlation between insulin and leptin at euglycemic clamp indicates that there exist correlation between these parameters in human).