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J Hrnciar

Publications and source records attributed to J Hrnciar.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Insulin resistance and arterial hypertension].

The hypothesis of insulin resistance in the pathogenesis of arterial hypertension as part of the hormonal metabolic X syndrome and our 5H syndrome resp. (association of hyperinzulinism with hyperglycaemia-NIDDM-hyperlipoproteinaemia, hypertension and a hyperandrogenic state in women) is based on sympathomimetic, sodium retention and trophic effects of insulin. In the submitted paper the authors review opinions supporting and refuting the validity of this hypothesis. Based on the results of different studies in recent years another genetic predisposition comes also to the foreground, i.e. reduced vascularization of the skeletal muscles which on the background of insulin resistance leads to enhanced development of hypertension with subsequent hypertrophy of the vascular wall and left ventricle and to the development of arteriosclerosis. From the clinical aspect this stimulating pathogenetic concept within the framework of the hormonal and metabolic X syndrome and 5H syndrome makes it possible to use a more adequate approach to prevention and treatment not only of arterial hypertension but also of associated phenomena which enhance the risk of cardiovascular morbidity and mortality in the population. The authors summarize factors which during non-pharmacological treatment promote insulin resistance and those which improve it. When drugs are selected for pharmacological treatment, priority is given to those which improve the insulin sensitivity index (ACE-inhibitors, alpha blockers) or are at least neutral in this respect (Ca antagonists, beta blockers with ISA and cardioselective). The drugs must not enhance associated hyperlipoproteinaemia, hypercoagulability, hyperviscosity, hyperuricaemia) and they should exert a positive effect on the regression of hypertrophic vascular walls and the left ventricle.

Diabetes Mellitus, Type 2↗
PubMed1995

[Hyperandrogenic states in women (polycystic ovary syndrome) and insulin resistance].

In the submitted paper the authors try to explain the relationship between hyperinsulinism as the cause and the polycystic ovary syndrome as the consequence of hyperinsulinism. This takes place via the insulin like growth factor I, the luteinizing hormone, sex binding hormone globulin, insulin like growth factor I binding protein and growth hormone. By varying interactions of the regulatory hormones gradually the granulosa cells are destroyed and replaced by androstendione producing thecal and stromal cells with impaired folliculogenesis. Chronic hyperestrogenism interferes also with hypothalamic regulation in the nucleus arcuatus. As almost identical changes are found in polycystic ovary syndrome and puberty, genetic and/or environmental factors certainly play a part. Their more detailed specification is a task for the future.

Female↗
PubMed1995

[Clinical manifestations of the insulin resistance syndrome. The hormonal-metabolic syndrome X, the 5H syndrome and their etiopathogenesis].

The author summarizes mechanisms by which insulin resistance and compensatory hyperinsulinism are manifested in the clinical picture. He divides the mechanisms into prereceptor, receptor and postreceptor mechanisms. The latter dominate in the population quantitatively and thus also by their impact because they create the so-called 5H syndrome (association of hyperinsulinism with hyperglycaemia (NIDDM), hyperlipoproteinaemia, hypertension, hirsutism and the polycystic ovary syndrome) or the so-called hormonal metabolic syndrome X, lethal tetrad, metabolic syndrome, syndrome of insulin resistance). The term syndrome X does not appear suitable as it is frequently mistaken for coronary X syndrome which probably is also conditioned by hyperinsulinism, for the hormonal metabolic X syndrome and probably also fot the "fragile X syndrome" in genetics. The 5H syndrome is caused by a postreceptor disorder of insulin efficiency for which so far the molecular basis and dominating organ site have not yet been defined adequately. Hyperinsulinism is conceived as an insulin resistance compensating phenomenon. In its development participates, however, in addition to compensatory hypersecretion also impaired insulin utilization (liver, muscles) and an impaired primary secretory response caused probably by a disorder of blood sugar control (glucokinase, GLUT 2). This is suggested by the frequently inadequate response of the blood sugar level, IRI and C-peptide during the oral glucose tolerance test (OGGT). A hyperinsulinaemic response may be encountered when the blood sugar curve is normal, flat, in impaired glucose tolerance and in diabetes. Thus OGGT alone is not suited for the early detection of the 5H syndrome unless concurrently the IRI and C-peptide response is recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus, Type 2↗
PubMed1995

[The effect of long-term treatment of arterial hypertension with Ca antagonists on the renin-angiotensin-aldosterone system in diabetics. Hyporeninemic hypoaldosteronism].

During long-term treatment of arterial hypertension with calcium antagonists of the dihydropyridine type activation of the sympathetic nervous system and subsequently also of the renin-angiotensin-aldosterone system persists, while the haemodynamic reaction to vasodilatation, manifested by an elevated pulse rate and minute volume from the initial stage of therapy, recedes. In type II diabetics the basal and stimulated response of the renin-angiotensin-aldosterone system is reduced. The administration of calcium antagonists of the dihydropyridine type does not stimulate significantly the renin-angiotensin-aldosterone system as the starting function of the sympathetic nervous system is impaired within the framework of vegetative neuropathy. In almost 20% NIDDM plasma renin activity and aldosterone do not respond to furosemide administration and the vertical posture. In others the response is found but takes place at reduced levels. Hyporeninaemic hypoaldosteronism is thus manifested not so much by a drop of plasma renin and aldosterone beneath the lower range of reference values as by a reduced response to stimulation. Functional hyporeninaemic hypoaldosteronism is another, frequent late complication of diabetes. In advanced forms a further block of the renin-angiotensin-aldosterone system by ACE inhibitors can then produce, even in the absence of diabetic nephropathy, in the stage of chronic renal failure dangerous hyperkaliaemia which may threaten the patient. Dynamic examination of the sympathetic nerve and the renin-angiotensin-aldosterone system makes it possible to predict this condition. In practice it is necessary in diabetics with arterial hypertension after starting with ACE inhibitors during the first days to monitor repeatedly plasma potassium and creatinine. ACE inhibitors and calcium antagonists are otherwise for diabetics drugs of first choice which can arrest the progression of nephropathy, effectively reduced the blood pressure without causing deterioration of insulin resistance and hyperlipoproteinaemia and lead even to regression of hypertrophy of the vascular wall and left ventricle.

Aged↗
PubMed1994

[The importance of studying the renin-angiotensin-aldosterone system in essential arterial hypertension in clinical practice. Activity of the renin-angiotensin-aldosterone system during treatment of hypertension with ACE-inhibitors and beta blockers].

The authors assessed in 20 subjects with mild or medium severe arterial hypertension basal and stimulated values of plasma renin activity (PRA) and aldosterone before onset of treatment and after 6-week therapy with enalapril (ENAP KRKA) or metoprolol (Vasocardin Slovakofarma). PRA and aldosterone secretion was stimulated by a vertical position and by administration of 40 mg furosemide by the i.v. This test proved suitable for assessment of secondary arterial hypertension in different forms of primary hyperaldosteronism and for expressing suspicion of renovascular hypertension and hypertension with affection of the renal arteries resp. Based on PRA levels, arterial hypertension can be divided into normorenin, high-renin and low-renin hypertension. This classification is, however, of no value for selection of treatment and the prognosis of hypertension. Each level of PRA can be associated with three different aldosterone levels. PRA and aldosterone did not correlate with urinary K, Na excretion nor with blood pressure. During treatment with ACE inhibitor PRA rose while basal as well as stimulated aldosterone levels declined. After administration of betablockers basal as well as stimulated PRA and aldosterone levels declined.

Adult↗
PubMed1994

[Thyrotoxic crisis].

A thyrotoxic Crisis is an acute or subacute metabolic explosion caused by uncontrolled release of tyronines from the thyroid gland (more frequently a diffuse thyroid gland) following its injury: strumectomy, administration of a therapeutic dose of I131, inflammations, or excessive stimulation (massive release of TSIg by stress lympholysis, low iodine doses). Concurrently a massive conversion of T4 to T3 in tissues must occur which is enhanced by discontinuation of beta-blockers, thyrostatics, synthetic glucocorticoids and administration of drugs replacing T4 from the bond to plasma carries (salicylates, sodantone, furosemide, barbiturates etc.) during stress. The trigger mechanism of the crisis is any severe stress (surgery, accidents, infection, childbirth) and the administration of iodine preparations. Their effect depends, however, on the dose, period of administration and the functional and morphological state of the thyroid gland. Small doses of iodine administered for a short period stimulate hormonogenesis, large doses (more than 10 mg/day), on the other hand, block the iodine pump, T4 and T3 secretion by the thyroid gland and conversion of T4 to T3 in tissues. In therapy specific procedures are involved: I. Block of T4, T3 synthesis and secretion a) ipodate, ioipanoic acid, Lugol's solution i.v. b) propycil, methimasol c) in iodine-basedowized goitres perchlorate and lithium II. Block of T4 to T3 conversion (iodine preparations, incl. amiodarone, beta-blockers, propycil, dexamethasone). III. Reduction of hypermetabolism (beta-blockers, Ca inhibitors) IV. Reduction of free T4 and T3 in blood stream (by plasmapheresis, haemoperfusion, haemodialysis) V. General provisions in intensive therapy (control of hyperpyrexia, dehydration, hypoxia, supraventricular arrhythmia and circulatory decompensation).

Humans↗
PubMed1993

[Methods of measuring hyperinsulinism and insulin resistance].

The author gives an account of methods used for evaluation of hyperinsulinism and insulin resistance such as: hyperinsulinaemic, euglycaemic and hyper- and hypoglycaemic "clamp", minimal model of glucose and insulin kinetics. They evaluate specially indexes used in clinical practice such as: I/G, (insulin/glucose--the so-called insulinogenic index), the G/I index, (the so-called index of insulin resistance) and the index of C-peptide/IRI, basal and during the oral glucose tolerance test. In epidemiological studies of the prevalence of the X syndrome (5H) he recommends to use the G/I index basal and minimal two hours after a glucose load, along with assessment of C-peptide. It is thus possible to estimate not only insulin resistance but also hyperinsulinism and the ratio of distribution-utilization factors in the development of this hyperinsulinism. Hyperinsulinism need not be only hypersecretory but may be also associated with a reduced insulin utilization in the liver and peripheral target tissues. A hyperinsulinaemic response may be observed in four types of glycaemic curves after a glucose load: a in a normal curve, a flat curve, in impaired glucose tolerance and in a diabetic curve. According to the author the limiting value of the I/G index is 0.4 and the limiting value of the G/I index is 6 when the insulinaemia is expressed in mIU/l and the blood sugar level in mg%. The limiting level of insulinaemia after two hours is 63 mIU/l. The ratio of C-peptide: IRI basal is cca 5:1 after a glucose load 2.5:1 when expressed in moles.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1992

[How should we implement the basic principles of treatment of type 2 diabetes mellitus from the aspect of the hormono-metabolic syndrome X (5H)?].

The authors summarize the principles of the therapeutic approach to the 5H syndrome [1. hyperinsulinism, 2. hyperglycaemia (NIDDM), 3. hyperlipoproteinaemia (obesity), 4. hypertension, 5. hirsutism], in particular its two components, i.e. NIDDM and arterial hypertension. The authors found that early treatment of hyperinsulinism, e.g. already in the stage of impaired glucose tolerance or NIDDM with oral antidiabetics, their disproportionate increase with regard to the blood sugar level and glycosylated haemoglobin without making "hygienic" provisions (radical weight reduction; increased physical activity to the maximum possible individual level; energy restricted diet in particular as regards carbohydrates and fat) does not prevent progression of the components of the 5H syndrome to the clinical stage. In treatment of arterial hypertension associated with 5H syndrome non-selective beta-blockers and thiazide diuretics are unsuitable because they worsen the HPLP and enhance insulin resistance. Suitable preparations are combinations of ACE-inhibitors, calcium antagonists, selective beta-blockers in particular with ISA and beta-blockers with a partial selective sympathomimetic activity (devalol and celiprolol). Hygienic provisions must be started in childhood, or when hyperinsulinism is detected.

Blood Glucose↗
PubMed1992

[Insulin resistance and arterial hypertension. Hyperinsulinism as a basic etiopathogenic factor in essential arterial hypertension and associated phenomena].

In 50 normotonic patients with type 2 diabetes (NIDDM) and controls matched for sex and age with NIDDM and hypertension a statistically significant difference was found as regards S-peptide values on fasting, cholesterol, triglycerides, BMI and atherogenic index (cholesterol/HDL, p < 0.01). C-peptide values correlated positively with values of the systolic and median BP and the atherogenic index in both groups. In normotonic diabetics there was also a positive correlation with the BMI and in hypertonic subjects with the triglyceride levels. The results confirm the hypothesis that in NIDDM there is a direct relationship between arterial hypertension, unfavourable lipid parameters and insulin resistance and compensatory hyperinsulinism resp. The authors discuss possible mechanisms by which hyperinsulinism mediates a rise of BP, hyperlipoproteinaemia, hyperglycaemia and hirsutism (hormonal metabolic syndrome X and 5H resp.). These phenomena are the main risk factors of cardiovascular diseases and lead via heart attacks and cerebrovascular attacks (IHD and stroke) to a high cardiovascular morbidity and mortality in our population. The morbidity and mortality is steadily increasing and thus we are among civilized countries among those with the highest morbidity and mortality.

Diabetes Mellitus, Type 2↗
PubMed1992

[The dilemma of syndrome X].

The term X syndrome involves several dilemmas. The terminological dilemma is that this term is used to describe microvascular angina pectoris, as well as Reaven's metabolic-hormonal syndrome and our 5H syndrome [association of hyperinsulinism with arterial hypertension, hyperlipoproteinaemia, hyperglycaemia (NIDDM) and hirsutism]. It is probable that the coronary X syndrome is frequently conditioned by the hormonal-metabolic X syndrome. The pathogenetic dilemma is that it is not clear why in microvascular angina pectoris the coronary circulation does not possess an adequate reserve for vasodilatation during exercise or in response to some pharmacological stimuli. This could condition hyperinsulinism in hypertonic subjects with NIDDM with an early disorder of paracrine endothelial relaxation mechanisms (EDRF-NO), with a predominance of vasoconstrictor mechanisms (endothelin-1). In Reaven's syndrome X it is not clear whether insulin resistance of the postreceptor type is a primary inborn phenomenon which is compensated by insulin hypersecretion or whether it is a secondary phenomenon, which develops ex post and by which the target tissues defend themselves against an excessive effect of insulin (e.g. down regulation receptors) in primary disorders of its secretion.

Angina Pectoris↗
PubMed1992

[Hyperinsulinism and the coronary syndrome].

In one third of patients who suffered an infarction NIDDM and arterial hypertension are present. In the absolute majority of patients with IHD, as apparent from the IRI and C-peptide response after a glucose load, hyperinsulinism is present. The blood sugar response can have the character of diabetes or of impaired glucose tolerance, the curve may be very flat or normal while the IRI and C-peptide response are excessive. Hyperinsulinism has a hypersecretory origin as suggested by the concurrently elevated C-peptide level but also reduced insulin utilization in the liver and peripheral target organs. Hyperinsulinism is thus a regular associated phenomenon of IHD and is a special risk factor independent on hyperglycaemia and associates with the other main risk factors of IHD such as arterial hypertension, HPLP (android obesity), hyperglycaemia (NIDDM) and hirsutism as a manifestation of a hyperandrogenic state in the female organism with the syndrome of polycystic ovaries. Hyperinsulinism plays an indirect role in the pathogenesis of coronary syndrome via the main risk factors (5H syndrome--hyperinsulinism, hypertension, HPLP, hyperglycaemia, hirsutism) and also directly by its action on endothelial paracrine mechanism of the coronary circulation where in the early stage vasoconstrictor factors predominate (endothelin-1, PGF2-alpha) over physiological vasodilatating factors (EDRF-NO, PGE2, PGI2) and this leads then to functional spasms. It seems that also the coronary X syndrome develops very frequently on the background of the hormonal metabolic X syndrome or the 5H syndrome.

Adult↗
PubMed1992

[Clinical manifestations of insulin resistance. The hormonal-metabolic syndrome X (5H), its prevalence and impact on cardiovascular morbidity and mortality. I].

Insulin resistance (prereceptor, receptor, postreceptor) is a complex phenomenon. It penetrates into the clinical picture via hyperinsulinism as impaired glucose tolerance, or NIDDM, as hyperlipoproteinaemia, arterial hypertension and hirsutism in women (syndrome 5H) associated with the polycystic ovary syndrome or the HAIR-AN syndrome. Based on a group of their 480 patients with NIDDM, 108 women with hirsutism, 320 patients with myocardial infarction and the results of the national cardiovascular programme the authors estimate the prevalence of the 5H syndrome as follows: in the general population 5-10%, in patients with arterial hypertension 15-30%, in NDDM 65-90%, in hirsutic women 10-20% and in patients with myocardial infarction 30-50%. These figures could be, however, substantially higher if as the criterion the IRI response was taken or that of C-peptide in OGTT or the results of the hyperinsulinaemic euglycaemic clamp. The clinical 5H syndrome is a phenomenon of latent insulin resistance perceived late by doctors and patients.

Adult↗
PubMed1992

[Hyperinsulinism as a major etiopathogenic link with arterial hypertension, hyperlipoproteinemia and hirsutism. II].

The authors analyze mechanism by which hyperinsulinism causes NIDDM, hypertension, hyperlipoproteinaemia and hirsutism (5H syndrome). They demonstrate on a group of their 100 patients with NIDDM and arterial hypertension that, as compared with matched pairs without arterial hypertension, they have significantly higher levels of C-peptide and less favourable parameters of dyslipoproteinaemia. Hirsutism occurs in 10-15% of the adult female population, but in 18.4% women with NIDDM. However, in a group of 48 hirsutic women with NIDDM they did not find, as compared with matched pairs (i.e. women with NIDDM of analogous age, BMI and BP) significantly higher C-peptide and lipid levels. According to the authors congenital insulin resistance modified by numerous endogenous and exogenous factors is eventually manifested in the phenotype, in particular via hyperinsulinism as NIDDM, hypertension, associated with dyslipoproteinaemia and obesity which then, as the main risk factors, condition a high cardiovascular morbidity and mortality. Although hirsutism and the polycystic ovary syndrome are associated with hyperinsulinism, their interrelation is probably less close and thus has not such a negative impact on national health.

Adult↗
PubMed1992

[Primary hyperaldosteronism, problems in diagnosis and therapy in clinical practice].

The paper summarizes data from the recent literature on pathogenetic variants of primary hyperaldosteronism, screening, diagnosis and therapy of this secondary form of arterial hypertension. On examples from their own practice the authors draw attention to the that the diagnosis and treatment of this disease is not always as straightforward as might appear from the literature. The solution is simple, effective screening in every hypertensive patient by examination of the kalaemia before treatment of arterial hypertension is started. In case of hypokalaemia the subsequent procedure should be the concern of specialized departments.

Aged↗
PubMed1991

[Autoimmune mechanisms in endocrinology--the polyglandular autoimmune endocrine syndrome].

Autoimmune endocrinopathies belong to so-called organ specific autoimmune diseases. These diseases combine very often and from the polyglandular autoimmune endocrine syndrome (PAES), where autoantibodies either destroy or stimulate individual endocrine glands or hormone receptors in target tissues. Thus a wide range of combinations of hypofunctional or hyperfunctional clinical syndromes develops. PAES is a good natural model of endocrine polyautoaggressiveness. In its development the following aetiopathogenetic factors participate: 1. Hereditary familial disposition, expressed e.g. by certain inherited HHS genes (e.g. A1, B8, DR 3, 4). 2. Aberrant expression of these DR genes on endocrine organs due to bacterial or viral infections, pregnancy, stimulation of the thyroid gland by TSH or immunoglobulins (TSIg). 3. Antigenic mimicri and the presentation of autoantigens to immunocompetent cells. 4. Impaired immunoregulation--antigen specific insufficiency of suppressor T lymphocytes. 5. Local and general amplification reaction to an autoimmune process. 6. The development and autoreproduction of organ specific autoimmune endocrine disease and its development into the final stage of endocrine disease where autoantibodies may disappear. The diagnosis of PAES in clinical practice is difficult. Common immunological tests are not very conclusive. To assess a polyglandular affection we found useful the multiaxial synchronous test where stimulation of several hypothalamic releasing hormones combined with a hypoglycaemic stimulus is used. Autoimmune lymphocytic hypophysitis is part of PAES. In clinical practice this syndrome is therefore frequently incorrectly diagnosed and then incorrectly treated.

Autoimmune Diseases↗
PubMed1990

[Diagnosis of acute dissection of the aorta].

The authors present a group of 14 patients (9 men and 5 women) aged 38-76 years (mean age 59 years) who were hospitalized during the five-year period between 1984 and 1988 at the medical department A of the Regional Institute of National Health in Banská Bystrica on account of acute dissection of the aorta. The authors describe clinical manifestations which can lead to suspicion of this serious disease. They make the readers familiar with their experience with ultrasonic and X-ray examination (in particular aortography and computed tomography). They analyze their contribution to the diagnosis of acute dissection of the aorta.

Acute Disease↗