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Kun Imre Zoltán, Kun Ildikó and Kolcsár Melinda

Abstract

Polycystic ovary syndrome (PCOS) is the most frequent endocrine disease among women with childbearing potential, the best-known cause of hirsutism, with a hypothesized prevalence of 8-22%. The first part of the paper discusses the conceptional evolution of the syndrome, from its description in 1935 by Stein and Leventhal till today. It describes the changes in the criteria systems, emphasizing that the Rotterdam criteria, proposed in 2003 by the European Society for Human Reproduction and Embryology/American Society for Reproductive Medicine, are still valid today. This system basically differs from earlier (1990) NIH-criteria in one aspect: it introduced two newer phenotypes, one without hyperandrogenism and the other with ovulatory cycles, so it distinguishes 4 phenotypes. The etiology and pathogenesis of PCOS is heterogeneous, multifactorial, poorly understood. We present the 3 leading hypotheses (1 - hypothalamo-hypophyseal disturbances, 2 – primary enzyme disorders in ovarian, or ovarian/adrenal steroidogenesis, resulting primarily in hyperactivity of 17alpha-hydroxylase/17,20-lyase, 3 – insulin resistance-hyperinsulinism and other metabolic dysfunctions). We emphasize the role of genetically determined hyperandrogenism, that of insulin resistance-hyperinsulinism and the importance of reinforcing each other. Subsequently, the aggravating aspects of the frequently associated metabolic syndrome are discussed, and then the effects of the mentioned pathological processes on the endocrine and other organ structures participating in the regulation of sexual functions. We stress the hypothetical role of perinatal and pubertal androgen exposition in the pathogenesis of PCOS. The mechanisms of anovulation and those of the endometrial lesions are discussed, too. The clinical manifestations, the paraclinical and laboratory examinations, the positive and differential diagnosis and the complications are also presented. We intend to deal with the therapeutic aspects of PCOS in an upcoming paper.

Open access

Kolcsár Melinda, Gáll Zsolt, Bába László-István and Kun Imre Zoltán

Abstract

The relationship between antidepressants (AD) and metabolic syndrome (MS) can be approached from many perspectives. We can start from the mutuality of depression and MS: depression often causes MS and vice versa; however, the two diseases aggravate each other. Altered glucocorticoid secretion - among others - may be a common etiological factor for depression and MS. Enhanced glucocorticoid production leads both to sleep disorders and insulin resistance, and several antidepressants cause obesity and insulin resistance. In addition, sympathetic nervous system activity increases in depression, together with the elevated production of counter-insulin hormones such as catecholamines (adrenaline) and glucocorticoids. From the components of MS, body weight changes can be most easily followed by the patient. The obesogenic mechanisms of AD drugs are different. The H1-receptor blocking agents have the most important weight gaining effect, followed by the 5-HT2c-receptor blocking and/or down-regulating ADs. The fattening effect of mirtazapine, paroxetine, and tricyclic antidepressants are based on such central mechanisms. Blocking of alpha1-receptors contributes to the obesogenic effects of certain drugs by inducing sedation: this has been confirmed in case of imipramine, amitriptyline, and doxepin. Fluoxetine behaves differently depending on the dose and duration of treatment: while at the usual doses it induces weight loss at the beginning of therapy, its initial anorexigenic effects reverses during prolonged use; while its activation effect at high doses is favorable in bulimia. The selective noradrenaline reuptake inhibitor reboxetine reduces appetite, similarly to bupropion, which inhibits dopamine reuptake as well. We highlight the effect of fluoxetine on direct adipogenicity, mentioning its preadipocyteadipocyte transformation-reducing and adipocyte proliferation-inhibiting activity, as well as its ability to enhance fat cell autophagy.

Open access

Elod Nagy, Imre Zoltan Kun and Piroska Kelemen

Abstract

Background: there is an overt bias between cardiovascular morbidity and mortality in male and female patients. Research of the past decades postulated that this difference could be due to the lipid-lowering effect of male sexual-steroids, that show decreased values in cardiovascular disease.

Methods: the aim of our study was to determine total serum testosterone and dehydroepiandrosterone sulfate (DHEA-S) on a peripheral arterial disease patient’s cohort (n=35), in comparison with a healthy control group, (n=23) and to establish correlations with other biological risk factors like serum lipids, C-reactive protein, plasma fibrinogen, and the ankle-brachial pressure index.

Results: our results showed that total serum testosterone and DHEA-S were significantly decreased in PAD patients in comparison to the control group. We could not observe any significant correlation with the presence of critical ischemia, the levels of total cholesterol, HDL-cholesterol, triglycerides, lipoprotein (a), C-reactive protein or plasma fibrinogen.

Conclusion: these results express that low androgen levels could be implicated in the pathogenesis of peripheral arterial disease, but testosterone and DHEA-S are not markers of disease severity. The elucidation of their exact role needs larger, population-based studies.

Open access

Anna David, Imre Zoltán Kun, Gábor Nyírő, Zsuzsánna Szántó and Attila Patócs

Abstract

Introduction: Isolated Short Stature Homeobox (SHOX) gene haploinsufficiency can be found in 2-15% of individuals diagnosed with idiopathic short stature determining different skeletal phenotypes.

Case presentation: We present the history of an 11-year-old female patient diagnosed with idiopathic short stature. Clinically, she was moderately disproportionate, with cubitus valgus and palatum ogivale. Her breast development was in Tanner stage 1 at the time of diagnosis. The endocrine diagnostic tests did not reveal any abnormalities except a slightly elevated thyroid stimulating hormone. We have also assessed the bone radiological findings. Multiplex Ligation-dependent Probe Amplification technique used for the identification of SHOX gene haploinsufficiency showed a heterozygous deletion spanning exons 4-5 of SHOX gene.

Conclusions: This case is determined by deletions in exons 4-5 of SHOX gene and indicates the necessity of screening for SHOX deletions in patients diagnosed with idiopathic short stature, especially in children having increased sitting height-to-height ratio or decreased extremities-to-trunk ratio.

Open access

László-István Bába, Zsolt Gáll, István Lóránt Bíró, Tibor Mezei, Imre Zoltán Kun and Melinda Kolcsár

Abstract

This study aims to investigate the effects of chronic fluoxetine (FLX) treatment on preadipocyte factor-1 (Pref-1) expression in subcutaneous, visceral and brown adipose tissues, and on the size of vacuoles in a dipocytes obtained from the perirenal regions in rats. Twenty-eight Wistar rats were treated with FLX at two different doses and fourteen animals received vehicle. After 40 days of treatment, the subcutaneous, perirenal and interscapular adipose tissues were collected. Pref-1 expression was examined using an immunohistochemical method and the vacuolar area was measured in stained sections. In the low dose FLX group, the size of vacuoles increased both in male and female animals. The high dose of FLX also induced a significant increase of vacuole size, but only in male animals. Neither of the two doses of FLX has significantly affected the Pref-1 expression in any type of adipose tissue.