[Primary aldosteronism in gravidity]. / Primárny aldosteronizmus v gravidite.

Endocrinology and obstetrics have one thing in common--diagnosis and treatment endocrine diseases in gravidity. These are modified by physiological changes in gravidity, often missing data and tests in normal condition and the influence of diagnosis and treatment on the pregnant female and fetus have also to be taken into consideration. If diagnosis of primary aldosteronism is suspected, suprimed plasmatic renin activity is determinant indicator (disregarding arterial hypertension, hypokaliaemia, hyperkaliuresis and proteinuria) as well as ultrasound diagnostics or adrenal gland diagnostics means magnetic resonance imaging. Aldosteron produced adenomas may by treated by adrenalectomy in the second trimester, late diagnosed adenoma and hyperplastic forms are treated by the administration of the respective medicaments.

[Dehydrdoepiandrosterone, dehydroepiandrosteron-sulfate and insulin in acute myocardial infarct]. / Dehydroepiandrosterón, dehydroepiandrosterón-sulfát a inzulín u akútneho infarktu myokardu.

The authors discuss the relationship between dehydroepiandsoterone, its sulphate conjugate and insulin and ischaemic heart disease in patients with acute myocardial infarction. In the examined group of patients they found lower values of dehydroepiandosterone and its sulphate in men, lower values of dehydroepiandosterone in women as compared with mean values with regard to age and a close inverse correlation of insulin and dehydroepiandrosterone and insulin and dehydroepiandrosterone sulphate. Whether dehydroepiandosterone is the "missing link" of hyperinsulinaemia and arterosclerosis is so far only a theoretical issue.

Primary aldosteronism caused by aldosterone-producing adenoma in pregnancy--complicated by EPH gestosis.

Pregnancy in conjunction with primary aldosteronism is an unusual occurrence. We report a 28-year-old woman who presented with mild hypertension and hypokalemia as manifestations of primary aldosteronism caused by an aldosterone-producing adenoma in the left adrenal gland during pregnancy. Although the diagnosis was straightforward, the patient refused to undergo the proposed operation during the second trimester of her pregnancy. She was not admitted to hospital until she developed EPH gestosis in the 27th week of gestation, which had an unfavourable outcome for the infant who died nine days after delivery. The patient underwent a laparoscopic adrenalectomy which resulted in normalization of blood pressure and blood potassium levels. In cases of aldosterone-producing adenoma, surgery in the second trimester is the most appropriate option to avoid a poor obstetric outcome.

[The polycystic ovary syndrome and insulin resistance]. / Syndróm polycystických ovárií a inzulínová rezistencia.

The insulin resistance syndrome and the polycystic ovary syndrome (PCOS) appear to have some following coincidences: the existence of subclinical acanthosis nigricans in PCOS hyperinsulinemic women, correlation of insulin levels and free testosterone, insulin-like growth factor I binding protein (IGFIBP), and sex-hormone binding globulin. Insulin and IGFI act synergically with luteinizing hormone increasing the activity of cytochrome P450c17 and its enzymatic activity in the adrenals. The decrease in IGFI level and IGFI receptors in the ovarian granulosa cells reduce the steroids aromatisation. The increased expression of IGFI receptors in the theca cells favours the androgens' synthesis. Long-term insulin therapy results in an increase in ovary volume and the blood androgens levels. The deterioration of insulin resistance in PSOC women progresses also by the reduction of type I of skeletal muscle fibres which are sensitive to insulin, and the increase of type II fibres which are resistant to insulin in hyperandrogenemia. Testosterone deteriorates the skeletal as well as hepatic insulin sensitivity by both its facilitating effect on lipolysis and the increase of free fatty acids. Abdominal obesity seen in PCOS and insulin resistance is composed by adipocytes with glucocorticoid receptors, which after cortisol stimulation activate the lipoprotein lipase and fat accumulation. Gynoid obesity with the preferential aromatisation of steroids is not evolved because of the low estrogens and progesterone levels in PCOS. Low progesterone levels (with anticortisol effect) support the development of abdominal obesity. Ultimately, the early peak of insulin secretion (4-8 min) in PCOS is higher. This fact should testify a certain diabetic disposition. (Ref. 37.)

[Initial experience with laparoscopic adrenalectomy]. / Prvé skúsenosti s laparoskopickou adrenalektómiou.

We present the first experience with laparoscopic adrenalectomy, which was in Slovakia introduced to the surgical practice on March 3, 1996. We analyse first seven patients who underwent completed laparoscopic adrenalectomy (five leftsided, two right-sided). Four patients had cortex adenoma (clinically 2 incidentalomas and 2 Cishing syndroma), three patients had cortex hyperplasia (clinically Conn syndroma). Average duration of operation was 120 minutes, there were no postoperative complications. Average postoperative hospital stay was 5 days. Our initial experiences are comparable with that of surgical departments which has more than two-years experiences. Laparoscopic adrenalectomy is a perfect method for the small adrenal tumors and it is better than traditional transabdominal approach.

[Successful treatment of agranulocytosis caused by carbimazole using recombinant granulocyte-macrophage colony stimulating factor]. / Uspesná liecba agranulocytózy vyvolanej karbimazolom pomocou rekombinantného granulocyty-makrofágy kolónie stimulujúceho faktora.

The authors describe a patient with hyperthyroidism who developed after three weeks' treatment with carbimazole agranulocytosis and the condition was complicated by septic shock. The authors used for treatment in addition to antibiotics and corticoids, for the first time in their practice, human recombinant granulocyte macrophage colonies stimulating factor (rHuGM-CSF) which produced a very favourable effect. In the meantime the patient was prepared for goitrectomy, operated and discharged in a satisfactory condition to have ambulatory treatment.

[Hyperandrogenic states in women (polycystic ovary syndrome) and insulin resistance]. / Hyperandrogénne stavy u zien (SPO) a inzulínová rezistencia.

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.

[Primary hyperaldosteronism, problems in diagnosis and therapy in clinical practice]. / Primárny hyperaldosteronizmus, problémy jeho diagnózy a liecby v klinickej praxi.

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.