Abstract
Obesity is the underlying cause of a great number of “civilization” diseases on which special attention should be focused in the years to come. The discovery of leptin marks the beginning of the “leptin era” in the views and concepts for the neuroendocrine mechanisms regulating food intake. Synthesized and secreted by adipocellular tissue, leptin is a hormone functioning as an afferent signal in a negative feedback regulating body weight. Defect in the leptin signalling pathway leads to obesity in test animal models. However mutations in the leptin gene or leptin receptor are found in few obese persons, with most instances of overweight in humans being associated with elevated leptin levels. This is most likely attributable to a state of leptin resistance. The continuous detection of novel leptin actions implies that leptin should be by all means considered as more than just an “antiobesity” hormone. It is believed that leptin triggers the onset of puberty, exerts influence on fetal growth, regulates glucose homeostasis through affecting insulin secretion and activity, participates in the pathogenesis of metabolic syndrome, stimulates hematopoiesis and the like. Presumably leptin or its antagonists are potentially involved in diagnosing, pathophysiology and management of a number of human disease.

KEY WORDS: leptin, obesity, hypothalamus, diabetes mellitus, metabolic (X) syndrome. 

Abstract
Overweight is taken to be an independent risk factor of cardiovascular complications development among diabetic patients. The presence of interdependence between plasma levels of leptin ­ a hormone regulating body weight ­ and cardiovascular risk factors is a disputable issue.
It is the purpose of the study to assay the correlation existing between leptin and the single components of metabolic (X) syndrome. Serum leptin levels are measured using RIA kit (DSL ­ USA) in 45 women (norm 5,8­10,4 ng/ml) ? 25 men (norm 1,3­3,4 ng/ml). Significant correlations are documented with the body mass index (??I) (r=0,58 for women and r=0,76 for men), cholesterol (r=0,38 women and r=0,31 men), triglycerides (r=0,76 women and r=0,79 men), LDL cholesterol (r=0,24 women and r=0,37 men), LDL/HDL ratio (r=0,23 women and r=0,36 men), non-HDL cholesterol (r=0,26 women and r=0,27 men), fasting plasma glucose (r=0,79 women and r=0,79 men) and systolic blood pressure (r=037 women and r=0,47 men).
In conclusion it is assumed that leptin most likely affects some cardiovascular risk factors relating to the metabolic syndrome through mechanisms still not enough clarified.

KEY WORDS: leptin, obesity, cardiovascular risk factors, metabolic (x) syndrome.

?bstract
Serum prolactin levels (PRL) exceeding 100 ng/ml are universally accepted as characteristic of true prolactinomas, while levels in the range 30 to 100 ng/ml are associated with functional disorders or normal inhibitory control impairment by dopamine as the result of pituitary stalk compression, caused by nonfunctioning pituitary adenomas (NFPA). The absence of clinical manifestation, evidence of hormone hypersecretion or low biological activity of hormones interfere greatly with making exact NFPA diagnosis. In nearly 10 per cent, NFPA are capable to synthesize and secrete hCG b. It is the aim of the study to assess the contribution of serum hCG b levels in identifying pituitary adenomas. Forty-four women of reproductive age presenting mild hyperprolactinemia are covered by the study. Serum hCG b levels in patients with pituitary microadenomas, associated with mild hyperprolactinemia, are significantly higher, and differ from the ones in patients with mild idiopathic hyperprolactinemia and patients with microadenomas and moderately elevated PRL levels (>100 ng/ml). The heterogeneity of hCG b levels in patients with microadenoma, accompanied by mild hyperprolactinemia, warrant the assumption of a morphological heterogeneity of pituitary tumors. As shown by the results, evaluation of serum hCG b levels contribute to differentiate hyperprolactinemia genesis, and may be used as an additional method in diagnosing pituitary tumors.

KEY WORDS: mild hyperprolactinemia, b-subunit of chorionic gonadotropin, nonfunctionic pituitary adenoma, pituitary microadenoma. 

Abstract
The aim of this study is to determine the impact of hypermagnesiemia on bone metabolism in predialysis patients with chronic renal failure (CRF). Forty-six patients were examined ­ 21 men and 25 women aged 20­60. Serum creatinine, total and ionized calcium, alkaline phosphatase, serum magnesium, intact parathormone and serum osteocalcin were analyzed. A dual-energy X-ray absorptiometry (”Lunar”) and computed tomographic osteometry of lumbar vertebrae were implemented in all patients. In those at first stage of CRF the serum magnesium shows a trend toward increase while in patients at second and third stage of CRF it is authentically increased ­ 1,043±0,074 mmol/l, and in eight of them (28,57%) it exceeds the reference limits. The intact parathormone in patients with hypermagnesiemia ­ 170,85±41,40 pg/ml does not differ significantly from that in patients at II and III stage of CRF ­ 153,47±23,63. The same dependence is valid for serum osteocalcin ­ 113,51±37,26 ng/ml in patients with hypermagnesiemia versus 120,56±22,61. Three of all patients at an opening stage of CRF have osteoporosis and 7 ­ osteopenia, while 8 of those at II and III stage of CRF have osteoporosis and 10 ­ osteopenia. A moderate positive correlation (r=0,34) was found between magnesium and intact parathormone in the patients at I stage of CRF. No significant correlation was found between magnesium and osteodensitometric indices. The existing slight to moderate hypermagnesiemia in predialysis patients with CRF does not reduce the level of intact parathormone and serum osteocalcin. The obtained data rule out the independent use of serum magnesium as a noninvasive marker for bone turnover assessment.

KEY WORDS: chronic renal failure, magnesium, renal osteodystrophy, parathormone, osteocalcine.

Abstract
The study covers a series of 184 patients with Cushing's syndrome of which 155 present Cushing's disease, 23 ­ corticosteromas and 6 ­ ectopic ACTH secretion.
Osteoporosis is observed in 89,6 per cent of Cushing's disease, 56,5 per cent of those with corticosteromas, and in all cases with ectopic ACTH secretion.
An assessment is also done of the relationship existing between cortisol levels in the various pathomorphological forms of Cushing's disease and bone mass changes.
In the event of hypercortisolicism accompanied by carbohydrate metabolism impairment, the incidence rate and severity of osteoporosis are rather markedly expressed.
Bone densitometry of the forearm, performed in 15 patients with Cushing's syndrome, is not informative insofar as the forearm bones are not a predilection site of glucocorticoid action.

KEY WORDS: Cushing's syndrome, cortisol, bone mineral density, osteoporosis. 

Abstract
This is a report on 49 patients presenting diabetes mellitus type 1 divided up into two groups, as follows: group one ­ free of diabetes mellitus complications (DM-1, n=28), and group two ­ with diabetic microangiopathy (DM-1C, n=21). Twenty healthy persons of comparable age are investigated for control purpose.
The goal of the study is to perform serum evaluation using biochemical methods with a view to characterize and compare the oxidative stress situation in either group of patients.
A significantly reduced serum superoxide-dismutase (SOD) activity is documented in both groups, as compared to controls. Total antioxidant capacity (TAOCS) is significantly lower in group one and two, by comparison with controls. In DM-1 it amount to 22,55±8,99 mmol/H2O2/ml/min­1, and in the controls accordingly 34,1±5,28 mmol/H2O2/ml/min­1 (?<0,001). In DM-1C it is 24,5±12,4 mmol/H2O2/ml/min­1 and relative to controls ?<0,01. TAOCS does not reveal significant differences between the two groups of patients. Lipid peroxides (LP) are significantly increased. In DM-1 they amount to 2,87±0,95 nmol/l, and in the controls 2,07±0,65 nmol/l, at significant difference (?<0,01). In DM-1C ­ 3,1±1,02 nmol/l, and relative to controls ?<0,001. Lipid peroxides do not show differences between the two groups. 
The obtained results point to presence of oxidative stress in diabetic patients type 1, expressed by the decrease in TAOCS, increased amount of LP, increased FA and reduced SOD level, as compared to controls. SOD activity is lower among patients with complications.

KEY WORDS: oxidative stress, free radicals, diabetes.

Abstract
Opinions on the optimal therapeutic approach to hyperthyroidism are conflicting, with three procedures being mainly used: antithyroid drug therapy, subtotal thyroidectomy and radioiodine (I131) therapy. Antithyroid drug therapy is usually given preference by most clinicians, although relapses often occur. It is the purpose of the study to assay the effect of some demographic and clinical factors on the outcome of treating Graves' disease patients with antithyroid drugs (ATD). One-hundred twenty patients with Graves' disease (96 women, 24 men) at mean age 41,93±12,61 years are covered by the study; in 53 of the total (44,2%) relapses are noted following treatment with methimazole (MMI) over periods ranging from 12 to 24 months. Remission is deemed as attained in patients remaining euthyroid for minimum 15 months after ATD therapy discontinuation. The incidence rate of Graves' disease recurrences depends on the patient's age, size of goiter, presence of ophthalmopathy and severity of the disease. The role played by the presence of acute inflammatory process as a factor triggering the onset of hyperthyroidism is also assayed. The positive familial history of thyroid autoimmune diseases, chronic stress situations and gastrointestinal infection are all factors that may influence the incidence rate of Graves' disease relapses.

KEY WORDS: Graves' disease, antithyroid therapy, recurrence.