Browsing by Author "Micić, Dragan (7006038410)"

Maintaining body homeostasis is a prerequisite for normal reproductive function, which is vital for the survival of the species and an important process of natural selection. Body weight is an independent regulator of the hypothalamic–pituitary–gonadal axis activity. © 2016, International Society of Gynecological Endocrinology.

Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß-cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß-cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIRG), as well as Si by minimal model analysis. Si was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p<0.05), but no difference in AIRG existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p<0.05). BMI and WHR correlated negatively with Si (r = -0.43; r = -0.289, p<0.001, respectively), but not with AIRG (r = 0.116; r = -0.02, p>0.05, respectively). Increasing age correlated negatively with AIRG (r = -0.285, p<0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on Si as well as between age and PCOS on AIRG. Thus, patients below the age of 25 with PCOS showed enhanced AIRG (89.5 ± 7.1 vs. 65.1 ± 6.7, p<0.05) and decreased Si (2.43 ± 0.25 vs. 4.52 ± 0.62, p<0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. © 2022 Mirjana Šumarac-Dumanović et al.

Insulin resistance is believed to be an integral component of the polycystic ovary syndrome (PCOS). Beta (ß) cell dysfunction is also found in PCOS. In the study, we determined the influence of age, body mass index (BMI), and waist-to-hip ratio (WHR) on insulin response to oral glucose load (OGTT) and on insulin sensitivity (Si) and ß-cell function in young women with PCOS. One hundred fourteen patients with PCOS and 41 controls with normal basal plasma glucose were studied. A 75-g OGTT was performed to determine glucose tolerance and insulin response. Insulin sensitivity and ß-cell function were studied using a modified frequently sampled IV glucose tolerance test (FISGTT) to determine the acute insulin response (AIRG), as well as Si by minimal model analysis. Si was decreased in PCOS women (2.49 0.18 vs. 3.41 ± 0.36, p<0.05), but no difference in AIRG existed between the PCOS and control group (75.1 ± 4.6 vs. 63.4 ± 4.6, p<0.05). BMI and WHR correlated negatively with Si (r = -0.43; r = -0.289, p<0.001, respectively), but not with AIRG (r = 0.116; r = -0.02, p>0.05, respectively). Increasing age correlated negatively with AIRG (r = -0.285, p<0.001). There was a significant interaction between disease (PCOS), BMI, and WHR on Si as well as between age and PCOS on AIRG. Thus, patients below the age of 25 with PCOS showed enhanced AIRG (89.5 ± 7.1 vs. 65.1 ± 6.7, p<0.05) and decreased Si (2.43 ± 0.25 vs. 4.52 ± 0.62, p<0.05) compared to age-matched controls. In conclusion, these data suggest that not all patients with PCOS have basal and stimulated hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Based on these data in young PCOS subjects, the development of insulin resistance and T2DM may be prevented with appropriate treatment strategies. © 2022 Mirjana Šumarac-Dumanović et al.

Introduction Premature ovarian failure (POF) is characterized by amenorrhea, hypergonadotropism and hypoestrogenism in women bellow 40 years. Osteoporosis is one of the late complications of POF. Objective To correlate collagen type I alpha1 (COLIA1) gene polymorphism with bone mineral density (BMD) in women with POF. Methods We determined the COLIA1 genotypes SS, Ss, ss in 66 women with POF. Single nucleotide polymorphism (G to T substitution) within the Sp 1-binding site in the first intron of the COLIA1 gene was assessed by polymerase chain reaction (PCR) followed by single-stranded conformation polymorphism (SSCP) analysis. Bone mineral density (BMD) was measured at the lumbar spine region by dual X-ray absorptiometry. Statistics: Kruskal-Wallis ANOVA, Chi-square test, Spearman correlation test. Results The relative distribution of COLIA1 genotype alleles was SS - 54.4%, Ss - 41.0% and ss - 4.5%. No significant differences were found between genotype groups in body mass index, age, duration of amenorrhea or BMD. A significant positive correlation was observed between BMI and parity. Conclusion The COLIA1 gene is just one of many genes influencing bone characteristics. It may act as a marker for differences in bone quantity and quality, bone fragility and accelerated bone loss in older women. However, in young women with POF, COLIA1 cannot identify those at higher risk for osteoporosis.

Background/Aims: Exaggerated adrenocorticotropic hormone (ACTH) and cortisol responses to ghrelin in Cushing's disease (CD) have previously been reported, similarly to responses to corticotropin-releasing hormone (CRH). We assessed the ability of ghrelin to enhance ACTH and cortisol responses when added to CRH stimulation in CD patients. Methods: In 21 CD patients (18 females, 3 males; age 49.8 ± 10.2 years; BMI 29.8 ± 0.8) and 8 healthy subjects (7 females, 1 male; age 40.6 ± 5.3 years; BMI 29.9 ± 1.2), we administered (1) ghrelin 100 μg i.v. bolus, (2) CRH 100 μg i.v. bolus, and (3) ghrelin + CRH combination. ACTH and cortisol were analyzed by commercially available kits from samples taken at 0, 15, 30, 45, 60, 90 and 120 min. ACTH and cortisol responses were calculated as peak and area under the curve (AUC0-120 min). Results: ACTH and cortisol at baseline and stimulated with ghrelin and/or CRH (peak and AUC0-120 min) were significantly higher in CD patients compared to controls (p < 0.01). ACTH and cortisol responses to ghrelin or CRH were similar in CD patients. Combined ghrelin + CRH administration in CD patients produced the highest ACTH response (peak and AUC0-120 min) compared to ghrelin or CRH alone (p < 0.01). Cortisol responses after ghrelin + CRH were uncoupled with ACTH responses and similar to the response to ghrelin or CRH alone in both groups. ACTH and cortisol responses, during all three tests, were similar in CD patients with micro- or macroadenomas. Conclusion: Ghrelin administration causes exaggerated ACTH and cortisol responses in CD patients compared to healthy controls. In combination with CRH, it additionally enhances ACTH secretion without further additive effect on cortisol output. © 2016 S. Karger AG, Basel.

Background/Aims: Exaggerated adrenocorticotropic hormone (ACTH) and cortisol responses to ghrelin in Cushing's disease (CD) have previously been reported, similarly to responses to corticotropin-releasing hormone (CRH). We assessed the ability of ghrelin to enhance ACTH and cortisol responses when added to CRH stimulation in CD patients. Methods: In 21 CD patients (18 females, 3 males; age 49.8 ± 10.2 years; BMI 29.8 ± 0.8) and 8 healthy subjects (7 females, 1 male; age 40.6 ± 5.3 years; BMI 29.9 ± 1.2), we administered (1) ghrelin 100 μg i.v. bolus, (2) CRH 100 μg i.v. bolus, and (3) ghrelin + CRH combination. ACTH and cortisol were analyzed by commercially available kits from samples taken at 0, 15, 30, 45, 60, 90 and 120 min. ACTH and cortisol responses were calculated as peak and area under the curve (AUC0-120 min). Results: ACTH and cortisol at baseline and stimulated with ghrelin and/or CRH (peak and AUC0-120 min) were significantly higher in CD patients compared to controls (p < 0.01). ACTH and cortisol responses to ghrelin or CRH were similar in CD patients. Combined ghrelin + CRH administration in CD patients produced the highest ACTH response (peak and AUC0-120 min) compared to ghrelin or CRH alone (p < 0.01). Cortisol responses after ghrelin + CRH were uncoupled with ACTH responses and similar to the response to ghrelin or CRH alone in both groups. ACTH and cortisol responses, during all three tests, were similar in CD patients with micro- or macroadenomas. Conclusion: Ghrelin administration causes exaggerated ACTH and cortisol responses in CD patients compared to healthy controls. In combination with CRH, it additionally enhances ACTH secretion without further additive effect on cortisol output. © 2016 S. Karger AG, Basel.

Introduction Androgen insensitivity syndrome (AIS) belongs to disorders of sex development, resulting from complete or partial resistance to the biological actions of androgens in persons who are genetically males (XY) with normally developed testes and age-appropriate for males of serum testosterone concentration. Case Outline A 21-year-old female patient was admitted at our Clinic further evaluation and treatment of testicular feminization syndrome, which was diagnosed at the age of 16 years. The patient had never menstruated. On physical examination, her external genitalia and breast development appeared as completely normal feminine structures but pubic and axillary hair was absent. Cytogenetic analysis showed a 46 XY karyotype. The values of sex hormones were as in adult males. The multisliced computed tomography (MSCT) showed structures on both sides of the pelvic region, suggestive of testes. Bilateral orchiectomy was performed. Hormone replacement therapy was prescribed after gonadectomy. Vaginal dilatation was advised to avoid dyspareunia. Conclusion The diagnosis of complete androgen insensitivity is based on clinical findigs, hormonal analysis karyotype, visualization methods and genetic analysis. Bilateral gonadectomy is generally recommended in early adulthood to avoid the risk of testicular malignancy. Vaginal length may be short requiring dilatation in an effort to avoid dyspareunia. Vaginal surgery is rarely indicated for the creation of a functional vagina. © 2015, Serbia Medical Society. All rights reserved.

Climacterium is the phase in women’s life beginning with the first menopausal symptom and cycle irregularities and ending 1 year after the last menstruation. Endocrinological, biological and clinical changes become apparent at that time. © 2016, International Society of Gynecological Endocrinology.

Introduction/Objective There are controversial data in the literature on the topic of effects of alcohol on insulin secretion, apoptosis, and necrosis of the endocrine and exocrine pancreas. The goal of this research was to determine how alcohol affects the insulin secretion and viability of human adult pancreatic islets in vitro during a seven-day incubation. Methods Human pancreatic tissue was digested with Collagenase XI, using a non-automated method. Cultures were incubated in Roswell Park Memorial Institute (RPMI) medium containing alcohol (10 μl of alcohol in 100 ml of medium). Insulin stimulation index (SI) and viability of the islets were determined on the first, third, and seventh day of cultivation. Results Analysis of the viability of the islets showed that there wasn’t significant difference between the control and the test group. In the test group, viability of the cultures declined with the time of incubation. SI of the test group was higher compared to the control group, by 50% and 25% on the first and third day of cultivation, respectively. On the seventh day, insulin secretion was reduced by 25%. The difference was not statistically significant (p > 0.05). In the test group, significant decline in insulin secretion was found on the third and seventh day of incubation (p ≤ 0.05). Conclusion Alcohol can increase or decrease insulin secretion of islets cultures, which may result in an inadequate response of pancreatic β-cells to blood glucose, leading to insulin resistance, and increased risk of developing type 2 diabetes. © 2017, Serbia Medical Society. All rights reserved.

It is well known that hypertension can be primary or secondary. However, among secondary causes of hypertension, gender-specific hypertension is one lately recognized. © 2016, International Society of Gynecological Endocrinology.

Introduction/Objective Hot flashes are one of the first clinical symptoms of menopause. The mechanism of hot flashes is still not fully understood. Changes in concentrations of the circulating follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, and other hormones can lead to thermoregulatory dysfunction. The aim of this study was to examine the association between dynamic changes in concentrations of sex hormones and the presence of vasomotor symptoms in menopausal women. Methods The study involved 36 women divided into two groups: in the first group there were 24 women with hot flashes, BMI 26.16 ± 3.42 kg/m2; the control group comprised 12 women, BMI 26.82 ± 3.89 kg/m2. Data on the presence of hot flashes were based on medical history data. Venous blood samples were collected for the analyses of FSH, LH, prolactin, estradiol, progesterone, testosterone, sex hormone binding globulin, dehidroepiandrosteron sulfate, thyroid-stimulating hormone, and thyroxin. During the subjective feeling of hot flashes, three blood samples during the day and night were collected to determine the mean levels of FSH, LH, and estradiol in women with hot flashes. Results Women with hot flashes had significantly higher prolactin (389.58 ± 123.69 mIU/L to 258.19 ± 122 mIU/L, p < 0.01) and dehydroepiandrosterone sulfate (3.60 ± 2.49 nmol/L vs. 1.88 ± 1.27 nmol/L, p < 0.05) levels, as well as lower mean values of FSH during hot flashes during the day (69.08 ± 28.84 IU/L vs. 107.18 ± 39.11 IU/L, p < 0.01) and night (60.72 ± 21.89 IU/L vs. 104.57 ± 38.06 IU/L, p < 0.01). Conclusion Women with hot flashes had significantly lower mean FSH levels during hot flashes during the day and night than the control group. © 2018, Serbia Medical Society. All rights reserved.

Introduction/Objective The development of acute insulin resistance after surgery intervention is associated with the type and magnitude of operation and tissue injury. The aim of our study was to compare insulin sensitivity assessed by homeostatic model assessment of insulin resistance (HOMA-IR) and C-reactive protein (CRP) before and after laparoscopic and open cholecystectomy during seven days follow-up. Methods In total, 92 patients were divided into two groups: laparoscopic cholecystectomy (Group 1) (n = 61) and open cholecystectomy (Group 2) (n = 31). Glucose, insulin and CRP levels were measured at day 0 and at postoperative days one, three and seven. Glucose, insulin and CRP were determined using commercial assay on Roche Cobas 6000 automated analyzer (Roche Diagnostics, Manheim, Germany). Results There was no statistical difference between studied groups concerning age (p = 0.626), body mass index (p = 0.548), glucose (p = 0.947), insulin (p = 0.212), HOMA-IR (p = 0.390) and CRP (p = 0.546) at day 0. At day one, higher values of CRP were found in group 2 compared with group 1 (p = 0.046). At day three, significantly higher values of glucose and HOMA-IR were found in group 2 compared with group 1 (p = 0.025, p = 0.036, respectively). Conclusion Increase in CRP precedes deterioration of insulin sensitivity measured by HOMA-IR after cholecystectomy. Impairment of insulin sensitivity was more pronounced at postoperative day three in group with open cholecystectomy. On the basis of our results, laparoscopic cholecystectomy induced less impairment in insulin sensitivity and lower inflammatory response. © 2023, Serbia Medical Society. All rights reserved.

Objective: A high prevalence of insulin resistance (IR) has proven to manifest in patients with adrenal incidentalomas (AI). It has been demonstrated that an increase in IR is related to the size of tumourous masses; additionally, luteinizing hormone (LH)-dependent adrenal pathologies are well documented in patients with LH-responsive adrenal tumours occurring under conditions of physiologically elevated LH. We hypothesized that an association between LH and insulin might play a role in adrenal tumourigenesis and steroidogenesis. Design: The aim of our study was to investigate the association between LH and IR; adrenal tumour size (ATS) and IR; LH and cortisol after the 1 mg overnight dexamethasone test (1 mg DST); and ATS and 1 mg DST cortisol in AI patients. This was a case-control study conducted in the Clinic for Endocrinology, Diabetes and Metabolic Diseases in Belgrade, Serbia. The total study group consisted of 105 menopausal women: 75 AI patients [27 with nonfunctional AI (NAI) and 48 with (possible) autonomous cortisol secretion ((P)ACS)] and 30 age-, BMI-, LH- and menopause duration-matched healthy control (HC) women. To estimate IR, we used homeostasis model assessment (HOMA-IR). Results: Luteinizing hormone and ATS are in a significant positive correlation with HOMA-IR and 1 mg DST cortisol in menopausal patients with AI and (P)ACS. Conclusions: Our data point to a possible cause-effect relationship between LH and insulin in patients with AI and (P)ACS adding to the body of evidence of their involvement in adrenal tumourigenesis and steroidogenesis. © 2017 John Wiley & Sons Ltd

Objective: A high prevalence of insulin resistance (IR) has proven to manifest in patients with adrenal incidentalomas (AI). It has been demonstrated that an increase in IR is related to the size of tumourous masses; additionally, luteinizing hormone (LH)-dependent adrenal pathologies are well documented in patients with LH-responsive adrenal tumours occurring under conditions of physiologically elevated LH. We hypothesized that an association between LH and insulin might play a role in adrenal tumourigenesis and steroidogenesis. Design: The aim of our study was to investigate the association between LH and IR; adrenal tumour size (ATS) and IR; LH and cortisol after the 1 mg overnight dexamethasone test (1 mg DST); and ATS and 1 mg DST cortisol in AI patients. This was a case-control study conducted in the Clinic for Endocrinology, Diabetes and Metabolic Diseases in Belgrade, Serbia. The total study group consisted of 105 menopausal women: 75 AI patients [27 with nonfunctional AI (NAI) and 48 with (possible) autonomous cortisol secretion ((P)ACS)] and 30 age-, BMI-, LH- and menopause duration-matched healthy control (HC) women. To estimate IR, we used homeostasis model assessment (HOMA-IR). Results: Luteinizing hormone and ATS are in a significant positive correlation with HOMA-IR and 1 mg DST cortisol in menopausal patients with AI and (P)ACS. Conclusions: Our data point to a possible cause-effect relationship between LH and insulin in patients with AI and (P)ACS adding to the body of evidence of their involvement in adrenal tumourigenesis and steroidogenesis. © 2017 John Wiley & Sons Ltd

Objective The aim of this study was to estimate insulin sensitivity (IS) in nondiabetic patients with adrenal incidentalomas (AI): nonfunctional adrenal incidentalomas (NAI) and patients with AI and subclinical Cushing's syndrome (SCS). Methods Based on the inclusion criteria (normal fasting glucose levels, no previous history of impaired fasting glucose and/or diabetes, and no medications or concomitant relevant diseases) and the exclusion criteria (pheochromocytoma, overt hypercortisolism, hyperaldosteronism, adrenal carcinoma, metastasis of extra-adrenal tumors, extra-adrenal malignancies), 142 subjects were drawn from a series of patients with AI. The subjects were age-, sex- and body mass index (BMI)-matched: 70 with NAI (50 women and 20 men), 37 with AI and SCS (31 women and 6 men) and 35 healthy control (HC) subjects (30 women and 5 men). The oral glucose tolerance test (OGTT) and several indices of insulin sensitivity (IS) were used: homeostasis model assessment (HOMA), quantitative insulin sensitivity check index (QUICKI), triglycerides and glucose index (TyG), index of whole-body insulin sensitivity (ISI-composite) and glucose to insulin ratio (G/I). Results There was a significant difference in IS between subjects with NAI and HC (HOMA, p = 0.049; QUICKI, p = 0.036; TyG, p = 0.002; ISI-composite, p = 0.024) and subjects with SCS and HC (AUC insulin, p = 0.01; HOMA, p = 0.003; QUICKI, p = 0.042; TyG, p = 0.008; ISI-composite, p = 0.002). There was no difference in the tested indices of IS between subjects with NAI and SCS (p > 0.05). However, subjects with SCS had a significantly higher prevalence of impaired glucose tolerance and higher area under the curve for glucose than subjects with NAI (p = 0.0174). The linear regression analysis showed that 1 mg-DST cannot be used as a predictor of HOMA (R2 = 0.004, F = 0.407, p = 0.525). Significant relationship was found between 1 mg-DST and ISI-composite (R2 = 0.042, F = 4.981, p = 0.028) but this relationship was weak and standard error of estimate was high. The linear regression model also showed that ACTH cannot be used as a predictor of HOMA (R2 = 0.001, F = 0.005, p = 0.943) or ISI-composite (R2 = 0.015, F = 1.819, p = 0.187). Conclusions Insulin resistance is a major cardiovascular risk factor; therefore, the assessment of IS in patients with AI, even nonfunctional, has a valuable place in the endocrine workup of these patients. © 2013 Elsevier Inc.

Objective The aim of this study was to estimate insulin sensitivity (IS) in nondiabetic patients with adrenal incidentalomas (AI): nonfunctional adrenal incidentalomas (NAI) and patients with AI and subclinical Cushing's syndrome (SCS). Methods Based on the inclusion criteria (normal fasting glucose levels, no previous history of impaired fasting glucose and/or diabetes, and no medications or concomitant relevant diseases) and the exclusion criteria (pheochromocytoma, overt hypercortisolism, hyperaldosteronism, adrenal carcinoma, metastasis of extra-adrenal tumors, extra-adrenal malignancies), 142 subjects were drawn from a series of patients with AI. The subjects were age-, sex- and body mass index (BMI)-matched: 70 with NAI (50 women and 20 men), 37 with AI and SCS (31 women and 6 men) and 35 healthy control (HC) subjects (30 women and 5 men). The oral glucose tolerance test (OGTT) and several indices of insulin sensitivity (IS) were used: homeostasis model assessment (HOMA), quantitative insulin sensitivity check index (QUICKI), triglycerides and glucose index (TyG), index of whole-body insulin sensitivity (ISI-composite) and glucose to insulin ratio (G/I). Results There was a significant difference in IS between subjects with NAI and HC (HOMA, p = 0.049; QUICKI, p = 0.036; TyG, p = 0.002; ISI-composite, p = 0.024) and subjects with SCS and HC (AUC insulin, p = 0.01; HOMA, p = 0.003; QUICKI, p = 0.042; TyG, p = 0.008; ISI-composite, p = 0.002). There was no difference in the tested indices of IS between subjects with NAI and SCS (p > 0.05). However, subjects with SCS had a significantly higher prevalence of impaired glucose tolerance and higher area under the curve for glucose than subjects with NAI (p = 0.0174). The linear regression analysis showed that 1 mg-DST cannot be used as a predictor of HOMA (R2 = 0.004, F = 0.407, p = 0.525). Significant relationship was found between 1 mg-DST and ISI-composite (R2 = 0.042, F = 4.981, p = 0.028) but this relationship was weak and standard error of estimate was high. The linear regression model also showed that ACTH cannot be used as a predictor of HOMA (R2 = 0.001, F = 0.005, p = 0.943) or ISI-composite (R2 = 0.015, F = 1.819, p = 0.187). Conclusions Insulin resistance is a major cardiovascular risk factor; therefore, the assessment of IS in patients with AI, even nonfunctional, has a valuable place in the endocrine workup of these patients. © 2013 Elsevier Inc.

Introduction Losartan, the angiotensin type 1 receptor blocker (ARB) exercises its main antihypertensive effect by vasodilatation of peripheral arteries. Objective The aim of this study was to evaluate the antihypertensive effect and safety of losartan in patients with mild and moderate arterial hypertension (AH). Methods This was an open post-marketing study with losartan as monotherapy in previously treated or untreated patients with AH. Primary efficacy parameter was the percentage of patients that achieved target blood pressure after 8-week treatment with a single daily dose of losartan of 50-100 mg. Safety parameters were assessed according to the percentage of adverse events and metabolic effects of therapy. Results The study included 550 patients with AH (59% female and 41% male), mean age 56.8±11.4 years, BMI=27±4 kg/m2. Losartan was applied in 31% of untreated and 69% of previously treatment-resistant patients After 8 weeks target blood pressure was achieved in 67.8% (SBP) and in 81.1% (DBP) of patients, respectively. The mean decrease was 21.8% for SBP and 21.1% for DBP (p<0.001). Out of all, 65% of patients achieved both target SBP and DBP values. Hydrochlorothiazide was added to the therapy in 11.6% of patients. There were no significant differences in drug efficacy between the entire group and subgroups of patients with diabetes mellitus and impaired renal function (p=ns). Adverse events were rare and metabolic effect was favorable. Conclusion Monotherapy with losartan in a dosage of 50-100 mg applied during 8 weeks resulted in achieving target values of blood pressure in 65% of patient with mild and moderate hypertension, also including the patients with diabetes mellitus and impaired renal function. Losartan is a safe and metabolically neutral medication.

Premature ovarian failure (POF) is the occurrence of hypergonadotropic hypoestrogenic amenorrhea in women under the age of forty years. It is idiopathic in 74-90% patients. Known cases can be divided into primary and secondary POF. In primary POF genetic aberrations can involve the X chromosome (monosomy, trisomy, translocations, deletions) or autosomes. Genetic mechanisms include reduced gene dosage and non-specific chromosome effects impairing meiosis, decreasing the pool of primordial follicles and increasing atresia due to apoptosis or failure of follicle maturation. Autoimmune ovarian damage is caused by alteration of T-cell subsets and T-cell mediated injury, increase of autoantibody producing B-cells, a low number of effector/cytotoxic lymphocyte, which decreases the number and activity of natural killer cells. Bilateral oophorectomy, chemotherapy, radiotherapy and infections cause the secondary POF. Symptoms of POF include irritability, nervousness, loss of libido, depression, lack of concentration, hot flushes, weight gaining, dry skin, vaginal dryness, frequent infections etc.The diagnosis is confirmed by the level of FSH of over 40IU/L and estradiol below 50 pmol/L in women aged below 40 years. Biochemical and other hormonal analysis (free thyroxin,TSH, prolactin, testosterone), karyotype (>30 years of age), ultrasound of the breasts and pelvis are advisable. Optimal therapy is combined estrogen progestagen therapy given in a sequential rhythm, after excluding absolute contraindications.Testosterone can be added to adnexectomized women and those with a low libido. Sequential estrogen progestagen replacement therapy is the first line therapy for ovulation induction in those looking for pregnancy and after that oocyte donation will be advised. Appropriate estro-progestagen therapy improves the quality of life and prevents complications such as cardiovascular diseases, osteoporosis, stroke etc.

Introduction. Juxtaglomerular cell tumor (JGCT) or reninoma is a very rare cause of curable hypertension among young people. The early diagnosis is the most important based on the clinical presentation, hormonal and radiological findings observed on computed tomography (CT) and/or magnetic resonance imaging (MRI). The final confirmation of the JGCT is the lateralization of the plasma renin activity (PRA) during the selective renal venous sampling. Case report. This report presents a typical case of young women with JGCT which was manifested for the first time with severe hypertension during the pregnancy and was the reason of fetal death. After the miscarriage, the diagnosis of JGCT was made by the CT scanning and confirmed by the selective renal venous sampling. After the partial nephrectomy, the blood pressure and serum potassium normalized without the medications. Conclusion. Reninoma should be considered in the differential diagnosis as a cause of severe hypertension in pregnancy and also should be suspected in young hipertensives (especially females) with hypokalemia and secondary hyperaldosteronism after the exclusion of other causes particularly renal artery stenosis. A dynamic contrastenhanced CT, MRI and selective renal venous sampling are the most important tools in the diagnosis of JGCT. © 2017, Institut za Vojnomedicinske Naucne Informacije/Documentaciju. All Rights Reserved.

Introduction Adenocarcinoma of the small bowel is a rare gastrointestinal neoplasm usually affecting the distal duodenum and proximal jejunum. Because of their rarity and poorly defined abdominal symptoms, a correct diagnosis is often delayed. Case Outline We present a 43-year-old woman admitted at the Clinic for Endocrinology due to a large tumor (over 7 cm) of the left adrenal gland. The tumor was detected by ultrasound and confirmed by CT scan. The patient complained of abdominal pain in the left upper quadrant, fatigue and septic fever. Normal urinary catecholamines excluded pheochromocytoma. The endocrine evaluations revealed laboratory signs of subclinical hypercorticism: midnight cortisol 235 nmol/L, post 1 mg - overnight Dexamethasone suppression test for cortisol 95.5 nmol/L and basal ACTH 4.2 pg/mL. Plasma rennin activity and aldosterone were within the normal range. Surgery was performed. Intraoperative findings showed signs of acute peritonitis and a small ulceration of the jejunum below at 70 cm on the anal side from the Treitz's ligament. Adrenal glands were not enlarged. Patohistology and immunochemistry identified adenocarcinoma of the jejunum without infiltration of the lymphatic nodules. The extensive jejunal resection and lavage of the peritoneum were performed. Due to complications of massive peritonitis, the patient died seven days after surgery. Conclusion Poorly defined symptoms and a low incidence make the diagnosis of small bowel carcinoma, particularly of the jejunal region, very difficult in spite of the new endoscopic techniques.