Browsing by Author "Vujović, Svetlana (57225380338)"

Introduction Neurofibromatosis type 1 is one of the most common genetically transmitted diseases with a high index of spontaneous mutations and extremely varied and unpredictable clinical manifestations. It is diagnosed by the existence of certain clinical criteria. The presence of numerous localised cutaneous neurofibromas or a plexiform neurofibroma is virtually pathognomonic of neurofibromatosis type 1. The incidence of pheochromocytoma in neurofibromatosis type 1 is 0.1-5.7%. Case Outline A 56-year old female patient was admitted for further evaluation of incidental adrenal tumour previously diagnosed on computerized tomography (CT). She had previously unrecognized neurofibromatosis type 1 and a clinical picture which could remind of pheochromocytoma. None of the catecholamine samples in 24 hr urine indicated functionally active pheochromocytoma. Chromogranin A was moderately increased. Decision for operation was made after performing the image techniques. Adrenal incidentaloma had features of pheochromocytoma on abdominal magnetic resonance imaging (MRI), with positive 131I-MIBG (iodine 131-labelled metaiodobenzylguanidine scintigraphy). After being treated with phenoxybenzamine and propranolol, she was operated on. The pathohistological finding showed the case of left adrenal pheochromocytoma. Conclusion Detailed diagnostic procedure for pheochromocytoma should be performed with patients having neurofibromatosis type 1 and adrenal incidentaloma. Pheochromocytomas are rare tumours with fatal outcome if not duly recognized and cured.

Estradiol promotes neuronal growth, transmission, survival, myelinization, plasticity, synaptogenesis, and dendritic branching and it improves cognitive function. Alzheimer’s disease (AD) is characterized by amyloid plaques, neurofibrillary tangles, and the loss of neuronal connection in the brain. Genomic analysis has concluded that hypoestrogenism influences the APOE gene and increases the risk of AD. Premature ovarian insufficiency (POI) is defined as oligo/amenorrhea in women below 40 years of age, low estradiol, and high-gonadotropin levels. Early symptoms and signs of POI must be detected in time in order to prevent subsequent complications, such as Alzheimer’s disease. Meta-analysis has shown favorable effects of estrogen in preventing Alzheimer’s. We measured some of the typical markers of AD in women with POI such as interleukin 6 (IL-6), interleukin 8 (IL-8), tissue necrosis factor α (TNFα), TAU1, TREM2, and amyloid precursor proteins (APP). While FSH, LH, and IL-8 were significantly higher in POI group, compared to controls, testosterone and DHEAS were lower. A significant decrease in IL-6 was found in the POI group during a 6-month therapy, as well as an increase in amyloid precursor proteins. CONCLUSION: Neurological complications of POI, such as declining short-term memory, cognitive function, and dementia, have to be promptly stopped by initiating estro-progestogen therapy in POI. A long-term continuation of the therapy would be strongly advised. © 2023 by the authors.

Estradiol promotes neuronal growth, transmission, survival, myelinization, plasticity, synaptogenesis, and dendritic branching and it improves cognitive function. Alzheimer’s disease (AD) is characterized by amyloid plaques, neurofibrillary tangles, and the loss of neuronal connection in the brain. Genomic analysis has concluded that hypoestrogenism influences the APOE gene and increases the risk of AD. Premature ovarian insufficiency (POI) is defined as oligo/amenorrhea in women below 40 years of age, low estradiol, and high-gonadotropin levels. Early symptoms and signs of POI must be detected in time in order to prevent subsequent complications, such as Alzheimer’s disease. Meta-analysis has shown favorable effects of estrogen in preventing Alzheimer’s. We measured some of the typical markers of AD in women with POI such as interleukin 6 (IL-6), interleukin 8 (IL-8), tissue necrosis factor α (TNFα), TAU1, TREM2, and amyloid precursor proteins (APP). While FSH, LH, and IL-8 were significantly higher in POI group, compared to controls, testosterone and DHEAS were lower. A significant decrease in IL-6 was found in the POI group during a 6-month therapy, as well as an increase in amyloid precursor proteins. CONCLUSION: Neurological complications of POI, such as declining short-term memory, cognitive function, and dementia, have to be promptly stopped by initiating estro-progestogen therapy in POI. A long-term continuation of the therapy would be strongly advised. © 2023 by the authors.

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.

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.

More empathized approach is required and is obligatory to women with premature ovarian insufficiency (POI) interested for pregnancy. In order to improve fertility rate in POI patients our suggestions would be: (1) To decrease FSH value to 10–15 IU/L by increasing estrogen. Oocyte donation can be suggested after a minimum of six month interval from FSH between 10–15 IU/L and when no dominant follicles are found. (2) To perform oral glucose tolerance test (OGTT). Insulin sensitizing agents has to be included, when indicated, 3–6 month before pregnancy. (3) TSH has to be 1–2.5 mM/L during 3–6 months before pregnancy. (4) Tests for thrombophyllia (Leiden V, FII, MTHFR, PAI) have to be obligatory. They are less expensive than those repeated in vitro fertilizations. Therapy has to be included according to the indications. (5) In order to regulate disturbed immune response in POI patients with endometriosis oral contraceptive therapy is needed for atleast six months prior to the pregnancy. (5) Encourage the patients and advice them about healthy life style and eating habits. (6) Add other drugs, when they are indicated. Complex interplay between endocrine, immunological, haematological, and psychological factors are very often underdetected in POI patients. It is very important to find out the real time for oocyte donation after correcting all the disturbances, improving endometrium receptivity and reaching women’s acceptable psychological status. Untreated disturbances induce cardiovascular diseases, diabetes mellitus, thyroid diseases, coagulopathioes etc. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.

More empathized approach is required and is obligatory to women with premature ovarian insufficiency (POI) interested for pregnancy. In order to improve fertility rate in POI patients our suggestions would be: (1) To decrease FSH value to 10–15 IU/L by increasing estrogen. Oocyte donation can be suggested after a minimum of six month interval from FSH between 10–15 IU/L and when no dominant follicles are found. (2) To perform oral glucose tolerance test (OGTT). Insulin sensitizing agents has to be included, when indicated, 3–6 month before pregnancy. (3) TSH has to be 1–2.5 mM/L during 3–6 months before pregnancy. (4) Tests for thrombophyllia (Leiden V, FII, MTHFR, PAI) have to be obligatory. They are less expensive than those repeated in vitro fertilizations. Therapy has to be included according to the indications. (5) In order to regulate disturbed immune response in POI patients with endometriosis oral contraceptive therapy is needed for atleast six months prior to the pregnancy. (5) Encourage the patients and advice them about healthy life style and eating habits. (6) Add other drugs, when they are indicated. Complex interplay between endocrine, immunological, haematological, and psychological factors are very often underdetected in POI patients. It is very important to find out the real time for oocyte donation after correcting all the disturbances, improving endometrium receptivity and reaching women’s acceptable psychological status. Untreated disturbances induce cardiovascular diseases, diabetes mellitus, thyroid diseases, coagulopathioes etc. © 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.

Many of the presenting features in women with Cushing's syndrome (CS) are similar to those observed for patients with polycystic ovary syndrome (PCOS). The aim of this study was to compare gonadotropin pulsatility characteristics in CS and PCOS. We evaluated 32 females divided into three groups. The first group comprised 12 females with clinically and biochemically proven CS, subsequently confirmed by histology (seven with Cushing's syndrome, five with adrenal adenoma). The second group comprised ten females with clinical, endocrine and ultrasonographic parameters for PCOS, while the third group comprised ten healthy females with regular menstrual cycles to serve as controls. Blood samples were taken at 15-min intervals for 6 h in the follicular phase, for determination of luteinizing hormone (LH) and follicle-stimulation hormone (FSH). Pulse analysis was carried out using the PulsDetekt program, and statistical analysis was done using the Rruskal-Wallis test. The following data, presented as median (minimum-maximum), were found for the three groups respectively. Number of LH pulses: 0 (0-5), 7 (3-8) and 3 (2-7); LH pulse amplitude: 2.29 (1.98-3.49), 2.27 (1.15-5.90) and 2.03 (1.02-4.46) mU/l; LH pulse mass: 17.81 (14.82-26.20) 29.85 (8.59-185.82) and 27.57 (7.63-66.69) mU/l × min. Number of FSH pulses: 3 (0-3), 2 (0-5) and 3 (1-5); FSH pulse amplitude: 1.62 (1.29-1.94), 1.49 (1.19-4.40) and 2.02 (1.37-2.52) mU/l; FSH pulse mass: 12.17 (9.64-41.69), 11.18 (8.92-33.02) and 15.16 (10.31-18.93) mU/l × min. Only the number of pulses was compared because other parameters of pulsatile secretion cannot be estimated when no pulses are detected. The difference in number of LH pulses between groups was statistically significant (p < 0.05); however, there was no difference in the number of detected FSH pulses between groups (p > 0.05). Attenuation of pulsatile LH secretion indicating gonadotropin deficiency in the majority of women with CS is mostly due to alterations in serum cortisol levels. Our data also suggest that different mechanisms alter LH pulsatile secretion in CS and PCOS. © 2005 Taylor & Francis Group Ltd.

Many of the presenting features in women with Cushing's syndrome (CS) are similar to those observed for patients with polycystic ovary syndrome (PCOS). The aim of this study was to compare gonadotropin pulsatility characteristics in CS and PCOS. We evaluated 32 females divided into three groups. The first group comprised 12 females with clinically and biochemically proven CS, subsequently confirmed by histology (seven with Cushing's syndrome, five with adrenal adenoma). The second group comprised ten females with clinical, endocrine and ultrasonographic parameters for PCOS, while the third group comprised ten healthy females with regular menstrual cycles to serve as controls. Blood samples were taken at 15-min intervals for 6 h in the follicular phase, for determination of luteinizing hormone (LH) and follicle-stimulation hormone (FSH). Pulse analysis was carried out using the PulsDetekt program, and statistical analysis was done using the Rruskal-Wallis test. The following data, presented as median (minimum-maximum), were found for the three groups respectively. Number of LH pulses: 0 (0-5), 7 (3-8) and 3 (2-7); LH pulse amplitude: 2.29 (1.98-3.49), 2.27 (1.15-5.90) and 2.03 (1.02-4.46) mU/l; LH pulse mass: 17.81 (14.82-26.20) 29.85 (8.59-185.82) and 27.57 (7.63-66.69) mU/l × min. Number of FSH pulses: 3 (0-3), 2 (0-5) and 3 (1-5); FSH pulse amplitude: 1.62 (1.29-1.94), 1.49 (1.19-4.40) and 2.02 (1.37-2.52) mU/l; FSH pulse mass: 12.17 (9.64-41.69), 11.18 (8.92-33.02) and 15.16 (10.31-18.93) mU/l × min. Only the number of pulses was compared because other parameters of pulsatile secretion cannot be estimated when no pulses are detected. The difference in number of LH pulses between groups was statistically significant (p < 0.05); however, there was no difference in the number of detected FSH pulses between groups (p > 0.05). Attenuation of pulsatile LH secretion indicating gonadotropin deficiency in the majority of women with CS is mostly due to alterations in serum cortisol levels. Our data also suggest that different mechanisms alter LH pulsatile secretion in CS and PCOS. © 2005 Taylor & Francis Group Ltd.

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.

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.

Background: Disrupted sleep affects cardio-metabolic and reproductive health. Obstructive sleep apnea syndrome represents a major complication of obesity and has been associated with gonadal axis activity changes and lower serum testosterone concentration in men. However, there is no consistent opinion on the effect of obstructive sleep apnea on testosterone levels in men. Objective: The aim of this study was to determine the influence of obstructive sleep apnea on total and free testosterone levels in severely obese men. Materials and methods: The study included 104 severely obese (Body Mass Index (BMI) ≥ 35 kg/m2) men, aged 20 to 60, who underwent anthropometric, blood pressure, fasting plasma glucose, lipid profile, and sex hormone measurements. All participants were subjected to polysomnography. According to apnea-hypopnea index (AHI) patients were divided into 3 groups: <15 (n = 20), 15 - 29.9 (n = 17) and ≥ 30 (n = 67). Results: There was a significant difference between AHI groups in age (29.1 ± 7.2, 43.2 ± 13.2, 45.2 ± 10.2 years; p < 0.001), BMI (42.8 ± 5.9, 43.2 ± 5.9, 47.1 ± 7.8 kg/m2; p = 0.023), the prevalence of metabolic syndrome (MetS) (55%, 82.4%, 83.6%, p = 0.017), continuous metabolic syndrome score (siMS) (4.01 ± 1.21, 3.42 ± 0.80, 3.94 ± 1.81, 4.20 ± 1.07; p = 0.038), total testosterone (TT) (16.6 ± 6.1, 15.2 ± 5.3, 11.3 ± 4.44 nmol/l; p < 0.001) and free testosterone (FT) levels (440.4 ± 160.8, 389.6 ± 162.5, 294.5 ± 107.0 pmol/l; p < 0.001). TT level was in a significant negative correlation with AHI, oxygen desaturation index (ODI), BMI, MetS and siMS. Also, FT was in a significant negative correlation with AHI, ODI, BMI, age, MetS and siMS. The multiple regression analysis revealed that both AHI and ODI were in significant correlation with TT and FT after adjustment for age, BMI, siMS score and MetS components. Conclusion: Obstructive sleep apnea is associated with low TT and FT levels in severely obese men. © Copyright © 2021 Tančić-Gajić, Vukčević, Ivović, Marina, Arizanović, Soldatović, Stojanović, Đogo, Kendereški and Vujović.

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.

Premature ovarian insufficiency (POI) (also known as premature menopause) is a heterogeneous disorder of multifactorial origin defined as the occurrence of secondary amenorrhoea, hypergonadotropism (follicle-stimulating hormone above 40 IU/L) and hypoestrogenism (oestradiol below 50 pmol/L) in women under the age of 40 years. © 2015, International Society of Gynecological Endocrinology.

Premature ovarian insufficiency (POI) is a delicate medical problem in young women. This condition is not unchangeable and permanent but is associated with intermittent and unpredictable ovarian activity, resulting in low conception rate. Over the period of 8 years, the evaluation of secondary amenorrhea was conducted in 90 patients below the age of 40 who wished to restore fertility. Having confirmed the diagnosis and investigated the etiology of POI, hormone replacement therapy was applied (sequential administration of estradiol and norethisterone acetate) in the first 30 patients (group A). Estrogen–progestogen therapy with daily supplementation of 25 mg of micronized oral dehydroepiandrosterone (DHEA) was conducted in 44 patients (group B), whereas a combined regime (estrogen–progestogen therapy, DHEA supplementation in daily dose of 25 mg, and melatonin supplementation in daily dose of 3 mg) was conducted in 16 patients (group C). In the course of our study, 16 pregnancies were realized (18% of all cases: 17% in group A; 18% in group B; 19% in group C) 6 to 20 months after the initiation of hormone therapy, and there have been 13 completed term pregnancies so far with normal fetal growth and development. We concluded that estrogen–progestogen therapy combined with DHEA and melatonin could optimize fertility and lead to successful pregnancy in POI patients. © 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group.

Premature ovarian insufficiency (POI) is a delicate medical problem in young women. This condition is not unchangeable and permanent but is associated with intermittent and unpredictable ovarian activity, resulting in low conception rate. Over the period of 8 years, the evaluation of secondary amenorrhea was conducted in 90 patients below the age of 40 who wished to restore fertility. Having confirmed the diagnosis and investigated the etiology of POI, hormone replacement therapy was applied (sequential administration of estradiol and norethisterone acetate) in the first 30 patients (group A). Estrogen–progestogen therapy with daily supplementation of 25 mg of micronized oral dehydroepiandrosterone (DHEA) was conducted in 44 patients (group B), whereas a combined regime (estrogen–progestogen therapy, DHEA supplementation in daily dose of 25 mg, and melatonin supplementation in daily dose of 3 mg) was conducted in 16 patients (group C). In the course of our study, 16 pregnancies were realized (18% of all cases: 17% in group A; 18% in group B; 19% in group C) 6 to 20 months after the initiation of hormone therapy, and there have been 13 completed term pregnancies so far with normal fetal growth and development. We concluded that estrogen–progestogen therapy combined with DHEA and melatonin could optimize fertility and lead to successful pregnancy in POI patients. © 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group.

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.