ACTA ENDOCRINOLOGICA (BUC)

Introduction. Fahr’s syndrome is an infrequent disorder characterized by bilateral symmetrical calcification of basal ganglia and the cerebral cortex. It can be seen genetic, idiopathic, or secondary to endocrine diseases. This disease is related to different metabolic disorders particularly with diseases of the parathyroid gland. Case 1. A 63-year-old female patient applied to our clinic due to having hypoparathyroidism with bilateral basal ganglia calcification in head computed tomography(CT). She had subtotal thyroidectomy 25 years ago. In the neurological examination, mild symmetrical parkinsonism was determined. In laboratory examination Ca:8 mg/dL (8.6- 10.2), P:5.1 mg/dL (2.3-4.5), PTH:9.53 pg/mL (15-65) were detected. Calcitriol 0.25 μ/day was added to her treatment. Her parkinsonism disappeared after the treatment. Case 2. A 49-year-old male patient was consulted when he was admitted to the department of neurology in our hospital. The physical examination demonstrated the characteristics of Albright’s hereditary osteodystrophy. The neurological examination shows bilateral symmetrical bradykinesia, dysphagia, and moderate dysarthria. In the laboratory examination PTH: 46.5 ng/L(15-65), Ca:8.6 mg/dL (8.6-10.2), P:2.7 mg/dL (2.3-4.5) were detected and were all within the normal ranges. Consequently, pseudopseudohypoparathyroidism was decided as a diagnosis. G protein alpha subunit mutation (Gsα) was not detected due to technical limitations. Conclusion. When a patient is diagnosed as Fahr’s syndrome, we should keep in mind parathyroid disorders. Fahr’s syndrome must be evaluated in patients showing intracranial calcification accompanied by parathyroid diseases.

The aim of this study is to investigate the possible association between hormonal status and adipose tissue characteristics in obese and non-obese subjects. Fourteen obese and 15 nonobese premenopausal female patients were enrolled in the study. Stromal vascular cells were isolated and cultured using modified procedures described by Entenmann and Hauner. In the non-obese group, omental SVCs seeded at a density of 4.12?1.1x103/cm2 in 25-cm2 in culture flasks for measuring cell proliferation and subcutaneus SVCs seeded at a density of 2.05?0.76x103/cm2 in 25-cm2 at culture flasks. In the obese group, omental SVCs seeded at a density of 6.11?1.98x103/cm2 in 25-cm2 at culture flasks for measuring cell proliferation and subcutaneous SVCs seeded at a density of 2.94?0.75x103/cm2 in 25-cm2 in culture flasks. Mean GPDH activity levels were significantly higher in SVCs from the omentum in obese compared to those from the omentum in nonobese (651.9?65.7 vs 405.1?60.1 mU/mg protein). However, GPDH activities were similar in SVCs from the subcutaneous SVCs in obese subjects, compared to those from the subcutaneous SVCs in non-obese subjects (303.5?63.2 vs 367.4?73.7 mU/mg protein). In obese group, omental SVCs number was positively correlated with plasma estradiol (E2) (r=0.604, p=0.017), and fasting insulin levels (r=0.843, p=0.01). It was negatively correlated with plasma progesterone (r=-0.793, p=0.006), prolactin (r=-0.655, p=0.008) and free T3 (FT3) levels(r=-0.630, p=0.01). These findings suggest that there are differences in adipose tissue proliferation capacity and metabolic activity between obese and non-obese subjects. In obese group, the number of omental stromal vascular cells was positively correlated with plasma estradiol and insulin levels.

Objective. Gestational diabetes mellitus (GDM) is defined as glucose intolerance that\r\nis detected for the first time during pregnancy. Normal pregnancy induces insulin resistance\r\nthrough the diabetogenic effects of placental hormones. Glucose tolerance test results in\r\ntwin and singleton pregnancies were compared in this study.\r\nSubjects and Methods. A total of 360 pregnant women were studied. 200 women\r\n(mean age 31.60?2.10 yr) had singleton pregnancies (Group I) and 160 women (mean age\r\n28.20?2.70 yr) had twin pregnancies (Group II). 50- g, 1- hour glucose tolerance test was\r\nconducted on the first prenatal visit. An abnormal glucose screen defined as glucose > 140\r\nmg/dL was followed by a 100g, 3-hour glucose tolerance test. Gestational diabetes was\r\ndefined as the presence of two or more abnormal values during the 3-hour test.\r\nResults. Gestational diabetes was found in 4 of the 200 (2%) singleton pregnant\r\nwomen and 8 of the 160 (5%) twin pregnant women. Group I (Singleton) was further\r\ndivided into two subgroups according to whether the 1-hr plasma glucose level was < 140\r\nmg/dl (Group Ia) or >140 mg/dL (Group Ib). Likewise, Group II pregnancies was also\r\ndivided into two subgoups on the same basis. Mean screening test glucose levels were found\r\nto be 127.8?14.94 mg/dL in Group Ia and 150.8 ? 18.1 mg/dL in Group Ib women. Mean\r\nscreening test glucose levels of Group IIa subjects was 92.80 ? 18.30 mg/dL while that of\r\nGroup IIb subjects was 154.8 ? 27.0 mg/dL. Mean 1st h glucose levels of 100-g glucose\r\ntolerance test was found to be 131.4 ? 32.58 mg/dL in Group I, and 112.5 ? 39.6 mg/dL in\r\nGroup II. Mean 2nd h glucose tolerance test values were 133.2 ? 28.8 mg/dL in Group I and\r\n100.6?28.8 mg/dL in Group II. Mean 3rd h glucose tolerance test values were 107.6 ? 23.58\r\nmg/dl in Group I and 72?16.9 mg/dL in Group II.\r\nConclusion: Glucose screening results and 100-g, 3- hour glucose tolerance test\r\nvalues have been found to be lower in twin pregnancies than in singleton pregnancies.\r\nTherefore, we suggest that these findings be taken into account in developing diagnostic\r\ncriteria for gestational diabetes in twin or more pregnancies.

Adipocytokines involved in inflammation and the acute phase responders have been found to be increased in the metabolic syndrome (MS). The aim of the study was to compare the ‘normal’ weight women’s fibrinogen, hsCRP, adiponectin, TNF-α, vascular cell adhesion molecule (VCAM) with obese patients with MS, and to evaluate the association between fibrinogen, hsCRP, adiponectin, TNF-α, VCAM and insulin resistance. The study included 52 obese women who met the criteria for MS defined as in 2001, the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) ATP III and 24 normal women. Serum concentrations of glucose (FBG), triglyceride, total and HDL-Cholesterol were determined by enzymatic procedures, serum insulin was measured by chemiluminescence, plasma levels of adiponectin, TNF-α and VCAM by Elisa, hsCRP by immunoturbimetric assay and fibrinogen by coagulation method. Measurements of insulin resistance were obtained using the homeostasis model assessment. Mean plasma levels of adiponectin, TNF-α, VCAM, fibrinogen and hsCRP were found 6.11±2.39 mg/ml, 3.10±3.30 pg/ml, 14.21±4.00 ng/ml, 375.49±49.67 mg/dl, 0.33±0.10 mg/dl in the obese with MS; 6.20±2.48 mg/ml, 3.01±1.68 pg/ml, 12.63±2.54 ng/ml, 304.06±49.52 mg/dl, 0.30±0.19 mg/dl in the normal women, respectively. Mean fasting insulin level and HOMA-IR were measured 13.80±6.32 mU/ml and 3.69±1.90 mU/ml, respectively in obese with MS. In normal women, fasting insulin level and HOMA-IR were measured 8.30±3.08 mU/ml and 1.49±0.37, respectively. Mean levels of adiponectin were positively correlated with mean TNF-α levels in the obese with MS (r=0.472, p=0.001). VCAM was negatively correlated with TNF-α levels (r=-0.301, p=0.038) in the obese with MS. This study demonstrated that TNF-α showed a positive association with adiponectin and a negative association with VCAM in the obese women with MS.

Objective. This study aims to investigate the factors affecting development of acute kidney injury (AKI) in patients with severe hypothyroidism. Methods. This retrospective observational study involved patients with primary hypothyroidism and thyroid stimulating hormone (TSH) levels of more than 50 mIU/L at their review in the endocrinology outpatient clinic, between January 2015 and April 2021. Factors affecting the development of AKI were examined by logistic regression analysis. Results. A total of 100 patients, 20 (11 male (M), 9 female (F)) in the AKI (case) group and 80 (23 M, 57 F) patients in control group, were included in our study. The median age of the case group (56 years, interquartile range (IQR) 44.3–68.5) was significantly higher than the control group (49 years, IQR 32.3–60; p = 0.027), and the ratio of males to females was significantly higher in the case group (p = 0.001). Multivariate logistic regression analyses showed that hypothyroidism diagnosed after the age of 60 years (odds ratio (OR) 59.674, 95% confidence intervals (CI) 5.955–598.031; p = 0.001), free triiodothyronine (FT3) < 1.3 pg/mL (OR 17.151, 95% CI 2.491–118.089; p = 0.004) and creatine kinase (CK) > 1000 U/L (OR 1.522, 95% CI 1.602– 82.848; p = 0.015) were predictors for the development of AKI in patients with severe hypothyroidism. Conclusion. We recommend close follow-up and monitoring of patients with AKI caused by severe hypothyroidism if patients who are diagnosed at age > 60 years, CK > 1000 U/L or FT3 < 1.3 pg/mL.