Mehtap Evran

Background: Suppression of thyroid-stimulating hormone (TSH) can adversely affect bone tissue in individuals with differentiated thyroid cancer (DTC). This study aims to examine bone mineral density (BMD) and vertebral fractures (VF) in DTC patients receiving levothyroxine (LT4) suppression therapy. Methods: A total of 990 patients with differentiated thyroid cancer who had undergone total thyroidectomy and received levothyroxine suppression therapy for a minimum of one year were included in the study. Clinical and laboratory data obtained at the most recent visit were extracted from patient records. Bone mineral density (BMD) measurements of the lumbar spine and femoral regions, assessed by dual-energy X-ray absorptiometry (DXA) within the preceding year, were recorded. When available, lateral vertebral radiographs were also evaluated. Results: The study included 990 patients with differentiated thyroid cancer (DTC). According to DXA results, 545(55.2%) had normal BMD, 363 (36.6%) had osteopenia, and 82 (8.2%) had osteoporosis. Osteoporotic patients were older and had lower BMI (p = 0.001 for both), while TSH levels were similar across groups. Among 476 patients with vertebral radiographs, 131 (27.5%) had moderate to severe vertebral fractures (VF). Fracture rates were significantly higher in patients with severe TSH suppression compared to other groups (p = 0.013). Patients with VF were older and had lower femoral neck and L1–L4 BMD (p = 0.001). Regression analysis showed that disease duration, FT4 levels, and femoral neck BMD were associated with fracture risk (p = 0.001). Multivariate analysis identified age, femoral neck BMD, L1–L4 BMD, and osteocalcin as independent predictors of osteoporosis (p = 0.001). TSH subgroups showed no differences in BMD values. Conclusion: Findings suggest that DTC patients undergoing TSH suppression have a significant risk of VF. Assessments of VF should be integrated into routine care for DTC survivors to ensure long-term skeletal safety.

Objectives: The predictive role of macroalbuminuria in the development of hypoglycemia in patients with type 2 diabetes mellitus was investigated. Methods: Ninety-two patients diagnosed with type 2 diabetes mellitus who presented to Çukurova University Faculty of Medicine between January 2014 and January 2015 were included in the study. At the beginning of the study, the glomerular filtration rate values of 92 patients with type 2 diabetes mellitus were calculated using creatinine levels. The study was designed as a single-blind study. There were 14 patients with proteinuria at the level of macroalbuminuria (stage IV diabetic nephropathy) in the study group (group 1) and 78 patients without proteinuria at the level of macro-albuminuria (stage I–III diabetic nephropathy) in the control group (group 2). Thyroid-stimulating hormone, blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, sodium, potassium, C-peptide, and HbA1c levels were measured in all patients at baseline and at 6 months. If adrenergic symptoms of hypoglycemia developed together with a capillary glucose level below 70 mg/dL, or if a measurement below 55 mg/dL was obtained regardless of the presence of hypoglycemic symptoms, the episode was recorded as a hypoglycemic event. Results: The study was completed with 70 patients, 12 of whom were in the first group and 58 of whom were in the second (control) group. Statistical analysis was performed using SPSS version 24 after the 6-month follow-up. Twenty-six hypoglycemic attacks occurred in the macroalbuminuria group (group 1), and 37 hypoglycemic attacks occurred in the control group (group 2). The Mann–Whitney U test was applied. Conclusion: The presence of macroalbuminuria was found to be significant for the development of hypoglycemia at the p

Backgound: Suppression of thyroid-stimulating hormone (TSH) can adversely affect bone tissue in individuals with differentiated thyroid cancer (DTC).In a multi-center setting, this study aim to examine vertebral fractures (VF) and bone mineral density (BMD) in DTC patients receiving levothyroxine (LT4) suppression therapy. Methods: Clinical measurements done in the last visit, laboratory and radiologic data extracted from patients files. Serum TSH concentrations were divided into four groups based on the American Thyroid Association’s guidelines for TSH suppression: 0.01 mu/L, 0.01-0.1, 0.1–0.5 mu/L, and >0.5 mu/L. Within the preceding year, the BMD measurements obtained in the lumbar and femoral regions with a DXA scanner were recorded. Lateral spinal X-rays obtained within the previous year were evaluated. Results: The study comprised 990 people with DTC. The DXA showed 545 patients with normal BMD, 82 (8.2%) with osteoporosis, and 363 (36.6%). patients had osteopenia. The osteoporotic group exhibited older age (p = 0.001), lower BMI (p = 0.001), and comparable TSH levels compare to the osteopenia and normal BMD groups. In 476 lateral vertebral x-rays, 200 (42%), 131 (27.5%) were significant or severe VF. The severe TSH suppression group had a greater fracture rate than the moderate, mild, and non-suppressed groups(p=0.013). VF patients were older (p = 0.001) and had lower femur neck and L1-L4 BMD. Disease duration, FT4 level, and femur neck BMD affected fracture risk (p = 0.001, pseudo R2: 0.028). Age, femur neck BMD, L1-L4 BMD, and osteocalcin levels were linked with osteoporosis in a multivariate analysis (p = 0.001, pseudo R2: 0.427). TSH subgroups had similar femur neck (p = 0.61) and L1-L4 BMD (p = 0.89). Conclusion: Findings suggest that DTC patients undergoing TSH suppression have a significant risk of VF. Assessment of VF should be integrated into the routine care of DTC survivors to ensure long-term skeletal safety.

Objective: Patients with impaired glucose metabolism have increased thyroid volume and a higher prevalence of nodules. Yet, some studies show that there is an improvement in these thyroid parameters after diabetes treatment. Our observational study aimed to reveal the effect of treatment on thyroid function, thyroid volume, and the presence of nodules in newly diagnosed type 2 diabetes mellitus (T2DM) patients who were started on metformin treatment. Methods: Euthyroid and subclinically hypothyroid patients with a serum TSH level of <10 mU/L, who were newly diagnosed with T2DM and started on metformin as an antidiabetic treatment and not used any thyroid medication previously, were included in our study. Patients' characteristics were recorded. Baseline and 6th-month serum thyroid function tests were scheduled. Baseline and 6th-month thyroid gland characteristics were examined by thyroid ultrasonography. Results: A total of 101 (37 males, 64 females) newly diagnosed T2DM patients with euthyroid (n=95) or subclinical hypothyroidism (n=6) were included in the study. The mean age of the patients was 53.02 ± 11.9 years, and the mean BMI was 29.60 ± 3.9 kg/m2. Fifty-two (52%) patients were classified as obese. Body weight, BMI, serum TSH, ALT, Anti-TPO levels, and thyroid volume decreased significantly in the 6th-month compared to baseline values (p = 0.000; p = 0.000; p = 0.011; p = 0.022; p = 0.000, respectively). Serum anti-Tg, fT4, fT3 levels, and thyroid nodule count did not change significantly. A high agreement was found between the baseline and 6thmonth nodule counts (gamma= 0.886; p <0.001) and the presence of multi-nodularity in the thyroid (gamma= 0.941; p <0.001), but no significant change was observed. Anti-TPO levels showed a significant decrease in both with and without obesity groups at the end of 6 months (p = 0.003, p = 0.009, respectively). Serum TSH level decreased significantly only in non-obese subjects (p = 0.004), and thyroid volume decreased significantly only in obese subjects (p = 0.000). Conclusion: Our results suggest that metformin treatment significantly reduces body weight, BMI, thyroid volume, and serum TSH, ALT, and Anti-TPO levels in patients with newly diagnosed T2DM. Moreover, serum TSH levels showed a significant decrease in non-obese subjects, while thyroid volume showed a significant decrease in obese subjects.

Sexual health is an important part of a healthy life. The aim of this study is to define Behçet’s sexual dysfunction and the factors affecting it. Sixty-nine patients with Behçet’s disease (BD) and 74 healthy controls were included in the study. International Index of Erectile Function (IIEF), the Female Sexual Function Index (FSFI), the Beck Depression Inventory (BDI), and the Short Form Health Survey (SF-36) were filled out by patients and healthy control group (HCG). Follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin and estradiol or testosterone levels according to gender were measured in Behçet’s patients. The rate of sexual dysfunction and its relationship with gonadal hormones, Beck depression and SF 36 subgroups were evaluated in Behçet’s patients. Sixty-nine patients with BD (mean age 39.55 ± 11.7) and 74 HCG (mean age 36.9 ± 6.84) were included in the study. Sexual dysfunction was observed in 74% (49) of BD and 59.5% (44) of HCG (p = 0.047). Prolactin level is within normal limits in all patients. Although there are abnormal levels of gonadal hormones, no relationship was found with sexual dysfunction. Depression especially is more prevalent compared to the healthy population (p = 0.016). The presence of depression negatively affects sexual life. Depression, SF 36 physical role limitations, energy vitality, vitality and mental health were associated with sexual dysfunction in patients with Behçet’s disease. Sexual dysfunction was associated with the presence of depression and SF-36 subscales in Behçet’s patients.

Introduction: Addison’s Crisis is extremely rare entity that is difficult to diagnose in the emergency department. Here we present a case of Addison’s crisis diagnosed in the emergency department who complained of vomiting after consuming extract of Momordica charantia fruit for gastric pain. Case Report: A 29-year-old female was admitted to the ED with complaints of nausea and vomiting after consuming Momordica charantia extract for stomach pain. The patient had tachypnea, tachycardia, hypoglycemia, and hypotension. Blood tests revealed elevated anion gap (24 mEq/L) metabolic acidosis, +4 acetone, normokalemia, and hyponatremia. Although it was impossible to exclude intoxication immediately, 100 mg hydrocortisone was given due to possible Addison’s crisis after obtaining blood samples for hormone testing and excluding other causes of shock. The tests revealed very high ACTH (1.250 pg/mL) and low cortisol (1.23 ug/dL) levels, and the patient was diagnosed with primary adrenal insufficiency. Conclusion: This case illustrates the importance of comprehensive examination and management of profound hypotension and hypoglycemia in the ED and of emergency physicians diagnosing and initiating appropriate treatment for Addison’s crisis.

Purpose There is no clear information about the level of Apelin-13 in patients with diabetic nephropathy (DN). In this study, we investigated whether there is a relationship between Apelin-13 level and the severity of the disease in patients with DN. Methods In our case–control study, we included patients who applied to the endocrinology outpatient clinic in 2019. Patients without a history of diabetes were determined as the healthy group (group 1). The patients were divided into 4 groups according to their microalbumin and creatinine levels. Venous blood samples were obtained from all patients for routine laboratory parameters and Apelin-13 levels. Homeostatic Model Assessment-Insulin Resistance (HOMA-IR) for insulin resistance was calculated using the formula: plasma glucose X insulin level/405. Results Albumin was found to be significantly lower in group 5 (p = 0.032), hemoglobin A1c, microalbumin/creatinine and HOMA-IR values were found to be significantly lower in group 1 (p < 0.001 for each). Apelin-13 level was found to be significantly higher in group 4 and group 5 (p < 0.001). A negative correlation was found between Apelin-13 and GFR (r = − 0.286, p = 0.003). A positive correlation was found between Apelin-13 and HOMA-IR (r = 0.309, p = 0.009) and microalbumin/creatinine (r = 0.296, p < 0.001). Conclusion In patients with DN, Apelin-13 level increases with the severity of the disease and can be used as a biomarker for staging of DN.

Purpose To investigate the possibility of distinguishing between nonfunctioning adrenal incidentalomas (NFAI) and autonomous cortisol secreting adrenal incidentalomas (ACSAI) with a model created with magnetic resonance imaging (MRI)–based radiomics and clinical features. Methods In this study, 100 adrenal lesions were evaluated. The lesions were segmented on unenhanced T1-weighted in-phase (IP) and opposed-phase (OP) as well as on T2-weighted (T2-W) 3Tesla MRIs. The LASSO regression model was used to select potential predictors from 108 texture features for each sequence. Subsequently, a combined radiomics score and clinical features were created and compared. Results A significant difference was found between median rad-scores for ACSAI and NFAI in training and test sets (p < 0.05 for all sequences). Multivariate logistic regression analysis revealed that the length of the tumor (OR = 1.09, p = 0.007) was an independent risk factor related to ACSAI. Multivariate logistic regression analysis was used for building clinical-radiomics (combined) models. The Op, IP, and IP plus T2-W model had a higher performance with area under curve (AUC) 0.758, 0.746, and 0.721 on the test dataset, respectively. Conclusion ACSAI can be distinguished from NFAI with high accuracy on unenhanced MRI. Radiomics analysis and the model constructed by machine learning algorithms seem superior to another radiologic assessment method. The inclusion of chemical shift MRI and the length of the tumor in the radiomics model could increase the power of the test.

Pseudohypoparathyroidism is a rare inherited metabolic disorder that associated with parathormone resistance. Low serum calcium, high phosphates and raised parathormone levels suggesting parathormone resistance are biochemical characteristic features of disorder . Pseudohypoparathyroidism type 1 is known as Albright’s hereditary osteodystrophy that characterized by a typical phenotype. This syndrome encompasses multiple clinical findings such as brachydactyly, rounded face, short stature, central obesity, and variable degrees of mental retardation. Here, we present a patient with pseudohypoparathyroidism which is rare cause of hypocalcemia and parathormone resistance .