Endocrine disruptors (ED) are exogenous agents that interfere with the normal function of the endocrine system and they are considered environmental chemicals with estrogen-like and/or anti-androgenic activity with important impact on the reproductive axis. They act via nuclear receptors, non-nuclear steroid receptors, nonsteroidal receptors, orphan receptors, and different enzyme pathways involved in the biosynthesis and/or metabolism of steroids. The molecules identified as ED and sources of exposure are diverse and vary worldwide, including from natural chemicals found in human and animal food (the main source) up to synthetic chemicals, such as as solvents, plasticizers, pesticides, fungicides, pharmaceuticals etc. ED are incriminated in the occurrence of malignant tumors, birth defects, attention deficit disorders, cognitive impairment, brain development, deformations of the body (including limbs), disturbance of sexual development, menstrual irregularity, precocious puberty, feminizing or masculinizing effects, abortion, not least obesity and decreased fertility. The principles of action are still studied and controversial, therefore, it is difficult to determine the minimum level at which adverse effect occurs and further studies are required.

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Introduction. Current studies support the implication of metabolic changes associated with type 2 diabetes in altering bone metabolism, structure and resistance. Objective. We conducted a cross-sectional study on postmenopausal women aimed to analyze the differences in metabolic and bone profile in patients with and without type 2 diabetes Methods. We analyzed the metabolic and bone profile in postmenopausal women with and without type 2 diabetes (T2DM). Clinical, metabolic, hormonal parameters, along with lumbar, hip and femoral bone mineral density (BMD) and trabecular bone score (TBS) were evaluated. Results. 56 women with T2DM(63.57±8.97 years) and 83 non-T2DM (60.21±8.77 years) were included. T2DM patients presented a higher value of body mass index (BMI) and BMD vs. control group (p = 0.001; p = 0.03-lumbar level, p = 0.07-femoral neck and p = 0.001-total hip). Also, BMI correlated positively with lumbar-BMD and glycated hemoglobin (HbA1c) (r = 0.348, p = 0.01; r = 0.269, p = 0.04), correlation maintained even after age and estimated glomerular filtration rate (eGFR) adjustment (r = 0.383, p = 0.005; r = 0.237, p = 0.08). Diabetic patients recorded lower levels of 25(OH)D(p = 0.05), bone markers (p ≤ 0.05) and TBS(p = 0.07). For the entire patient group we found a negative correlation between HbA1c level and bone markers: r = -0.358, p = 0.0005-osteocalcin, r = -0.40, p = 0.0005-P1NP, r = -0.258, p = 0.005-crosslaps. Conclusions. Our results indicate the presence of altered bone microarchitecture in T2DZ patients according to the TBS score, combined with lower levels of bone markers, with a statistically significant negative correlation between HbA1c level and bone markers.

Primary hyperparathyroidism (PHPT), an endocrine condition caused by a parathyroid adenoma (PTA) in 80-85% of the cases, has shifted in the modern era to a mildly symptomatic phenotype due to the prompt recognition of hypercalcemia and to a minimally invasive surgical approach which has a curative potential. Clinical complications of PHTH are either related to high calcium or parathyroid hormone [also parathormone (PTH)] or both, while the originating tumor typically is small, without local mass effects. A distinct entity is represented by giant PTA (GPTA) which is considered at a weight of more than 3 (3.5) grams. The present article is a review of the literature involving practical points of non-syndromic PHPT-related GPTA. Most authors agree that pre-operatory calcium and PTH are higher in GPTA vs. non-GPTA. However, the clinical presentation of PHPT may be less severe, probably due to local mass effects that bring the patient to an early medical evaluation. Age distribution, sex ratio, rate of successful pre-operatory location do not differ from non-giant PTA. Hypovitaminosis D is more frequent in PTA of higher dimensions. Post-operative hypocalcemia, but not recurrent/persistent PHPT, is expected, even hungry bone disease. A higher rate of atypia is described although the tumor is mostly benign. Unusual presentations such as cystic transformation, initial diagnosis during pregnancy or auto-infarction have been reported. The ectopic localization of PTA presented in almost 15% of all cases may also be found in GPTA. What are the exact cutoffs for defining GPTA is still an open issue. Contents 1. Introduction 2. Aim 3. Giant parathyroid adenoma: Concept around the size considerations 4. Pre-operative biological correlates 5. Relationship with vitamin D status 6. Histological issues 7. Ectopic PTA of large dimensions 8. Risk of post-operative hypocalcemia 9. Future considerations 10. Conclusions