ACTA ENDOCRINOLOGICA (BUC)

Context. Adipokines secreted by fat cells are vital to the control of energy metabolism, communicating the nutrient status with the tissues responsible for controlling both energy intake and expenditure and insulin sensitivity. Objective. We aimed to prove in an experimental animal study that maternal obesity has long term adverse fetal metabolic consequences, which pass on even to the next generation of descendants. Design. The effects of maternal obesity have been studied on animal model using 50 obese female Wistar rats, in which we induced obesity by high-calorie high-fat diet administered by gavage. Subjects and Methods. Obese rat females were sacrificed at gestation term and we analyzed the secretion of adipokines from maternal venous blood: leptin and adiponectin, placental, pancreatic, liver and brain homogenates lipid peroxidation levels estimated by: MDA (malonyl-dialdehyde), total thiols and GSH – as antioxidant factors and routine biochemistry. Results. Low levels of adiponectin and increased levels of leptin positively correlated with the value of placental and fetal tissue lipid peroxidation (from the liver, pancreas and brain) measured by elevated MDA and total thiols and low levels of GSH. The lipid peroxidation in the organs examined generated consistent results, showing high levels of peroxidation expressed through high values of MDA in the groups with Omega 6 supplements respectively no supplementation, and low levels of antioxidants expressed through glutathione and thiols. Conclusions. Endocrine secretion of adipokines from the adipocytes and the recruited macrophages of obese mothers is positively correlated with placental and tissue lipid peroxidation level and routine biochemical parameters.

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Acute or chronic burn injuries require hormonal responses that significantly influence patient prognosis. Elevated cortisol, catecholamines, and glucagon levels, lead to important metabolic changes, such as hyperglycaemia, insulin resistance, protein catabolism, free fatty acids oxidation, and secondary metabolic acidosis. These alterations impair immune function and wound healing and trigger a systemic inflammatory response. A multidisciplinary approach is needed in order to correctly manage the aforementioned endocrine and metabolic changes. During the acute phase, glucose monitoring, corticosteroid administration for transient or iatrogenic adrenal insufficiency and electrolyte balance maintenance are critical. Chronic phase requires hormonal replacement, nutritional optimization, and anabolic agents administration to counteract catabolic states. Despite continuous advances in burn care, understanding the complex interplay between hormonal changes and immune dysfunction remains challenging. Managing burn-associated endocrine responses could lead to the development of new therapeutic strategies, including personalised and stage- adapted treatment.

Context. Neoangiogenesis and lymphangiogenesis are essential for the growth of tumor and progression of malignancy. Objective. The study examined the significance of VEGF-C expression in comparison to classical prognostic factors in differentiated thyroid carcinoma (DTC), as well as an independent prognostic marker in DTC. Design. The study included 81 patients with DTC allocated in two groups according to the type of cancer (follicular versus papillary) and then compared to expression of VEGF-C and clinicopathological features. Methods. Expression of VEGF-C was identified with anti-VEGF-C antibody using tris-EDTA buffer Antigen Retrieval Protocol. Each specimen was scored with a semiquantitative score system (H-score). Results. The analysis of T staging system showed a linear correlation between the size of a tumor, expression of VEGF-C and recurrence of a disease, with a statistical significance (p < 0.0001). There was a clear and significant correlation between VEGF-C expression and T stage in patients with papillary carcinoma (p = 0.0294). Analysis of invasion of a surgical margin demonstrated significant positivity in patients with papillary thyroid cancers who expressed VEGF-C (p = 0.0207) indicating the worse prognosis of a disease. Also a statistically significant correlation was between VEGF-C and extrathyroid extension, indicating the worse prognosis (p = 0.0133) in papillary cancers. The level of VEGF-C expression was statistically significant in patients with papillary thyroid cancer (p = 0.039). Conclusions. This study undoubtedly demonstrates that VEGF-C expression is an evident negative prognostic factor in patients with papillary thyroid carcinoma, along with the classic prognostic factors, such as a larger tumor size, tumor margin involvement, extrathyroid extension, i.e. local aggressiveness.

Pituitary adenomas are fully characterized only by immunohistochemistry. The technical limitations, gaps and peculiarities influence the pathology diagnosis. More and more data shows that clinically nonfunctioning pituitary adenomas could synthesize or secrete hormones or their subunits. The tumor pathology is monomorphous or polymorphous, difficult to differentiate from normal adjacent tissue. Light microscopy (LM) qualitative analysis using basic or special stains can differentiate between tumor and normal tissue and allows elimination of artifacts. Electron microscopy (EM) completes the diagnosis in selected cases. Pituitary adenomas immunohistochemistry was done by LM in 120 cases (84 ? clinically nonfunctioning adenomas ? NFA and 36 acromegalics with or without PRL secreting adenomas - ACM) using the avidine-biotin complex method. In 26 cases we determined by EM the immunoreactive cells (17 NFA and 9 ACM) using the immunogold method. We observed high tumor immunoreactivity (mono or plurihormonal) in 43/84 (51%) NFA, 13/36 (36%) ACM respectively. Serum excess hormones and tissue immunoreactivity were significantly concordant for prolactin in NFA cases and for GH, in ACM cases (p<0.05). Mute pituitary adenomas have no clinical expression of hormonal products either they produce biologically inactive components or they synthesize but do not secrete hormones in sufficient amounts to increase serum level and to determine a systemic response. A concordance between LM and EM immunoreactivity was observed only for GH in ACM patients group (p<0.05). The differences could be due to dimensions of the samples or the number of granules inside of the cells (sparsely granulated adenomas are negative or low immunoreactive at the LM level). EM evaluation of NFA identified 2 oncocytomas and 4 null cell adenomas. The complete evaluation of pituitary adenomas includ a qualitative and quantitative analysis at the LM level using special methods, validated at the EM level in order to identify clinically mute immunoreactive cells ? a possible target for specific drugs therapies in the future.

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Context. SARS-CoV-2 infection was declared a pandemic in 2020 and affected millions of people worldwide. Angiotensin-converting enzyme-2 receptors, through which coronavirus enters the cells of different organs, have been detected in the thyroid gland. The most common cause of thyrotoxicosis is Graves’ disease in which thyroid-receptors antibodies (TRAb) stimulate the TSH receptor, increasing thyroid hormone production and release. Case presentation. A 22-year-old woman had symptoms of palpitation, tremor, muscle weakness, anxiety and sleep disturbance. 3 weeks before the onset of these symptoms, the patient suffered from COVID-19, which lasted 14 days and was characterized by a course of moderate severity with fever up to 38˚C, general weakness without shortness of breath. The patient had no pre-existing thyroid problems. Her TSH was <0.01 mU/L, FT4, FT3 and TRAb were increased. Antithyroid drugs, glucocorticosteroids and β-blockers were prescribed. During 3 months of treatment doses of methimazole, methylprednisolone and bisoprolol were gradually reduced due to the improvement of the patient’s condition and thyroid tests normalization. Conclusions. COVID-19 infection can cause Graves’ disease and thyrotoxicosis. The onset of this disease after SARS-CoV-2 does not depend on the presence of preexisting thyroid pathology and requires the appointment of glucocortisteroids.

Background. Arecoline, a plant alkaloid of betel nut, is consumed by millions of people, for increased capacity of work. It causes immunosuppression, hepatotoxicity, and disturbance in antioxidant production, but it stimulates HPA axis and induces thyroid dysfunction.\r\nAim. To investigate the role of arecoline on adrenal activity, glycemia and glycogen profile in mice.\r\nMaterials and methods. Arecoline was injected intraperitoneally at a dose of 10 mg/kg body wt for 20-60 min for acute administration. In chronic administration the same dose was used daily for 15 days. Corticosterone, epinephrine, norepinephrine, blood glucose and liver glycogen profiles were measured after 20, 40 and 60 min, in acute administration and after 15 days in chronic administration.\r\nResults. Arecoline in acute administration increased corticosterone, norepinephrine and epinephrine levels and induced hyperglycemia with depletions of liver glycogen. But\r\nchronic arecoline administration with the same dose for 15 days caused ultrastructural degenerations of adrenal cortex and medulla with the elevation of corticosterone, and\r\ndepletions of norepinephrine and epinephrine levels. Arecoline also caused hypoglycemia and elevated liver glycogen. Atropine (arecoline receptor antagonist) prevented arecoline action on adrenal activity or blood glucose ? liver glycogen interaction.\r\nConclusion. The findings indicate that arecoline initially stimulates adrenal activity, but subsequently inhibits it with alterations of glycemic and glycogen profiles. Arecoline action is mediated by arecoline receptor in mice. Arecoline may have immunological action via adrenal hormonal suppression in mice.

Introduction. Genetic disorders associated with the development of the pituitary gland and cranial bones may cause a genetic tendency toward Sheehan’s syndrome (SS). Our aim in this study was to investigate expression disorders in the genes responsible for the development of the pituitary gland and cranial bones in patients with SS. Materials and Methods. Forty-four patients who were previously diagnosed with SS and 43 healthy women were compared in terms of the mean expression values of genes including the prophet of PIT-1 (PROP1), HESX homeobox 1 (HESX1), POU class 1 homeobox 1 (POU1F1), LIM homeobox 3 (LHX3), LHX4, glioma-associated oncogene homolog 2 (GLI2), orthodenticle homeobox 2 (OTX2), SIX homeobox 3 (SIX3), SIX6, T-box transcription factor 19 (TBX19), transducin-like enhancer protein 1 (TLE1), TLE3, distal-less homeobox 2 (DLX2), DLX5, MSH homeobox 2 (MSX2), and paired box 3 (PAX3). Results. The mean expression values of the HESX1, TLE1, TLE3, and MSX2 genes were significantly different in the SS group from the healthy control group, while the mean expression values of the remaining genes were similar. Conclusion. The present study concludes that abnormal expressions of HESX1, TLE1, TLE3, and MSX2 genes may cause a genetic predisposition to the development of SS.