ACTA ENDOCRINOLOGICA (BUC)

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Background. The use of nutrient supplements along with medication to optimize the treatment of diseases yields desirable outcomes. Hypothyroidism causes abnormalities in cells, and organs, and induces gene expression changes. The use of salt supplements and vitamins considerably helps to treat hypothyroidism. Objectives. To evaluate the effect of a food supplement containing iron, iodine, and folic acid on thyroid hormones changes as well as the quality and quantity of hypothyroid female rat’s offspring. Materials and Methods. In the current experimental study, 40 female rats were divided into six experimental and two control groups. The study was conducted in three phases. In the first phase, the role of a combinatory supplement along with levothyroxine to treat hypothyroidism by assessing T3, T4, and TSH hormones was investigated. In the second phase, the dose-depended effects of a combinatory supplement were investigated. Additionally, in the third phase, the quality and quantity of the next generation were measured in the hypothyroid female rats receiving the salt supplement. Results. The plasma level of T3, T4 and TSH in hypothyroid rats receiving nutrient supplements indicated that the use of combinatory supplements along with levothyroxine could have desirable effects on the treatment of hypothyroidism to such an extent that the level of T3 and T4 hormones in the intervention group was significantly higher than that of the control group (P≤0.01). The second phase demonstrated that the desired effects of combinatory supplements on the serum levels of T3, T4, and TSH hormones were dose-dependent so that by increasing the dosage of supplementation, a significant decrease in the TSH level was observed (P <0.05), while T3 and T4 levels increased (P <0.01). The results of the third phase demonstrated that salt supplements could be effective in reducing the number of dead or preterm pups, and the use of mineral salts along with levothyroxine could promote a healthy birth. Conclusion. Salt supplements have considerable effects on the health status of the offspring of hypothyroid rats, resulting in the birth of more healthy pups and reducing the rate of abortion or preterm births.

Objective. After total thyroidectomy, radioiodine (131I) treatment is a usual treatment in patients with differentiated thyroid cancer (DTC). Since most of ingested 131I is excreted by the kidneys, one of the procedures for enhancement of 131I excretion from the body is the use of diuretics. The aim of study was to investigate the effect of hydrochlorothiazide (HCTZ) administration on the excretion of 131I in the urine in patients with DTC treated with 131I. Design. Study included 90 patients with DTC, normal renal function and low 131I uptake in the thyroid gland region. Patients were divided into two groups: the group taking HCTZ and the control group. All patients underwent whole-body measurements of the radioactivity of 131I in the urine and in blood samples. Results. Blood radioactivity was significantly higher in the HCTZ group as compared to the control group (16380.89 vs. 11731.61cpm/mL/GBq; P=0.007). The residual radioactivity in the body and the exposed dose were higher in patients taking HCTZ (71.61 vs. 60.70MBq/ GBq and 7.05% vs. 6.14%) but this difference was not significant. During the first 36h from 131I administration the patients taking HCTZ excreted a higher percentage of the 131I than the controls (65.45±12.12% vs. 62.21±11.25%, P=0.032). During the second part of the hospitalization (36- 72h) the urinary excretion as reversed, so after 72h patients taking HCT excreted less 131I than controls, however, this difference was not significant (P=0.084; 76.54±10.16% vs. 83.81±13.46%). Conclusions. HCTZ given as additional treatment decreases urinary excretion of 131I as and should not be administered in patients under 131I treatment for DTC.

Background. The purpose of this study was to observe the effects of denosumab on bone mineral density (BMD), bone turnover markers and serum calcium in patients with primary hyperparathyroidism (PHPT) and osteoporosis. Methods. Seven consecutive patients with PHPT were administered a single subcutaneous injection of denosumab, 60 mg. The subjects were followed up to 6 months: serum calcium on days 1,3,7,14,30 and at 3 months and 6 months; serum intact parathyroid hormone (iPTH), C-telopeptide (CTX) and N-mid osteocalcin at baseline, 3 months and 6 months. BMD by DXA, at the femoral neck (FN) and lumbar spine (LS), were measured at baseline and at 6 months. Results. The patients (mean age= 69.8 yrs, range 62-81) had mild PHPT (mean total calcium = 10.8 mg/dL; mean PTH = 148.9 pg/mL); all had osteoporosis and four were currently treated with various bisphosphonates (BP). After 6 months mean LS BMD increased significantly by 4.5 % (p = 0.04) and mean FN BMD by 2.4% (p= 0.09 two-tailed; p = 0.047 one-tailed). Serum CTX decreased significantly by 90% at 3 months (p = 0.04), and by 48% at 6 months (p = 0.02); the similar changes for serum osteocalcin were 41% and 42% (p = 0.07, onetailed), respectively. In the first two weeks, serum total Ca variably decreased vs. baseline (0.5 to 2.8 mg/dL) in six out of seven patients. After 6 months mean total serum Ca nonsignificantly increased vs. baseline (11.4 mg/dL vs. 10.8 mg/dL, p = 0.1). Serum iPTH levels did not significantly change at both 3 and 6 months; after 6 months there was a trend toward decreased values (p = 0.03 onetailed). Conclusion. Denosumab increased BMD at both lumbar spine and femoral neck, and significantly decreased bone resorption in patients with PHPT. The effects on hypercalcemia were mild and transient, with a numerical increase after 6 months.

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Context. Hyperparathyroidism-jaw tumour (HPTJT) syndrome is a rare autosomal dominant cause of familial hyperparathyroidism associated with ossifying fibromas (OF) of the maxillofacial bones and increased risk of parathyroid carcinoma, caused by inactivating germline mutation of the cell division cycle 73 (CDC73) gene. Objective. To report the first Romanian family with HPT-JT and genetic screening of CDC73 gene. Subjects and Methods. Mutational analysis of the CDC73 gene and genetic screening of the family of a proband with HPT-JT. Histological diagnosis of parathyroid tumors (WHO criteria) and immunohistochemistry (parafibromin) were performed. Results. Three of the six screened family members had evidence of PHPT and surgically proven parathyroid tumours. Two of the three affected members had parathyroid carcinomas and one had two parathyroid adenomas. Genetic screening of CDC73 gene revealed that 4 of 6 patients showed a heterozygous germline deletion of one nucleotide: c.128-IVS1+1 delG. All the three affected patients, resulted to be carriers of the CDC73 mutation, but each one bearing a different CDC73 polymorphism. Conclusions. We identified a new CDC73 germline mutation in a Romanian family of HPT-JT. Analysis of clinical phenotypes in the four mutated individuals confirmed the incomplete penetrance and the variable clinical expression of the disease.

Context. Infertility affects more and more younger patients nowadays. Life-saving cancer treatments - chemotherapy and radiation therapy unfortunately damage oocytes and reduce the window of fertility in women. There were an estimated 14.1 million cases of cancer worldwide in 2012, of which 6.7 million were in women. Aim. We are reviewing fertility options and treatments for women fighting oncological diseases. It is important to promote that there is a possibility for these patients to know all they can do in order to preserve their fertility and our government should help all these young patients. The trend of delayed childbearing has increased worldwide duet o increased life costs, difficulty of finding a suitable partner and carier options, while the number of women facing a cancer diagnosis is rising. Material and methods. We describe a review regarding the impact of these treatments for the fertility of these patients. Results. Show that informed patients can better cope with their diagnostic and have a better prognosis. Conclusions. Improving survival rates and current data have created a new medical field oncofertility. The term was first introduced in 2015 and is being used all over clinics that treat young patients nowadays.

The detection of thyroid nodules in a patient with Graves&#8217; disease is not a rare event.\r\nThe management of these cases still represents a controversial problem for clinical practice.\r\nThis paper describes the case of a patient with Graves&#8217; disease and a concurrent\r\nfollicular thyroid carcinoma, presenting as a clinical palpable nodule in the right lobe.\r\nThyroid function tests confirmed thyrotoxicosis. Immunological investigations showed high\r\nlevels of TSH-R antibodies. Thyroid ultrasound revealed an increased thyroid volume with\r\na diffuse low echogenicity of parenchyma and in the right lobe a single homogeneous\r\nhypoechoic nodule. The scintiscan indicated the presence of a &#8220;cold nodule&#8221; in the right lobe\r\nand increased uptake in the rest of parenchyma. Antithyroid drug therapy was\r\nrecommended. Cytological exam indicated an &#8220;indeterminate&#8221; smear. After euthyroidism\r\nwas achieved, surgical therapy was recommended and near total thyroidectomy was\r\nperformed. The morphopathological exam revealed an invasive follicular carcinoma on a\r\ndiffuse thyroid hyperplasia (Graves&#8217; disease). This case report is followed by a discussion\r\nabout the incidence of malignancy in thyroid nodules concurrent with Graves&#8217; disease. The\r\ncriteria that raised concern about a possible malignancy of the nodule are presented.\r\nIn conclusion, we recommend that patients with Graves&#8217; disease should undergo a\r\nregular examination of the thyroid gland for an early detection of possible malignant\r\nnodules. The intervention of choice in these cases should be near total or total\r\nthyroidectomy, if malignancy cannot be excluded by preoperative evaluation.

Gastrointestinal effects of estrogens are emerging as an important topic in colorectal cancer management. Current research demonstrated the link between inflammation and this malignancy, so important estrogen dependent mediators of the inflammatory response have been identified. Radioresistance and chemoresistance still represent an important cause of therapeutic failure in colorectal cancer and lead to further studies of colorectal carcinogenesis and predictive markers.

Background. People chew betel nut (Areca catechu) for physical work and stress reduction, but it contains arecoline, which has both therapeutic value and untoward effects on endocrine and gonadal functions. Objective. Aim of the present study is to investigate its role on adrenal with its target in metabolic stress in mice. Materials and methods. Mice were deprived of water / food, each for 5 days / treated with arecoline (10 mg / kg body wt daily for 5 days) / arecoline after water or food deprivation, for 5 days each. Results. Water or food-deprivation caused adrenocortical hyperactivity, evident from abundance of enlarged mitochondria and smooth endoplasmic reticulum (SER) with elevation of corticosterone level (C: 68.31 ± 2.30, WD: 159.31 ± 4.10 / FD: 194.12 ± 3.40 μg/ mL). Arecoline treatment alone or in water deprivation (C: 68.31 ± 2.30, AR: 144.50 ± 4.33, AR+WD: 194.42 ± 3.35 μg/ mL) / food deprivation (AR + FD: 180.89 ± 4.51 μg/ mL) stress also stimulated adrenocortical activity as recorded in metabolic stress. In contrast, adrenomedullary activity was not altered following water/ food deprivation. Arecoline treatment alone or in metabolic stress suppressed adrenomedullary activity by showing depletion of chromaffin granules (E/NE?), epinephrine (E) and norepinephrine (NE) concentrations. Both the stress decreased blood glucose and liver glycogen levels. Arecoline treatment decreased blood glucose level, with a rise in liver glycogen level, but elevated blood glucose level in water deprivation unlike in starvation. Conclusion. Arecoline alone or in metabolic stress involves adrenal and probably other endocrine glands (pancreas, posterior pituitary and rennin-angiotensin system) to maintain homeostasis in metabolic stress in mice.