ACTA ENDOCRINOLOGICA (BUC)

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Long lasting hypocalcemia, hyperphosphatemia, low calcitriol and high fibroblast growth factor 23 could result in progressive parathyroid gland hyperplasia with high, uncontrolled, parathormone production, e.g. severe secondary hyperparathyroidism (sHPT), in 10% of dialysis patients. Parathyroidectomy (PTX) could be a solution, but has inherent (low) surgical risks and although dramatically decreases parathormone levels, could induce hypoparathyroidism (50-66%) and low turnover bone disease. Moreover, the rate of recurrences is 15-20% at 10 years. Total and subtotal PTX with autografting are equally safe and effective with similar recurrences rates. Calcimimetics are efficient drugs, but with limited effectiveness in sHPT, as only 25% of patients responded to cinacalcet. In the USA, they are more cost-effective than PTX only in patients with >2 years expected dialysis duration. As there are not randomized studies to compare surgical to medical therapy, the strength of evidence allows only for suggestions in guidelines. In countries like Romania, where dialysis vintage is high because of the low transplantation rate and calcimimetics are costly, PTX seems a better solution when parathyroid glands are large (diameter >1cm or\r\ntotal mass >500mg), parathormone levels >800pg/mL, in patients who are not candidates for renal transplantation or are anticipated to stay >2 years on dialysis.

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Background. Antineutrophil cytoplasmic antibodies (ANCA) positivity is usually determined in vasculitis of medium and large arteries. In literature, data related to the prevalence of ANCA positivity and the development of antibodies after antithyroid therapy in Graves’ disease are quite rare. Aim. To investigate the titers of myeloperoxidase (MPO)-ANCA and proteinase 3 (PR3)-ANCA in Graves’ patients treated with propylthiouracil (PTU) and to determine the factors that may contribute to ANCA positivity. Subjects and Methods. Fifty-two Graves’ patients treated with propylthiouracil (PTU) were included into the study. The control group consisted of 37 healthy subjects. MPO-ANCA and PR3-ANCA titers were measured in both groups. Results. Mean titer of PR3-ANCA in Graves’ group was significantly higher than in controls (p=0.025), but no significant difference was found in the titer of MPOANCA between two groups (p=0.060). A positive correlation was observed between PR3-ANCA titer, and anti-thyroid peroxidase antibody and anti-thyroglobulin antibody levels in Graves’ patients (p=0.001, r=0.447 and p=0.030, r=0.310, respectively). PR3-ANCA titer in anti-thyroglobulin antibody positive patients was higher than those with negative antibody (p=0.018). A positive correlation was detected between the duration of treatment and PR3-ANCA titer (p=0.024, r=0.314). Both MPO-ANCA and PR3-ANCA were positive in two Graves’ patients, while only MPO-ANCA was positive in two patients. No signs of vasculitis in ANCA positive patients were observed. Conclusion. Propylthiouracil (PTU) may cause ANCA positivity, but no vasculitis may develop in most of the cases. A correlation was determined between PR3- ANCA titer, and thyroid autoantibodies and the duration of treatment.

Context. Platelet indices change in relation to cardiovascular risk factors, including type 2 diabetes mellitus (T2DM). An increase of platelet indices over time in patients undergoing percutaneous coronary intervention (PCI) could be a predictor of mortality. The objective of this study was to assess differences in platelet indices in patients with and without T2DM undergoing PCI, prior and more than one month after the procedure. Subjects and Methods. In this retrospective observational study, patients undergoing PCI were included. Data were extracted from PCI Registry of the Emergency Institute for Cardiovascular Diseases and Transplantation of Tirgu Mures, Romania. Results. Of the 718 patients included in the study, 222 (30.9%) had T2DM; 61% of patient underwent PCI for SCAD, the rest for NSTE-ACS or STEMI. Prior to PCI, MPV, PDW and P-LCR were not higher in T2DM patients irrespective of the indication for PCI. At a follow-up time of 69 (46-98) days, platelet indices were not different between TD2M+ and T2DM-, except from MPV (11.0 vs. 10.6, p=0.02) which were higher in TD2M patients with SCAD. Intraindividual variability of platelet indices was not different in diabetics, but MPV, PDW and platelet count decreased over time (3.5% and 8.4% respectively) in diabetics with STEMI (p=0.02). Conclusions. Platelet indices were not higher in patients with T2DM undergoing PCI, but we observed an important variation in platelet indices in diabetics after STEMI related PCI.

Calcitonin (CT) is a polypeptidic hormone specifically secreted by the thyroid parafollicular cells (C cells) and tangentially involved in human phosphocalcic and bone metabolism. CT from other species (e.g. salmon) is more potent than human CT and has limited therapeutic applications. The neoplastic proliferation of C cells leads to medullary thyroid carcinoma (MTC) generally characterized by an increase of CT secretion. Serum CT is therefore the ideal marker for MTC and can confirm its presence at an early stage, as well as the follow up of its remission or progression/relapse/survival after surgery. There are, however, controversies such as the necessity of CT screening in patients with thyroid nodules, or particular situations causing false positive or false negative results. Our minireview also deals with an up-to-date of surgical procedures for MTC, as well as with non-surgical therapy.

Context. Melanoma is the most aggressive skin cancer, with significant morbidity and mortality, and one factor that may influence the course of disease is stress. Objective. Our aim was to evaluate the effect of corticosterone, norepinephrine, epinephrine on murine B16F10 melanoma cells in vitro proliferation. Methods. B16F10 melanoma cells were treated with different concentrations of tested hormones. The proliferative capacity of melanoma cells was quantified by MTS assay and the cell viability was quantified as membrane integrity evaluation measured by lactate dehydrogenase (LDH) release. Results. B16F10 cells treated with corticosterone showed no significant changes. In contrast, norepinephrine exposure stimulated the cell proliferation (P = 0.0003). Treatment with 1 μM norepinephrine induced the highest increase in cell proliferation (OD 492 = 0.27 ± 0.02) statistically significant to both control (OD 492 = 0.17 ± 0.01; p = 0.0003), 10 nM norepinephrine (OD 492 = 0.16 ± 0.00; p = 0.0004) and 100 nM norepinephrine (OD 492 = 0.19 ± 0.01; p = 0.002). Likewise, treatment with epinephrine increased cell proliferation (p = 0.0004). Exposure to 5 μm epinephrine induced a stimulation of cell proliferation (OD 492 = 0.28 ± 0.02) significantly higher compared to controls (OD 492 = 0.17 ± 0.01; p = 0.0004), 50 nM epinephrine (OD 492 = 0.17 ± 0.00; p = 0.001) and 500 nM epinephrine (OD 492 = 0.173 ± 0.00; p = 0.001). Conclusions. Our results may open new perspectives concerning the link between stress hormones and melanoma, emphasizing a direct stimulating in vitro effect induced by catecholamines on melanoma B16F10 cells proliferation.

The conventional treatment of hypoparathyroidism consists of vitamin D analogues in combination with oral calcium\r\nsupplementation. This treatment modalities induce chronic hypercalciuria which leads to nephrocalcinosis, nephrolithiasis and renal insufficiency. Here we report the case of a 32-year-old woman who developed hypocalcemia and hypercalciuria under treatment with high doses of vitamin D\r\nanalogs and oral calcium. She had cerebral calcification, nephrocalcinosis under this treatment. Stable calcium levels were achieved with synthetic human parathyroid hormone treatment that was given in alternate days. PTH appears to be an alternative and effective treatment in hypoparathyroidism.

Context. Stress hyperglycemia has been studied in numerous critical illnesses for several decades. Despite the extensive accumulation of knowledge about this topic, the definition of stress hyperglycemia is not updated since 2007. Subjects and Methods. We performed a narrative review about stress hyperglycemia in acute myocardial infarction (AMI), aiming to improve its current definition and to give evidence supporting this. Results. The definition of stress hyperglycemia in 2021 we recommend is: “SH is a high ABGly in an AMI patient irrespective of DM status. It can be calculated as e.g., “stress hyperglycemia ratio” or “admission glucose delta”/“glycemic gap”. This definition may serve to start a consensus document of the experts in the field. The evidence accumulates supporting the possibility to recognize stress hyperglycemia also in AMI patients with diabetes mellitus (DM) by calculating glycemia during the previous 2-3 months using glycated hemoglobin. Moreover, it is now obvious that 2007 definition of stress hyperglycemia did not take into account the necessity to separate cut-offs for the subgroups with vs. without DM. Conclusions. We demonstrated the insufficiency of the current 2007 definition of stress hyperglycemia, provided evidence-based recommendation for the improvement and suggested the need for a consensus of the experts on this topic. In order to optimize the treatment of stress hyperglycemia in numerous critical illnesses, we ought to have its universal definition (as we already have the universal definition of AMI).