Starting from the metabolic profile of type 2 diabetes mellitus (T2DM), we hypothesized that the mechanisms of ¹³¹I-induced cardiotoxicity differ between patients diagnosed with differentiated thyroid cancer (DTC) with/without T2DM, with metformin potentially acting as a cardioprotective agent by mitigating inflammation in patients with T2DM. To address this hypothesis, we quantified, using ELISA, the serum concentration of several key biomarkers that reflect cardiac injury (NT-proBNP, NT-proANP, ST2/IL-33R, and cTn I) in 74 female patients with DTC/−T2DM and 25 with DTC/+T2DM treated with metformin. All patients received a cumulative oral dose of 131I exceeding 150 mCi (5.55 GBq) over approximately 53 months. Our results showed the following: (i) In DTC/−T2DM patients, high-cumulative 131I doses promote a pro-inflammatory state that accelerates the development of cardiotoxicity. Monitoring NT-proBNP, ST2/IL-33R, and cTn I in these patients may help identify those at risk of developing cardiac complications. (ii) In patients with DTC/+T2DM, high-cumulative 131I doses lead to the release of NT-proANP (r = 0.63), which signals that the atria are under significant stress. (iii) In patients with DTC/+T2DM, metformin suppresses inflammation, leading to a dose-dependent reduction in cTn I (r = −0.59). Monitoring cTn I and NT-proANP, and considering the use of metformin as part of the therapeutic strategy, could help manage cardiotoxicity in T2DM patients undergoing 131I therapy.

ntroduction: The thyroid hormone secretion disorders may be hyperthyroidism (reduced TSH levels and increased levels of FT3 and FT4) and subclinical hyperthyroidism (decreased concentration of TSH with normal FT3 and FT4).Aim: To investigate levels of thyroid hormones (TSH, FT3, and FT4) in patients with hyperthyroidism or subclinical hyperthyroidism treated at Tuzla Blue Clinic.Materials and methods:The study included 120 patients divided into three groups: a control group, groups with respondents who have hyperthyroidism, and a group of patients with subclinical hyperthyroidism. The concentrations of the hormones TSH, FT3, and FT4 were analyzed. The determination was carried out on the device IMMULITE 1 Siemens using the immunochemistry method. Results:TSH between our group investigated the existence of significant statistical differences between the control group and the group with hyperthyroidism (p<0.0001) and between the control group and the group withsubclinical hyperthyroidism (p=0.0001), and the parameter FT3 showed that a statistically significant difference exists between the control group and the group with hyperthyroidism (p<0.0001), and between patients with hyperthyroidism andsubclinical hyperthyroidism (p<0.0001). For FT4, we found a statistically significant difference between the control group and the group with hyperthyroidism (p<0.0001) and between groups with hyperthyroidism and subclinical hyperthyroidism (p <0.0001).Conclusions: The concentration of TSH is reduced in both hyperthyroidism and subclinical hyperthyroidism. The serum concentrations of FT3 and FT4 are elevated in hyperthyroidism, while in subclinical hyperthyroidism, the serum concentrations of FT3 and FT4 stand in the reference area.Keywords:Thyrotropin, thyroxine, TSH, FT3, FT4, hyperthyroidism

Aim To investigate the serum value of brain derived neurotrophic factor (BDNF), proteins S-100, NSE, IL-6 in normal pressure patients (NPH) compared to control (healthy) group and also a possible correlation with radiological findings in NPH patients. Methods Study patients were included during the period of 2020- 2022. All NPH patients met the diagnostic criteria for probability of NPH. Control patients group included patients without known brain disorder, without clinical symptoms of NPH. Blood samples were taken before planned surgery for NPH. BDNF serum concentrations were assessed by a sensitive ELISA kit, and serum concentrations of S-100, NSE and IL-6 were assessed by using ECLIA technology for immunoassay detection. Results Among 15 patients who were included, seven NPH patients were compared to eight control patients. Non-significant decrease in BDNF serum concentrations, an increase of protein S-100 serum concentrations, a decrease of NSE serum concentrations, as well as an increase of IL-6 serum concentrations in NPH patients compared to healthy controls was found. Strong positive correlation between BNDF and Evans index was observed (p=0.0295). Conclusion We did not find a significant difference of BDNF, protein S-100, IL-6 and NSE between serum concentration in NPH and healthy patients. More future research is needed to find the role of BDNF in NPH patients.

Abstract Background: Low-grade chronic inflammation is an important feature of chronic kidney disease (CKD). Aim: To determine the values of C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) in patients with different stages of CKD and to examine how they change depending on the progression of renal damage. Materials and methods: A cross-sectional descriptive comparative study included 157 subjects at different stages of CKD which was assessed based on glomerular filtration rate (GFR) calculated according to the MDRD equation. CRP was analyzed by an immunoturbidimetric method. NLR and PLR were calculated by a mathematical calculation after a blood count was performed. Results: The present study showed an increase in serum creatinine, CRP, and NLR values with progression of renal failure. There was a statistically significant difference in the creatinine and CRP concentrations between groups with different stages of CKD (p <0.001 for all comparisons). A significant positive correlation was found between NLR and CRP, while negative, significant correlations were observed between NLR and eGFR as well as between PLR and eGFR. There was a slight increase in PLR value with the progression of renal impairment, but the correlation between PLR and CRP was not significant. Conclusion: These results suggest that NLR, together with CRP, may serve as an indicator of systemic low-grade inflammation progression in patients with CKD. Larger prospective studies are required to observe the possibility of using NLR as a surrogate marker for CRP in patients with CKD.