As apoptosis and genome instability in children with autoimmune diseases (AIDs) are insufficiently investigated, we aimed to analyse them in peripheral blood lymphocytes (PBLs) of children and adolescents with Hashimoto's thyroiditis (HT), Graves' disease (GD) and type 1 diabetes mellitus (T1DM), including possible factors that could affect their occurrence. The study population included 24 patients and 19 healthy controls. Apoptotic cells were detected using an Annexin V-FITC/7-AAD kit. Genome instability was measured as micronuclei (MNs) frequency using the cytokinesis-block MN assay. In addition, comet assay was performed for determination of genome instability as genome damage index (GDI) in new subpopulation of patients with T1DM. The percentage of apoptotic PBLs in patients with AID was significantly lower than in control subjects. There was a positive correlation between thyroid-stimulating homone (TSH) concentration and the proportion of cells in late stage apoptosis in patients with autoimmune thyroid diseases (AITDs). The MN frequency in patients was significantly higher than in controls. Individuals with HT or T1DM had a significantly higher MN frequency than those with GD. Similarly, the value of GDI in patients with T1DM was significantly higher than in controls. The level of apoptosis was positively correlated with MN frequency as well as with GDI in patients with AID. In conclusion, children with AITD (HT and GD) and T1DM have a significantly lower level of apoptosis in PBLs and significantly higher MN frequency as GDI than healthy subjects. Apoptosis and the level of genome instability in these patients with AID are positively correlated.

Bearing in the mind that a variety of agents can contribute to genome instability, including viral infections, the aim of this study was to analyze DNA damage in hospitalized COVID-19 patients and its relationship with certain laboratory parameters. The potential impact of applied therapy and chest X-rays on DNA damage was also estimated. The study population included 24 severely COVID-19 patients and 15 healthy control subjects. The level of DNA damage was measured as genetic damage index (GDI) by comet assay. The standard laboratory methods and certified enzymatic reagents for the appropriate autoanalyzers were performed for the determination of the biochemical and hematological parameters. COVID-19 patients had significantly higher level of DNA damage compared with control subjects. The absolute number of neutrophil leukocytes was statistically higher, while the absolute number of lymphocytes was statistically lower in COVID-19 patients than in healthy controls. The analysis of the relationship between DNA damage and laboratory parameters indicated that GDI was positively correlated with interleukin 6 (IL-6) concentration and negatively with platelet count in COVID-19 patients. The level of DNA damage was slightly higher in female patients, in whom it was demonstrated a positive correlation of GDI with C-reactive protein (CRP) and procalcitonin. Likewise, there was a negative relationship of GDI and platelet count, and positive relationship of GDI and activated partial thromboplastin time (aPTT) in female population. The applied therapy (antibiotics, corticosteroid, anticoagulant, and antiviral therapy) as well as chest X rays has been shown to have genotoxic potential. The level of DNA damage significantly corresponds to the inflammatory markers and parameters of hemostasis in COVID-19 patients. In conclusion, inflammation, smoking habit, applied therapy, and chest X rays contribute to a higher level of DNA damage in COVID-19 patients.

Background and Objectives: Chronic kidney disease (CKD) is a growing public health problem and one of the leading causes of premature death worldwide. The progressive nature of CKD is associated with serious complications that can reduce the quality of life in CKD patients. Additional factors that can worsen well-being include dialysis treatment, malnutrition, inflammation, and lack of social support. The aim of our study was to analyze the quality of life of CKD patients undergoing hemodialysis and its association with certain biochemical and immunonutritional parameters, as well as with social support. Materials and Methods: This research was conducted as a cross-sectional study that included 170 patients, divided into two groups: a group of patients undergoing hemodialysis (HD group) (n = 85), and a control group of non-hemodialysis patients (group with CKD stage 3–4) (n = 85). The Health-Related Quality of Life (HRQoL) score was used to assess the quality of life of the study population. Measurement of biochemical and immunonutritional parameters was also performed in all patients. The Oslo-3 Social Support Scale (OSSS-3) was used to analyze social support. Results: The HRQoL score was significantly lower in HD patients compared to patients with CKD stage 3–4 (0.701 ± 0.137 vs. 0.832 ± 0.122, p < 0.001). It declined significantly as the concentrations of urea (β = −0.347, p < 0.001), creatinine (β = −0.699, p = 0.005), uric acid (β = −0.184, p = 0.016), β2-microglobulin (β = −0.432, p < 0.001), and parathormone (β = −0.209, p = 0.006) increased in HD patients. In addition to uremic toxins, an increase in glucose (β = −0.278, p = 0.010) and triglyceride (β = −0.354, p = 0.001) concentrations was associated with poor HRQoL in patients with CKD stage 3–4. There was a significant connection between the Hemoglobin, Albumin, Lymphocyte, and Platelet (HALP) score and HRQoL in HD patients (β = 0.229, p = 0.035). Additionally, C-reactive protein (β = −0.361, p < 0.001) and neutrophil-to-lymphocyte ratio (β = −0.288, p < 0.001), as markers of systemic inflammation, directly affected HRQoL in HD patients. In both study groups, perceived social support positively influenced the HRQoL scores (β = 0.192, p = 0.012 for hemodialysis; β = 0.225, p = 0.038 for non-hemodialysis). Conclusions: There is a decline in HRQoL in chronic hemodialysis patients, significantly affected by certain biochemical and immunonutritional parameters, along with perceived social support.

THE ASSOCIATION OF CIRCULATING SCLEROSTIN LEVEL WITH MARKERS OF BONE METABOLISM IN PATIENTS WITH THYROID DYSFUNCTION