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Öğe Endothelium-derived microparticles are increased in teenagers with cobalamin deficiency(Wolters Kluwer Health, 2021) Dündar, Mehmet Akif; Altuner Torun, Yasemin; Çetin, Feyza; Oz, Hatice T.Introduction: Vitamin B12 (cobalamin) deficiency may be a significant cause of hyperhomocysteinemia, and high homocysteine (Hcy) levels are associated with an increased risk of cardiovascular disease. Endothelium-derived microparticles (EMPs) are a new marker in endothelial dysfunction and atherosclerosis, which play a role in cardiovascular diseases’ pathogenesis. This study aimed to evaluate the EMPs, the markers of endothelial dysfunction and atherosclerosis, and lipid profile in teenagers with cobalamin deficiency. Materials and Methods: This prospective study included 143 teenagers, 75 vitamin B12 deficient patients and 68 healthy controls between 11 and 18 years of age. Routine laboratory tests, hemogram, vitamin B12, folic acid, ferritin, Hcy, lipid profile and EMPs were examined and compared. EMP subgroups were analyzed by flow cytometry method according to the expression of membranespecific antigens. The microparticles released from the endothelium studied were VE-cadherin (CD144), S-endo1 (CD146), and Endoglin (CD105). Results: The present study demonstrates that circulating CD105+ EMP, CD144+ EMP, CD146+ EMPs, and Hcy were increased, and high-density lipoprotein (HDL) cholesterol was reduced in teenagers with cobalamin deficiency. Vitamin B12 showed a negative correlation with EMPs and Hcy, positive correlation with folate and HDL. All EMPs showed a significant positive correlation with triglyceride, vitamin B12, and HDL. Conclusion: Vitamin B12 deficiency may predispose to endothelial damage and atherosclerosis by increasing EMPs and harms lipid metabolism in the long term.Öğe Genetic, immunological, and clinical features of 32 patients with autosomal recessive STAT1 deficiency(American Association of Immunologists, 2021) Voyer, Tom Le; Sakata, Sonoko; Tsumura, Miyuki; Khan, Taushif; Esteve-Sole, Ana; Al-Saud, Bandar K.; Güngör, Hatice Eke; Altuner Torun, YaseminAutosomal recessive (AR) STAT1 deficiency is a severe inborn error of immunity disrupting cellular responses to type I, II, and III IFNs, and IL-27, and conferring a predisposition to both viral and mycobacterial infections.We report the genetic, immunological, and clinical features of an international cohort of 32 patients from 20 kindreds: 24 patients with complete deficiency, and 8 patients with partial deficiency. Twenty-four patients suffered from mycobacterial disease (bacillus Calmette Guerin = 13, environmental mycobacteria = 10, or both in 1 patient). Fifty-four severe viral episodes occurred in sixteen patients, mainly caused by Herpesviridae viruses. Attenuated live measles, mumps, and rubella and/or varicella zoster virus vaccines triggered severe reactions in the five patients with complete deficiency who were vaccinated. Seven patients developed features of hemophagocytic syndrome. Twenty-one patients died, and death was almost twice as likely in patients with complete STAT1 deficiency than in those with partial STAT1 deficiency. All but one of the eight survivors with AR complete deficiency underwent hematopoietic stem cell transplantation. Overall survival after hematopoietic stem cell transplantation was 64%. A diagnosis of AR STAT1 deficiency should be considered in children with mycobacterial and/or viral infectious diseases. It is important to distinguish between complete and partial forms of AR STAT1 deficiency, as their clinical outcome and management differ significantly.Öğe Reduced antioxidant capacity in children with iron deficiency and iron-deficiency anemia(2021) Aslaner, Humeyra; Dundar, Mehmet Akif; Arslan, Alev; Karakukcu, Cigdem; Altuner Torun, YaseminObjective: This study aimed to assess the relationship between antioxidant enzymes such as glutathione peroxidase (GSH-Px), glutathione reductase (GSH-R), and paraoxonase (PON1) and carotid intima-media thickness (CIMT) and investigate susceptibility to atherosclerosis with decreasing antioxidant capacity in adolescent patients with iron deficiency (ID) and irondeficiency anemia (IDA). Material and methods: Twenty-five patients with IDA (14.9±1.8 years; 14 female and 11 male patients), 25 patients with ID (14.1±2.24 years; 13 female and 12 male patients) and 21 healthy controls (14.04±2.01 years; 11 female and 10 male individuals) were included in the study. Serum PON1, GSH-Px, GSH-R, and CIMT were measured in all cases. After 3-month oral iron therapy for the group with IDA, the same measurements were performed again. Results: CIMT was statistically significantly higher in patients with ID and IDA than in the control group (p<0.05). PON1, GSH-Px, and GSH-R activities decreased and were statistically significantly low in patients with IDA compared to the control group (p<0.05). Serum PON1 activity was statistically significantly lower in patients with ID than in the control group (p<0.05). Post-treatment PON1, GSH-Px, and GSH-R activities in patients with IDA got back to normal and were statistically significantly higher compared to pre-treatment values. Conclusions: Antioxidant capacity decreases in patients with IDA and ID, which causes atherosclerotic changes. Therefore, patients with iron deficiency must be treated without the development of iron-deficiency anemia.Öğe Soluble Receptor for Advanced Glycation End Products (sRAGE) Level and Its Prognostic Significance in Children with Acute Lymphoblastic Leukemia(Mdpi, 2024) Ozkan, Busra; Altuner Torun, Yasemin; Karakukcu, Cigdem; Celik, BinnazAcute lymphoblastic leukemias are the most common malignancies in childhood. Although its etiology is still unclear, it is thought that disorders in oxidative stress metabolism may contribute to leukemogenesis. Advanced glycation end products (AGEs) are formed as a result of the non-enzymatic binding of sugars to biomolecules. Oxidation reactions are triggered through AGE-Receptor (RAGE) interaction, resulting in the formation of reactive oxygen species. These can play crucial roles in cancer pathogenesis and leukemogenesis. It is thought that sRAGE (soluble RAGE) is the end product of glycation and circulates freely in the circulation by binding to RAGE ligands. We investigate novel leukemia biomarkers and focus on soluble RAGE (sRAGE) for acute lymphoblastic leukemia (ALL) diagnosis and prognosis. Thirty children (1-17 years) diagnosed with ALL were included in the study. Patients were divided into standard, medium, and high risk groups according to the Berlin-Frankfurt-Munster (BFM) treatment protocol. Patients were evaluated twice; at the time of diagnosis and at the sixth month of remission. sRAGE and blood parameters were compared with healthy controls (n = 30, 1-17 years). The sRAGE levels in ALL patients at diagnosis (138.7 +/- 177.3 pg/mL) were found to be significantly higher than they were during the sixth month of remission (17.6 +/- 21.1 pg/mL) and in healthy controls (22.2 +/- 23.7 pg/mL). The cut-off value of the sRAGE level for the diagnosis of ALL was found to be 45 pg/mL in ROC analysis (sensitivity: 73.3%, specificity: 86.7%, AUC: 0.681). At the same time, the sRAGE level was found to be significantly higher in T-ALL patients (490.9 +/- 236.9 pg/mL) than in B-ALL patients (84.5 +/- 82.7 pg/mL). No significant difference was found in terms of the sRAGE level between standard (45.8 +/- 33.1 pg/mL), medium (212 +/- 222.1 pg/mL), and high (143.9 +/- 111.5 pg/mL) risk group ALL patients classified according to the BFM protocol. Despite the fact that this was a small, single-center study, our findings highlight the potential use of sRAGE as a biomarker for diagnosing ALL and assessing response to treatment.
