Cumali Karatoprak

Objective: Iron deficiency anemia is primarily evaluated using hematological and iron‐related parameters; however, these markers may not fully reflect the systemic metabolic consequences of impaired oxygen delivery and altered iron availability. This study aimed to characterize serum metabolomic alterations associated with iron deficiency anemia using an untargeted LC‐HRMS approach. Materials and Methods: Serum samples from 47 individuals with iron deficiency anemia and 50 healthy controls were analyzed by LC‐HRMS in positive and negative ionization modes. Data processing and metabolite annotation were performed using MassCube and MZmine workflows. Multivariate and univariate analyses, covariate‐adjusted models, metabolite set enrichment analysis, correlations with hematologic/iron indices, and internally cross‐validated exploratory ROC analyses were performed. Results: PCA showed partial separation between iron deficiency anemia and control groups, while OPLS‐DA demonstrated clearer group discrimination. Differential metabolites indicated prominent alterations in amino acid, central carbon, nitrogen‐related, and redox‐associated pathways. The principal amino‐acid/nitrogen‐related differences remained significant after adjustment for age, sex, albumin, and total protein. In the full cohort, several discriminatory metabolites correlated with hemoglobin, ferritin, and transferrin saturation, although these correlations did not remain FDR‐significant within the IDA group alone. Repeated stratified 5‐fold cross‐validation yielded a mean AUC of 0.964 for the three‐metabolite model comprising isoleucine, isonicotinic acid, and phenylalanine. Conclusion: Untargeted serum metabolomics revealed a distinct metabolic signature in iron deficiency anemia, mainly involving amino acid remodeling, central carbon metabolism, nitrogen balance, and redox‐associated pathways. These findings provide a basis for future targeted and externally validated metabolomics studies.

Iron deficiency anemia is a prevalent type of anemia globally, caused mainly by the deficiency of iron, which is an essential component of various metabolic pathways. In this study, we aimed to investigate the changes in metabolite profiles resulting from alterations in these interconnected pathways. We selected 48 patients with IDA and 48 healthy participants based on diagnostic criteria for iron deficiency. NMR spectroscopy was utilized for metabolite profiling. Chenomx, MetaboAnalyst, and R were employed for data analysis. NMR analysis identified and quantified 119 metabolites. Significant metabolites between the two groups were determined using fold change (FC) analysis and t-test results. The FC values of the metabolite group ranked the following compounds in descending order: Acetoin, 2-Hydroxy-3-methylvalerate, Homogentisate, 3-Methylxanthine, Desaminotyrosine, Succinate, Methylguanidine, Guanidinosuccinate, 3-Methylglutarate, Ethanol, Carnosine, SN-Glycero-3-phosphocholine, and Homocysteine. The IDA patients had increased levels of Acetoin, 2-Hydroxy-3-methylvalerate, Homogentisate, 3-Methylxanthine, Succinate, Guanidinosuccinate, Ethanol, Carnosine, and SN-Glycero-3-phosphocholine, while decreased levels of Desaminotyrosine, Methylguanidine, and 3-Methylglutarate were observed. Our findings provide valuable insights into the different metabolites and pathways associated with IDA. Further molecular research is needed to validate these findings.

OBJECTIVE: This study aimed to evaluate the SARS-CoV-2 immunoglobulin G (IgG) levels after 6 months of polymerase chain reaction (PCR) negative but assumed to be COVID-19 positive cases to investigate the relationship between IgG levels and thoracic computed tomography (CT) findings.METHODS: This was a single-center study that included patients whose PCR test results were negative at least three times using nasopharyngeal swabs but had clinical findings of COVID-19 and thoracic CT findings compatible with viral pneumonia. Six months after discharge, the IgG antibodies were analyzed. The cutoff value for negative and positive serology was defined as = 1.4 (index S/C), respectively. In addition, the patients were categorized according to their thoracic CT findings as high (typical) and low (atypical). Also, the patients were grouped into classes as = 5% lung involvement.RESULTS: The patients' mean age was 49.78 +/- 12.96 years. PCR was negative, but patients with COVID-19 symptoms who had SARS-CoV-2 IgG positive were 81.9% (n=95). The antibody titer and lung involvement >= 5% were statistically significantly higher in SARS-CoV-2 IgG positive cases (p<0.001 and p=0.021). Age and chest CT findings were the risk factors for lung involvement (OR=1.08, p= 5%) of lung involvement appears to be associated with high and persistent IgG antibody titers. In probable cases of COVID-19, even if the PCR test is negative, high IgG titers 6 months after discharge can predict the rate of lung parenchymal involvement.

OBJECTIVE: Beta-thalassemia minor is a blood disease caused by a hereditary decrease in beta-globin synthesis, frequently leading to hypochromic microcytic anemia. Formerly called endothelial cell-specific molecule 1, endocan is a proteoglycan released by vascular endothelial cells in many organs. Our aim was to investigate the relationship between the beta-thalassemia minor patients and the healthy control group in terms of serum endocan level. METHODS: The study was performed in a total of 80 subjects. They were divided into two groups, the beta-thalassemia minor group (n=40) and the healthy control group (n=40). Serum endocan levels, age, sex, body mass index value, and tobacco use data of these groups were compared. RESULTS: No statistically significant difference was detected between the two groups in terms of age, sex, and body mass index values (p>0.05). Endocan levels were measured to be 206.85 +/- 88.1 pg/mL in the beta-thalassemia minor group and 236.1 +/- 162.8 pg/mL in the control group with no significant difference between the groups in terms of serum endocan levels (p>0.05). CONCLUSIONS: In our study, there was no change in endocan level in beta-thalassemia minor. This might be because serum endocan levels are affected by multi-factorial reasons. Serum endocan levels may be altered secondarily to decreased beta-globin chain, increased sympathetic activity due to anemia, or platelet dysfunction induced by oxidative stress in beta-thalassemia minor. Further multicenter studies involving more patients are necessary to demonstrate this.

Background/aim: Vitamin D, adropin, proinflammatory cytokines, and oxidative stress closely related with metabolic homeostasis and endothelial dysfunction. The aim of the present study is to investigate how vitamin D levels affect serum adropin, IL-1ß, IL-6, and oxidative stress. Materials and methods: A total of 77 female subjects were divided into 3 groups according to vitamin D levels. Biochemical parameters, adropin, IL-1ß, IL-6, oxidative stress markers were studied in these groups, and the results were compared statistically. Results: Serum adropin, IL-1ß, IL-6, total oxidant status (TOS) and total antioxidant status (TAS) and oxidative stress index (OSI) levels differed significantly between the vitamin D groups (p < 0.05). A significant positive correlation was detected between vitamin D, and adropin and TAS (r = 0.807; p < 0.001, r = 0.814; p < 0.001, respectively). A significant negative correlation was detected between vitamin D, and IL-1ß, IL-6, TOS, OSI (r = -0.725; p < 0.001, r = -0.720; p < 0.001, r = -0.238; p = 0.037, r = -0.705; p < 0.001, respectively). Conclusions: Vitamin D could show its effects through vitamin D receptors on tissues or on the ENHO gene in adropin secreting tissues via direct or indirect mechanisms. Proinflammatory cytokines, oxidative stress, and adropin targeted studies could contribute to the prevention and treatment of diseases associated with vitamin D deficiency in future.

OBJECTIVE: Many chronic diseases such as malignancy, cardiovascular diseases, endothelial dysfunction, and autoimmune diseases, which have been shown to be related to vitamin D in various studies; have similar relations with CTRP-9, TNF alpha, and thiol-disulfide hemostasis. We aimed to contribute to the literature by evaluating the relationship between CTRP-9, TNF alpha, and thiol-disulfide hemostasis and vitamin D levels, which we thought may have some effects on the pathogenesis of vitamin D deficiency. METHODS: In our study, 78 female volunteers older than 18 years were included. Volunteers were divided into three groups according to the reference values of vitamin D levels. Biochemical parameters, CTRP-9, TNF alpha, and thiol/disulfide hemostasis tests taken from all volunteers were studied. RESULTS: In this study, there was a significant difference in CTRP-9, TNFa, total thiol (TT), native thiol (NT), DIS (disulfide), TT/DIS, and NT/DIS levels in vitamin D groups (p<0.05). There was a significant negative correlation between vitamin D and TNF alpha and DIS, while a significant positive correlation was found with CTRP-9, TT, NT, TT/DIS, and NT/DIS (p<0.05). CONCLUSIONS: It was determined that vitamin D deficiency causes a significant decrease in CTRP-9 level and a significant increase in TNF alpha level, as well as an increase in thiol/disulfide hemostasis in favor of disulfide, which may be a risk factor for increased oxidative stress. We considered that these changes may play mediator roles for many chronic diseases and metabolic disorders that are increasing in frequency due to vitamin D deficiency.

Giriş: Son zamanlarda D vitamini eksikliğinin kemik metabolizma hastalıkları dışında, alzheimer, parkinson, multiple sklerozis, diyabet, kardiyovasküler hastalıklar gibi pek çok hastalığın oluşmasında rolü olabileceğini destekleyen çalışmalar artmaktadır. Biz de çalışmamızda D vitamini düzeyinin, kardiyovasküler erken risk belirteçleri olarak kabul edilen serum endocan ve ADMA düzeyleri arasındaki ilişkiyi araştırmayı amaçladık.Materyal- Metod: Çalışmada Vitamin D düzeyi 30 ng/ml olan 35 kişiden (grup2) oluşan iki grup oluşturuldu. Grupların VKİ, serum vitamin D, Endocan, ADMA, PTH, TSH, Glikoz, HOMA-IR, HDL kolesterol, LDL kolesterol, Trigliserit, düzeyleri karşılaştırıldı.Bulgular: Çalışmaya dahil edilen toplam 77 hastanın sonuçları karşılaştırıldı. Her iki grubun yaş, cinsiyet ve BMI değerleri karşılaştırıldığında anlamlı fark olmadığı saptandı (sırasıyla p:0.67, p:0.69, p:0.052). Grup 1 de serum ADMA düzeyi 104.5 ± 44 μmol/L olarak, grup 2’de 90.42 ± 29 μmol/L tespit edildi (p:0.31). Endocan düzeyi ise grup 1’de 549.5 ± 245 ng/L ve grup 2’de 465.99 ± 207 ng/L tespit edildi (p:0.12). Vitamin D düzeyi ile endocan düzeyi arasında anlamlı negatif korelâsyon saptandı (r:-0.26 p:0.02). Serum endocan ve ADMA arasında da anlamlı bir korelâsyon izlenmedi (r:0.19, p:0.1). Gruplar arası PTH, ALT, ALP, HDL kolesterol ve Trigliserit düzeylerinde istatistiksel olarak anlamlı fark tespit edilirken diğer parametrelerde anlamlı olarak fark tespit edilemedi.Sonuç: Kardiyovasküler riski değerlendirmek üzere endotel disfonksiyonu göstergelerinden serum endocan ve ADMA düzeylerini incelediğimiz çalışmada vitamin D düşüklüğü olan hastalarda anlamlı bir değişim saptamadık. Bu parametreler üzerinden yalnızca vitamin D düşüklüğünün endotel disfonksiyonu üzerine bir etki saptayamadığımızı söyleyebiliriz. Ancak çalışma sınırlı sayıda gönüllü ile yapıldığından daha kesin sonuçlara ulaşmak için daha büyük çalışmalara ihtiyaç olduğunu düşünüyoruz.