Investigation of the Relationship between Inflammation and Oxidative Stress Markers and Treatment Response in First-Attack Major Depression Patients: A Follow-Up Study. / Ilk Atak Major Depresyon Hastalarinda Inflamasyon ve Oksidatif Stres Belirteçleri ile Tedavi Yaniti Iliskisinin Incelenmesi: Bir Izlem Çalismasi.

OBJECTIVE: There is a need to biomarkers for major depression (MD). The goals of this study are to compare serum levels of oxidative stress markers malondialdehyde (MDA) and F2-isoprostane and inflammation markers tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and C-reactive protein (CRP) between patients with first-episode MD and healthy controls, to investigate the change of these markers after treatment and to investigate the relationship between levels of these markers and treatment response. METHOD: Our study was performed in 30 first-episode MD patients and 30 healthy volunteers. During the clinical evaluation Hamilton Depression Rating Scale and Clinical Global Impression Scale were applied to the participants. Serum levels of markers were measured at the baseline and after 8 weeks of treatment. RESULTS: Compared to the control group, first-episode MD patients had significantly higher IL-6, CRP and MDA levels and lower F2- isoprostane levels. There was no difference between the groups in terms of TNF-α levels. TNF-α, IL-6, MDA and F2-isoprostane levels decreased significantly after treatment, whereas there was no significant change in CRP levels with treatment. Baseline F2-isoprostane levels were found to be significantly higher in treatment responders than nonresponders (p<0.05). CONCLUSION: In our study, it was shown that there are irregularities related to inflammatory processes and oxidative stress in MD, even in patients who had their first-episode and did not take medication, and these irregularities can be resolved after treatment. While there was a relationship between treatment response and baseline F2-isoprostane levels, there was no relationship with other biomarkers.

Assessment of ADAM17 and ADAM10 proteins with CXCL10 and thyroid autoimmunity in vitiligo pathogenesis.

Introduction: Vitiligo is an acquired chronic pigmentation disorder. The etiopathogenesis is still not fully understood. Aim: To research the correlation of ADAM proteins, shown to be associated with autoimmune diseases like rheumatoid arthritis and lupus erythematosus, with vitiligo also considered to be an autoimmune disease. Material and methods: The study included a patient group of 45 patients with the diagnosis of vitiligo and a control group of 45 healthy adults. The ADAM10 and ADAM17 protein serum levels and CXCL10 and thyroid autoantibody anti-TG and anti-TPO levels along with FT3, FT4, and TSH hormone levels were determined with the ELISA method. Statistical analysis of results was made with the SPSS 22.0 program. Results: In vitiligo patients, the ADAM10 levels (2.34 ±0.80 pg/ml) were statistically significantly low compared to the control group (10.29 ±1.71 pg/ml) (p < 0.05), while the ADAM17 levels (128.51 ±14.37 pg/ml) were statistically significantly high compared to the control group (16.30 ±6.31 pg/ml) (p < 0.05). Additionally, the CXCL10 levels were observed to be statistically significantly higher in the patient group (275.11 ±62.36) than in the control group (107.08 ±33.12). Thyroid autoimmunity test results (anti-TG, anti-TPO, and TSH) were shown to be different to a statistically significant degree in the patient group compared to the control group (p < 0.001, p < 0.000, p = 0.003, respectively). Statistical analyses used the Kolmogorov-Smirnov, Mann-Whitney U test, and the independent T-test. Conclusions: We obtained data that are important in terms of understanding the pathogenesis. ADAM10 and ADAM17 proteins may be new targets for future therapeutic approaches.

Elevated Serum Endocan Levels in Patients with Rosacea: A New Therapeutic Target?

BACKGROUND: Rosacea is a chronic inflammatory skin disease whose etiopathogenesis is still unknown. Previous studies have shown a relationship between certain inflammatory disorders and serum endocan levels. Endocan (previously known as endothelial cell-specific molecule 1) might play a role in the pathogenesis of various inflammatory diseases. AIMS AND OBJECTIVES: Our study aimed to evaluate serum endocan levels in patients with rosacea to investigate the association of endocan with the demographic data. MATERIALS AND METHODS: The study recruited individuals aged ≥18 years who voluntarily agreed to participate in the study. The participants included 37 women (mean age: 48.29 ± 12.08 years) and 13 men (mean age: 52.23 ± 13.34 years) diagnosed with rosacea, and 37 women (mean age: 49.18 ± 16.6 years) and 13 men (mean age: 53.69 ± 11.30 years) selected as controls. Both groups were matched according to age and sex. The rosacea diagnosis was based on clinical examination findings, and serum endocan levels were measured using the method of enzyme-linked immunosorbent assay (ELISA). The statistical significance of the data was determined by the Mann-Whitney U test, and a value of P < 0.05 was considered statistically significant. RESULTS: Serum endocan levels differed significantly between the patients with rosacea and the control group (P < 0.05). CONCLUSION: Circulating endocan might be a new marker related to disease progression in patients with rosacea. Further investigation is needed to determine whether endocan levels could become a new therapeutic target in rosacea, a disease that still cannot be fully cured.

Serum brain-derived neurotrophic factor in the diagnosis of febrile seizure.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) is a noncovalently linked homodimer protein from the neurotrophic growth factor family. Although it is expressed throughout the brain, it is produced more intensively in the entorhinal cortex and hippocampus and can cross the blood-brain barrier in two directions easily. The aim of this study is to understand, for the first time, whether there is a relationship between febrile seizure (FS) and BDNF. METHODS: The study included cases diagnosed with FS and febrile illness, of similar age, weight, and height, between 6 months and 6 years. Samples for serum BDNF measurement were taken within the first 24-48 h of admission at the hospital and levels were measured using the commercial enzyme-linked immunosorbent assay kit and expressed in ng/mL. RESULTS: Eighty cases (40 FS, 40 febrile illness) were included in the study. The mean serum BDNF was found to be 6.7 ± 2.4 ng/mL in the FS group and 4.5 ± 2.6 ng/mL in the febrile illness group (P = 0.001). No relation was found between gender, age, body weight, length, and platelet counts and serum BDNF levels. The optimal cut-off value for serum BDNF was found to be 5.2 ng/mL (75% sensitivity, 62.5% specificity, AUC: 0.723) to distinguish between FS and febrile illness. CONCLUSIONS: Excluding demographic variables such as gender, age, weight, length, and platelet counts serum BDNF levels have increased in children with FS. Considering the hippocampal origin of FS, we can suggest that the pathophysiology of FS may be related to the BDNF.