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Background: Inflammation has been implicated in core features of depression pathophysiology and treatment resistance. Therefore, new challenges in the discovery of inflammatory mediators implicated in depression have emerged. MicroRNAs (miRNAs) have been found aberrantly expressed in several pathologies, increasing their potential as biomarkers and therapeutical targets. In this study, the aim was to assess the changes and biomarker potential of inflammation-related miRNAs in depression patients. Methods: Depression diagnosis was performed according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). 40 healthy controls and 32 depression patients were included in the study. The levels of inflammatory cytokines were measured in plasma, and expression levels of cytokines and inflammation-related miRNAs were evaluated in peripheral blood mononuclear cells (PBMCs). Results: Depression patients were found to have a pro-inflammatory profile in plasma, with significantly higher levels of TNF-α and CCL2 compared with controls. In PBMCs of depression patients, TNF-α and IL-6 expression levels were significantly up and downregulated, respectively. Moreover, miR-342 levels were found upregulated, while miR-146a and miR-155 were significantly downregulated. miR-342 expression levels were positively correlated with TNF-α. Importantly, when analyzed as a diagnostic panel, receiver operating characteristics (ROC) analysis of miR-342, miR-146a, miR-155 in combination, showed to be highly specific and sensitive in distinguishing between depression patients and healthy controls. Conclusion: In summary, these findings suggest that inflammation-related miRNAs are aberrantly expressed in depression patients. Moreover, we show evidences on the potential of the combination of dysregulated miRNAs as a powerful diagnostic tool for depression. [ABSTRACT FROM AUTHOR]

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Aims: In heart failure patients, anemia and iron deficiency are predictors of poor outcome. We studied the association of anemia, iron deficiency and related hematological parameters with short-term rehospitalization, short-term all-cause mortality and end of follow-up all-cause mortality in heart failure patients. Material and Methods: Anemia, iron deficiency, red cell distribution width and erythropoietin were assessed in patients hospitalized with acute decompensated heart failure. Univariate Cox proportional hazard model was used to assess the relationship between variables and outcomes. Results: 65 patients were followed for a median of 13.7 (Q1-Q3 6.7-18.9) months. Mean age was 79.2 (SD 10.8) years. The mean left ventricular ejection fraction was 50.38 ± 19.07 %. Variables associated with an increased risk for short-term rehospitalization were red cell distribution width (HR 1.35; 95% CI 1.16- 1.58), anemia (HR 3.81; 95% CI 1.29-11.28) and anemia with iron deficiency (HR 3.50; 95% CI 1.30-9.38). Increased risk for short-term mortality was associated with red cell distribution width (HR 1.83; 95% CI 1.29-2.59), erythropoietin (HR 1.38; 95% CI 1.04-1.82), absolute iron deficiency (HR 7.22; 95% CI 1.50-34.81) and anemia with iron deficiency (HR 4.48; 95% CI 1.26-15.88). Variables associated with increased risk for end of follow-up mortality were red cell distribution width (HR 1.31; 95% CI 1.12-1.54) and erythropoietin (HR 1.29; 95% CI 1.11-1.49). Conclusions: Conclusions: Anemia and red cell distribution width correlated with higher risk for short-term rehospitalization. Absolute iron deficiency, red cell distribution width and erythropoietin were associated with higher risk for short-term mortality. Red cell distribution width and erythropoietin were associated with higher risk for end of follow-up mortality. [ABSTRACT FROM AUTHOR]

Copyright of Galicia Clínica is the property of Sociedad Gallega de Medicina Interna and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)