RESUMO
Background Iron deficiency is a prevalent and clinically significant comorbidity in patients with heart failure with reduced ejection fraction (HFrEF). Despite its high prevalence, its impact on clinical outcomes, mortality, and various physiological parameters remains a subject of ongoing investigation. The findings of this study are anticipated to contribute valuable insights into the management and prognosis of patients with HFrEF, potentially informing future interventions and improving patient outcomes. This study aimed to assess the clinical profile of iron deficiency and its implications on morbidity and mortality in patients with HFrEF. Methodology A prospective cohort study was conducted at King Edward Memorial Hospital, India, involving 371 patients with HFrEF. Participants underwent comprehensive clinical and laboratory assessments, evaluating iron deficiency with signs, symptoms, comorbidities, dyspnea, elevated jugular venous pressure (JVP), past medical history, and various hematological and biochemical parameters. Results Overall, 50% of HFrEF participants were iron deficient (n = 185), of whom 80% (n = 148) had anemia against 43% (n = 81) anemics in iron repletes (n = 186). Of the 185 iron-deficient patients, 44 (11.86%) had absolute iron deficiency and 141 (38%) had functional iron deficiency. Iron deficiency significantly correlated with increased mortality in HFrEF patients (χ2 (1, N = 371) = 3.88, p = 0.048). A large positive correlation was observed between absolute iron deficiency and dyspnea severity (r2 = 0.949, p = 0.026). Statistically significant differences were found in hemoglobin (anemia), serum iron, serum ferritin, total iron-binding capacity, and transferrin saturation between iron-deficient and iron-replete patients (p < 0.05). However, no statistically significant difference in left ventricular ejection fraction between iron-deficient and replete patients was noted. Conclusions Iron deficiency emerges as more than a mere comorbidity in heart failure, becoming a prognostic factor with multifaceted outcomes. Its impact extends beyond cardiovascular consequences, encompassing adverse manifestations such as anemia, ascites, edema, dyspnea, elevated JVP, and a heightened risk of mortality. This intricate interplay positions iron deficiency as a critical determinant, significantly influencing the clinical trajectory and outcomes for patients with HFrEF.
RESUMO
BACKGROUND: A rise in secondary fungal infections during the COVID-19 pandemic necessitates a deeper understanding of the associated immunological perturbations. OBJECTIVES: To evaluate the clinical and immunological characteristics observed in patients with COVID-19 associated mucormycosis (CAM) infection. PATIENTS/ METHODS: Cases of mucormycosis with or post-COVID-19 infection were compared with cases of acute COVID-19 and convalescent COVID-19. Lymphocyte subsets, cytokines and other laboratory markers were compared between the groups. RESULTS: The frequency of proposed risk factors for CAM was diabetes mellitus (77%), recent history of steroid use (69%) and hypoxia during COVID-19 infection (52%). Iron metabolism was dysregulated in CAM patients with low TIBC and total iron. Further, CAM was accompanied with lymphopenia with drastic reduction in B cell counts; however, plasmablasts were not altered. Further, CAM patients had low immunoglobulin levels and antibodies specific to mucor peptide did not increase in CAM suggesting dysfunction in B-cell response. There was increase in activated effector cytotoxic CD8 T cells and NK cells in CAM compared with COVID-19 infection and healthy controls. Among T helper cells, Tregs were reduced and Th-1 frequency was increased in CAM compared with COVID-19 infection. A distinct cytokine signature was evident in CAM with increase in IL-1ß, IFN-γ, IL-6, IL-22, IL-17A, IL-10, IL-2, IL-8, IL-7, IL-21 and GM-CSF. CONCLUSION: This is the first study on immunophenotyping in CAM suggesting the need for long-term monitoring of B-cell function after SARS-CoV-2 in patients with dysregulated glycaemic control and the possible benefit of therapeutic supplementation with intravenous immunoglobulins in CAM.