ABSTRACT
In this study, it was aimed to evaluate the relationship between the clinical course of the disease and hematological data, serum 25-hydroxyvitamin D (25 (OH) D), iron (Fe), free iron-binding capacity (UIBC), and D-dimer levels in calves with diarrhea in the neonatal period. Within the scope of the study, 10 healthy calves (group-I) and 30 diarrheal calves in the neonatal period of different races, ages and genders were used. Calves with diarrhea were divided into mild (group-II, n=10), moderate (group-III, n=10) and severe (group-IV, n=10) groups. Blood samples were taken from calves in all groups at once. Hematological analyzes were performed using a veterinary-specific hematology analyzer device. In serum samples, 25 (OH) D3, Fe and UIBC levels were determined with an autoanalyzer, and D-dimer levels were determined with an automatic immunoassay analyzer. In the hematological analysis, an increase was observed in the number of LYMs (lymphocytes) in group-II (5.04±1.3) and III (5.2±3.3) compared to group-I (4.47±1.2), and a decrease was observed in group IV (2.76±0.9) (P<0.05). Fe levels in group-II (59±56), group III (56±52) and group IV (72±63) were found to be decreased compared to group-I (131±66) (P<0.05). It was determined that the 25 (OH) D3 level of group IV (13.4±8.5) was higher than that of group-I (6.12±2.73) (P<0.05). D-dimer levels of group-III (1.15±1.13) and group-IV (0.96±0.88) were found to be higher than group-I (0.10±1.46) (P<0.05).
ABSTRACT
Transfusion-dependent thalassemia patients undergo transfusion immunomodulating effects, which result in a general immune response depression and, consequently, an increase in the frequency of infectious episodes and neoplastic events due to a reduction in phagocytic function. Altered natural killer functions and IL-2-mediated lymphocytic response, defects in antigen presentation due to monocyte–macrophage cells, and decreases in bone marrow precursors and HLA II+ cells all play key roles in immunodepression in thalassemia major. SARS-CoV-2 infection presents marked lymphopenia, occurring in 96.1% of severe cases. COVID-19-related lymphopenia is due to various mechanisms, which lead to an increase in lymphocytic apoptosis. Post-COVID-19 lymphocytic quantitative and functional disorders may compromise immune response and promote the onset of infections via opportunistic pathogens. Herein, we report a case of a thalassemia major patient who developed severe post-COVID-19 lymphocytopenia, which may have facilitated the onset of a severe Klebsiella Pneumoniae infection.