Our results suggest that higher depression and anxiety scores in COVID-19 patients are associated with an enhanced inflammatory state, as assessed by higher hematological inflammatory markers including RDW and PLR. However, PLR was also associated with stress in participants.
There are several theoretically viable hypotheses that can be used to justify the potential prognostic role of anisocytosis in COVID-19, including direct cytopathic injury disease associated of circulating erythrocytes or their bone marrow precursors, indirect erythrocyte damage caused by hemolytic anemia or intravascular coagulopathy, and profound iron metabolism disruption caused by the sustained inflammatory response [15]. All of these factors would eventually lead to deranged erythrocyte biology and explain the wide range of erythrocyte sizes in circulation. The dramatic derangement of erythrocyte biology in patients with SARS-CoV-2 infection could also be explained by a coexisting indirect injury. First, cases of autoimmune hemolytic anemia have been linked to SARS-CoV-2 infection [33] a phenomenon that has been attributed to the high molecular similarity between the SARS-CoV-2 spike protein and the protein ankyrin 1 found on RBC surfaces [34]In COVID-19 patients who develop severe or critical illness, intravascular coagulopathy, either localized to the lung parenchyma or disseminated, is also common [35]. The formation of micro- and macrothrombi in various blood veins is a well-known cause of erythrocyte injury, which would contribute to the existence of RBCs with numerous morphological defects high size heterogeneity in the circulation [36].
Coronavirus infection is associated with alterations in the white blood cell count. Alteration in the white blood cell count are linked to Coronavirus infection. A Wuhan study found no significant change in WBC counts, a reduction in the severity of symptoms, and a complete recovery, especially in individuals with no co–morbidities. So, when comparing severe and non-severe patients, total leukocyte counts have a wide range of findings in the literature. The mechanism behind this phenomenon is unknown, while some researchers believe it is linked to the worsening of cytokine storm syndrome, a clinical state of hyper inflammation caused by the production of pro-inflammatory cytokines and inflammatory cytokines. Multi organ failure, which can be dangerous, can occur as a result of cytokine storm syndrome [16].
A higher WBC count has been identified in depressed and anxious people in several investigations [10, 37]. After 5 years of follow-up, the participants with recurring depressive symptoms have higher WBC counts [10]. In one study results showed that after adjusting for age and cigarette smoking, there is still a link between major depressive illness and leukocyte counts for males but not for women [38]. Furthermore, Pitsavos et al. discovered that anxiety score is positively connected with WBC count in women, but not in men [39]. Another study found that WBC count and related indicators are associated with depressed symptoms, particularly in women [40]. In depressed patients, Darko and colleagues discovered relative lymphopenia, absolute neutrophilia, and leukocytosis. However, the authors speculated that leukocytosis and neutrophilia could be a side effect of taking specific medications [41]. Similarly, when compared to control subjects, newly diagnosed antidepressant-naive patients had a decreased lymphocyte count [42]. A number of studies have demonstrated a link between depression and inflammation, and some have even suggested that depression is an inflammatory disease. Since WBC count is an independent predictor of atherosclerosis and cardiovascular disease, it's possible that higher WBC counts or the related inflammatory state could explain some of the elevated cardiac events shown in depressed people [43, 44].
NLR was considerably higher in ICU patients than in non-ICU patients, indicating that it is a useful severity indicator. NLR was also proven to be an effective predictor of critical disease risk in other trials[45]. Another study indicated that patients with NLR >3 were more likely to have severe illness in the population under 50 years old. All of these investigations concluded that the NLR was the most important prognostic factor for patients with serious illnesses [46].
Another study found that patients with major depressive disorder had significantly higher RDW and Neutrophil/Lymphocyte ratio (NLR) levels than the control group [47, 48]. May and colleagues also discovered a link between rising RDW levels and a prospective depression diagnosis, which remained after controlling for risk factors, medications, and indicators of other disease states [49]. MCV, MCH, MCHC, and RDW were not significantly different between major depressed subjects and normal controls in another study [50]. RDW has received a lot of attention in the last decade because of its ability to successfully predict the risk of death in the general population [51], patients with non-cardiovascular critical illness, sepsis, pneumonia, and other respiratory tract infections [52, 53]. It is not surprising that our findings show RDW to be a significant and independent predictor of disease severity and kidney injury in patients infected with SARS-CoV-2. Remarkably, after managing for confounding variables, an increased value of this laboratory variable was associated with a 9.2- and 16.0-fold higher risk of estimating severe illness and AKI, respectively, with predictive precision as high as 73 percent and 80 percent and suggested that RDW should be part of routine laboratory assessment and monitoring of COVID-19 [15]. Wang et al. measured RDW in 45 COVID-19 patients with moderate to severe illness over a nearly 20-day period in this latter study. Patients with severe COVID-19 had significantly higher RDW values than those with a milder form of the disease. Furthermore, both RDWs were found to be significant predictors of severe illness, with diagnostic accuracy ranging from 65 to 76 percent [54].
Many other research, however, reveal that thrombocytopenia is a common characteristic in severe COVID-19 patients. Although, few investigations found no variations in platelet count between patients with severe disease and those with mild disease. Regarding the authors' conflicting observations, new research suggests that coagulopathy is a known hazard of COVID-19 [55]. The PLR, a general inflammatory marker, represents a concurrent interaction of platelet count and lymphocyte count, and it indicates aggregation as well as inflammatory pathways. It has been reported to be increased in response to a variety of acute and chronic proinflammatory conditions, and it has been linked to a poor prognosis in individuals with COPD and carcinomas [19, 55–57]. A previous study has found a relationship between elevated PLR and a poor prognosis of sepsis-induced acute renal injury and mortality [58]. In COVID19 patients, the change in PLR from baseline appears to be linearly associated with severity of illness and length of hospital stay [59]. PLR appeared as an independent predictive factor for prolonged hospitalization in one study's multivariate analysis. A high PLR may indicated a more intense cytokine storm as a result of increased platelet activation [60]. No major differences in PLR were seen in Tiwari's investigative process, as was observed in the current study. However, because platelets are a dynamic variable, the validity of PLR can only be determined by collecting follow-up samples at different time points [16].