ABSTRACT
Due to the importance of control and prevention of COVID-19-correlated long-term symptoms, the present review article has summarized what has been currently known regarding the molecular and cellular mechanisms linking COVID-19 to important long-term complications including psychological complications, liver and gastrointestinal manifestations, oral signs as well as even diabetes. COVID-19 can directly affect the body cells through their Angiotensin-converting enzyme 2 [ACE-2] to induce inflammatory responses and cytokine storm. The cytokines cause the release of reactive oxygen species [ROS] and subsequently initiate and promote cell injuries. Another way, COVID-19-associated dysbiosis may be involved in GI pathogenesis. In addition, SARS-CoV-2 reduces butyrate-secreting bacteria and leads to the induction of hyperinflammation. Moreover, SARS-CoV-2-mediated endoplasmic reticulum stress induces de novo lipogenesis in hepatocytes, which leads to hepatic steatosis and inhibits autophagy via increasing mTOR. In pancreas tissue, the virus damages beta-cells and impairs insulin secretion. SARS-COV-2 may change the ACE2 activity by modifying ANGII levels in taste buds which leads to gustatory dysfunction. SARS-CoV-2 infection and its resulting stress can lead to severe inflammation that can subsequently alter neurotransmitter signals. This, in turn, negatively affects the structure of neurons and leads to mood and anxiety disorders. In conclusion, all the pathways mentioned earlier can play a crucial role in the disease's pathogenesis and related comorbidities. However, more studies are needed to clarify the underlying mechanism of the pathogenesis of the new coming virus.
ABSTRACT
BACKGROUND: The aim of this study was to investigate changes in some laboratory parameters in response to four independent variables (COVID-19, diabetes, gender, and age) using univariate and multivariate analysis. METHODS: We measured WBC (neutrophil and lymphocytes), RBC and platelet counts, and hemoglobin, lactate dehydrogenase, C-reactive protein, IL-2, IL-4, and vitamin D3 levels in 30 hospitalized patients with severe COVID-19 and in 30 healthy people in terms of COVID-19. The population was divided into groups based on each of the variables of age, gender, COVID-19, and type 2 diabetes. Then they were subjected to univariate and multivariate analysis of logistic regression. RESULTS: Based on CBC data, leukocytosis (in 70% of COVID-19 patients, 61.1% of diabetic patients, and 70.9 ± 18 years old), neutrophilia (in 73.3% of patients with COVID-19, 61.1% of diabetic patients, and 66 ± 18.6 years old), neutropenia (in 6.7% of patients with COVID-19, 27.8% of diabetic patients, and 33.6 ± 12.7 years old), lymphocytosis (10% of patients with COVID-19, 33.3% of diabetic patients, and 35.4 ± 15.5 years old), and lymphocytopenia (in 76.7% of patients with COVID-19, 66.7% of diabetic patients, and 67.1 ± 18.8 years old) were observed in the population. The elderly and those with COVID-19 had significant abnormal RBC and platelet counts. Increased LDH and CRP levels and abnormal hemoglobin level were related to elderly, COVID-19, and diabetes conditions. Although the levels of IL-2 and -4 were significant in patients with COVID-19 and elderly; however, the changes were not significant in diabetic patients. Changes in serum vitamin D levels were not significant in any of the sub-groups. CONCLUSIONS: We showed that leukocytosis, neutrophilia, lymphocytopenia, abnormal counts of RBCs and platelets, the elevated levels of LDH and CRP, and abnormal hemoglobin levels in blood are considered as poor prognostic factors for COVID-19.