الفهرس 
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Abstract
Summary and Conclusion
Coronaviruses are important pathogens in humans that can cause diseases ranging from the common cold to more severe and even fatal respiratory infections. Since the outbreak of the novel COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019 in Wuhan, China, more than 2 million cases have been diagnosed globally to date and the number is still growing rapidly.
Patients infected with COVID-19 develop from mild, self-limiting respiratory tract illness to severe progressive pneumonia associated with multi-organ failure.
A wide range of clinical outcomes has been observed in patients with COVID-19, from mild and moderate disease to severe and rapidly progressive pneumonia evolving in acute respiratory distress syndrome (ARDS) and multi-organ failure
The correlation between the immune system, especially the innate immune system, the inflammation, and the coagulations system is well-known and has been addressed in different contexts
In particular, COVID‐19 has been shown to exert significant effects on the hematopoietic system and hemostasis, Studies have emphasized that patients diagnosed with COVID‐19 are susceptible to hypercoagulation and thrombotic events.
coagulation dysfunction is commonly found in COVID-19 patients, and the symptoms range from mild disorders of coagulation indicators to disseminated intravascular coagulation (DIC). The exact etiology of COVID-19-associated coagulopathy is unclear, diverse and multifactorial, and may include direct attack by the SARS-CoV-2 on vascular endothelial cells, cytokine storm-mediated inflammation–coagulation cascades, hypoxia, and complication with sepsis. Coagulation dysfunction or thrombocytopenia is closely associated with the severity and poor prognosis in COVID-19 patients.
Routine laboratory data in the early stage of COVID-19 epidemic are similar to common viral infection: lymphopenia, prolonged prothrombin time, elevated D-dimer, liver enzymes (alanine aminotransferase), total bilirubin, and lactate dehydrogenase, with worsening data in ICU cases.
Aim of the work in this study, to investigate the effect of COVID‐19 disease on coagulation cascade in mild, moderate and critically ill patients of this disease, and to analyze the coagulation parameters of patients with COVID-19 pneumonia admitted to Sohag university hospital, determine whether coagulation factors consumption occurs.
This study was conducted on forty COVID‐19 patients diagnosed by PCR, the patients were classified into 3 subgroups according to the severity of pneumonia mild, moderate and critical groups, compared with 20 persons of healthy control group.
The results of the current study illustrated that the absolute lymphocyte counts and The neutrophil count were significantly lower in moderate and critical groups comparing to healthy control group, also NLR show significant difference between the same groups.
MPV also show significant increase in mild, moderate and critical group comparing to healthy control group, the PCT also show Significant difference between mild group with moderate and healthy control group.
As regards prothrombin concentration was significantly lower in moderate group comparing to healthy control group, concerning d-dimer and vWF:Ag, demonstrated significant elevations mild, moderate and critical group comparing to healthy control group.
Regarding anti-coagulant profile, Protein C show lower level comparing mild group to moderate and critical groups, and Anti-Thrombin was significantly lower in moderate and critical groups comparing to mild and healthy control groups.