Discussion
Coronavirus disease 2019 (COVID-19) is the seventh known human coronavirus[2]. It is a new coronavirus caused by SARS-COV-2 coronavirus. The new virus has an envelope[3], consisting of a single strand of RNA.Sars-cov-2 is thought to have originated in bats, with 89% to 96% of its nucleic acid sequence identical to that of the virus carried by bats[4]. SARS-CoV-2 is believed to have originated in bats, similar to many other coronaviruses, because it shares 89% to 96% nucleotide identity with bat coronaviruses. Sars-cov-2 mainly transmitted through droplets, but can also be transmitted by aerosols. The median incubation period of the virus is 4-5 days, and 97.5% of patients develop symptoms at 11.5 days after infection. At the start of the pandemic, The median period from clinical symptoms onset to progression to death is about 14 days[5]. Morbidity and mortality varied from time to time and region to region, for reasons that may be related to virus variation in addition to regional differences.
For its infectiousness, the number of cases increases exponentially without control measures. The hyperinflammatory response triggered by SARS-CoV-2 is the principal causes of death in infected patients[6].The most common symptoms are fever and tussiculation, some patients appear runny nose, sneezing, a small number of patients develop nausea, vomiting or diarrhea. Part of the population can have no symptoms, or tends to improve after the infection, some people can appear rapid progression such as respiratory failure even to death[7]. The mortality increased significantly in patients with cardiovascular diseases, diabetes, COPD and hypertension[8]. Fatality increases with the progression of the severity of disease.  We analyzed some relevant indicators and outcomes of patients diagnosed with COVID-19 in a hospital in wuhan in order to provide guidance for the treatment and prognosis of patients with coronavirus pneumonia.
The study included 239 patients with confirmed COVID-19. All patients were assessed until disease outcome( improve or dead). The study showed that 140 patients were discharged with a better health condition and 99 patients died. There was a statistically significant difference in age between the two groups, suggesting that old age is a risk factor for the disease, which is usually accompanied by a variety of complications, resulting in complicated conditions.
Data from the Chinese Center for Disease Control and Prevention showed that 80% patients experienced mild disease or even non-symptom and 20% developed severe symptoms such as respiratory failure and multiple organ failure. Previous observational studies reported patients with old age and comorbidities were more likely to deteriorate. It was later found that previously healthy patients also developed severe hypoxemia and respiratory failure, which were caused by inflammatory cascades[6, 9]. Pathological examination showed lesions involved multiple organs in severe patients[10].
Studies have shown that inflammatory markers C-reactive protein and neutrophil-to-lymphocyte ratio are risk factors in COVID patients[11-13]. Excessive inflammatory responses, including high levels of cytokines, lymphocytosis, and mononuclear macrophage infiltration, are considered important reasons for the rapid progression of the disease[6]. Our study found significant differences in white blood cell counts, neutrophil counts and lymphocyte counts between the improvement group and the death group, CRP was also associated with the risk of death, suggesting that excessive inflammation is a risk factor for patients and should be controlled clinically. Given the consideration of the importance of white blood cell and neutrophil counts for the COVID-19, we also plot the two factors in the survival curve.
In our study, survival analysis suggests that renal function factor such as blood urea nitrogenis was associated with a risk of death in patients. The differences of urea nitrogen and creatinine between the improvement group and the death group were statistically significant. Data from complete autopsy including histopathologic and virologic analysis in 12 patients who died from COVID-19 showed that high viral RNA titers were detected in kidney[14]. A study[15] involving 701 patients with COVID-19 found that 5.1% patients experienced acute kidney injury. The mechanism involved acute tubular injury may be associated with infiltration of lymphocytes and monocytes in renal tissue. In addition, cytokine injury and organ interference may also play a role in some biological processes. Patients with renal dysfunction who are infected with SARS-CoV-2 coronavirus will face an increased risk of death, suggesting that effective renal function control should be paid attention into the clinical treatment. Serum albumin levels partially reflect body’s immune state. Patients with bad nutritional status are more likely to experience lower serum albumin levels, which is harmful to the antibody production and virus clearance, and should be given high attention. Recent study suggest [9]showed that poor nutritional status was significant risk factors for severe COVID-19 infection. Severe anorexia, and malnutrition may increase risks for respiratory failure and even required noninvasive ventilation[16].
Assessment of the risk factors of the disease is helpful for clinicians to timely understand the risk of disease progression, so as to carry out appropriate and multifaceted intervention earlier to achieve the best therapeutic purpose. There were a few limitations in our study. Our data sources were single-center and the sample size was not large enough to represent all infected people. Highly subjective outcomes such as pain may bias the accessment results. Patients without access to treatment were not included. Some patients were complicated with uremia, resulting in a large degree of dispersion of creatinine values in samples.