Objective:We aim to systematically review the clinical characteristics of Coronavirus disease 2019 .Methods: Seven datebases were searched to collect studies about the clinical characteristics of COVID-19 from 1 January 2020 to 28 February 2020. Then, meta-analysis was performed by using Stata12.0 software. Results:A total of 38 studies involving 3 062 COVID-19 patients were included.Meta-analysis showed that a higher proportion of infected patients were male (56.9%).The incidence rate of respiratory failure or ARDS was 19.5% and the fatality rate was 5.5%. Fever (80.4%), fatigue (46%), cough (63.1%) and expectoration (41.8%) were the most common clinical manifestations. Other common symptoms included muscle soreness (33%), anorexia (38.8%), chest tightness (35.7%), shortness of breath (35%), dyspnea (33.9%). Minor symptoms included nausea and vomiting (10.2%), diarrhea (12.9%), headache (15.4%), pharyngalgia(13.1%), shivering (10.9%) and abdominal pain (4.4%). Patients with asymptomatic was 11.9%. Normal leukocytes counts (69.7%), lymphopenia (56.5%), elevated C-reactive protein levels (73.6%), elevated ESR (65.6%) and oxygenation index decreased (63.6%) were observed in most patients. About 37.2% of patients with elevated D-dimer, 25.9% of patients with leukopenia, along with abnormal levels of liver function (29%) and renal function (25.5%). Other findings included leukocytosis (12.6%) and elevated procalcitonin (17.5%). Only 25.8% of patients had lesions involving single lung and 75.7% of patients had lesions involving bilateral lungs. Conclusions:The most commonly experienced symptoms of COVID-19 patients were fever, fatigue, cough and expectoration. A relatively small percentage of patients were asymptomatic. Most patients showed normal leucocytes counts, lymphopenia, elevated levels of C-reactive protein and ESR. Bilateral lungs involvement was common.

The renin-angiotensin system (RAS) is undisputedly one of the most prominent endocrine (tissue-to-tissue), paracrine (cell-to-cell) and intracrine (intracellular/nuclear) vasoactive systems in the physiological regulation of neural, cardiovascular, blood pressure, and kidney function. The importance of the RAS in the development and pathogenesis of cardiovascular, hypertensive and kidney diseases has now been firmly established in clinical trials and practice using renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, type 1 (AT1) angiotensin II (ANG II) receptor blockers (ARBs), or aldosterone receptor antagonists as major therapeutic drugs. The major mechanisms of actions for these RAS inhibitors or receptor blockers are mediated primarily by blocking the detrimental effects of the classic angiotensinogen/renin/ACE/ANG II/AT1/aldosterone axis. However, the RAS has expanded from this classic axis to include several other complex biochemical and physiological axes, which are derived from the metabolism of this classic axis. Currently, at least five axes of the RAS have been described, with each having its key substrate, enzyme, effector peptide, receptor, and/or downstream signaling pathways. These include the classic angiotensinogen/renin/ACE/ANG II/AT1 receptor, the ANG II/APA/ANG III/AT2/NO/cGMP, the ANG I/ANG II/ACE2/ANG (1–7)/Mas receptor, the prorenin/renin/prorenin receptor (PRR or Atp6ap2)/MAP kinases ERK1/2/V-ATPase, and the ANG III/APN/ANG IV/IRAP/AT4 receptor axes. Since the roles and therapeutic implications of the classic angiotensinogen/renin/ACE/ANG II/AT1 receptor axis have been extensively reviewed, this article will focus primarily on reviewing the roles and therapeutic implications of the vasoprotective axes of the RAS in cardiovascular, hypertensive and kidney diseases.

Our study aimed to assess the existing evidence on whether severe coronavirus disease 2019 (COVID-19) is associated with elevated inflammatory markers. The PubMed, Embase, Web of Science, Scopus, Chinese National Knowledge Infrastructure, WanFang, and China Science and Technology Journal databases were searched to identify studies published between January 1 and April 21, 2020 that assayed inflammatory markers in COVID-19 patients. Three reviewers independently examined the literature, extracted relevant data, and assessed the risk of publication bias before including the meta-analysis studies. Fifty-six studies involving 8719 COVID-19 patients were identified. Meta-analysis showed that patients with severe disease showed elevated levels of white blood cell count (WMD: 1.15, 95% CI: 0.78–1.52), C-reactive protein (WMD: 38.85, 95% CI: 31.19–46.52), procalcitonin (WMD: 0.08, 95% CI: 0.06–0.11), erythrocyte sedimentation rate (WMD: 10.15, 95% CI: 5.03–15.46), interleukin-6 (WMD: 23.87, 95% CI: 15.95–31.78), and interleukin-10 (WMD: 2.12, 95% CI: 1.97–2.28). Similarly, COVID-19 patients who died during follow-up showed significantly higher levels of white blood cell count (WMD: 4.11, 95% CI: 3.25–4.97), C-reactive protein (WMD: 74.18, 95% CI: 56.63–91.73), procalcitonin (WMD: 0.26, 95% CI: 0.11–0.42), erythrocyte sedimentation rate (WMD: 10.94, 95% CI: 4.79–17.09), and interleukin-6 (WMD: 59.88, 95% CI: 19.46–100.30) than survivors. Severe COVID-19 is associated with higher levels of inflammatory markers than a mild disease, so tracking these markers may allow early identification or even prediction of disease progression.