Demographic characteristics
In this study, a total of 197 patients with COVID-19 were confirmed from Taihe Hospital and Jinzhou central hospital. The demographic and clinical characteristics are shown in Table 1. The median age of the patients was 66.5 years (IQR 7–76), and 97 (49.2%) patients were older than 60 years. 120 (60.9%) patients were males. And less than 20% of patients had a smoking history. Of the 197 patients, 72 (36.5%) had at least one underlying chronic diseases, including hypertension (25.9%), diabetes (20.8%), COPD (18.8%), cardiovascular disease (10.2%), cerebrovascular diseases (9.1%), malignancy (8.1%), chronic kidney disease (7.6%), chronic liver disease (10.2%), HIV infection (4.6%). Further, COVID-19 patients with ACEI/ARB therapy were enrolled, and we found that about 50.7% of patients had taken ACEI/ARB in the progression group, which is much higher than that of the control group (25%). In addition, of these patients, 36 (18.3%) were infected medical staff.
Table 1
Clinical characteristics of the two groups
Clinical characteristics | Total patients (n = 197) | Non-aggravation (n = 109) | Aggravation (n = 88) | p value |
Age (year, IQR) | 66.5 (7–76) | 60 (47.5–67) | 53 (32–64) | < 0.001 |
Male (n/%) | 120 (60.9%) | 59 (54.1%) | 61 (69.3%) | < 0.001 |
Medical workers (n/%) | 36 (18.3%) | 33 (30.3%) | 3 (3.40%) | < 0.001 |
Smoking history (n/%) | 31 (15.74%) | 14 (12.84%) | 17 (19.32%) | 0.473 |
Comorbidity (n/%) | | | | |
Hypertension | 51 (25.9%) | 21 (19.3%) | 30 (34.1%) | 0.018 |
Diabetes | 41 (20.8%) | 14 (12.8%) | 27 (30.7%) | 0.002 |
ACEI or ARB(n = 92) | 38/92(41.3%) | 9/35 (25.7%) | 29/57(50.7%) | 0.003 |
COPD | 37 (18.8%) | 13 (11.9%) | 24 (27.3%) | 0.006 |
Cardiovascular disease | 22 (11.2%) | 9 (8.3%) | 13 (14.8%) | 0.149 |
Cerebrovascular disease | 18 (9.1%) | 7 (6.4%) | 11 (12.5%) | 0.141 |
Cancer | 16 (8.1%) | 10 (9.2%) | 6 (6.8%) | 0.547 |
Chronic liver disease | 20 (10.2%) | 9 (8.3%) | 11 (12.5%) | 0.626 |
Chronic kidney disease | 15 (7.6%) | 9 (8.3%) | 6 (6.8%) | 0.705 |
HIV infection | 9 (4.6%) | 4 (3.7%) | 5 (5.7%) | 0.501 |
Signs and symptoms at admission (n/%) | | | |
Fever | 159 (80.7%) | 89 (81.7%) | 70(79.5%) | 0.82 |
Dry cough | 157 (79.7%) | 88(80.7%) | 69(78.4%) | 0.687 |
Productive cough | 40 (20.3%) | 18(16.5%) | 22(25.0%) | 0.16 |
Nasal congestion | 15 (7.6%) | 10(9.2%) | 5(5.7%) | 0.358 |
Rhinorrhea | 9 (4.6%) | 6(5.5%) | 3(3.4%) | 0.484 |
Myalgia or arthralgia | 45(22.8%) | 21(19.3%) | 24(27.3%) | 0.805 |
Headache and dizziness | 29 (14.7%) | 16(14.7%) | 13(14.8% | 0.985 |
Runny nose | 9 (4.6%) | 6(5.5%) | 3(3.4%) | 0.484 |
Fatigue | 125 (63.5%) | 63(57.8%) | 62(70.5%) | 0.067 |
Chest distress | 76 (38.6%) | 34(31.2%) | 42(47.7%) | 0.018 |
Chest pain | 15 (7.6%) | 6(5.5%) | 9(10.2%) | 0.214 |
Chills | 23 (11.7%) | 10(9.2%) | 13(14.8%) | 0.224 |
Sneeze | 8 (4.1%) | 5(4.6%) | 3(3.4%) | 0.677 |
Dyspnea | 46 (23.4%) | 16(14.7%) | 30(34.1%) | 0.001 |
Abdominal pain | 19 (9.6%) | 9(8.3%) | 10(11.4%) | 0.463 |
Nausea or vomiting | 22 (11.2%) | 12(11.% | 10(11.4% | 0.937 |
Conjunctival hyperemia | 11 (5.6%) | 5(4.6%) | 6(6.8%) | 0.498 |
Oxygen partial pressure(%) | 94 (87–97) | 97(94–99) | 88(80–93) | < 0.001 |
Onset of symptom to hospital admission | 5(3–8) | 5(3–9) | 5(3–7) | 0.4 |
Data are median (IQR), n (%). |
Signs and symptoms of the patients on admission are shown in Table 1. The most common symptoms at the onset of illness were fever (81.5%), dry cough (79.7%), followed by fatigue (63.5%), chest distress (38.6%), dyspnea (23.4%). The majority of patients (76.6%) had both fever and cough. 89 (45.3%) had a fever with fatigue, and 72 (36.8%) patients had a fever with dyspnea; The less common symptoms were rhinorrhea (4.6%), runny nose (7.6%), and chest pain (7.6%). Notably, we found that 24 (12.7%) patients represented at least one gastrointestinal symptom including abdominal pain (9.6%) nausea or vomiting (11.2%). Besides, 11 (5.6%) patients were clinically characterized by conjunctival hyperemia. Though, these digestive and ocular symptoms were less common in COVID-19 patients, special attention should be paid to the care of this unique group of patients. The median time from onset to hospital admission was 5.0 days (3.0–8.0).
Laboratory findings
The laboratory findings of the confirmed patients are summarized in Table 2. Of 197 patients, 62 (31.5%) cases showed an increased presence of neutrophils, and 92 (46.7%) cases had lymphocytopenia. Severe patients showed liver injury with elevated level of aspartate aminotransferase (AST, 34%), alanine aminotransferase (ALT, 36.5%), total bilirubin (TBIL, 7.6%), direct bilirubin (DBIL, 12.2%), Albumin (17.3%). Approximately one-quarter of patients exhibited myocardial injury with elevated lactate dehydrogenase (LDH, 52.4%), myoglobin (MYO, 27.1%), Cardiac Troponin I (CTnI, 35.6%), N-terminal-pro-B-type natriuretic peptide (ProBNP, 23.5%). Some patients exhibited kidney injury indicated by elevated plasma urea (30.5%) and serum creatinine (10.2%). Some patients showed increased high sensitivity C-reactive protein (CRP, 54.4%) and procalcitonin (PCT, 32.6%). In addition, some patients showed coagulation dysfunction with elevated prothrombin time (PT, 17.9%), activated partial thromboplastin time (APTT, 24.1%), D-dimer (27.2%), fibrinogen (Fbg, 21.3%).
Table 2
Initial Laboratory Indices of Patients with COVID-19.
Variables | Normal range | No. of patients | Median (IQR) | No. of patients with value deviation (%) |
Hematologic *109/L | | | | |
White blood cells | 3.5–9.5 | 197 | 5.78 (4.56–9.13) | 68(34.5%)a |
Neutrophils | 1.8–6.3 | 197 | 3.94 (2.48–8.14) | 62(31.5%) a |
Lymphocytes | 1.1–3.2 | 197 | 1.17 (0.71–1.78) | 92(46.7%)b |
Platelets | 125–350 | 197 | 197 (156–266) | 37(18.8%) b |
CD3 | 723–2737 | 162 | 812 (395–1128) | 77(47.5%) b |
CD4 | 404–1612 | 177 | 427 (190–615) | 83(46.9%) b |
CD8 | 220–1129 | 173 | 291 (151–460) | 66(38.2%) b |
CD16 + CD56 | 80–610 | 153 | 154 (117–251) | 23(19%) b |
CD19 | 84–724 | 167 | 154 (105–254) | 66(39.5%) b |
Biochemical | | | | |
AST, U/L | 15–40 | 197 | 24 (16–38) | 67(34%) a |
ALT, U/L | 9–50 | 197 | 27(18–55) | 72(36.5%) a |
ALP, U/L | 10–60 | 197 | 58 (48.4–79) | 68(34.5%) a |
Total bilirubin, µmol/L | 0–23 | 197 | 8.9 (6.8-11.65) | 15(7.6%) a |
Direct bilirubin µmol/L | 0–8 | 197 | 4.6 (4-7.4) | 24(12.2%) a |
Albumin, g/L | 40.0–55.0 | 197 | 37 (32.9–39.5) | 34(17.3%) a |
PCT, mg/L | < 0.05 | 184 | 0.09 (0.04–1.44) | 60(32.6%) a |
BUN, mmol/L | 3.1-8 | 197 | 4.63 (3.95–7.35) | 60(30.5%) a |
Creatinine, µmol/L | 57–97 | 197 | 55 (49–99) | 20(10.2%) a |
Creatinine kinase, µM | < 171 | 178 | 62 (40-114.75) | 17(9.6%) a |
CK-MB, U/L | < 25 | 176 | 1.7 (1-5.21) | 48(27.3%) a |
MYO, µg/L | 0-100 | 192 | 56.6 (33.8–113) | 52(27.1%) a |
CTnI, ng/mL | 0-0.04 | 146 | 0.016(0.006–0.08) | 52(35.6%) a |
ProBNP | | 149 | 106.5 (38.1–551) | 35(23.5%) a |
LDH, U/L | 125–243 | 189 | 246 (172–375) | 99(52.4%) a |
Potassium, mmol/L | 3.5–5.5 | 191 | 140 (138–142) | 91(47.6%) a |
Sodium, mmol/L | 135–145 | 191 | 3.89 (3.6–4.37) | 51(26.7%) a |
PT, s | 9.4–12.5 | 195 | 11.8 (11.1–12.5) | 35(17.9%) a |
APTT, s | 25.1–36.5 | 190 | 28.9 (26.3–31) | 28(24.1%) a |
D-dimer, mg/mL | 0-0.55 | 195 | 0.8 (0.3–6.12) | 53(27.2%) a |
Fbg, g/L | 2–4 | 183 | 3.33 (2.68–4.83) | 39(21.3%) a |
Inflammation immunologic related indices |
CRP, mg/L | 0–10 | 169 | 14.1 (5–73) | 92(54.4%) a |
Serum ferritin, ng/mL | < 300 | 197 | 276 (230–445) | 67(34.0%) a |
Procalcitonin, ng/mL | < 0.1 | 174 | 0.34 (0.06–1.49) | 60(32.6%) a |
IL-6, pg/L | ≤ 20 | 197 | 18.6 (14.5–27) | 71(36.6%) a |
IL-10, pg/L | ≤ 5.9 | 197 | 5.58 (4.2–10.2) | 76(38.6%) a |
TNF, pg/L | ≤ 5.5 | 197 | 4.8 (4.2–6.6) | 62(31.5%) a |
aAbove reference. b Below reference. Data are median (IQR), n (%). |
There existed many differences in laboratory parameters between patients with disease progression and non-progression patients in Table 3. In the aggravation group, the total lymphocyte was significantly decreased in comparison with the non-aggravation group (P = 0.001). The cell count of the lymphocyte subtype was then further analyzed, which revealed that the count of CD3+, CD4+ and CD8+ T cell in aggravation group was significantly lower than that of the non-aggravation group (P < 0.05), but there was no difference in the counts of CD16+ and CD19+ cells (P > 0.05). We also found that the number of neutrophils was notably increased in the patients of aggravation group (P < 0.001). Blood biochemical examination results suggested that patients with disease progression demonstrated higher levels of AST, Albumin, BUN, Creatinine, CK-MB, CTnI, ProBNP, LDH. At present, some researchers reported that the coagulation function would be dysregulation with the aggravation of the disease. We concluded that the levels of D-dimer, and Fbg were remarkably elevated in the aggravation patients. Table 3. also revealed the differences in inflammation immunologic related indices between the two groups. It suggested that the level of CRP, serum ferritin, procalcitonin, and IL-6 were significantly higher in the aggravation group.
Table 3
Laboratory findings of patients infected with COVID-19.
Variables | Non-aggravation (n = 109) | Aggravation (n = 88) | p value |
Hematologic *109/L | | | |
White blood cells | 5.47 (3.56–7.18) | 6.8 (4.44–13.13) | 0.06 |
Neutrophils | 2.81 (2.31–4.06) | 7.75 (4.32–11.77) | < 0.001 |
Lymphocytes | 1.56 (1.12–1.96) | 0.755 (0.5–1.12) | 0.001 |
Platelets | 229 (159–266) | 192 (150–218) | 0.014 |
CD3 | 985 (812–1311) | 395 (113–641) | 0.001 |
CD4 | 558 (400–804) | 235 (198–401) | 0.001 |
CD8 | 378 (274–526) | 191 (73–307) | < 0.001 |
CD16 + CD56 | 104 (70–196) | 98 (58–183) | 0.13 |
CD19 | 152 (117–251) | 154 (76–256) | 0.176 |
Biochemical | | | |
AST, U/L | 22 (15–33) | 26 (21-48.5) | 0.01 |
ALT, U/L | 26(13–54) | 29(23–55) | 0.06 |
ALP, U/L | 55.7 (45–73) | 58 (48.4–73) | 0.783 |
Total bilirubin, µmol/L | 9 (6.6–11.3) | 8.6(7-13.79) | 0.318 |
Direct bilirubin µmol/L | 4 (3.9-5) | 7.8 (4.6–11.4) | 0.001 |
Albumin, g/L | 38.8 (37-41.8) | 35.9 (30.1–34.4) | 0.16 |
BUN, mmol/L | 4.04 (3.924.89) | 7.82 (4.64–11.4) | 0.001 |
Creatinine, µmol/L | 52 (49–72) | 69 (45.3-120.8) | 0.04 |
Creatinine kinase, µM | 60 (39–89) | 69 (54.5–158) | 0.055 |
CK-MB, U/L | 1.02 (0.48–3.6) | 2.5 (1.58–6.92) | 0.001 |
MYO, µg/L | 89 (21.4–97.4) | 97.8 (48.3–234) | 0.071 |
CTnI, ng/mL | 0.006(0.005–0.03) | 0.034 (0.015–0.426) | 0.001 |
ProBNP | 38.1 (30.5–234) | 209 (44–921) | < 0.001 |
LDH, U/L | 199(161–253) | 355 (264–589) | 0.002 |
Potassium, mmol/L | 116 (103–140) | 121 (88–140) | 0.314 |
Sodium, mmol/L | 3.94 (3.7–4.63) | 3.7 (3.3–4.27) | 0.065 |
Coagulation function | | | |
PT, s | 11.2 (11-11.9) | 12 (11.7–13.4) | 0.059 |
APTT, s | 27.9 (25.4–30.5) | 29.05 (26.9–32) | 0.119 |
D-dimer, mg/mL | 0.32 (0.15–0.8) | 6.03 (0.9–18.6) | 0.001 |
Fbg, g/L | 2.87 (2.18–4.3) | 3.63 (3.0-4.94) | 0.001 |
Inflammation immunologic related indices | | |
CRP, mg/L | 5 (1-15.5) | 26.6 (10.7–122) | 0.001 |
Serum ferritin, ng/mL | 258 (208–303) | 288 (254–699) | 0.001 |
Procalcitonin, ng/mL | 0.037 (0.027–0.06) | 1.06 (0.11–3.26) | 0.01 |
IL-6, pg/L | 16.7 (14.4–20.4) | 25 (17.6–64.5) | 0.002 |
IL-10, pg/L | 5.57 (4.2–11.4) | 6.1 (4.64–9.95) | 0.42 |
TNF, pg/L | 4.64 (4.12-6) | 4.9 (4.32–8.4) | 0.245 |
Data are median (IQR), n (%). |
Chest imaging features and pathogens examination
The Chest imaging features on admission are summarized in Table 4. The median interval between symptom onset and CT examination was 7 days. Of the 197 patients with a chest CT scan on admission, the majority (164, 83.2%) showed abnormal results, consisting of 107 cases (59.4%) of multiple ground-glass opacities and 115 cases (72.3%) of no bilateral lobular and subsegmental consolidation areas. 64.4% of patients showed diffuse infiltration or white lung in both lungs, and about 42.4% had diffuse patch shadow with interstitial involvement. Compared with the patients of non-aggravation, the aggravation group showed more bilateral ground-glass opacity and subsegmental areas of consolidation as well as the lung interstitial involvement. Most of the lesions were localized in the periphery then the center follows and the last was both the periphery and center of the lung (105, 53.3% vs 18, 9.1% vs 74, 37.6%). In the non-aggravation patients, the lesions were more localized in the periphery rather than the center of the lung. However, the lesions would spread to the center of bronchus and gradually to the whole lung in aggravation patients. Therefore, the lesion was more likely located in both the periphery and center of the lung in the disease progression group (54.5% vs 23.9%). The SARS-CoV-2 PCR assay demonstrated that 167 (84.8%) cases showed positive results at the first test, and 30 (15.2%) cases showed negative results. Besides SARS-CoV-2, we also detected other pathogens within the same patients, including epsteinbarr virus (EBV, 22, 13.90%), mycoplasma pneumonia (32, 16.20%), influenza B virus (28, 14.2%), parainfluenza virus (17, 8.6%), cytomegalovirus (CMV, 15, 7.6%). There were no significant differences between the disease progression group and the control group.
Table 4
Radiological data and pathogens test of the patients.
Clinical characteristics | Total patients (n = 197) | Non-aggravation (n = 109) | Aggravation (n = 88) | P |
Chest Imaging features | 164 (83.2%) | 87 (79.8%) | 77 (87.5%) | 0.151 |
Ground-glass opacity | 107 (59.4%) | 59 (68.6%) | 48 (54.5%) | 0.01 |
Consolidation | 115 (72.3) | 62 (65.3%) | 53 (82.8%) | 0.015 |
Bilateral infiltration | 103 (64.4%) | 47 (51.1%) | 56 (82.4%) | 0.01 |
Interstital involvement | 61 (42.4%) | 32 (35.6%) | 29 (53.7%) | 0.03 |
Lesion location | | | | |
Peripheral | 105(53.3%) | 75 (79.3%) | 30 (19.3%) | < 0.001 |
Central | 18 (9.1%) | 8 (6.7%) | 10 (5.8%) | |
Both peripheral and central | 74 (37.6%) | 26 (39.6%) | 48 (14.9%) | |
Pathogens test | | |
SARS-CoV-2 PCR assay+ | 167 (84.8%) | 93 (85.3%) | 74 (84.1%) | 0.81 |
SARS-CoV-2 PCR assay± | 30 (15.2%) | 16 (14.7%) | 14 (15.9%) | 0.78 |
EBV | 22 (13.9%) | 15 (15.2%) | 7 (11.9%) | 0.754 |
Mycoplasma pneumonia | 32 (16.2%) | 23 (21.1%) | 9 (10.2%) | 0.426 |
Influenza B virus | 28 (14.2%) | 15 (13.8%) | 13(14.8%) | 0.84 |
Parainfluenza virus | 17 (8.6%) | 9 (8.3%) | 8 (9.1%) | 0.836 |
CMV | 15 (7.6%) | 8 (7.3%) | 7 (8%) | 0.871 |
Data are median (IQR), n (%). |
Nucleic acid testing is the standard method for the diagnosis of COVID-19 infections. However, some research suggested that this method usually showed lower positive rates due to poor RNA stability, different specimen position, and quality. Therefore, the IgM-IgG combined assay was recommended to increase the sensitivity of COVID-19 diagnoses especially in patients with suspected SARS-CoV-2 infection. In this study, the dynamic changes of IgM-IgG antibody levels were detected. The specific IgG and IgM antibodies can be detected 4–7 days after onset of illness. The IgM antibody titers increased sharply and notably in the initial two weeks and peaked at 1–2 week after symptom onset and significantly declined after 21 days. The IgG antibodies titers increased over time peaking at 4–5 week after onset of illness, and then maintained higher levels for the whole observation period (Fig. 1a). In addition, we compared the IgM-IgG levels between the two groups and found that there was no difference in the levels of IgM between the aggravation group and the non-aggravation group during the first two weeks. After that, the aggravation group tended to have a more vigorous IgM response against SARS-CoV-2 and displayed a higher peak, which suggested that serum IgM antibody levels were significantly correlated with disease progression from day 3-week onward (Fig. 1b). However, the levels of IgG in aggravation group were markedly lower compared to the non-aggregation group in the early stage of infection, and then it experienced a rapid growth and exceed those of the non-aggravation group Fig. 1c.
Treatments and clinical outcomes
All of the confirmed patients were isolated and treated in a negative pressure ward with applicable protective equipment. Table 5. includes details of the outcomes associated with COVID-19 infections and treatments administered. Most patients received combination therapy with oxygen support, antibiotics, antiviral, and glucocorticoids. 139 (68%) patients received multiple antiviral treatments including cephalosporins, quinolones, carbapenems, tigecycline. More than one intravenous antibiotic was given to 65 (42.8%) patients and 87 (57.2%) received an antibiotic only. The patients prescribed antibiotics treatment with a duration of 3–21 days (median, 5 days [IQR 3–6]. Most patients (155, 83.8%) were given antibiotic treatment including ganciclovir, oseltamivir, ritonavir, and lopinavir with a median duration of 5 days [IQR 3–8]. Among the 86 patients who required systemic glucocorticoid therapy (methylprednisolone, dexamethasone) over the treatment period, 49 (57%) patients were given low-dose glucocorticoids and 37 (43%) were given standard-dose glucocorticoids at the initiation of treatment. The median time on glucocorticoid therapy was 7.5 days [IQR 5–13]. 21 (61.4%) received Chinese traditional medicine treatment, which has been demonstrated to play an important role in resistance to viral infections. The duration of Chinese medicine treatment was 9 days [IQR 6.5–15]. Of the 197 patients, more than two-thirds of the patients required oxygen therapy. 105 (55.6%) patients were treated with high-flow oxygen. 43(44.8%) were given non-invasive mechanical ventilation to assist ventilation for 4 days [IQR 5–13]. And 23(25.6%) patients used invasive mechanical ventilation (4d [IQR 2–10]) respectively. The study also indicated that antibiotics, corticosteroids and oxygen therapy were necessary more often in the aggregation patients than in the non-aggregation patients (50.5% vs 89.8%, 28.90% vs 69.00%, 42.60%vs100.0%).
Table 5
Treatment and outcome of COVID-19 patients.
Treatments | Total | Non-aggravation | Aggravation | p value |
Antibiotics (n/%) | 139 (68%) | 55 (50.5%) | 79 (89.8%) | < 0.001 |
Treatment period (d) | 6 (4–9) | 5 (3–9) | 8 (6–12) | 0.001 |
Antiviral (n/%) | 155 (83.8%) | 91 (83.5%) | 74 (85.2%) | 0.12 |
Treatment period (d) | 5 (3–8) | 6 (3–7) | 7 (3.75-9) | 0.07 |
Corticosteroids (n/%) | 86 (48.6%) | 26 (28.9%) | 60 (69%) | 0.01 |
Treatment period (d) | 7.5 (5–13) | 7 (5-8.5) | 11 (6–15) | 0.001 |
Interferon (n/%) | 134 (68.4%) | 66 (61.1%) | 68 (77.3%) | 0.08 |
Treatment period (d) | 7 (5–11) | 7 (4.25-11) | 8 (5–13) | 0.155 |
Chinese medicine (n/%) | 121 (61.4%) | 64 (58.7%) | 57 (64.8%) | 0.385 |
Treatment period (d) | 9 (6.5–15) | 9 (6–15) | 9 (7–15) | 0.681 |
Oxygen treatment (n/%) | 134 (68.4%) | 46 (42.6%) | 88 (100%) | < 0.001 |
High-flow oxygen therapy (n/%) | 105 (55.6%) | 40 (39.2%) | 65 (74.7%) | 0.001 |
Treatment period (d) | 5.5 (4-18.5) | 7 (4–15) | 8 (5-13.5) | 0.149 |
Noninvasive mechanical ventilation (n/%) | 43 (44.8%) | 1 (4.2%) | 42 (58.3%) | 0.001 |
Treatment period (d) | 7 (5–13) | - | 7 (5–13) | - |
Invasive mechanical ventilation | 23 (25.6%) | 2 (7.7%) | 21 (32.8%) | 0.013 |
Treatment period (d) | 4 (2–10) | - | 4 (2–10) | - |
Outcomes (n/%) | | | | |
ARDS | 59 (34%) | 10 (11.5%) | 49 (59%) | 0.01 |
Septic shock | 29 (17.4%) | 9 (10.2%) | 20 (25.3%) | 0.01 |
DIC | 15 (7.8%) | 3 (2.9%) | 12 (13.6%) | 0.005 |
Fungal infections | 27 (16.4%) | 11 (12%) | 16 (21.9%) | 0.81 |
Acute cardiac injury | 32 (18%) | 11 (11.6%) | 21 (25.3%) | 0.017 |
Acute kidney injury | 25 (14%) | 5 (5.3%) | 20 (24.1%) | 0.02 |
ICU admission | 57 (28.9%) | 8 (7.34%) | 49 (55.7%) | < 0.001 |
Length of ICU stay (d) | 7 (2–13) | 5 (2–8) | 7 (2–13) | 0.15 |
Length of hospital stay (d) | 14 (9–21) | 10 (9–19) | 15 (13–22) | 0.003 |
Duration of viral shedding after onset (d) | 11(6.5–17) | 9(6–14) | 13(8–18) | 0.039 |
Data are median (IQR), n (%). |
By the end of Mar 10, 151 (77%) patients were improved and discharged. The median length of stay of discharged patients was 14 days [IQR 9–21]. 46 (23%) patients had died from ARDS, shock and multiple organ damage. Of the 88 aggravation patients, 49 (55.7%) patients were admitted to the ICU for 8 days, which was significantly higher than that of the non-aggravation patients (5, 5.3%) for 5 days. To evaluate the prognosis of COVID-19 patients, we performed the Kaplan-Meier analysis, and the composite endpoint (event) was ICU transfer or death within 25 days from the date of admission to the hospital. The cumulative event-free survival curve was plotted in Fig. 1d, which suggested that 61.6% of patients had not experienced ICU transfer or survival from the hospital. During the course of the disease, about 103 (52.3%) patients presented with functional damage involving multiple vital organs, including ARDS (59, 34%), septic shock (29, 17.4%), DIC (15, 7.8%), fungal infections (27, 16.4%), acute cardiac injury (32, 18%), and acute kidney injury (25, 14%). And patients with disease progression showed higher complication rates than that of the patients without Table 5.
Risk factors for disease progression
To investigate the risk factors for disease progression, we compared the epidemiological, clinical characteristics, laboratory, and radiological findings of COVID-19 patients between the two groups. In univariate logistic regression analysis, we found that the older age, male, underlying diseases (hypertension, diabetes), dyspnea, chest tightness were more frequently administered to patients in the progression group. It revealed that lymphopenia, neutrophilia, high levels of AST, lactic acid, Urea, Creatinine kinase, LDH, CTnI, ProBNP, Fbg, D-dimer, Serum ferritin, Procalcitonin, IL-6 were all significantly correlated with disease progression. Then, these variables were included in the multivariable logistic regression model, which indicated that older age, hypertension, diabetes, dyspnea, lymphocytes, Fbg, LDH, CTnI, serum ferritin, IL-6 were all independently associated with disease progression Table 6.
Table 6
Bivariate cox regression of factors associated with disease progression of COVID-19.
Variables | Univariate analysis | Multivariate analysis |
OR | 95% CI | P | OR | 95% CI | P |
Age (≥ 60 years vs. <60 years) | 4.17 | 2.3–7.59 | < 0.001 | 2.74 | 1.03–7.27 | 0.04 |
Gender (male vs female) | 1.91 | 1.06–3.45 | 0.03 | 1.03 | 0.99–1.07 | 0.09 |
Comorbidity (yes vs no) | | | | | | |
Hypertension | 3.00 | 1.46–6.19 | 0.002 | 3.64 | 1.28–10.3 | 0.015 |
Diabetes | 2.17 | 1.13–4.15 | 0.001 | 8.31 | 2.92–23.6 | 0.001 |
Signs and symptoms (yes vs no) | | | | | |
Dyspnea | 2.01 | 1.13–3.61 | 0.018 | 6.17 | 2.01–18.9 | 0.001 |
Chest distress | 3.0 | 1.51–6.01 | 0.001 | 1.85 | 0.76–4.5 | 0.18 |
Hematologic | | | | | | |
Neutrophils | 6.83 | 3.53–17.6 | < 0.001 | 0.99 | 0.96–1.01 | 0.41 |
Lymphocytes | 8.58 | 4.5–16.3 | 0.001 | 0.29 | 0.10–0.86 | 0.02 |
CD3 | 0.08 | 0.04–0.17 | 0.002 | 0.101 | 0.01–1.78 | 0.12 |
CD4 | 0.74 | 0.59–0.93 | 0.01 | 0.88 | 0.21–3.7 | 0.86 |
CD8 | 0.25 | 0.13–0.49 | 0.03 | 1.01 | 0.99–1.03 | 0.16 |
Coagulation function | | | | | | |
Fbg | 4.35 | 2.33–8.14 | 0.002 | 9.72 | 2.6–36.4 | 0.001 |
D-dimer | 9.59 | 4.48–20.51 | < 0.001 | 1.75 | 0.37–8.24 | 0.48 |
Biochemical | | | | | | |
AST | 2.09 | 1.11–3.93 | 0.03 | 0.99 | 0.93–1.07 | 0.98 |
lactic acid | 2.6 | 1.363–4.96 | 0.001 | 1.75 | 0.37–8.24 | 0.47 |
Urea | 5.17 | 2.66-10 | 0.001 | 1.19 | 0.96–1.46 | 0.11 |
Creatinine kinase | 11.67 | 2.58–52.8 | 0.001 | 1.09 | 0.96–1.24 | 0.19 |
LDH | 8.6 | 4.43–16.69 | 0.001 | 1.01 | 1-1.02 | 0.046 |
CTnI | 4.78 | 2.15–10.6 | 0.002 | 10.06 | 2.44–41.2 | 0.001 |
ProBNP | 5.89 | 3.64–9.04 | 0.001 | 0.10 | 0.93–1.07 | 0.98 |
Infection-related indices | | | | | | |
IL-6 | 3.26 | 1.77–5.99 | 0.001 | 1.03 | 1.01–1.06 | 0.02 |
CRP | 5.99 | 1.18–30.3 | 0.03 | 1.01 | 0.99–1.03 | 0.33 |
PCT | 3.73 | 1.96–7.12 | 0.001 | 2.11 | 0.67–6.62 | 0.2 |
Serum ferritin | 2.30 | 1.26–4.2 | 0.006 | 1.01 | 1.0-1.02 | 0.04 |