Comorbidities are associated with the severity of coronavirus disease 2019 . This meta-analysis aimed to explore the risk of severe COVID-19 in patients with pre-existing chronic obstructive pulmonary disease (COPD) and ongoing smoking history. A comprehensive systematic literature search was carried out to find studies published from December 2019 to 22 March 2020 from five databases. The languages of literature included English and Chinese. The point prevalence of severe COVID-19 in patients with pre-existing COPD and those with ongoing smoking was evaluated with this meta-analysis. Overall 11 case series, published either in Chinese or English language with a total of 2002 cases, were included in this study. The pooled OR of COPD and the development of severe COVID-19 was 4.38 (fixed-effects model; 95% CI: 2.34-8.20), while the OR of ongoing smoking was 1.98 (fixed-effects model; 95% CI: 1.29-3.05). There was no publication bias as examined by the funnel plot and Egger's test (P = not significant).The heterogeneity of included studies was moderate for both COPD and ongoing smoking history on the severity of COVID-19. COPD and ongoing smoking history attribute to the worse progression and outcome of COVID-19.COPD, COVID-2019, smoking 2.34-8.20), heterogeneity among the different studies being moderate (I 2 = 41%; P = .08). Sensitivity analysis showed that the results were not affected by any individual study. Publication bias, as accessed by funnel plot ( Figure 2B) and Egger's test, showed no publication bias in this analysis (P for Egger's test was 0.5492). | Pre-existing COPD and mortalityOnly two of the included studies reported the association between death and pre-existing COPD. 11,12 Death was reported in 6 of 10 (60%) of patients with COPD and 80 of 233 (34.3%) of non-COPD patients. The pooled OR of COPD for death was 1.93 (95%CI: 0.59-7.43); however, the heterogeneity in this analysis (I 2 = 61%; P = .11) was quite high. | Smoking history and the severity of COVID-19Seven studies reported the relationship between active smoking and the severity of 8,[11][12][13]16,17 The exact duration of smoking was not reported in most studies. The pooled OR is summarized in Figure 2C, which shows that smoking increases the risk of severe COVID-19 (fixed-effects model; OR = 1.98; 95% CI: 1.29-3.05) by around twofolds. The heterogeneity among the different studies was moderate (I 2 = 44%; P = .10). Sensitivity analysis by excluding each study one by one showed that the study from Guan 6 was a major source of heterogeneity. After excluding this F I G U R E 3 Subgroup analysis for the impact of COPD and smoking histology on the severity of COVID-19. CI, confidence interval; COPD, chronic obstructive pulmonary disease; COVID-19, coronavirus disease 2019; ICU, intesive care unit; OR, odds ratio ZHAO ET AL.| 5 overall sample size could be a possible explanation. When the study with the largest sample size was excluded from sensitivity analysis, the effect of smoking on the severity of COVID-19 was no longer significant. An...

BACKGROUND The outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has posed great threat to human health, which has been declared a public health emergency of international concern (PHEIC) by the WHO. T cells play a critical role in antiviral immunity but their numbers and functional state in COVID-19 patients remain largely unclear. METHODS We retrospectively reviewed the counts of total T cells, CD4+, CD8+ T cell subsets, and serum cytokine concentration from inpatient data of 522 patients with laboratory-confirmed COVID-19, admitted into two hospitals in Wuhan from December 2019 to January 2020, and 40 healthy controls, who came to the hospitals for routine physical examination. In addition, the expression of T cell exhaustion markers PD-1 and Tim-3 were measured by flow cytometry in the peripheral blood of 14 COVID-19 cases. RESULTS The number of total T cells, CD4+ and CD8+ T cells were dramatically reduced in COVID-19 patients, especially among elderly patients (≥60 years of age) and in patients requiring Intensive Care Unit (ICU) care. Counts of total T cells, CD8+T cells or CD4+T cells lower than 800/μL, 300/μL, or 400/μL, respectively, are negatively correlated with patient survival. Statistical analysis demonstrated that T cell numbers are negatively correlated to serum IL-6, IL-10 and TNF-α concentration, with patients in decline period showing reduced IL-6, IL-10 and TNF-α concentrations and restored T cell counts. Finally, T cells from COVID-19 patients have significantly higher levels of the exhausted marker PD-1 as compared to health controls. Moreover, increasing PD-1 and Tim-3 expression on T cells could be seen as patients progressed from prodromal to overtly symptomatic stages, further indicative of T cell exhaustion. CONCLUSIONS T cell counts are reduced significantly in COVID-19 patients, and the surviving T cells appear functionally exhausted. Non-ICU patients, with total T cells, CD8+T cells CD4+T cells counts lower than 800/μL, 300/μL, and 400/μL, respectively, may still require aggressive intervention even in the immediate absence of more severe symptoms due to a high risk for further deterioration in condition.

BACKGROUND The outbreak of a novel coronavirus (SARS-CoV-2, previously provisionally named 2019 novel coronavirus or 2019-nCoV) since December 2019 in Wuhan, China, has become an emergency of major international concern. Apart from the respiratory system, it is unclear whether SARS-CoV-2 can also directly infect other tissues such as the kidney or induce acute renal failure. METHODS We conducted a retrospective analysis of estimated glomerular filtration rate (eGFR) along with other clinical parameters from 85 patients with laboratory-confirmed COVID-19 admitted to a hospital in Wuhan from January 17, 2020 to March 3, 2020. Kidney tissues from six patients with postmortem examinations were analyzed by Hematoxylin and Eosin (H&E) and in situ expression of viral nucleocaspid protein (NP) antigen, immune cell markers (CD8, CD68 and CD56) and the complement C5b-9 was detected by immunohistochemistry. Moreover, the viral particles in kidneys were also investigated by transmission electronic microscope (EM). RESULTS 27.06% (23/85) patients exhibited acute renal failure (ARF). The eldery patients and cases with comorbidities such as hypertension and heart failure more easily developed ARF (65.22% vs 24.19%, p< 0.001; 69.57% vs 11.29%, p< 0.001, respectively). H&E staining demonstrated kidney tissues from postmortems have severe acute tubular necrosis and lymphocyte infiltration. Immunohistochemistry showed that SARS-CoV-2 NP antigen was accumulated in kidney tubules. EM observation also demonstrated that viruses- like particles are visible in the kidneys. Viral infection not only induces CD68+ macrophages infiltrated into tubulointerstitium, but also enhances complement C5b-9 deposition on tubules. CONCLUSIONS SARS-CoV-2 induces ARF in COVID-19 patients. Viruses directly infect human kidney tubules to induce acute tubular damage. The viruses not only have direct cytotoxicity, but also initiate CD68+ macrophage together with complement C5b-9 deposition to mediate tubular pathogenesis.

Objectives: Coronavirus Disease 2019 is a new respiratory and systemic disease which needs quick identification of potential critical patients. This meta-analysis aimed to explore the relationship between lymphocyte count and the severity of COVID-19. Methods: A comprehensive systematic literature search was carried out to find studies published from December 2019 to 22 March 2020 from five databases. The language of literatures included English and Chinese. Mean difference (MD) of lymphocyte count in COVID-19 patients with or without severe disease and odds ratio (OR) of lymphopenia for severe form of COVID-19 was evaluated with this meta-analysis. Results: Overall 13 case-series with a total of 2282 cases were included in the study. The pooled analysis showed that lymphocyte count was significantly lower in severe COVID-19 patients (MD -0.31 Â10 9 /L; 95%CI: -0.42 to -0.19 Â 10 9 /L). The presence of lymphopenia was associated with nearly threefold increased risk of severe COVID-19 (Random effects model, OR = 2.99, 95% CI: 1.31-6.82). Conclusions: Lymphopenia is a prominent part of severe COVID-19 and a lymphocyte count of less than 1.5 Â 10 9 /L may be useful in predicting the severity clinical outcomes.

Background and aims Metabolic associated fatty liver disease (MAFLD) is a novel concept proposed in 2020, the utility of which has not been tested and validated in real world. We aimed to compare the characteristics of MAFLD and non‐alcoholic fatty liver disease (NAFLD). Methods The data was retrieved from the third National Health and Nutrition Examination Surveys of the United States, which is an unbiased survey dataset and frequently used for the study of fatty liver disease. Results A total of 13 083 cases with completed ultrasonography and laboratory data were identified from the NHANES III database. MAFLD was diagnosed in 4087/13 083 (31.24%) participants, while NAFLD in 4347/13 083 (33.23%) amongst the overall population and 4347/12 045 (36.09%) in patients without alcohol intake and other liver diseases. Compared with NAFLD, MAFLD patients were significantly older, had higher BMI level, higher proportions of metabolic comorbidities (diabetes, hypertension) and higher HOMA‐IR, lipid and liver enzymes. MAFLD patients with alcohol consumption were younger than those without, and more likely to be male. They had less metabolic disorder but higher liver enzymes. There were more cases with advance fibrosis in MAFLD patients with alcohol consumption. Conclusion MAFLD definition is more practical for identifying patients with fatty liver disease with high risk of disease progression.