Survival Rates and Prognostic Factors in Patients with Coronavirus Disease 2019: A Registry-Based Retrospective Cohort Study
Open accessAbstract
Background: Coronavirus disease 2019 (COVID-19) is a contagious disease caused by a newly identified coronavirus. Our knowledge about the survival rate and prognostic factors of the disease is not established well. Therefore, this study aimed to identify the risk factors associated with the survival of COVID-19 cases in Hamadan province, West of Iran. Study design: A retrospective cohort study Methods: This retrospective cohort study was performed in Hamadan province, West of Iran. The study included patients that referred to the provincial hospitals from February 20 to September 20, 2020. The follow-up of each subject was calculated from the date of onset of respiratory symptoms to the date of death. Demographic and clinical characteristics were extracted from patients’ medical records. Kaplan-Meier method, Flemington-Harrington test, and Cox regression were used for data analysis. Results: The overall 1, 5, 10, 20, 30 and 49-day survival rates were estimated at 99.57%, 95.61%, 91.15%, 87.34%, 86.91%, and 86.74%, respectively. Furthermore, survival time showed a significant association with age, gender, history of traveling to contaminated areas, co-morbidity, neoplasms, chronic diseases, and hospital units. Conclusions: In conclusion, elderly people, male gender, and comorbidities presented a greater risk of death. Therefore, it is important to pay more attention to this group of people to reduce the incidence and consequences after infection.
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Other key innate cytokines elevated during COVID-19 include TNFα and IL-6, which is increased by IL-1β.
“Other key innate cytokines that are elevated during COVID-19 include TNF α and IL-6, which is increased by IL-1 β . 137-142”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [139]
The Discussion (page unavailable) mentions systemic inflammatory responses in COVID-19 but does not identify TNFα, IL-6, or IL-1β. Searches for those cytokines and the proposed IL-1β–IL-6 relationship found no passage addressing the claim. (LLM, conf=0.76)
Experimental — accuracy not yet measuredSARS-CoV-2 infection strongly activates complement and other innate immune pathways such as TLR4 and the inflammasome, leading to increased IL-1β and IL-18 levels.
“SARS-CoV-2 infection has been documented to strongly activate complement and to activate other innate immune pathways such as TLR4 and the inflammasome, which leads to increased IL-1 β and IL-18 levels. 137-142”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [139]
The Discussion mentions systemic inflammatory responses as a possible mechanism of adverse COVID-19 outcomes, but does not address complement, TLR4, the inflammasome, or IL-1β and IL-18. Searches for those pathways and cytokines found no passage supporting the claimed activation sequence; the paper instead focuses on survival and prognostic factors. (LLM, conf=0.76)
Experimental — accuracy not yet measuredTim-3 and IL-10 upregulation is observed in patients with COVID-19.
“Tim-3 and IL-10 upregulation is also observed in patients with COVID-19. 139”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [139]
The Results and Discussion report COVID-19 survival, mortality, and risk factors, but do not address Tim-3 or IL-10 expression. Searches for “Tim-3 and IL-10 upregulation” and the expanded marker names found no relevant passage in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThe Tim-3/IL-10 pathway may be responsible for the inhibited T-cell responses reported during COVID-19 in some patients.
“This pathway may be responsible for the inhibited T-cell responses that have been reported during COVID-19 in some patients. 138,139”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [139]
The Discussion (page unavailable) mentions a weakened immune system as a possible contributor to adverse COVID-19 outcomes, but does not discuss Tim-3, IL-10, or inhibited T-cell responses. Searches for the Tim-3/IL-10 pathway and T-cell inhibition found no passage addressing the proposed mechanism. (LLM, conf=0.76)
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COVID-19, Myocarditis and Pericarditis
Fairweather, D., Beetler, D. J., Di Florio, D. N., Musigk, N., Heidecker, B., & Cooper, L. T. (2023) · Circulation Research · doi:10.1161/circresaha.123.321878 · Cited by 181 · see citing works
- Authors
- Shahbazi, F., Karami, M., Mirzaei, M., & Mohammadi, Y.
- Affiliations
- Hamedan University of Medical Sciences (IR)
- Corresponding author
- Mohammadi, Younes
- Venue
- Journal of Research in Health Sciences
- Publisher
- Maad Rayan Publishing Company
- Published
- 2021-04-24
- Volume
- 21
- Issue
- 2
- Pages
- e00515-e00515
- ISSN
- 2228-7795 (ISSN-L)
- 2228-7809
- PMC
- PMC8957676
- OpenAlex
- W3169548406
- Cited by
- 6
- References
- 1
- Citations by year
- 2026: 1 · 2023: 1 · 2022: 1 · 2021: 3
- FWCI
- 0.40
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Locations
- Journal of Research in Health Sciences (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Hamadan University of Medical Sciences
- Hamedan University of Medical Sciences
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Physical Sciences › Mathematics › Modeling and Simulation › COVID-19 epidemiological studies
- Health Sciences › Medicine › Oncology › COVID-19 and healthcare impacts
- Keywords
- COVID-19 pandemic, survival rate, prognostic factors, mortality risk factors, comorbidities, age, sex differences, travel history, hospitalized patients, Hamadan Province
- MeSH terms
- COVID-19, SARS-CoV-2, Adult, Age Factors, Aged, Chronic Disease, Female, Hospitalization, Hospitals, Humans, Iran, Male, Middle Aged, Neoplasms, Prognosis, Registries, Retrospective Studies, Risk Factors, Sex Factors, Travel, Comorbidity, Survival Rate, Survival Analysis, Hospital Mortality, Pandemics
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