Does this enzyme raise the chance of COVID-related death?

Researchers discovered an enzyme that is genetically related to a key enzyme in snake venom and was found in COVID-19 fatalities in doses 20 times the safe amount.

By JERUSALEM POST STAFF   SEPTEMBER 4, 2021 19:37

A study from the University of Arizona discovered that an enzyme with a key role in severe inflammation may be a vital mechanism in COVID-19 severity and could provide a new target for medicine development.The researchers collaborated with Stony Brook University and Wake Forest School of Medicine to analyze blood samples from two COVID-19 patients and discovered that the circulation of the sPLA2-11A enzyme may be an important method in predicting which patients would die of COVID-19.At high levels, the enzyme has the ability to “shred” the membranes of vital organs. “It’s a bell-shaped curve of disease resistance versus host tolerance,” said Floyd (ski) Chilton, senior author on the paper and director of the U Arizona Precision Nutrition and Wellness Initiative at the university. “In other words, this enzyme is trying to kill the virus, but at a certain point it is released in such high amounts that things head in a really bad direction, destroying the patient’s cell membranes and thereby contributing to multiple organ failure and death.” “The idea to identify a potential prognostic factor in COVID-19 patients originated from Dr. Chilton,” said Maurizio Del Poeta, a co-author of the study. “He first contacted us last fall with the idea to analyze lipids and metabolites in blood samples of COVID-19 patients.” The research team analyzed thousands of patient data points. The team focused on traditional risk factors like age, body mass index and preexisting conditions, but they also focused on biochemical enzymes and patients’ levels of lipid metabolites.

“In this study, we were able to identify patterns of metabolites that were present in individuals who succumbed to the disease,” said Justin Snider, an assistant research professor at the University of Arizona and lead study author. “The metabolites that surfaced revealed cell energy dysfunction and high levels of the sPLA2-11A enzyme. The former was expected but not the latter.”The analysis showed that most healthy people have approximately half a nanogram of the enzyme per milliliter, 63% of people who had severe COVID-19 and died had more than 10 nanograms per milliliter.”Some of the patients who died from COVID-19 had some of the highest levels of this enzyme that have ever been reported,” said Chilton.Previous research into the enzyme shows that it has similar genetic ancestry to a key enzyme contained in snake venom. “Like venom coursing through the body, [the enzyme] has the capacity to bind to receptors at neuromuscular junctions and potentially disable the function of these muscles,” said Chilton.”Roughly a third of people develop long COVID, and many of them were active individuals who now cannot walk 100 yards,” he added. “The question we are investigating now is: if this enzyme is still relatively high and active, could it be responsible for part of the long COVID outcomes that we’re seeing?”

First case of postmortem study in a patient vaccinated against SARS-CoV-2

Author:TorstenHansenaUlfTitzeaNidhi Su AnnKulamadayil-HeidenreichbSabineGlombitzacJohannes, et. al.

Highlights

• We report on a patient with a single dose of vaccine against SARS-CoV-2.

• He developed relevant serum titer levels but died 4 weeks later.

• By postmortem molecular mapping, we found viral RNA in nearly all organs examined.

• However, we did not observe any characteristic morphological features of COVID-19.

Immunogenicity might be elicited, while sterile immunity was not established.

Abstract

A previously symptomless 86-year-old man received the first dose of the BNT162b2 mRNA COVID-19 vaccine. He died 4 weeks later from acute renal and respiratory failure. Although he did not present with any COVID-19-specific symptoms, he tested positive for SARS-CoV-2 before he died. Spike protein (S1) antigen-binding showed significant levels for immunoglobulin (Ig) G, while nucleocapsid IgG/IgM was not elicited. Acute bronchopneumonia and tubular failure were assigned as the cause of death at autopsy; however, we did not observe any characteristic morphological features of COVID-19. Postmortem molecular mapping by real-time polymerase chain reaction revealed relevant SARS-CoV-2 cycle threshold values in all organs examined (oropharynx, olfactory mucosa, trachea, lungs, heart, kidney and cerebrum) except for the liver and olfactory bulb. These results might suggest that the first vaccination induces immunogenicity but not sterile immunity.

Keywords

SARS-CoV-2VaccineAutopsyHistologyRT-PCR

We report on an 86-year-old male resident of a retirement home who received vaccine against SARS-CoV-2. Past medical history included systemic arterial hypertensionchronic venous insufficiencydementia and prostate carcinoma. On January 9, 2021, the man received lipid nanoparticle-formulated, nucleoside-modified RNA vaccine BNT162b2 in a 30 μg dose. On that day and in the following 2 weeks, he presented with no clinical symptoms (Table 1). On day 18, he was admitted to hospital for worsening diarrhea. Since he did not present with any clinical signs of COVID-19, isolation in a specific setting did not occur. Laboratory testing revealed hypochromic anemia and increased creatinine serum levels. Antigen test and polymerase chain reaction (PCR) for SARS-CoV-2 were negative.

For More Information: https://www.sciencedirect.com/science/article/pii/S1201971221003647

Prophylaxis against covid-19: living systematic review and network meta-analysis

Authors: Jessica J Bartoszko, methodologist,1 ,*Reed A C Siemieniuk, methodologist, internist,1 ,*Elena Kum, methodologist,1 ,*Anila Qasim, methodologist,1 ,*Dena Zeraatkar, methodologist,1 ,*Long Ge, methodologist,2 ,*Mi Ah Han, methodologist,3Behnam Sadeghirad, assistant professor,1,4Arnav Agarwal, methodologist, internist,1,5Thomas Agoritsas, methodologist, internist,1,6Derek K Chu, methodologist, immunologist,1,7Rachel Couban, librarian,4Andrea J Darzi, methodologist,1Tahira Devji, methodologist,1Maryam Ghadimi, methodologist,1Kimia Honarmand, methodologist, critical care physician,8Ariel Izcovich, methodologist, internist,9Assem Khamis, data analyst,10Francois Lamontagne, methodologist, critical care physician,11Mark Loeb, methodologist, infectious disease physician,1,7Maura Marcucci, methodologist, internist,1,7Shelley L McLeod, methodologist, assistant professor,12,13Sharhzad Motaghi, methodologist,1Srinivas Murthy, clinical associate professor, paediatric critical care, infectious diseases physician,14Reem A Mustafa, methodologist, nephrologist,15John D Neary, methodologist, internist,7Hector Pardo-Hernandez, methodologist,16,17Gabriel Rada, methodologist,18,19Bram Rochwerg, methodologist, critical care physician,1,7Charlotte Switzer, methodologist,1Britta Tendal, methodologist,20Lehana Thabane, professor,1Per O Vandvik, methodologist, internist,21Robin W M Vernooij, methodologist,22,23Andrés Viteri-García, methodologist,18,24Ying Wang, methodologist, pharmacist,1Liang Yao, methodologist,1Zhikang Ye, methodologist, pharmacist,1Gordon H Guyatt, methodologist, internist,1,7 and Romina Brignardello-Petersen, methodologist1

BMJ. 2021; 373: n949.Published online 2021 Apr 26. doi: 10.1136/bmj.n949

Abstract

Objective

To determine and compare the effects of drug prophylaxis on SARS-CoV-2 infection and covid-19.

Design

Living systematic review and network meta-analysis.

Data sources

World Health Organization covid-19 database, a comprehensive multilingual source of global covid-19 literature to 25 March 2021, and six additional Chinese databases to 20 February 2021.

Study selection

Randomized trials of people at risk of covid-19 who were assigned to receive prophylaxis or no prophylaxis (standard care or placebo). Pairs of reviewers independently screened potentially eligible articles.

Methods

Random effects Bayesian network meta-analysis was performed after duplicate data abstraction. Included studies were assessed for risk of bias using a modification of the Cochrane risk of bias 2.0 tool, and certainty of evidence was assessed using the grading of recommendations assessment, development, and evaluation (GRADE) approach.

Results

The first iteration of this living network meta-analysis includes nine randomised trials—six of hydroxychloroquine (n=6059 participants), one of ivermectin combined with iota-carrageenan (n=234), and two of ivermectin alone (n=540), all compared with standard care or placebo. Two trials (one of ramipril and one of bromhexine hydrochloride) did not meet the sample size requirements for network meta-analysis. Hydroxychloroquine has trivial to no effect on admission to hospital (risk difference 1 fewer per 1000 participants, 95% credible interval 3 fewer to 4 more; high certainty evidence) or mortality (1 fewer per 1000, 2 fewer to 3 more; high certainty). Hydroxychloroquine probably does not reduce the risk of laboratory confirmed SARS-CoV-2 infection (2 more per 1000, 18 fewer to 28 more; moderate certainty), probably increases adverse effects leading to drug discontinuation (19 more per 1000, 1 fewer to 70 more; moderate certainty), and may have trivial to no effect on suspected, probable, or laboratory confirmed SARS-CoV-2 infection (15 fewer per 1000, 64 fewer to 41 more; low certainty). Owing to serious risk of bias and very serious imprecision, and thus very low certainty of evidence, the effects of ivermectin combined with iota-carrageenan on laboratory confirmed covid-19 (52 fewer per 1000, 58 fewer to 37 fewer), ivermectin alone on laboratory confirmed infection (50 fewer per 1000, 59 fewer to 16 fewer) and suspected, probable, or laboratory confirmed infection (159 fewer per 1000, 165 fewer to 144 fewer) remain very uncertain.

Conclusions

Hydroxychloroquine prophylaxis has trivial to no effect on hospital admission and mortality, probably increases adverse effects, and probably does not reduce the risk of SARS-CoV-2 infection. Because of serious risk of bias and very serious imprecision, it is highly uncertain whether ivermectin combined with iota-carrageenan and ivermectin alone reduce the risk of SARS-CoV-2 infection.

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8073806/

Characteristics of SARS-CoV-2 and COVID-19

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible and pathogenic coronavirus that emerged in late 2019 and has caused a pandemic of acute respiratory disease, named ‘coronavirus disease 2019’ (COVID-19), which threatens human health and public safety. In this Review, we describe the basic virology of SARS-CoV-2, including genomic characteristics and receptor use, highlighting its key difference from previously known coronaviruses. We summarize current knowledge of clinical, epidemiological and pathological features of COVID-19, as well as recent progress in animal models and antiviral treatment approaches for SARS-CoV-2 infection. We also discuss the potential wildlife hosts and zoonotic origin of this emerging virus in detail.

Introduction

Coronaviruses are a diverse group of viruses infecting many different animals, and they can cause mild to severe respiratory infections in humans. In 2002 and 2012, respectively, two highly pathogenic coronaviruses with zoonotic origin, severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), emerged in humans and caused fatal respiratory illness, making emerging coronaviruses a new public health concern in the twenty-first century1. At the end of 2019, a novel coronavirus designated as SARS-CoV-2 emerged in the city of Wuhan, China, and caused an outbreak of unusual viral pneumonia. Being highly transmissible, this novel coronavirus disease, also known as coronavirus disease 2019 (COVID-19), has spread fast all over the world2,3. It has overwhelmingly surpassed SARS and MERS in terms of both the number of infected people and the spatial range of epidemic areas. The ongoing outbreak of COVID-19 has posed an extraordinary threat to global public health4,5. In this Review, we summarize the current understanding of the nature of SARS-CoV-2 and COVID-19. On the basis of recently published findings, this comprehensive Review covers the basic biology of SARS-CoV-2, including the genetic characteristics, the potential zoonotic origin and its receptor binding. Furthermore, we will discuss the clinical and epidemiological features, diagnosis of and countermeasures against COVID-19.

Emergence and spread

In late December 2019, several health facilities in Wuhan, in Hubei province in China, reported clusters of patients with pneumonia of unknown cause6. Similarly to patients with SARS and MERS, these patients showed symptoms of viral pneumonia, including fever, cough and chest discomfort, and in severe cases dyspnea and bilateral lung infiltration6,7. Among the first 27 documented hospitalized patients, most cases were epidemiologically linked to Huanan Seafood Wholesale Market, a wet market located in downtown Wuhan, which sells not only seafood but also live animals, including poultry and wildlife4,8. According to a retrospective study, the onset of the first known case dates back to 8 December 2019 (ref.9). On 31 December, Wuhan Municipal Health Commission notified the public of a pneumonia outbreak of unidentified cause and informed the World Health Organization (WHO)9 (Fig. 1).

figure1
Fig. 1: Timeline of the key events of the COVID-19 outbreak.

By metagenomic RNA sequencing and virus isolation from bronchoalveolar lavage fluid samples from patients with severe pneumonia, independent teams of Chinese scientists identified that the causative agent of this emerging disease is a betacoronavirus that had never been seen before6,10,11. On 9 January 2020, the result of this etiological identification was publicly announced (Fig. 1). The first genome sequence of the novel coronavirus was published on the Virological website on 10 January, and more nearly complete genome sequences determined by different research institutes were then released via the GISAID database on 12 January7. Later, more patients with no history of exposure to Huanan Seafood Wholesale Market were identified. Several familial clusters of infection were reported, and nosocomial infection also occurred in health-care facilities. All these cases provided clear evidence for human-to-human transmission of the new virus4,12,13,14. As the outbreak coincided with the approach of the lunar New Year, travel between cities before the festival facilitated virus transmission in China. This novel coronavirus pneumonia soon spread to other cities in Hubei province and to other parts of China. Within 1 month, it had spread massively to all 34 provinces of China. The number of confirmed cases suddenly increased, with thousands of new cases diagnosed daily during late January15. On 30 January, the WHO declared the novel coronavirus outbreak a public health emergency of international concern16. On 11 February, the International Committee on Taxonomy of Viruses named the novel coronavirus ‘SARS-CoV-2’, and the WHO named the disease ‘COVID-19’ (ref.17).

The outbreak of COVID-19 in China reached an epidemic peak in February. According to the National Health Commission of China, the total number of cases continued to rise sharply in early February at an average rate of more than 3,000 newly confirmed cases per day. To control COVID-19, China implemented unprecedentedly strict public health measures. The city of Wuhan was shut down on 23 January, and all travel and transportation connecting the city was blocked. In the following couple of weeks, all outdoor activities and gatherings were restricted, and public facilities were closed in most cities as well as in countryside18. Owing to these measures, the daily number of new cases in China started to decrease steadily19.

However, despite the declining trend in China, the international spread of COVID-19 accelerated from late February. Large clusters of infection have been reported from an increasing number of countries18. The high transmission efficiency of SARS-CoV-2 and the abundance of international travel enabled rapid worldwide spread of COVID-19. On 11 March 2020, the WHO officially characterized the global COVID-19 outbreak as a pandemic20. Since March, while COVID-19 in China has become effectively controlled, the case numbers in Europe, the USA and other regions have jumped sharply. According to the COVID-19 dashboard of the Center for System Science and Engineering at Johns Hopkins University, as of 11 August 2020, 216 countries and regions from all six continents had reported more than 20 million cases of COVID-19, and more than 733,000 patients had died21. High mortality occurred especially when health-care resources were overwhelmed. The USA is the country with the largest number of cases so far.

Although genetic evidence suggests that SARS-CoV-2 is a natural virus that likely originated in animals, there is no conclusion yet about when and where the virus first entered humans. As some of the first reported cases in Wuhan had no epidemiological link to the seafood market22, it has been suggested that the market may not be the initial source of human infection with SARS-CoV-2. One study from France detected SARS-CoV-2 by PCR in a stored sample from a patient who had pneumonia at the end of 2019, suggesting SARS-CoV-2 might have spread there much earlier than the generally known starting time of the outbreak in France23. However, this individual early report cannot give a solid answer to the origin of SARS-CoV-2 and contamination, and thus a false positive result cannot be excluded. To address this highly controversial issue, further retrospective investigations involving a larger number of banked samples from patients, animals and environments need to be conducted worldwide with well-validated assays.

For More Information: https://www.nature.com/articles/s41579-020-00459-7

The incidence, clinical characteristics, and outcomes of pneumothorax in hospitalized COVID-19 patients: A systematic review

Authors: Woon H. Chong,a,⁎Biplab K. Saha,bKurt Hu,c and Amit Chopraa

Abstract

Background

Pneumothorax has been frequently described as a complication of COVID-19 infections.

Objective

In this systematic review, we describe the incidence, clinical characteristics, and outcomes of COVID-19-related pneumothorax.

Methods

Studies were identified through MEDLINE, Pubmed, and Google Scholar databases using keywords of “COVID-19,” “SARS-CoV-2,” “pneumothorax,” “pneumomediastinum,” and “barotrauma” from January 1st, 2020 to January 30th, 2021.

Results

Among the nine observational studies, the incidence of pneumothorax is low at 0.3% in hospitalized COVID-19 patients. However, the incidence of pneumothorax increases to 12.8–23.8% in those requiring invasive mechanical ventilation (IMV) with a high mortality rate up to 100%. COVID-19-related pneumothorax tends to be unilateral and right-sided. Age, pre-existing lung diseases, and active smoking status are not shown to be risk factors. The time to pneumothorax diagnosis is around 9.0–19.6 days from admission and 5.4 days after IMV initiation. COVID-19-related pneumothoraces are associated with prolonged hospitalization, increased likelihood of ICU admission and death, especially among the elderly.

Conclusion

COVID-19-related pneumothorax likely signify greater disease severity. With the high variability of COVID-19-related pneumothorax incidence described, a well-designed study is required to better assess the significance of COVID-19-related pneumothorax.

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8088235/

Anosmia and dysgeusia in SARS-CoV-2 infection: incidence and effects on COVID-19 severity and mortality, and the possible pathobiology mechanisms – a systematic review and meta-analysis

Authors: Endang Mutiawati, Conceptualization, Data Curation, Resources, Validation, Writing – Original Draft Preparation, Writing – Review & Editing,a,1,2Marhami Fahriani, Conceptualization, Data Curation, Investigation, Methodology, Validation, Writing – Original Draft Preparation, Writing – Review & Editing,3Sukamto S. Mamada, Data Curation, Investigation, Validation, Writing – Review & Editing,4Jonny Karunia Fajar, Conceptualization, Formal Analysis, Investigation, Methodology, Writing – Review & Editing,3,5Andri Frediansyah, Data Curation, Investigation, Writing – Original Draft Preparation, Writing – Review & Editing,6Helnida Anggun Maliga, Data Curation, Investigation, Validation, Writing – Review & Editing,7Muhammad Ilmawan, Data Curation, Investigation, Validation, Writing – Review & Editing,7Talha Bin Emran, Validation, Writing – Review & Editing,8Youdiil Ophinni, Investigation, Validation, Writing – Review & Editing,9Ichsan Ichsan, Validation, Writing – Review & Editing,3,10Nasrul Musadir, Validation, Writing – Review & Editing,1,2Ali A. Rabaan, Validation, Writing – Review & Editing,11Kuldeep Dhama, Supervision, Validation, Writing – Review & Editing,12Syahrul Syahrul, Supervision, Validation, Writing – Review & Editing,1,2Firzan Nainu, Data Curation, Investigation, Supervision, Validation, Writing – Review & Editing,4 and Harapan aPreparation, Writing – Review & Editing3,10,13

Abstract

Background: The present study aimed to determine the global prevalence of anosmia and dysgeusia in coronavirus disease 2019 (COVID-19) patients and to assess their association with severity and mortality of COVID-19. Moreover, this study aimed to discuss the possible pathobiological mechanisms of anosmia and dysgeusia in COVID-19.

Methods: Available articles from PubMed, Scopus, Web of Science, and preprint databases (MedRxiv, BioRxiv, and Researchsquare) were searched on November 10th, 2020. Data on the characteristics of the study (anosmia, dysgeusia, and COVID-19) were extracted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline. Newcastle–Ottawa scale was used to assess research quality. Moreover, the pooled prevalence of anosmia and dysgeusia were calculated, and the association between anosmia and dysgeusia in presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was assessed using the Z test.

Results: Out of 32,142 COVID-19 patients from 107 studies, anosmia was reported in 12,038 patients with a prevalence of 38.2% (95% CI: 36.5%, 47.2%); whereas, dysgeusia was reported in 11,337 patients out of 30,901 COVID-19 patients from 101 studies, with prevalence of 36.6% (95% CI: 35.2%, 45.2%), worldwide. Furthermore, the prevalence of anosmia was 10.2-fold higher (OR: 10.21; 95% CI: 6.53, 15.96, p < 0.001) and that of dysgeusia was 8.6-fold higher (OR: 8.61; 95% CI: 5.26, 14.11, p < 0.001) in COVID-19 patients compared to those with other respiratory infections or COVID-19 like illness. To date, no study has assessed the association of anosmia and dysgeusia with severity and mortality of COVID-19.

Conclusion: Anosmia and dysgeusia are prevalent in COVID-19 patients compared to those with the other non-COVID-19 respiratory infections. Several possible mechanisms have been hypothesized; however, future studies are warranted to elucidate the definitive mechanisms of anosmia and dysgeusia in COVID-19.

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7993408/

Clinical utility of cardiac troponin measurement in COVID-19 infection

Authors: David C Gaze 1 2

Abstract

The novel coronavirus SARS-CoV-2 causes the disease COVID-19, a severe acute respiratory syndrome. COVID-19 is now a global pandemic and public health emergency due to rapid human-to-human transmission. The impact is far-reaching, with enforced social distancing and isolation, detrimental effects on individual physical activity and mental wellbeing, education in the young and economic impact to business. Whilst most COVID-19 patients demonstrate mild-to-moderate symptoms, those with severe disease progression are at a higher risk of mortality. As more is learnt about this novel disease, it is becoming evident that comorbid cardiovascular disease is associated with a greater severity and increased mortality. Many patients positive for COVID-19 demonstrate increased concentrations of cardiac troponin, creating confusion in clinical interpretation. While myocardial infarction is associated with acute infectious respiratory disease, the majority of COVID-19 patients demonstrate stable cTn rather than the dynamically changing values indicative of an acute coronary syndrome. Although full understanding of the mechanism of cTn release in COVID-19 is currently lacking, this mini-review assesses the limited published literature with a view to offering insight to pathophysiological mechanisms and reported treatment regimens.

For More Information: https://pubmed.ncbi.nlm.nih.gov/32255359/

Cardiac Troponin-I and COVID-19: A Prognostic Tool for In-Hospital Mortality

Authors: Baher Al Abbasi 1Pedro Torres 1Fergie Ramos-Tuarez 2Nakeya Dewaswala 1Ahmed Abdallah 1Kai Chen 1Mohamed Abdul Qader 1Riya Job 1Samar Aboulenain 1Karolina Dziadkowiec 1Huzefa Bhopalwala 3Jesus E Pino 2Robert D Chait 2

Abstract

Background: The number of fatalities due to coronavirus disease 2019 (COVID-19) is escalating with more than 800,000 deaths globally. The scientific community remains in urgent need of prognostic tools to determine the probability of survival in patients with COVID-19 and to determine the need for hospitalization.

Methods: This is a retrospective cohort study of patients with a diagnosis of COVID-19 admitted to a tertiary center between March 2020 and July 2020. Patients age 18 years and older were stratified into two groups based on their troponin-I level in the first 24 h of admission (groups: elevated vs. normal). The aim of the study is to explore the utility of cardiac troponin-I level for early prognostication of patients with COVID-19.

Results: This cohort of 257 patients included 122/257 (47%) women with a mean age of 63 ± 17 years. Patients with an elevated troponin-I level were more likely to be older (77 ± 13 vs. 58 ± 16 years, P < 0.0001), have a history of hypertension (P < 0.0001), diabetes mellitus (P = 0.0019), atrial fibrillation or flutter (P = 0.0009), coronary artery disease (P < 0.0001), and chronic heart failure (P = 0.0011). Patients with an elevated troponin-I level in the first 24 h of admission were more likely to have higher in-hospital mortality (52% vs. 10%, P < 0.0001). Troponin-I level in the first 24 h of admission had a negative predictive value of 89.7% and a positive predictive value of 51.9% for all-cause in-hospital mortality.

Conclusions: Troponin-I elevation is commonly seen in patients with COVID-19 and is significantly associated with fatal outcomes. However, a normal troponin-I level in the first 24 h of admission had a high negative predictive value for all-cause in-hospital mortality, thereby predicting favorable survival at the time of discharge.

For More Information: https://pubmed.ncbi.nlm.nih.gov/33224386/

Risk for COVID-19 Infection, Hospitalization, and Death By Age Group

Authors: CDC

Rate ratios compared to 18- to 29-year-olds1

 0-4 years old5-17 years old18-29 years old30-39 years old40-49 years old50-64 years old65-74 years old75-84 years old85+ years old
Cases2<1x1xReference group1x1x1x1x1x1x
Hospitalization3<1x<1xReference group2x2x4x6x9x15x
Death4<1x<1xReference group4x10x35x95x230x600x

All rates are relative to the 18- to 29-year-old age category. This group was selected as the reference group because it has accounted for the largest cumulative number of COVID-19 cases compared to other age groups. Sample interpretation: Compared with 18- to 29-year-olds, the rate of death is four times higher in 30- to 39-year-olds, and 600 times higher in those who are 85 years and older. (In the table, a rate of 1x indicates no difference compared to the 18- to 29-year-old age category.)

For More Information: https://www.cdc.gov/coronavirus/2019-ncov/covid-data/investigations-discovery/hospitalization-death-by-age.html

Age-Adjusted Associations Between Comorbidity and Outcomes of COVID-19: A Review of the Evidence From the Early Stages of the Pandemic

Authors: Kate E. Mason*Gillian MaudsleyPhilip McHaleAndy PenningtonJennifer Day and Ben Barr

Objectives: Early in the COVID-19 pandemic, people with underlying comorbidities were overrepresented in hospitalised cases of COVID-19, but the relationship between comorbidity and COVID-19 outcomes was complicated by potential confounding by age. This review therefore sought to characterise the international evidence base available in the early stages of the pandemic on the association between comorbidities and progression to severe disease, critical care, or death, after accounting for age, among hospitalised patients with COVID-19.

Methods: We conducted a rapid, comprehensive review of the literature (to 14 May 2020), to assess the international evidence on the age-adjusted association between comorbidities and severe COVID-19 progression or death, among hospitalised COVID-19 patients – the only population for whom studies were available at that time.

Results: After screening 1,100 studies, we identified 14 eligible for inclusion. Overall, evidence for obesity and cancer increasing risk of severe disease or death was most consistent. Most studies found that having at least one of obesity, diabetes mellitus, hypertension, heart disease, cancer, or chronic lung disease was significantly associated with worse outcomes following hospitalisation. Associations were more consistent for mortality than other outcomes. Increasing numbers of comorbidities and obesity both showed a dose-response relationship. Quality and reporting were suboptimal in these rapidly conducted studies, and there was a clear need for additional studies using population-based samples.

Conclusions: This review summarizes the most robust evidence on this topic that was available in the first few months of the pandemic. It was clear at this early stage that COVID-19 would go on to exacerbate existing health inequalities unless actions were taken to reduce pre-existing vulnerabilities and target control measures to protect groups with chronic health conditions.

For More Information: https://www.frontiersin.org/articles/10.3389/fpubh.2021.584182/full