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1.
Revista Medica Clinica Las Condes ; 32(1):7-13, 2021.
Article in Spanish | Web of Science | ID: covidwho-1244819

ABSTRACT

This article presents a general history of historical epidemics, and new emerging diseases, pointing out their triggers. It is claimed that epidemics are inevitable, and that their risk increases in proportion to the size, complexity, and technological power of our societies. History teaches that epidemics have almost always been triggered by changes in the environment caused by human activities themselves. Infectious diseases are manifestations of an ecological interaction between the human species and another species of microorganisms. And epidemics are the result of a change in some environmental factor capable of influencing that interaction. Epidemic catastrophes are inevitable: firstly, because we cannot help but be part of trophic chains in which we eat and are eaten by microbes;secondly, because infections are evolutionary mechanisms and regulatory factors of ecological balance, which regulate especially the size of populations;and thirdly, because human technical interventions, in changing previous balances, create new balances that are more vulnerable. In this way human societies are more vulnerable the more complex. And human successes in modifying environmental conditions retain, or rather increase, the risk of epidemic catastrophes. All necessary epidemiological surveillance and control measures imaginable can lessen the damage caused by epidemics, but they can never prevent them.

2.
Astim Allerji Immunoloji ; 18(3):148-155, 2020.
Article in English | Web of Science | ID: covidwho-1031193

ABSTRACT

Objective: The outbreak of SARS-CoV-2 disease (COVID-19) emerged in 2019, and ultimately spread worldwide, being defined as a pandemic by the World Health Organization on March 11, 2020. The respiratory disease related to COVID-19 can range from being asymptomatic to presenting as devastating ARDS and death. The elderly and individuals with comorbidities and immunocompromised states are at a higher risk. Asthma is an inflammatory spasm of the airways with ACE2 overexpression at the alveolar level. ACE2 and TMPRSS2 expression mediate SARS-CoV-2 infection of host lung cells and hence might increase disease susceptibility in asthmatics. Materials and Methods: A literature review was done by searching the databases of Pubmed, WHO, clinicaltrials.gov, and Google Scholar, using the keywords of -COVID-19, SARS-CoV-2, coronavirus, asthma, and their combinations, following the timeline of December 2019 to August 10, 2020. We included patients with asthma diagnosed with COVID-19 while excluding non-COVID-19 patients, pregnant patients, and patients with other diseases or comorbidities. Primary outcomes included mortality and ICU admissions of both groups. Based on the available data, we conducted a meta-analysis via RevMan 5.4 using a random-effects model and 95% confidence intervals. Results: Patients with and without asthma were compared for risk outcomes of mortality. For the 755 COVID-19 patients with asthma and 4969 non-asthmatic COVID-19 patients, we found that the risk of mortality would increase by 9% in the asthmatic group (RR=1.09, CI= 0.58 to 2.03, I2=72%). There was an increased proportion of ICU admissions among the asthmatic group (RR=1.39, CI = 0.80 to 2.42). There was high heterogeneity among the studies (I-2 = 79%). Medications such as corticosteroids improve the mortality and ICU admission rates. Conclusion: Our results indicate that the number of COVID-19 cases in patients with asthma has been lower than those of the nonasthmatic group. COVID-19 patients with asthma were at increased risk of mortality and ICU admission due to underlying factors or predisposition. Finally, corticosteroids are considered safe and may confer protection against the severity of COVID-19 infection.

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