Coping Strategies and Stress Related Disorders in Patients with COVID-19.

Liana Dehelean,Daniela Violeta Mager,Ana-Maria Romosan,Ion Papava,Radu Stefan Romosan,Silvius Alexandru Pescariu,Talida Georgiana Cut,Ana-Maria Cristina Bortun,Mariana Bondrescu,Bianca Oana Bucatos,Roxana Paczeyka,Madalina Iuliana Musat,Ruxandra Laza,Felix Bratosin

doi:10.3390/brainsci11101287

Abstract

Patients with severe COVID-19 experience high-stress levels and thus are at risk for developing acute stress disorder (ASD) and/or post-traumatic stress disorder (PTSD). The present study aims to search for correlations between psychiatric response to stress and coping strategies among individuals with acute vs. remitted COVID-19. Ninety subjects with COVID-19 were included in the study, divided into two samples by disease category. Our focus was analysing the perceived stress intensity according to NSESSS and PCL-C-17 scales, and coping strategies with COPE-60. High NSESSS scores were found in 40% of acute patients, and 15.6% of remitted patients had high PCL-C-17 scores fulfilling the criteria for PTSD. We found a negative correlation between stress level and disease category. Acute patients used significantly more engagement and emotion-focused coping methods, but less disengagement types of coping than patients in the remitted phase. Remitted patients under high stress levels are prone to use disengagement and emotion-focused coping strategies. In conclusion, remitted COVID-19 patients experience lower levels of stress and use less emotion-focused strategies, except among those who developed PTSD post-COVID-19 infection, presenting with high-stress levels and using more disengagement and emotion-focused types of coping strategies.

Highlights

The current pandemic started 12 December 2019, in Wuhan, China, with a group of people suffering from atypical pneumonia
The present study aims to search for correlations between psychiatric response to stress and coping strategies among individuals with acute vs. remitted COVID-19
Since the actual knowledge of SARS-Cov-2 infection does not fully explain the diversity of its clinical manifestation, further elucidation has been sought in fields such as molecular biology research of the relationship between infection susceptibility and Human-Leukocyte Antigen (HLA), genetic polymorphism of the gene responsible for ACE2 synthesis, Single Nucleotide Polymorphisms (SNPs) implications in proinflammatory and anti-inflammatory cytokines synthesis and the interplay between genetic and -epigenetic mechanisms [5,10,11]

Summary

Introduction

The current pandemic started 12 December 2019, in Wuhan, China, with a group of people suffering from atypical pneumonia. The new coronavirus uses a membrane glycoprotein called spike protein S as a binding receptor to attach to the host cell. Another transmembrane protein-TMPRSS2- triggers protein S to split into two subunits, S1 causing the viral and the host cell membranes to merge. Protein S uses an angiotensin-converting enzyme (ACE2) to bind to the host cell. In organs such as lungs, kidneys, heart, and endothelium, where the ACE2 has greater expression, the clinical manifestation of the disease at these sites tends to be more intense [8,9]. Since the actual knowledge of SARS-Cov-2 infection does not fully explain the diversity of its clinical manifestation, further elucidation has been sought in fields such as molecular biology research of the relationship between infection susceptibility and Human-Leukocyte Antigen (HLA), genetic polymorphism of the gene responsible for ACE2 synthesis, Single Nucleotide Polymorphisms (SNPs) implications in proinflammatory and anti-inflammatory cytokines synthesis and the interplay between genetic and -epigenetic mechanisms [5,10,11]

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Conclusion