ABSTRACT
Background: The emotional experiences of healthcare workers during the first wave of COVID-19 warrant further investigation especially regarding gender differences. The purpose of this study was to determine the relationship between gender role, job role and risk and protective factors for the development of Post Traumatic Stress Disorder (PTSD). Methods: A total of 521 healthcare workers completed the survey during the first pandemic wave. Psychosocial Index (PSI) was used to assess stress, well-being, distress, illness behaviour, and quality of life;the distress caused by stressful events was evaluated with the Impact of Event Scale – Revised (IES-R) and resilience was measured with the Connor-Davidson resilience scale (CD RISC). Results: Associations were found between female gender and distress with and without sleep disturbance (p<0.0001). Assessment of PTSD symptoms showed significance on symptoms of avoidance (p=0.0006), intrusiveness of thought (p=0.0016), and hyperarousal (p=0.003) to the disadvantage of female compared to male. Nurses emerged as the most vulnerable professional role about distress (p<0.0001), sleep disturbance (p<0.0001), and abnormal illness behaviors (p<0.0001). Finally, the study of post-traumatic symptomatology showed significance for avoidance (p=0.0072), intrusive thinking (p=0.0071), and hyperarousal (p=0.0019) to the disadvantage of the medical and nursing role in the female gender compared to the medical and nursing role in the male gender and other professional role in the female gender. Conclusions: Such findings suggest, there are differences in gender, rather than professional role and resilience factor, in emotional management in a particularly stressful condition, such as that of the first pandemic wave © 2022. by the Author(s);licensee Mediterranean Journal of Clinical Psychology, Messina, Italy. This article is an open access article, licensed under a Creative Commons Attribution 4.0 Unported License
ABSTRACT
Introduction: At the end of April 2020, European clinicians warned the Public Health Agencies about an abnormal increase of Kawasakilike diseases and myocarditis requiring critical care support in the context of the ongoing COVID-19 epidemic in children. American clinicians also reported a large outbreak of severe inflammation in children following COVID-19 infection, a condition that is now named Pediatric Inflammatory Multisystemic Syndrome (PIMS) or Multisystem Inflammatory Syndrome in children (MIS-C). Objectives: As MIS-C combines clinical features of Kawasaki disease (KD) and Toxic Shock Syndrome (TSS), we aimed to compare the immunological profile of pediatric patients with these different conditions. Methods: We analysed blood cytokine expression, and the T cell repertoire and phenotype in 36 MIS-C cases, which were compared to 16 KD, 58 TSS, and 42 COVID-19 cases. Results: We observed an increase of serum inflammatory cytokines (IL-6, IL-10, IL-18, TNF-a, IFNg, CD25s, MCP1, IL-1RA) in MIS-C, TSS and KD, contrasting with low expression of HLA-DR in monocytes. We detected a specific expansion of activated T cells expressing the Vβ21.3 T cell receptor β chain variable region in both CD4 and CD8 subsets in 75% of MIS-C patients and not in any patient with TSS, KD, or acute COVID-19;this correlated with the cytokine storm detected. The T cell repertoire returned to baseline within weeks after MIS-C resolution. Vβ21.3+ T cells from MIS-C patients expressed high levels of HLA-DR, CD38 and CX3CR1 but had weak responses to SARS-CoV- 2 peptides in vitro. Consistently, the T cell expansion was not associated with specific classical HLA alleles. Conclusion: Thus, our data suggested that MIS-C is characterized by a polyclonal Vβ21.3 T cell expansion not directed against SARS-CoV-2 antigenic peptides, which is not seen in KD, TSS and acute COVID-19.