Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add filters

Database
Language
Document Type
Year range
1.
Eur J Neurol ; 28(10): 3418-3425, 2021 10.
Article in English | MEDLINE | ID: covidwho-1605552

ABSTRACT

BACKGROUND AND PURPOSE: Myasthenia gravis (MG) patients could be a vulnerable group in the pandemic era of coronavirus 2019 (COVID-19) mainly due to respiratory muscle weakness, older age and long-term immunosuppressive treatment. We aimed to define factors predicting the severity of COVID-19 in MG patients and risk of MG exacerbation during COVID-19. METHODS: We evaluated clinical features and outcomes after COVID-19 in 93 MG patients. RESULTS: Thirty-five patients (38%) had severe pneumonia and we recorded 10 deaths (11%) due to COVID-19. Higher forced vital capacity (FVC) values tested before COVID-19 were shown to be protective against severe infection (95% CI 0.934-0.98) as well as good control of MG measured by the quantified myasthenia gravis score (95% CI 1.047-1.232). Long-term chronic corticosteroid treatment worsened the course of COVID-19 in MG patients (95% CI 1.784-111.43) and this impact was positively associated with dosage (p = 0.005). Treatment using azathioprine (95% CI 0.448-2.935), mycophenolate mofetil (95% CI 0.91-12.515) and ciclosporin (95% CI 0.029-2.212) did not influence the course of COVID-19. MG patients treated with rituximab had a high risk of death caused by COVID-19 (95% CI 3.216-383.971). Exacerbation of MG during infection was relatively rare (15%) and was not caused by remdesivir, convalescent plasma or favipiravir (95% CI 0.885-10.87). CONCLUSIONS: As the most important predictors of severe COVID-19 in MG patients we identified unsatisfied condition of MG with lower FVC, previous long-term corticosteroid treatment especially in higher doses, older age, the presence of cancer, and recent rituximab treatment.


Subject(s)
COVID-19 , Coronavirus Infections , Myasthenia Gravis , Aged , COVID-19/therapy , Humans , Immunization, Passive , Myasthenia Gravis/complications , Myasthenia Gravis/drug therapy , Myasthenia Gravis/epidemiology , SARS-CoV-2 , COVID-19 Serotherapy
3.
Int J Mol Sci ; 22(12)2021 Jun 18.
Article in English | MEDLINE | ID: covidwho-1273461

ABSTRACT

COVID-19 is a pandemic respiratory disease caused by the SARS-CoV-2 coronavirus. The worldwide epidemiologic data showed higher mortality in males compared to females, suggesting a hypothesis about the protective effect of estrogens against severe disease progression with the ultimate end being patient's death. This article summarizes the current knowledge regarding the potential effect of estrogens and other modulators of estrogen receptors on COVID-19. While estrogen receptor activation shows complex effects on the patient's organism, such as an influence on the cardiovascular/pulmonary/immune system which includes lower production of cytokines responsible for the cytokine storm, the receptor-independent effects directly inhibits viral replication. Furthermore, it inhibits the interaction of IL-6 with its receptor complex. Interestingly, in addition to natural hormones, phytestrogens and even synthetic molecules are able to interact with the estrogen receptor and exhibit some anti-COVID-19 activity. From this point of view, estrogen receptor modulators have the potential to be included in the anti-COVID-19 therapeutic arsenal.


Subject(s)
COVID-19/pathology , Estrogen Receptor Modulators/pharmacology , SARS-CoV-2/drug effects , Breast Neoplasms/complications , Breast Neoplasms/drug therapy , Breast Neoplasms/pathology , COVID-19/complications , COVID-19/virology , Estrogen Receptor Modulators/metabolism , Estrogen Receptor Modulators/therapeutic use , Female , Humans , Receptors, Estrogen/chemistry , Receptors, Estrogen/metabolism , SARS-CoV-2/isolation & purification , SARS-CoV-2/physiology , Viral Matrix Proteins/antagonists & inhibitors , Viral Matrix Proteins/metabolism , Virus Internalization/drug effects , Virus Replication/drug effects
SELECTION OF CITATIONS
SEARCH DETAIL