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1.
Dermatol Ther ; 35(6): e15458, 2022 06.
Article in English | MEDLINE | ID: covidwho-1752529

ABSTRACT

Currently the most powerful tool in combating the COVID-19 pandemic is vaccination against SARS-CoV-2. A growing percentage of the world's population is being vaccinated. Various vaccines are worldwide on the market. Several adverse reactions have been reported as a part of post-marketing surveillance of COVID-19 vaccines. Among the possible adverse events, cutaneous vasculitis has occasionally been reported. We present a narrative review on cutaneous vasculitis related to COVID-19-vaccination to summarize clinical findings, histopathology, treatment and outcome. We searched for "COVID vaccine", "COVID vaccination" AND "cutaneous vasculitis" in PUBMED. Articles in English have been selected, from inception to December 2021, and analyzed for patient's characteristics, type of vaccine, time of appearance of cutaneous vasculitis and clinico-histopathologic type. Treatment and outcome have also been considered in this narrative review. Two new unpublished cases of ours were added. Cutaneous vasculitis is a rare adverse event to COVID-19 vaccination. It has been observed with mRNA and adenovirus-vector vaccines. IgA vasculitis, lymphocytic and ANCA-associated vasculitis, leukocytoclastic and urticarial vasculitis have been reported. This adverse event can occur after first or second shot. Most cases run a mild to moderate course. Cornerstone of medical treatment are systemic corticosteroids. Complete remission could be achieved in most patients. Vasculitis may not be considered as a contraindication of vaccination, being uncommonly reported and shows a favorable prognosis. The benefit of the vaccination remains high especially for immunocompromised patients. COVID-vaccine induced vasculitis is important in the differential diagnosis of purpuric and vasculitis disorders.


Subject(s)
COVID-19 Vaccines , COVID-19 , Vasculitis , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Humans , SARS-CoV-2 , Vaccination/adverse effects , Vasculitis/chemically induced , Vasculitis/diagnosis
3.
Am J Otolaryngol ; 42(6): 103080, 2021.
Article in English | MEDLINE | ID: covidwho-1230345

ABSTRACT

BACKGROUND: Acute invasive fungal rhinosinusitis (AIFRS) is aggressive morbidity affecting immunocompromised patients. Coronavirus disease 2019 (COVID-19) may allow secondary fungal disease through a propensity to cause respiratory infection by affecting the immune system leading to dysregulation and reduced numbers of T lymphocytes, CD4+T, and CD8+T cells, altering the innate immunity. The aim of this study is to evaluate the incidence of acute invasive fungal rhinosinusitis (AIFRS) in COVID-19 patients. METHODOLOGY: Data for acute invasive rhinosinusitis was obtained from the Otorhinolaryngology departments at our tertiary hospital at the period from January 2017 to December 2020. Then the risk factors of comorbid diseases and fungal types between post-COVID-19 and non-COVID-19 groups regarding the incidence of AIFRS are compared. RESULTS: Consequently, the incidence of AIFRS showed a more significant difference (P < 0.05) in post-COVID-19 patients than in non-COVID-19 especially in immunocompromised patients, diabetic, renal, and liver dysfunction patients as well as patients with risk factors of AIFRS. The most common organisms affecting patients with AIFRS are Rhizopus oryzae, Aspergillus fumigatus, and Absidia mucor. CONCLUSIONS: The incidence of AIFRS is markedly prominent in post-COVID-19 patients than in those of non-COVID-19, especially in immunocompromised, diabetic, renal, and liver dysfunction patients and patients with risk factors for rhinosinusitis.


Subject(s)
COVID-19/epidemiology , COVID-19/immunology , Disease Outbreaks , Invasive Fungal Infections , Rhinitis/epidemiology , Rhinitis/microbiology , Sinusitis/epidemiology , Sinusitis/microbiology , Absidia , Acute Disease , Aged , Aspergillus fumigatus , CD4-Positive T-Lymphocytes/immunology , CD8-Positive T-Lymphocytes/immunology , Female , Humans , Immunity, Innate/immunology , Immunocompromised Host/immunology , Incidence , Magnetic Resonance Imaging , Male , Middle Aged , Rhinitis/diagnostic imaging , Rhinitis/immunology , Rhizopus oryzae , Risk Factors , Sinusitis/diagnostic imaging , Sinusitis/immunology , Tomography, X-Ray Computed , Young Adult
4.
Pathogens ; 10(5)2021 May 07.
Article in English | MEDLINE | ID: covidwho-1224096

ABSTRACT

The pathogenesis of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is still not fully unraveled. Though preventive vaccines and treatment methods are out on the market, a specific cure for the disease has not been discovered. Recent investigations and research studies primarily focus on the immunopathology of the disease. A healthy immune system responds immediately after viral entry, causing immediate viral annihilation and recovery. However, an impaired immune system causes extensive systemic damage due to an unregulated immune response characterized by the hypersecretion of chemokines and cytokines. The elevated levels of cytokine or hypercytokinemia leads to acute respiratory distress syndrome (ARDS) along with multiple organ damage. Moreover, the immune response against SARS-CoV-2 has been linked with race, gender, and age; hence, this viral infection's outcome differs among the patients. Many therapeutic strategies focusing on immunomodulation have been tested out to assuage the cytokine storm in patients with severe COVID-19. A thorough understanding of the diverse signaling pathways triggered by the SARS-CoV-2 virus is essential before contemplating relief measures. This present review explains the interrelationships of hyperinflammatory response or cytokine storm with organ damage and the disease severity. Furthermore, we have thrown light on the diverse mechanisms and risk factors that influence pathogenesis and the molecular pathways that lead to severe SARS-CoV-2 infection and multiple organ damage. Recognition of altered pathways of a dysregulated immune system can be a loophole to identify potential target markers. Identifying biomarkers in the dysregulated pathway can aid in better clinical management for patients with severe COVID-19 disease. A special focus has also been given to potent inhibitors of proinflammatory cytokines, immunomodulatory and immunotherapeutic options to ameliorate cytokine storm and inflammatory responses in patients affected with COVID-19.

5.
Infect Prev Pract ; 2(4): 100081, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-764861

ABSTRACT

BACKGROUND: Healthcare workers have a higher risk of acquiring coronavirus disease 2019 (COVID-19). The process of requesting pathological investigations is usually handled manually through paper-based forms. This study evaluated the potential for paper-based request forms to transmit severe acute respiratory virus coronavirus-2 (SARS-CoV-2) to laboratory staff in order to make recommendations for dealing with hospital paperwork in a post-COVID-19 world. METHODS: Paper-based forms were tracked from the time of test ordering until the release of the pathology report by calculating the time taken for the forms to reach the laboratory, and the exposure of each staff group to forms received from both high and moderate COVID-19 risk areas. RESULTS: Four hundred and thirty-two (83%) of 520 forms were received in the laboratory within 24 h. The remaining 88 (17%) forms took ≥24 h to be handled by laboratory personnel. The mean daily exposure time to the paperwork for various laboratory staff was as follows: receptionists, 2.7 min; technicians, 5.5 min; and pathologists, 54.6 min. CONCLUSION: More than 80% of the forms were handled by laboratory personnel within 24 h, carrying a high potential risk for viral transmission. It is recommended that paper-based request forms should be replaced by electronic requests that could be printed in the laboratory if required. Another option would be to sterilize received paperwork to ensure the safety of laboratory personnel. More studies are needed to detect the stability of SARS-CoV-2 on different surfaces and determine the potential risk of COVID-19 transmission via paper.

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