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Human Vaccines & Immunotherapeutics Aug 2023Since COVID-19 became a global pandemic in 2020, the development and application of SARS-CoV-2 vaccines has become an important task to prevent the spread of the...
Since COVID-19 became a global pandemic in 2020, the development and application of SARS-CoV-2 vaccines has become an important task to prevent the spread of the epidemic. In addition to the safety and efficacy of COVID-19 vaccines, the adverse reactions caused by vaccines in a small number of people also deserve our attention. We aimed to discuss and analyze the possible causes of Sweet syndrome caused by the COVID-19 vaccine by integrating the effective information from 16 patients and combining it with the latest views on the innate immune mechanism. We searched the PubMed and Embase databases for published patient reports on the occurrence or recurrence of Sweet syndrome after COVID-19 vaccination. We summarized the basic information of the patients, the type of vaccination, the presence of underlying diseases, and the clinical manifestations, clinical treatment and prognosis of the patients. The results were reported in narrative methods and were sorted into tables. We initially identified 53 studies. 16 articles were included through full-text screening. Based on the table we compiled, we generally concluded that the first dose of any type of COVID-19 vaccine was more likely to cause Sweet syndrome than subsequent doses. Sweet syndrome may occur after COVID-19 vaccination. Clinicians should consider Sweet syndrome in addition to common adverse reactions such as anaphylaxis and infection when a patient presents with acute fever accompanied by nodular erythema, pustules, and edematous plaques after COVID-19 vaccination.
Topics: Humans; COVID-19; COVID-19 Vaccines; Pandemics; SARS-CoV-2; Sweet Syndrome
PubMed: 37313726
DOI: 10.1080/21645515.2023.2217076 -
Rheumatology International Jul 2024VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a newly discovered autoinflammatory condition characterised by somatic mutation of the UBA1... (Review)
Review Meta-Analysis
BACKGROUND
VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a newly discovered autoinflammatory condition characterised by somatic mutation of the UBA1 gene. The syndrome leads to multi-system inflammation affecting predominantly the skin, lungs and bone marrow.
METHODS
We undertook a systematic review of the multisystem features and genotypes observed in VEXAS syndrome. Articles discussing VEXAS syndrome were included. Medline, Embase and Cochrane databases were searched. Information was extracted on: demographics, type and prevalence of clinical manifestations, genetic mutations and treatment. Meta-analysis using a random effects model was used to determine pooled estimates of serum markers.
RESULTS
From 303 articles, 90 were included, comprising 394 patients with VEXAS. 99.2% were male, with a mean age of 67.1 years (SD 8.5) at disease onset. The most frequent diagnoses made prior to VEXAS were: relapsing polychondritis (n = 59); Sweet's syndrome (n = 24); polyarteritis nodosa (n = 11); and myelodysplastic syndrome (n = 10). Fever was reported in 270 cases (68.5%) and weight loss in 79 (20.1%). Most patients had haematological (n = 342; 86.8%), dermatological (n = 321; 81.5%), pulmonary (n = 297; 75.4%%) and musculoskeletal (n = 172; 43.7%) involvement, although other organ manifestations of varying prevalence were also recorded. The most commonly reported mutations were "c.122T > C pMET41Thr" (n = 124), "c.121A > G pMET41Val" (n = 62) and "c.121A > C pMet41Leu" (n = 52). Most patients received glucocorticoids (n = 240; 60.9%) followed by methotrexate (n = 82; 20.8%) and IL-6 inhibitors (n = 61, 15.4%). One patient underwent splenectomy; 24 received bone marrow transplants.
CONCLUSION
VEXAS syndrome is a rare disorder affecting predominantly middle-aged men. This is the first systematic review to capture clinical manifestations, genetics and treatment of reported cases. Further studies are needed to optimise treatment and subsequently reduce morbidity and mortality.
Topics: Humans; Male; Ubiquitin-Activating Enzymes; Female; Mutation; Syndrome; Aged; Middle Aged; Myelodysplastic Syndromes; Sweet Syndrome; Polyarteritis Nodosa; Hereditary Autoinflammatory Diseases
PubMed: 38129348
DOI: 10.1007/s00296-023-05513-0