ABSTRACT
Our patient is a 3-week-old female neonate, presented with complaints of low-grade fever and a congested nose for one day. Eventually, she developed progressive desaturation, hypotension, and poor perfusion due to severe pulmonary hemorrhage. Then, she developed cardiac arrest and was declared dead.
ABSTRACT
As the coronavirus disease 2019 (COVID-19) pandemic is ongoing, and new variants of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) are emerging, vaccines are needed to protect individuals at high risk of complications and to potentially control disease outbreaks by herd immunity. After SARS-CoV-2 vaccination, antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) presenting with a pulmonary hemorrhage has been described. Previous studies suggested that monocytes upregulate major histocompatibility complex (MHC) II cell surface receptor human leukocyte antigen receptor (HLA-DR) molecules in granulomatosis with polyangiitis (GPA) patients with proteinase 3 (PR3)- and myeloperoxidase (MPO)-ANCA seropositivity. Here, we present a case of new-onset AAV after booster vaccination with the Pfizer-BioNTech SARS-CoV-2 mRNA vaccine. Moreover, we provide evidence that the majority of monocytes express HLA-DR in AAV after SARS-CoV-2 booster vaccination. It is possible that the enhanced immune response after booster vaccination and presence of HLA-DR+ monocytes could be responsible for triggering the production of the observed MPO- and PR3-ANCA autoantibodies. Additionally, we conducted a systematic review of de novo AAV after SARS-CoV-2 vaccination describing their clinical manifestations in temporal association with SARS-CoV-2 vaccination, ANCA subtype, and treatment regimens. In light of a hundred million individuals being booster vaccinated for SARS-CoV-2 worldwide, a potential causal association with AAV may result in a considerable subset of cases with potential severe complications.
ABSTRACT
Extracorporeal membrane oxygenation (ECMO) therapy in patients with coronavirus disease 2019 (COVID-19) has a low frequency of use, and thus pathological findings in such patients are valuable. In this case report, a 62-year-old man with a history of hypertension presented with a runny nose. After an at-home COVID-19 positive test, he developed dyspnea and fever. Once admitted to our hospital, his oxygenation worsened, and ECMO was initiated. He died from respiratory failure 69 days after ECMO induction. Macroscopically, the lungs gained mass, were partially consolidated, and were airless. Histological analysis revealed diffuse bronchial epithelial metaplasia and adenoid metaplasia in the alveolar epithelium. Although the lung parenchyma was partially preserved, there was organizing and fibrosis that filled pulmonary alveolus due to COVID-19 and changes resulting from disuse and long-term ECMO.
ABSTRACT
A pericyte-centered theory suggesting that embolisms occurring within the microvasculature of a neurovascular unit that can result in either parenchymal hemorrhage or intravascular congestion is presented here. Dysfunctional microvascular pericytes are characterized by their location in the neurovascular unit, either on the arteriole or venule side. Pathophysiological and pathological changes caused by coronavirus disease 2019 (COVID-19) include pulmonary hypertension, edema, focal hemorrhage, microvascular congestion, and thrombosis. In this paper, the application of the pericytes-centered hypothesis to COVID-19 has been presented by proposing the concept of a pulmonary neurovascular unit (pNVU). The application of this concept implies that human lungs contain approximately 300 million pNVUs. This concept of existing local regulation of microvascular blood flow is supported by the observation of pathophysiology in pulmonary embolism and in acute high-altitude illness. The autonomic control seen in these three disease states matches blood flow with oxygen supply in each pNVU to maintain physiological blood oxygen saturation level. This paper illustrates how the malfunction of microvascular pericytes may cause focal hemorrhage, edema or microvascular congestion and thrombosis. A bypass existing in each pNVU would autonomically deviate blood flow from a COVID-19-affected pNVU to other healthy pNVUs. This action would prevent systemically applied medicines from reaching the therapeutic threshold in COVID-19-affected pNVUs. While testing this hypothesis with experimental evidence is urgently needed, supporting therapy aimed at improving microcirculation or rebuilding the physiological function of microvascular pericytes is recommended as a potentially effective treatment of COVID 19.