ABSTRACT
The global COVID-19 vaccination had an undeniable influence on the pandemic management, despite of having reported rare but life-threatening side-effects of vaccines. Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare autoimmune complication determined by thrombocytopenia and thrombosis propensity in the circulatory system. The activation of antibodies against platelet factor-4 (PF-4) which mimics the heparin-induced thrombocytopenia (HIT) characteristic is the main known pathogenicity of the disease. Herein, we reported a case of VITT in a middle-aged woman with no previous history of thrombophilia or other medical conditions who presented with thrombosis of the left superficial femoral artery 3-days after receiving the second dose of inactivated BBIBP-CorV (Sinopharm) vaccine. The patient underwent bypass vascular surgery and received none-heparin anticoagulation consistent with high-dose intravenous immunoglobin. Eight days after the discharge, she was subsequently referred to our center with the presentation of sub-massive pulmonary thromboembolism in spite of receiving the prophylactic anticoagulants during follow-up period. Details on side-effects of COVID-19 vaccines, specifically the inactivated ones are yet to be fully ascertained. Clinicians should consider the history of COVID-19 vaccines in thromboembolism patients who do not have well-acknowledged risk factors. Further studies about the necessity of prophylactic anticoagulants and clinical judgment for receiving other vaccines in such patients are required.
ABSTRACT
An amendment to this paper has been published and can be accessed via the original article.
ABSTRACT
BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has spread to almost 100 countries, infected over 31 M patients and resulted in 961 K deaths worldwide as of 21st September 2020. The major clinical feature of severe COVID-19 requiring ventilation is acute respiratory distress syndrome (ARDS) with multi-functional failure as a result of a cytokine storm with increased serum levels of cytokines. The pathogenesis of the respiratory failure in COVID-19 is yet unknown, but diffuse alveolar damage with interstitial thickening leading to compromised gas exchange is a plausible mechanism. Hypoxia is seen in the COVID-19 patients, however, patients present with a distinct phenotype. Intracellular levels of nitric oxide (NO) play an important role in the vasodilation of small vessels. To elucidate the intracellular levels of NO inside of RBCs in COVID-19 patients compared with that of healthy control subjects. METHODS: We recruited 14 COVID-19 infected cases who had pulmonary involvement of their disease, 4 non-COVID-19 healthy controls (without pulmonary involvement and were not hypoxic) and 2 hypoxic non-COVID-19 patients subjects who presented at the Masih Daneshvari Hospital of Tehran, Iran between March-May 2020. Whole blood samples were harvested from patients and intracellular NO levels in 1 × 106 red blood cells (RBC) was measured by DAF staining using flow cytometry (FACS Calibour, BD, CA, USA). RESULTS: The Mean florescent of intensity for NO was significantly enhanced in COVID-19 patients compared with healthy control subjects (P ≤ 0.05). As a further control for whether hypoxia induced this higher intracellular NO, we evaluated the levels of NO inside RBC of hypoxic patients. No significant differences in NO levels were seen between the hypoxic and non-hypoxic control group. CONCLUSIONS: This pilot study demonstrates increased levels of intracellular NO in RBCs from COVID-19 patients. Future multi-centre studies should examine whether this is seen in a larger number of COVID-19 patients and whether NO therapy may be of use in these severe COVID-19 patients.