Immune Thrombocytopenia Relapse in Patients Who Received mRNA COVID-19 Vaccines.

Background: Immune thrombocytopenia (ITP) is a blood disorder in which antibodies coating platelets cause platelet destruction in the spleen with a resultant low platelet count and an increased tendency for bleeding. Coronavirus disease 2019 (COVID-19) is an illness caused by SARS-CoV-2. Though pneumonia and respiratory failure are major causes of morbidity and mortality, multisystemic complications were identified, including hematological ones. Several ITP relapse cases post-mRNA SARS-CoV-2 vaccines have been reported, and different pathophysiological theories have been proposed. Purpose: The objective of this study is to identify the causal relationship between mRNA COVID-19 vaccines and ITP relapse, to highlight the longer-term effect of these vaccines on the platelet count more than 6 months after receiving the vaccine, and to identify if there is a statistical difference between Comirnaty and Spikevax vaccines on ITP relapse rate. Patients and Methods: In this retrospective study, 67 patients with known ITP were followed before and after receiving the mRNA COVID-19 vaccine. The follow-up parameters included platelet counts when available and bleeding symptoms. All patients were adults over 18 years old, with no other identified causes of thrombocytopenia. Forty-seven patients received the Comirnaty vaccine, and 20 patients received the Spikevax vaccine. Results: Data analysis showed 6% ITP relapse in the first 3 months, and a 10% relapse rate 3-6 months after receiving one of the mRNA COVID-19 vaccines, with no statically significant difference between the two vaccines. Conclusion: mRNA COVID-19 vaccines increase the risk of ITP relapse and can lead to a prolonged reduction in platelet count in a proportion of ITP patients, with no statistically significant difference between Comirnaty and Spikevax vaccines.

Adding colchicine to tocilizumab in hospitalized patients with severe COVID-19 pneumonia: An open-label randomized controlled trial.

INTRODUCTION: Colchicine acts upstream in the cytokines cascade by inhibiting the nod-like receptor protein 3 (NLRP3) inflammasome while interleukin 6 (IL-6) receptor antagonists, such as tocilizumab, block the end result of the cytokines cascade. Hence, adding colchicine to tocilizumab with the aim of blocking the early and end products of the cytokines cascade, might reduce the risk of developing cytokine storm. METHODS AND ANALYSIS: We aim to conduct an open-label randomized controlled trial to evaluate the efficacy and safety of adding colchicine to tocilizumab among patients with severe COVID-19 pneumonia to reduce the rate of invasive mechanical ventilation and mortality. We will include patients with severe COVID-19 pneumonia who received tocilizumab according to our local guidelines. Enrolled patients will be then randomized in 1:1 to colchicine versus no colchicine. Patients will be followed up for 30 days. The primary outcome is the rate of invasive mechanical ventilation and will be determined using Cox proportional hazard model. DISCUSSION: Given colchicine's ease of use, low cost, good safety profile, and having different anti-inflammatory mechanism of action than other IL-6 blockade, colchicine might serve as a potential anti-inflammatory agent among patients with severe COVID-19 pneumonia. This study will provide valuable insights on the use of colchicine in severe COVID-19 when added to IL-6 antagonists. ETHICS AND DISSEMINATION: The Medical Research Center and Institutional Review Board at Hamad Medical Corporation in Qatar approved the study protocol (MRC-01-21-299). Results of the analysis will be submitted for publication in a peer-reviewed journal.

Severe sinus bradycardia associated with favipiravir in a COVID-19 patient.

The antiviral medication "favipiravir" should be considered as a possible cause of unexplained sinus bradycardia.

Prevalence and clinical significance of antiphospholipid antibodies in patients with coronavirus disease 2019 admitted to intensive care units: a prospective observational study.

Coronavirus disease 2019 (COVID-19) increases the risk of coagulopathy. Although the presence of antiphospholipid antibodies (aPLs) has been proposed as a possible mechanism of COVID-19-induced coagulopathy, its clinical significance remains uncertain. Therefore, this study aimed to evaluate the prevalence and clinical significance of aPLs among critically ill patients with COVID-19. This prospective observational study included 60 patients with COVID-19 admitted to intensive care units (ICU). The study outcomes included prevalence of aPLs, and a primary composite outcome of all-cause mortality and arterial or venous thrombosis between antiphospholipid-positive and antiphospholipid-negative patients during their ICU stay. Multiple logistic regression was used to assess the influence of aPLs on the primary composite outcome of mortality and thrombosis. A total of 60 critically ill patients were enrolled. Among them, 57 (95%) were men, with a mean age of 52.8 ± 12.2 years, and the majority were from Asia (68%). Twenty-two patients (37%) were found be antiphospholipid-positive; 21 of them were positive for lupus anticoagulant, whereas one patient was positive for anti-ß2-glycoprotein IgG/IgM. The composite outcome of mortality and thrombosis during their ICU stay did not differ between antiphospholipid-positive and antiphospholipid-negative patients (4 [18%] vs. 6 [16%], adjusted odds ratio 0.98, 95% confidence interval 0.1-6.7; p value = 0.986). The presence of aPLs does not seem to affect the outcomes of critically ill patients with COVID-19 in terms of all-cause mortality and thrombosis. Therefore, clinicians may not screen critically ill patients with COVID-19 for aPLs unless deemed clinically appropriate.