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Levels of anti-annexin A2 antibodies at admission strongly predicted mortality among hospitalised COVID-19 patients. Given its critical protective function in the lung, annexin A2 antagonism may play an important role in the pathophysiology of COVID-19.https://bit.ly/2UMPr9w

BackgroundAnnexin A2 is a phospholipid-binding protein involved in fibrinolysis, cell membrane stabilization and repair, and ensuring the integrity of the pulmonary microvasculature. Given the autoantibodies observed in COVID-19 and that Annexin A2 is a known target of antiphospholipid antibodies, we studied autoimmunity directed against Annexin A2 among hospitalized COVID-19 patients.MethodsWe used ELISA to identify the levels of IgG autoantibodies recognizing Annexin A2 and A5 among 86 hospitalized cases of COVID-19. Using logistic regression, we analyzed the association between anti-Annexin A2 and A5 antibody levels with mortality after adjusting for age, sex, race and key comorbidities.ResultsWe found higher average levels of anti-Annexin A2 antibodies among hospitalized COVID-19 patients that died when compared with non-critical hospitalized COVID-19 patients (p-value = 0.006) and critically ill COVID-19 patients (p-value = 0.04). No significant differences in anti-Annexin A5 antibody levels were identified. Regression analysis showed that anti-Annexin A2 antibody levels as measured in relative units strongly predicted mortality with an odds ratio of 9.3 (95% CI: 1.9 to 44.6, p=0.005). In contrast, anti-Annexin A5 antibody levels were not associated with higher mortality (95% CI: 0.5 to 15.2, p=0.22).ConclusionsWe determined that anti-Annexin A2 antibodies were elevated among hospitalized COVID-19 patients and these levels predicted mortality. It is known that inhibition of Annexin A2 induces systemic thrombosis, cell death, and non-cardiogenic pulmonary edema. Autoimmunity to Annexin A2 is a potential mechanism that may explain the key clinical findings of severe COVID-19.

Purpose of review Community-acquired pneumonia (CAP) is a pervasive disease that is encountered in outpatient and inpatient settings. CAP is the leading cause of death from an infectious disease and accounts for significant worldwide morbidity and mortality. This update reviews current advances that can be used to promote improved outcomes in CAP. Recent findings Early recognition of CAP and its severe presentations, with appropriate site of care decisions, leads to reduced patient mortality. In addition to traditional prognostic tools, certain serum biomarkers can assist in defining disease severity and guide treatment and management strategies. The use of macrolides as part of combination antibiotic therapy has shown beneficial mortality effects across the CAP disease spectrum, especially for those with severe illness. When treating community-associated, methicillin-resistant Staphylococcus aureus pneumonia, use of an antitoxin antibiotic is likely to be valuable. Adjunctive therapy with corticosteroids may prevent delayed clinical resolution in selected patients with severe CAP. Recent data expand on the interaction of CAP with comorbid disease, particularly cardiovascular disease, and its impact on mortality in CAP patients. Summary Improved diagnostic tools, optimized treatment regimens, and enhanced understanding of CAP-induced perturbations in comorbid disease states hold promise to improve patient outcomes.

Kawasaki disease is an acute, self-limited, febrile vasculitis typically seen in early childhood. Pulmonary involvement is uncommon and is not part of the conventional diagnostic criteria. We add to the literature a unique case of a 22year-old male with Kawasaki disease and pulmonary involvement. It illustrates the importance of recognizing unusual presentations of Kawasaki disease and highlights the possibility of pulmonary abnormalities on physical and imaging examination. Awareness of such presentations can help avoid delayed diagnosis, prevent the development of coronary aneurysms, and allow careful observation for imaging resolution.

Human immunodeficiency virus (HIV) infection is associated with an increased risk of venous thrombosis compared to that of the general population. In addition to traditional risk factors for venous thromboembolism (VTE) such as age, smoking and hospitalization, several of which are more prevalent in HIV-infected individuals, HIV-specific factors including the degree of immunosuppression, presence of opportunistic infections and malignancy, HIV-related coagulation abnormalities and medications used in the treatment of HIV, also contribute to this increased risk. The incidence of arterial thrombosis and cardiovascular disease is also increased in HIV infection, and VTE and arterial thrombosis share many risk factors. Importantly, increased chronic inflammation and immune activation persist in HIV infection even despite effective antiretroviral therapy and play an important role in these disease processes. Given the increased incidence of thrombosis in HIV, it is important that clinicians are alert to the condition in this population. Additionally, a diagnosis of HIV should be considered in individuals presenting with unexplained VTE.

More than a decade in the making, a new, legally binding treaty on mercury will be adopted by governments in the fall of 2013. The treaty's objective is to protect human health and the environment from anthropogenic mercury emissions through a range of provisions - including an article devoted to reducing exposure to mercury. Global emissions have increased since 2005, with the environmental health burden increasingly shifting to developing countries. Time is of the essence to reduce pollution because (i) exposure risk to mercury is much greater than previously thought and (ii) mercury already in the environment can be re-emitted via processes in the natural cycle, resulting in a longer lag time before pollution reduction can have a demonstrable effect on the food chain. Health professionals can assist in reducing exposure, choosing mercury-free products and urging governments to ratify the treaty as quickly as possible so that it can take effect.

Community-acquired pneumonia (CAP) encompasses a broad spectrum of disease severity and may require outpatient, inpatient, or intensive care management. Successful treatment hinges on expedient delivery of appropriate antibiotic therapy tailored to both the likely offending pathogens and the severity of disease. This review summarizes key principles in starting treatment and provides recommended empiric therapy regimens for each site of care. In addition, we discuss the antimicrobial and anti-inflammatory role macrolides play in CAP, as well as specific information for managing individual CAP pathogens such as community-acquired methicillin-resistant Staphylococcus aureus and drug-resistant Streptococcus pneumoniae. We also examine several novel antibiotics being developed for CAP and review the evidence guiding duration of therapy and current best practices for the transition of hospitalized patients from intravenous antibiotics to oral therapy.

Community-acquired pneumonia (CAP) is the leading cause of death from infectious disease in North America, accounting for over 60,000 deaths in the United States in 2005 (1). CAP encompasses a wide range of clinical presentations resulting in variable clinical outcomes. While mild forms lead to mortality in less than 5% and may be safely treated in outpatient settings, more severe forms necessitate intensive care unit (ICU) admission and are associated with mortality rates exceeding 30% (2).

Published guidelines for community-acquired pneumonia (CAP) have informed management and treatment recommendations for 25 years. Since inception, CAP guidelines have been developed for nearly every region of world, in part owing to improved mortality, clinical outcomes, and costs associated with implementation of guideline based care. This review highlights reasons why guidelines remain useful, overviews the similarities and differences among global CAP guidelines, and focuses on the treatment principles underpinning management recommendations, and addresses treatment issues that should be resolved in future CAP guidelines.