SARS-CoV-2 is a new virus, to which herd immunity has not yet developed and both molecular and serological testing are not without flaws. The virus evokes a state of severe and widespread inflammation, and stimulates both innate and adaptive immune response. The angiotensin-converting enzyme 2 (ACE2), which acts as the SARS-CoV-2 receptor, is present in endothelial cells and has been noted within the human placenta. There are questions about whether pregnancy would increase the susceptibility of pregnant women to COVID-19 and disease severity within this population. In this report, we highlight physiological and immune/inflammatory considerations that may explain the susceptibility and disease pathology in response to SARS CoV-2 during pregnancy, explore testing considerations in asymptomatic individuals, discuss the potential role and of placental ACE2 receptor in the pathogenesis of COVID-19 in pregnancy and in pregnancy outcomes, and finally share our perspective with respect to an urgently needed change concerning involvement of pregnant women in research addressing COVID-19.

Vaccine-induced immune thrombotic thrombocytopenia (VITT) has been reported in association with the coronavirus disease 2019 preventative adenovirus vector-based vaccines ChAdOx1 nCoV-19 (Oxford/AstraZeneca) and Ad26.COV2.S (Janssen/Johnson & Johnson) in hundreds of recipients across the globe. VITT is characterized by thrombosis, typically at unusual sites, low fibrinogen, and elevated plasma D-dimer, generally manifesting between 4 and 28 days following vaccination. Detection of anti-platelet factor antibodies using an enzyme-linked immunosorbent assay (ELISA) is often confirmatory. Although several similar principles subside in most diagnostic criteria for VITT, the presentation of a positive ELISA assay, use of expert hematology and neurology opinion, and exclusion of possible VITT cases outside the “standard” 4 to 28-day timeframe have contributed a lack of global standardization for defining VITT. Accordingly, the global and regional incidence of VITT differs according to the diagnostic pathway and case definition used. This has influenced the public perception of VITT's severity and the decision to use adenovirus vector-based vaccines for limiting severe acute respiratory syndrome coronavirus 2 infection. We hereby delineate the recognized pathogenic mechanisms, global incidence, discrepancies in diagnostic criteria, recommended treatments, and global implications to vaccine hesitancy from this coagulopathy.

Thrombosis is one of the leading causes of death in cancer. Cancer-induced hypercoagulable state contributes to thrombosis and is often overlooked. Prostate cancer may not be of high thrombogenic potential compared with other cancers, but its high prevalence brings it into focus. Pathological evidence for venous thromboembolisms (VTEs) in prostate cancer exists. Factors such as age, comorbidities, and therapies increase the VTE risk further. There is a need to systematically identify the risk of VTE in regard to patient-, cancer-, and treatment-related factors to risk stratify patients for better-targeted and individualized strategies to prevent VTE. Sensitive tests to enable such risk assessment are urgently required. There is sufficient evidence for the utility of thromboelastography (TEG) in cancer, but it is not yet part of the clinic and there is only limited data on the use of TEG in prostate cancer. One study revealed that compared with age-matched controls, 68.8% of prostate cancer patients demonstrated hypercoagulable TEG parameters. The absence of clinical guidelines is a limiting factor in TEG use in the cancer population. Cancer heterogeneity and the unique cancer-specific microenvironment in each patient, as well as determining the hypercoagulable state in each patient, are added limitations. The way forward is to combine efforts to design large multicenter studies to investigate the utility and clinical effectiveness of TEG in cancer and establish longitudinal studies to understand the link between hypercoagulable state and development of thrombosis. There is also a need to study low thrombogenic cancers as well as high thrombogenic ones. Awareness among clinicians and understanding of test applicability and interpretation are needed. Finally, expert discussion is critical to identify the investigation priorities.

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