As the Coronavirus disease 2019 (COVID-19) pandemic, which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is spreading rapidly worldwide, it has emerged as a leading cause of mortality resulting in more than one million deaths over the past ten months. The pathophysiology of COVID-19 still remains unclear, posing a great challenge to the medical management of patients. Recent studies have reported unusually high prevalence of thromboembolic events in COVID-19 patients, although the mechanism remains elusive. Several studies have reported the presence of antiphospholipid antibodies in COVID-19 patients. We have noticed similarities between COVID-19 and the antiphospholipid syndrome, which is an autoimmune prothrombotic disease that is often associated with an infective aetiology. Molecular mimicry and endothelial dysfunction could plausibly explain the mechanism of thrombogenesis in acquired antiphospholipid syndrome. Here in this review, we discuss the clinicopathological similarities between COVID-19 and the antiphospholipid syndrome, and a potential role of therapeutic targets based on the antiphospholipid model for COVID-19 disease.

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Multiple myeloma is the second most common hematologic malignancy in the world. Despite improvement in outcome, the disease is still incurable for most patients. However, not all myeloma are the same. With the same treatment, some patients can have very long survival whereas others can have very short survival. This suggests that there is underlying heterogeneity in myeloma. Studies over the years have revealed multiple layers of heterogeneity. First, clinical parameters such as age and tumor burden could significantly affect outcome. At the genetic level, there are also significant heterogeneity ranging for chromosome numbers, genetic translocations, and genetic mutations. At the clonal level, there appears to be significant clonal heterogeneity with multiple clones coexisting in the same patient. At the cell differentiation level, there appears to be a hierarchy of clonally related cells that have different clonogenic potential and sensitivity to therapies. These levels of complexities present challenges in terms of treatment and prognostication as well as monitoring of treatment. However, if we can clearly delineate and dissect this heterogeneity, we may also be presented with unique opportunities for precision and personalized treatment of myeloma. Some proof of concepts of such approaches has been demonstrated.

We read with interest the recent editorial by B os et al. [1] on the perils of premature phenotyping in coronavirus disease 2019 (COVID-19). The authors concluded that a normal compliance variant of acute respiratory distress syndrome (ARDS) does not exist, based on two small cohort studies reporting low respiratory system compliance in COVID-19 patients [2, 3]. However, this assumption may be erroneous, as, first, the admission and intubation thresholds are highly variable across units, resulting in marked heterogeneity. Secondly, several studies demonstrate that a high proportion of mechanically ventilated COVID-19 patients exhibit near-normal lung compliance [4–6].