Therapeutic Plasma Exchange: A potential Management Strategy for Critically Ill COVID-19 Patients

In the 5 months since initial reports of COVID-19 came to light, the death toll due to SARS-CoV-2 has rapidly increased. The morbidity and mortality of the infection varies based upon patient age, comorbid conditions, viral load, and the availability of effective treatments. Findings from limited autopsies, clinical observations, and laboratory data suggest that high cytokine levels and a procoagulant state can precipitate acute respiratory distress syndrome and multi-organ dysfunction syndrome in critically ill patients. To complicate matters, comorbidities may affect the response to medical treatments currently in use, all of which are still in trial phase. Therapeutic plasma exchange (TPE) merits consideration in the treatment of critically ill COVID-19 patients and is an avenue for clinical trials to pursue. If efficacious, faster recovery of patients may lead to shorter intensive care unit stays and less time on mechanical ventilation. Herein, we briefly discuss some of the various approaches currently being investigated for the treatment of SARS-CoV-2 with a focus on potential benefits of TPE for selected critically ill patients. </jats:p

Paradoxical cadherin-catenin immunostaining in a case of invasive mammary carcinoma with ductal and lobular differentiation: A molecular correlation

We present a 66-year-old woman with right breast invasive mammary carcinoma with distinct areas consisting of lobular and tubular morphology. The areas with lobular morphology paradoxically demonstrated intact membranous expression of E-cadherin, membranous p120 expression, with loss of beta-catenin. In this lobular appearing area of tumor, massive parallel sequencing identified a p. Y835* (c.2504_2505del) variant in the CDH1 gene, which results in premature termination in the last exon and a truncated protein. The areas with tubular morphology unexpectedly demonstrated lack of E-cadherin and beta-catenin expression along with cytoplasmic p120 expression. In this tubular appearing area of tumor, massive parallel sequencing identified a variant in CDH1 at the exon–intron boundary (c.1711 G > A). Proposed mechanisms for absence of E-cadherin protein in this area include aberrant mRNA splicing or protein misfolding resulting from the missense alteration. Nevertheless, a genetic and phenotypic correlation in both morphologically distinct areas of the tumor is evident