Longer ICU stay and invasive mechanical ventilation accelerate telomere shortening in COVID-19 patients 1 year after recovery.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes virus-induced-senescence. There is an association between shorter telomere length (TL) in coronavirus disease 2019 (COVID-19) patients and hospitalization, severity, or even death. However, it remains unknown whether virus-induced-senescence is reversible. We aim to evaluate the dynamics of TL in COVID-19 patients 1 year after recovery from intensive care units (ICU). Longitudinal study enrolling 49 patients admitted to ICU due to COVID-19 (August 2020 to April 2021). Relative telomere length (RTL) quantification was carried out in whole blood by monochromatic multiplex real-time quantitative PCR (MMqPCR) assay at hospitalization (baseline) and 1 year after discharge (1-year visit). The association between RTL and ICU length of stay (LOS), invasive mechanical ventilation (IMV), prone position, and pulmonary fibrosis development at 1-year visit was evaluated. The median age was 60 years, 71.4% were males, median ICU-LOS was 12 days, 73.5% required IMV, and 38.8% required a prone position. Patients with longer ICU-LOS or who required IMV showed greater RTL shortening during follow-up. Patients who required pronation had a greater RTL shortening during follow-up. IMV patients who developed pulmonary fibrosis showed greater RTL reduction and shorter RTL at the 1-year visit. Patients with longer ICU-LOS and those who required IMV had a shorter RTL in peripheral blood, as observed 1 year after hospital discharge. Additionally, patients who required IMV and developed pulmonary fibrosis had greater telomere shortening, showing shorter telomeres at the 1-year visit. These patients may be more prone to develop cellular senescence and lung-related complications; therefore, closer monitoring may be needed.

Acquired von Willebrand Syndrome in a Patient Undergoing Extracorporeal Membrane Oxygenation: A Case Report.

Acquired von Willebrand syndrome (AvWS) is a rare bleeding disorder caused by dysfunction of the von Willebrand factor (vWF), leading to bleeding manifestations. It usually occurs due to an underlying disorder in patients with no family or personal history of bleeding diathesis. The exact mechanism causing this syndrome is not fully understood, but it involves a complex interplay of factors. Specifically, vWF deficiency or reduced activity can occur due to antibodies, adsorption of vWF onto tumor cells, shear stress, or increased proteolysis. We describe a patient with severe, right-sided heart failure secondary to idiopathic pulmonary hypertension. The patient was admitted to the intensive care unit to be placed on a venoarterial extracorporeal membrane oxygenation (VA ECMO) machine while awaiting bilateral lung transplantation. A few hours after initiation of VA ECMO, the patient experienced epistaxis and continuous bleeding from the cannula tips. The laboratory investigations were based on the measurements of vWF antigen (vWF:Ag), vWF ristocetin cofactor activity (vWF:RCo), and multimer analysis. The obtained results revealed a decreased VWF:RCo/VWF:Ag ratio (<0.7) and the loss of high-molecular-weight multimers of vWF, thus confirming the diagnosis of AvWS. This report reviews how to make the clinical diagnosis of AvWS, including a discussion of necessary laboratory results and their pitfalls, and highlights the importance of having a high index of suspicion of AvWS in the ECMO population so that laboratory values are obtained on time to allow for treatment and successful recovery.

Infiltración meníngea de linfoma linfoplasmocítico: síndrome de Bing-Neel / Meningeal infiltration by lymphoplasmacytic lymphoma: Bing-Neel syndrome

La macroglobulinemia de Waldenström es un linfoma linfoplasmocítico caracterizado por una proliferación monoclonal de linfocitos B productores de inmunoglobulina M que infiltran la médula ósea. Las manifestaciones neurológicas asociadas a la macroglobulinemia de Waldenström suelen ser debidas al fenómeno de hiperviscosidad o a neuropatías desmielinizantes mediadas por inmunoglobulina M. Cuando la afectación neurológica es debida a la infiltración del sistema nervioso central por las células linfoplasmocitoides, se produce un síndrome denominado de Bing-Neel, con baja prevalencia y variedad de manifestaciones clínicas. Se presenta el caso clínico de una mujer de 76 años con antecedentes de macroglobulinemia de Waldenström, con un cuadro neurológico repentino de alteración del lenguaje y torpeza en la mano derecha. Cabe destacar la relevancia del laboratorio clínico en el diagnóstico del síndrome de Bing-Neel y en el seguimiento del tratamiento (AU)

Waldenström macroglobulinemia is a lymphoplasmacytic lymphoma defined by a monoclonal proliferation of bone marrow infiltrating immunoglobulin M producing B lymphocytes. Neurological simptoms of Waldenström macroglobulinemia are mainly dominated by signs of hyperviscosity and autoimmune neuropathies mediated by immunoglobulin M. Neurological involvement secondary to the infiltration of IgM producing B lymphocytes, is defined as a Bing-Neel syndrome. This syndrome has a low prevalence and the clinical manifestations are variable. The case described is about a 76 year-old female with a history of Waldenström macroglobulinemia, who presents sudden neurological signs such as alteration of spoken language and clumsiness of the right hand. The clinical laboratory has a primary role in the diagnosis of Bing-Neel syndrome and monitoring of the treatment (AU)