Pleural Effusions Identified by Point-of-Care Ultrasound Predict Poor Outcomes in Decompensated Cirrhosis.

Chronic liver disease (CLD) may be associated with pleural effusions (PEs). This article prospectively evaluates whether detection of PEs on thoracic ultrasound (TUS) at the bedside independently predicts mortality and length of stay (LOS) in hospitalized patients with a decompensated CLD. A total of 116 consecutive inpatients with decompensated cirrhosis underwent antero-posterior chest radiographs (CXR) and TUS to detect PEs. Their median age was 54 y (interquartile range, 47-62), 90 (70.6%) were male, and 61 (52.6%) fell into the Child-Pugh class C categorization. TUS identified PEs in 58 (50%) patients, half of which were small enough to preclude thoracentesis. CXR failed to recognize approximately 40% of PEs seen on TUS. The identification of PEs by TUS was associated with a longer LOS (10 vs. 5.5 d, p < 0.001) and double mortality (39.7% vs. 20.7%, p = 0.021). In multivariate analysis, PEs were independently related to poor survival (hazard ratio 2.08, 95% confidence interval [CI] 1.02-4.25; p = 0.044). Patients with both Child-Pugh C stage and PEs had the lowest survival rate (70 vs. 317 d, p = 0.001). In conclusion, PEs identified by TUS in hospitalized patients with decompensated CLD independently predict a poor outcome and portend a longer LOS.

Altered detection of molecules associated with leukocyte traffic in HUVECs derived from newborns with a strong family history of myocardial infarction.

Atherosclerosis is a chronic inflammatory disease. As such, recruitment of immune cells is a significant event. Tightly controlled signaling molecules regulate leukocyte adhesion and migration to the tissues. The aim of this study was to determine if human umbilical vein endothelial cells (HUVECs) derived from healthy newborns with a strong family history of myocardial infarction (FHMI) showed variations in the presence of molecules related with leukocyte traffic and migration, in comparison to control healthy newborns. For this purpose, we evaluated the labeling of sialic acid containing glycoproteins, tight junction claudins and the cytoskeleton, using lectin- and immunocytochemistry in HUVECs from individuals with and without a strong FHMI. Our results show important differences in the labeling of alpha-2,3 or alpha-2,6 sialic acid-containing glycoconjugates, a disarrangement of actin filaments secondary to the absence of cytoplasmic claudin-5 immunopositivity and an increase in the binding of FHMI HUVECs to CD3+ Jurkat cells. It is possible that these differences relate to a predisposition for early appearance of atherosclerotic lesions.