Corrigendum: Platelet Counts and Patent Ductus Arteriosus in Preterm Infants: An Updated Systematic Review and Meta-Analysis

[This corrects the article DOI: 10.3389/fped.2020.613766.].Copyright © 2021 González-Luis, Ghirardello, Bas-Suárez, Cavallaro, Mosca, Clyman and Villamor

Platelet Counts and Patent Ductus Arteriosus in Preterm Infants: An Updated Systematic Review and Meta-Analysis

Background: A meta-analysis published in 2015 showed a significant association between low platelet counts in the first day(s) of life and risk of patent ductus arteriosus (PDA). The meta-analysis pooled data from 11 studies cohorts (3,479 preterm infants).Objective: To update the meta-analysis by adding new studies on the topic and including other platelet parameters different from platelet counts.Methods: PubMed/Medline and Embase databases were searched. Random-effects risk ratios (RR) and differences in means (DM) and 95% confidence intervals (CI) were calculated.Results: We included 31 studies (7,638 infants). Meta-analysis showed that the risk of developing any PDA was significantly associated with platelet counts<150 x 10(9)/L (11 studies, RR 1.58, 95% CI 1.28 to 1.95), and <100 x 10(9)/L (7 studies, RR 1.61, 95% CI 1.14 to 2.28), but not <50 x 10(9)/L (4 studies, RR 1.34, 95% CI 0.77 to 2.32). Risk of developing hemodynamically significant PDA (hsPDA) was significantly associated with platelet counts<150 x 10(9)/L (12 studies, RR 1.33, 95% CI 1.09 to 1.63), and <100 x 10(9)/L (7 studies, RR 1.39, 95% CI 1.06 to 1.82), but not <50 x 10(9)/L (6 studies, RR 1.24, 95% CI 0.86 to 1.79). Infants with hsPDA had significantly lower mean platelet counts (19 studies, DM 22.0 x 10(9), 95% CI 14.9 to 29.1) and platelet mass (11 studies, DM 214.4, 95% CI 131.2 to 297.5) and significantly higher platelet distribution width (PDW, 9 studies, DM -0.53, 95% CI -1.01 to -0.05) than infants without hsPDA. Meta-analysis could not demonstrate significant differences in mean platelet volume (MPV).Conclusion: Compared to the previous analysis, this updated meta-analysis included 21 additional studies that provide stronger evidence of the association between low platelet counts and PDA/hsPDA. Other platelet parameters such as platelet mass and PDW are also associated with hsPDA risk. However, the low number of platelets may be an epiphenomenon associated with the maturity and clinical stability of preterm infants rather than a contributing factor in the pathogenesis of PDA

Integrin α1β1 (VLA-1) mediates adhesion of activated intraepithelial lymphocytes to collagen

Intraepithelial lymphocytes (IELs) from human intestinal epithelium are memory CD8+ T cells that bind to epithelial cells through human mycosal lymphocyte (HML)-1 and to mesenchymal cells through very late activation antigen-4 (VLA-4). Their binding of extracellular matrix proteins and the mechanism involved were tested. Activated 51Cr-labelled lymphocytes were incubated in protein-coated microwells with various additives. After washing, the adherent cells were detected by radioactivity. The percentages of activated IELs that bound to collagen types I and IV were 20 and 31%, respectively; fewer bound to fibronectin or laminin. Compared to interleukin-2-activated peripheral blood CD8+ T lymphocytes, more IELs bound collagen IV and fewer bound fibronectin. IEL adhesion to collagen (but not fibronectin or laminin) was up-regulated by antibody ligation of CD2 or by protein kinase C stimulation by phorbol ester; staurosporine reduced binding, while herbimycin, phytohaemagglutinin and CD3 ligation had no effect. Antibody-blocking of integrin VLA-1 subunits α1 (CD49a) and β1 (CD18) inhibited adhesion to collagen type I by 82±6% and to type IV by 94±1% (P < 0·001), implicating VLA-1 as the main collagen receptor for IELs. Cell adhesion was dependent on extracellular divalent cations, a characteristic event of VLA-1 never before shown for IELs: manganese and magnesium ions supported binding in a dose-dependent manner; calcium ions inhibited their effectiveness. Therefore, IELs bind collagen through integrin α1β1 after protein kinase C activation. Adhesion is modulated by divalent cations