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Amniotic band syndrome: Reevaluation of its pathogenesis

  • Charles Lockwood
    Correspondence
    Reprint requests: Charles Lockwood, MD, Department of 'Maternal Fetal Medicine, Tufts University School of Medicine, St. Margaret's Hospital for Women, 90 Cushing Ave., Boston, MA 02125
    Affiliations
    Division of Maternal-Fetal Medicine, Department of Obstetris and Gynecology, Tufts University School of Medicine, Boston, and Yale Univesity School of Medicine, Boston, Massachusetts, and New Haven, Connecticut
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  • Alessandro Ghidini
    Affiliations
    Division of Maternal-Fetal Medicine, Department of Obstetris and Gynecology, Tufts University School of Medicine, Boston, and Yale Univesity School of Medicine, Boston, Massachusetts, and New Haven, Connecticut
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  • Roberto Romero
    Affiliations
    Division of Maternal-Fetal Medicine, Department of Obstetris and Gynecology, Tufts University School of Medicine, Boston, and Yale Univesity School of Medicine, Boston, Massachusetts, and New Haven, Connecticut
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  • John C. Hobbins
    Affiliations
    Division of Maternal-Fetal Medicine, Department of Obstetris and Gynecology, Tufts University School of Medicine, Boston, and Yale Univesity School of Medicine, Boston, Massachusetts, and New Haven, Connecticut
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      Abstract

      Amniotic band syndrome is a poorly defined entity characterized by protean fetal malformations and disruptions. The pathogenic theory widely accepted in the obstetric literature is that the formation of fibrous amniotic bands is the initiating event in the disorder and is responsible for subsequently pathologic conditions. A critical review of the recent clinical and experimental literature appears to contradict this hypothesis. Evidence suggests that amniotic band syndrome results from a multifactorial process in which vascular compromise, specifically hemorrhage, is the principal pathogenic stimulus and that the fibrous bands are a late, reparative event of little or no pathogenic significance. (AM J OBSTET GYNrECOL 1989;160:1030-3.)

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