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  Vol. 142 No. 1, January 1988 TABLE OF CONTENTS
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HIV Embryopathy and Neurocristopathies-Reply

ROBERT W. MARION, MD; ANDREW A. WIZNIA, MD; R. GORDON HUTCHEON, MD; ARYE RUBINSTEIN, MD
Department of Pediatrics Albert Einstein College of Medicine 1300 Morris Park Ave Bronx, NY 10461

Am J Dis Child. 1988;142(1):10-11.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In Reply.—Dr Calvani raises a tantalizing possible explanation for the craniofacial dysmorphism observed in children with evidence of intrauterine HIV infection.1,2 The basis of this theory is that some fundamental interference occurs with the development and migration of cells of the neural crest. This phenomenon would then lead to abnormalities in the structures derived from these cells, namely, the craniofacies, the cardiovascular system, the parathyroid glands, and the thymus. The possible causes of this interference are multiple and include single-gene mutations, chromosomal aberrations, and teratogenic agents. Dr Calvani proposes that in both the fetal AIDS syndrome and the retinoic acid embryopathy, the cause is a teratogen.

This theory has previously been advanced by Lammer et al3 for retinoic acid embryopathy. These authors, noting a recognizable pattern of altered morphogenesis involving the craniofacies, heart, thymus, and brain, postulated that a single mechanism, namely, a deficiency of branchial arch . . . [Full Text PDF of this Article]



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