Elsevier

The Journal of Pediatrics

Volume 97, Issue 5, November 1980, Pages 834-836
The Journal of Pediatrics

Brief clinical and laboratory observation
Cortical hyperostosis following long-term administration of prostaglandin E1 in infants with cyanotic congenital heart disease

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    Both can induce cortical hyperostosis when upregulated [25, 30, 31]. Long-term PGE administration in children with ductus-dependent cyanotic congenital heart disease is associated with new bone formation [30]. In Ghosal syndrome, the characteristic increased bone density with predominant diaphyseal involvement is believed to be the result of elevated levels of PGE caused by homozygous missense variants in TBXAS1, encoding the enzyme thromboxane synthase, which converts prostaglandins to thromboxane A2 [32].

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    Thus, suggesting inflammation in Caffey disease to be a local matrix-driven process. 3) Upregulation of COX2/PGE axis and transforming growth factor (TGFβ) signaling have been shown to cause cortical hyperostosis in humans [17,33]. Taken together, these observations argue for a pathogenesis driven not necessarily by gross structural or quantitative defects in type I collagen fibrils, but by a subtle alteration in ECM composition that may affect cell signaling as a result of impaired collagen interactions.

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