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Bone Modeling Alteration in Premature Infants

Stefano Mora, MD; H San Raffaele; Giovanna Weber, MD; Aldo Bellini, MD; Cesare Bianchi, MD; Giuseppe Chiumello, MD
Arch Pediatr Adolesc Med. 1994;148(11):1215-1217. doi:10.1001/archpedi.1994.02170110101021.
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Osteopenia is a well-recognized disorder of bone metabolism among premature infants.1 -6 Its cause is thought to be complex, with dietary deficiency being a major causative factor. Impairment of bone modeling has also been hypothesized, but extensive studies in infants have not been possible not only because of the invasive procedures required but also because of the lack of specificity of the widely used biochemical indexes of bone formation and resorption. Recently, new specific biochemical markers of bone modeling became available.

Type I collagen accounts for more than 90% of the organic bone matrix.7 It is derived from a larger protein, type I procollagen, which has propeptide extensions at both ends of the molecule.8 Procollagen type I carboxyterminal propeptide (PICP), a trimeric globular protein, is removed by specific proteinases before collagen molecules are assembled into fibers. Procollagen propeptides are released into circulation in a stoichiometric ratio of

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