Literature DB >> 15562030

Neonatal lethal osteochondrodysplasia with low serum levels of alkaline phosphatase and osteocalcin.

Myra H Wyckoff1, Chirine El-Turk, Abbot Laptook, Charles Timmons, Francis H Gannon, Xiafang Zhang, Steven Mumm, Michael P Whyte.   

Abstract

Neonatal lethal skeletal dysplasias are rare and typically involve thoracic malformations and severe limb shortening. We report on a newborn boy manifesting an osteochondrodysplasia associated with fatal respiratory insufficiency who had normal lung volumes and extremity lengths. His disorder featured aberrant skeletal patterning and defective ossification including a severely osteopenic skull, apparent absence of clavicles, and clefting of the mandible and vertebrae. Serum alkaline phosphatase and osteocalcin levels were markedly low. Biochemical studies suggested parathyroid insufficiency probably from critical illness. Histopathology at autopsy excluded impaired mineralization of skeletal matrix, but endochondral bone formation appeared disorganized with growth plate clustering of chondrocytes in hypertrophic zones and in zones of provisional calcification. Parathyroid glands were not found. Despite features of two distinctive heritable entities, hypophosphatasia and cleidocranial dysplasia, the cumulative findings did not match either condition, and no mutations were found in either the tissue nonspecific ALP isoenzyme or core-binding factor genes, respectively, or in the genes encoding osteocalcin or the osteoblast transcription factor osterix. This patient could represent the extreme of cleidocranial dysplasia (a disorder not always associated with structural mutation in core-binding factor A1), but more likely he defines a unique osteochondrodysplasia disrupting both intramembranous and endochondral bone formation.

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Year:  2004        PMID: 15562030     DOI: 10.1210/jc.2004-0251

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  4 in total

1.  Severe cleidocranial dysplasia and hypophosphatasia in a child with microdeletion of the C-terminal region of RUNX2.

Authors:  Areeg H El-Gharbawy; Joseph N Peeden; Ralph S Lachman; John M Graham; Stephen R Moore; David L Rimoin
Journal:  Am J Med Genet A       Date:  2010-01       Impact factor: 2.802

Review 2.  Hypophosphatasia.

Authors:  Agnès Linglart; Martin Biosse-Duplan
Journal:  Curr Osteoporos Rep       Date:  2016-06       Impact factor: 5.096

Review 3.  Hypophosphatasia: an overview of the disease and its treatment.

Authors:  M L Bianchi
Journal:  Osteoporos Int       Date:  2015-08-06       Impact factor: 4.507

Review 4.  Alkaline Phosphatase Replacement Therapy for Hypophosphatasia in Development and Practice.

Authors:  S A Bowden; B L Foster
Journal:  Adv Exp Med Biol       Date:  2019       Impact factor: 2.622

  4 in total

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