Literature DB >> 1934534

Laron-type dwarfism with apparently normal high affinity serum growth hormone-binding protein.

C R Buchanan1, H G Maheshwari, M R Norman, D J Morrell, M A Preece.   

Abstract

OBJECTIVE: Normal serum contains a high affinity GH-binding protein, which appears to be identical with the extracellular domain of the GH receptor. It is normally absent from the serum of patients with Laron-type dwarfism. We wished in this study to define the serum GH-binding protein status of a family with Laron-type dwarfism. DESIGN AND PATIENTS: We performed an open case study of an Asian family in which three sisters (aged 3 to 15 years) had the phenotype of Laron-type dwarfism. Sera from a fourth, unrelated girl with Laron-type dwarfism and subjects without endocrine disorders were used as control samples. MEASUREMENTS: Laron-type dwarfism was confirmed by demonstration of elevated serum GH levels and low serum IGF-I levels on immunoassay, with serum IGF-I levels failing to rise during treatment with GH. Serum GH-binding proteins were characterized using gel chromatography on Sephacryl S-100HR following incubation of serum with 125I-GH, Scatchard analysis of ligand binding, and by polyacrylamide gel electrophoresis after covalent cross-linking to 125I-GH.
RESULTS: All members of the family had high affinity serum GH-binding protein activity similar in size, circulating levels and apparent affinity for GH to that of normal subjects. This contrasted with the very low serum GH-binding protein activity in the unrelated child with Laron-type dwarfism and previous reports of serum GH-binding protein levels in this disorder.
CONCLUSIONS: The affected patients may possess a novel biochemical defect which results in GH-resistance and reduced production of IGF-I in the presence of normal serum GH-binding protein levels.

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Year:  1991        PMID: 1934534     DOI: 10.1111/j.1365-2265.1991.tb03518.x

Source DB:  PubMed          Journal:  Clin Endocrinol (Oxf)        ISSN: 0300-0664            Impact factor:   3.478


  3 in total

1.  Pseudoexon activation as a novel mechanism for disease resulting in atypical growth-hormone insensitivity.

Authors:  L A Metherell; S A Akker; P B Munroe; S J Rose; M Caulfield; M O Savage; S L Chew; A J Clark
Journal:  Am J Hum Genet       Date:  2001-07-20       Impact factor: 11.025

2.  An update on Laron syndrome.

Authors:  Z Laron
Journal:  Arch Dis Child       Date:  1993-03       Impact factor: 3.791

3.  A single amino acid substitution in the exoplasmic domain of the human growth hormone (GH) receptor confers familial GH resistance (Laron syndrome) with positive GH-binding activity by abolishing receptor homodimerization.

Authors:  P Duquesnoy; M L Sobrier; B Duriez; F Dastot; C R Buchanan; M O Savage; M A Preece; C T Craescu; Y Blouquit; M Goossens
Journal:  EMBO J       Date:  1994-03-15       Impact factor: 11.598

  3 in total

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