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Extra resources for Congenital Endocrinopathies

Sample text

Similar results on SGA but not in TS were found by Binder et al. [25]: these authors studied 2 cohorts of short subjects, 53 TS and 60 short SGA, in a retrospective way. The distribution of the GHR genotypes was not significantly different between controls, short children born SGA and TS girls. With regard to the efficacy of GH treatment, in TS the increment in GV in the first year of GH therapy was significantly higher in both the d3/d3 group as compared with the d3/fl ϩ fl/fl group and in the pooled d3 group compared to the sole homozygous fl subjects.

He inherited 2 different GHR mutations, each from a single parent. These were both nonsense mutations, leading to a stop codon. From the father he received a mutation in exon 4, already described, and from his mother a mutation in exon 3, where no mutation had been described before. The 2 heterozygous parents had a normal phenotype, both carrying a null GHR allele in combination with either a normal GHRfl or GHRd3 allele (in father and mother, respectively). Therefore, the authors could conclude that a single copy of either GHRfl or GHRd3 is sufficient for normal growth.

Additional neurodevelopmental Lin/Ferraz-de-Souza/Achermann 38 Pitx1 Tpit ␣-MSH/␤-MSH ␤-endorphin ACTH POMC PC1 Fig. 2. Diagrammatic representation of the processes involved in POMC synthesis and cleavage in the corticotrope. PC1 ϭ Prohormone convertase-1. (Modified with permission from Lin and Achermann [2]; copyright 2004, Blackwell Publishing Ltd). defects such as absent septum pellucidum or optic nerve hypoplasia may be present. A number of genetic causes of congenital hypopituitarism have been reported in the past decade.

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