Milo Zachmann

TL;DR: It is concluded that the clinical and biochemical expression of 11 beta-hydroxylase deficiency is variable, that hypertension in not directly related to deoxycorticosterone, and that, regardless of the intensity of the defect, there are patients in whom the 11 Beta-Hydroxylation of 17 alpha-hydroxyylated steroids only is impaired.

TL;DR: The nucleotide sequence of the two highly homologous genes encoding 3β–HSD isoenzymes in three classic 3β-HSD deficient patients belonging to two apparently unrelated pedigrees is described, providing the first elucidation of the molecular basis of this disorder.

TL;DR: Close genetic linkage between HLA-B and 21-hydroxylase deficiency was established and a link between congenital adrenal hyperplasia and HLA was established.

TL;DR: It is concluded that calculations based on coefficients and regression equations obtained from normal children (as in the Roche-Wainer-Thissen and Tanner methods) can only be used in normal children or in patients with normal growth potential under adequate treatment.

TL;DR: It is concluded that testosterone exerts its full growth-promoting action only in the presence of normal endogenous GH secretion or with sufficient hGH replacement and that both hormones should be continued simultaneously until final adult height is achieved.