Disorders of Adrenal Steroid Biogenesis

Bongiovanni, Alfred M.; Eberlein, Walter R.; Goldman, Alvin I.; New, Maria I.

doi:10.1016/b978-1-4831-9826-2.50012-x

Cited by 46 publications

(28 citation statements)

References 109 publications

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“…This relation is already known [7] but it does not explain the interrelation between sodium and cortisol. These children also have a very low ASR; thus, although the cortisol insufficiency associated with the salt loss could be a causative factor due to lack of the 'permissive' effect of cortisol [8], and although the presence of a salt-excreting factor in the precursors could play a role, the major factor may well be, quite simply, the inadequate ASR which is a constant association.…”

Section: Loras Haour and Bertrandmentioning

confidence: 99%

“…7,8,9, and 10) showed low sodium levels in plasma, and in the three cases in which it was studied, the Na, showed a severe deficit. The negative sodium balance in these infants would, therefore, appear to arise very early and, probably, as suggested by BONGIOVANNI et al [8] dates from the time of birth.…”

Section: Sodiummentioning

confidence: 99%

“…8,9, and lo), and in the other subjects during salt restriction (case nos. 15, 16, 21, and 25), clinical signs of salt loss appeared.…”

Section: Sodiummentioning

confidence: 99%

“…Three hypotheses have been put forward to explain the presence or absence of salt loss in CAH due to 21-hydroxylase deficiency [8]. Firstly, it has been suggested that there may be two adrenal 21-hydroxylases acting on two types of substrates, steroids with an hydroxyl group at C-17, and precursors of aldosterone.…”

Section: Factors Involved In Salt Lossmentioning

confidence: 99%

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Exchangeable Sodium and Aldosterone Secretion in Children with Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency

1970

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Aldosterone secretion rates (ASR) and exchangeable body sodium (Na,) have been measured simultaneously in 25 cases of congenital adrenal hyperplasia (CAH) with and without salt loss, both during normal and during low salt intake. The degree of 21 -hydroxylase deficiency was assessed from the cortisol secretion rate (CSR) and urinary excretion of pregnanetriol and 11-ketopregnanetriol. In cases with salt loss, the sodium equilibrium was unstable, even with optimum treatment and increased dietary salt intake. Clinical evidence of salt-losing crisis appeared when 15-25% of Na, was lost. In these subjects, a parallel decrease in ASR and CSR usually occurred. The ASR were somewhat elevated in the nonsalt-losing form. Speculation

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Section: Loras Haour and Bertrandmentioning

confidence: 99%

Section: Sodiummentioning

confidence: 99%

“…8,9, and lo), and in the other subjects during salt restriction (case nos. 15, 16, 21, and 25), clinical signs of salt loss appeared.…”

Section: Sodiummentioning

confidence: 99%

Section: Factors Involved In Salt Lossmentioning

confidence: 99%

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Exchangeable Sodium and Aldosterone Secretion in Children with Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency

1970

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“…Oestrogen inhibits 3-,B-hydroxysteroid dehydrogenase in the testes of some animals (Collenot 1964;Bongiovanni et al 1967;Botte and Delrio 1967) and causes a marked decrease in 171X-hydroxylase, 17,20-lyase, and 17 -,B-hydroxysteroid dehydrogenase (Samuels, Uchikawa, and Huseby 1967). Oestrogen also decreases the histochemical reaction of lactate dehydrogenase (LDH-X) (Zinkham, Blanco, and Clowry 1964), and glucose-6-phosphate dehydrogenase in the rat testis (Elkington and Blackshaw 1970).…”

Section: Introductionmentioning

confidence: 99%

Effect of Oestradiol-3,17ß Dipropionate on Spermatogenesis and Lysosomal Enzymes in the Rat Tests

Elkington¹,

Blackshaw²

1971

Aust. Jnl. Of Bio. Sci.

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Daily intramuscular injections (20 f-Lgjday) of oestradiol-3, 17,8 dipropionate in adult male rats depressed body growth and reduced the weight of the testes and seminal vesicles between 4 and 8 days of treatment.The proportion of soluble acid phosphatase (E.C. 3.1.3.2), acid proteinase (E.C. 3.4.4.23), and ,8-glucuronidase (E.C. 3.2.1.31), increased during oestradiol treatment. There was also an increase in the total amount of acid proteinase and ,8.glucuronidase but no significant change in total acid phosphatase activity with oestrogen treatment. These changes in hydrolase activity coincided with a decrease in the yield of late primary spermatocytes from early primary spermatocytes, and long spermatidsfromroundspermatids. Histochemical evidence supported the biochemical and histochemical findings, with increasing tubular staining of acid phosphatase and lipid in the testis during treatment.It is concluded that lysosomal enzymes are important in testicular degeneration and probably in normal spermatogenesis.

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Colonic Mucosal Potential Differences in the Management of 21-Hydroxylase Deficiency

Elias¹,

Grossman²,

Meshkinpour³

et al. 1980

Arch Intern Med

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Disorders of Adrenal Steroid Biogenesis

Cited by 46 publications

References 109 publications

Exchangeable Sodium and Aldosterone Secretion in Children with Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency

Exchangeable Sodium and Aldosterone Secretion in Children with Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency

Effect of Oestradiol-3,17ß Dipropionate on Spermatogenesis and Lysosomal Enzymes in the Rat Tests

Colonic Mucosal Potential Differences in the Management of 21-Hydroxylase Deficiency

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