Changes in steroid pattern following acute and chronic adrenocorticotropin administration in premature adrenarche

Toscano, Vincenzo; Balducci, R; Adamo, Maria; Mangiantini, A; Cives, C.; Boscherini, B

doi:10.1016/0022-4731(89)90271-9

Cited by 12 publications

(8 citation statements)

References 26 publications

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“…Toscano et al examined the levels of serum pregnenolone (50 ± 7 ng/dL), cortisol (13 ± 1.8 μg/dL) and 11-deoxycortisol (52 ± 3.6 ng/dL) in 20 children between ages 5.5 to 9 years (74). Several studies carried out in large cohorts of children between 2 to 12 years of age have established that serum cortisol levels do not increase in adrenarche (63, 75).…”

Section: Serum C21 Steroids In Adrenarchementioning

confidence: 99%

“…Toscano et al observed increase in plasma levels of C 21 steroids like pregnenolone and 17OHPreg along with the C 19 steroids like DHEA, DHEAS and androstenedione but with no change in cortisol or 11-deoxycortisol in PA children as compared to controls. They interpreted these steroid changes to suggest that the PA adrenal had decreased HSD3B2 activity and increased CYP17 activity (74). They also indicated that PA might not be exclusively dependent on ACTH regulation (74).…”

Section: Serum C19 Steroids In Adrenarchementioning

confidence: 99%

“…They interpreted these steroid changes to suggest that the PA adrenal had decreased HSD3B2 activity and increased CYP17 activity (74). They also indicated that PA might not be exclusively dependent on ACTH regulation (74). The levels of Adiol-G also increased in children with PA and showed a strong correlation with DHEA, DHEAS and androstenedione (115, 123-126).…”

Section: Serum C19 Steroids In Adrenarchementioning

confidence: 99%

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The steroid metabolome of adrenarche

Rege

Rainey

2012

Journal of Endocrinology

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Adrenarche is an endocrine developmental process whereby humans and select nonhuman primates increase adrenal output of a series of steroids, especially dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS). The timing of adrenarche varies between primates, but in humans, serum levels of DHEAS are seen to increase around 6 years of age. This phenomenon corresponds with the development and expansion of the zona reticularis (ZR) of the adrenal gland. The physiological phenomena that trigger the onset of adrenarche are still unknown; however the biochemical pathways leading to this event have been elucidated in detail. There are numerous reviews examining the process of adrenarche, most of which, have focused on the changes within the adrenal as well as the phenotypic results of adrenarche. This article reviews the recent and past studies that show the breadth of changes in the circulating steroid metabolome that occurs during the process of adrenarche.

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Section: Serum C21 Steroids In Adrenarchementioning

confidence: 99%

Section: Serum C19 Steroids In Adrenarchementioning

confidence: 99%

Section: Serum C19 Steroids In Adrenarchementioning

confidence: 99%

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The steroid metabolome of adrenarche

Rege

Rainey

2012

Journal of Endocrinology

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“…Androstenedione, 17OHP, 17PGN, DHA, and cortisol were measured by radioimmunoassay (RIA) after purification of plasma extracts by chromatography on Celite microcolumns as previously described [7, 8, 9, 10]. IGF1, DHA-S and cortisol were measured using commercial kits purchased from Diagnostic Systems Laboratories (Webster, Tex.).…”

Section: Methodsmentioning

confidence: 99%

Effects of Long-Term Growth Hormone Therapy on Adrenal Steroidogenesis in Turner Syndrome

Balducci

Toscano²,

Larizza³

et al. 1998

Horm Res Paediatr

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It has been shown that growth hormone (GH) and insulin-like growth factor-1 (IGF1) enhance steroidogenesis responsiveness to ACTH in cultured adrenal cells. To investigate the GH effect on adrenal steroidogenesis in non-GH-deficient subjects, we studied 9 girls with Turner syndrome (chronological age 5.5–7.2 years; bone age 5–7 years). In all subjects an ACTH test (Synacthen depot, 0.25 mg i.v. with blood samples at 0 and 60 min) was performed basally at 8–9 a.m. and 6 months after GH therapy (1 IU/kg/week). 17-Hydroxypregnenolone (17PGN), 17-hydroxyprogesterone (17OHP), dehydroepiandrosterone (DHA), its sulfate (DHA-S), androstenedione and cortisol were evaluated by radioimmunoassay. Two groups of normal girls were selected as controls: group A age-matched the patients at the start of the study, and group B age-matched the patients at the end of the study. The responsiveness of each hormone to ACTH was expressed as the difference between stimulated and basal values. A p value of < 0.01 was considered to indicate significance. There were no significant differences between pre- and posttreatment basal values of 17PGN, 17OHP, DHA, androstenedione and cortisol in the Turner syndrome patients, whereas a significant increase was observed for basal DHA-S (1.57 ± 0.31; 1.89 ± 0.43 µmol/l, p < 0.01). Comparison of increments before and after GH treatment showed a significant increase in responsiveness to ACTH after GH therapy DHA (p < 0.01). The increase in 17PGN was evident (p < 0.02), but the established significant p value was not reached. No differences for 17OHP, androstenedione and cortisol were found. The stimulated 17PGN/17OHP ratio was significantly higher (p < 0.01) after GH, whereas the 17OHP/androstenedione ratio was considerably lower, but the p value was < 0.02. No differences between pretreatment values with the control group androstenedione was found, whereas basal and stimulated posttreatment values of DHA and stimulated values of 17PGN were higher in patients after GH therapy than in control group B. No differences between the 2 control groups were found. In conclusion our study showed that adrenal steroid responsiveness to ACTH increases in Turner syndrome after long-term treatment with high GH doses. An increase in the number of ACTH adrenal receptors and/or a modulation of enzyme activities may be suggested. The positive or negative pharmacological implications of these data remain to be determined especially when taking into consideration the wide use of GH therapy in non-GH-deficient subjects.

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“…Na infância, tais precursores devem ser determinados após estímulo com ACTH, administrado de forma aguda ou crônica, pois os valores basais costumam ser normais. Pela sua maior praticidade, o teste do ACTH agudo foi incorporado como um método útil na investigação laboratorial de rotina da pubarca precoce (7,12,13).…”

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Pubarca precoce: estudo retrospectivo clínico e laboratorial

Borges

Paula

Nomeline

et al. 2000

Arq Bras Endocrinol Metab

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RESUMOAnalisaram-se 109 prontuários de pacientes atendidos no período de janeiro de 1990-2000, cujo diagnóstico era pubarca precoce, com o objetivo de se avaliar a etiologia e evolução destes pacientes. Os mesmos foram divididos em 4 grupos: G 1 , n=41 (35F/6M, idades entre 11 meses e 7anos e 11 meses, mediana: 7anos e 1 mês), nos quais foram dosados: 17-OH progesterona (17OHP), DHEA, DHEA-S, androstenediona, testosterona total e/ou livre, e feito teste de estímulo do LH e FSH com GnRH (Relisorm ® , 100mg iv); no grupo G 2 , n=28 (20F/8M, idades entre 9meses e 8anos e 11 meses, mediana: 7anos e10meses), além dos exames mencionados, investigou-se a deficiência da 21-hidroxilase através da dosagem de 17OHP sob estímulo agudo com ACTH (Cortrosina®, 250mg iv), O grupo G 3 , n=23 (19F/4M, idades entre 1ano e 2meses e 8anos e 10meses, mediana: 7anos e 6meses), além dos exames anteriores, foi investigado para deficiências de 11 b-hidroxilase e 3b-hidroxiesteróide desidrogenase pelas dosagens de 11-deoxicortisol, e relação DHEA/androstenediona, respectivamente. As dosagens de testosterona total e/ou livre, DHEA-S e estradiol (em meninas) foram feitas nos 3 grupos. No grupo G 4 , n=14 (12F/2M, idades entre 1ano e 1 mês e 8anos e 9meses, mediana: 6anos e 5meses) o diagnóstico foi feito apenas com dados clínicos. Três meninas (6meses, 2anos e 1 mês e 2anos e 7meses) foram consideradas à parte; tiveram puberdade precoce associada a hiperandrogenismo, como primeira manifestação de adenocarcinoma adrenal. A investigação demonstrou níveis muito elevados de DHEA-S e massas adrenais ressecadas posteriormente. Um grupo controle de 18 crianças normais pré-púberes (8F/10M) foi submetido ao teste agudo do ACTH. No estímulo com GnRH, um D LH ³ 7,0 foi considerado indicativo de resposta púbere. Andrógenos e estradiol foram dosados por RIE e kits comerciais DPC; LH e FSH foram dosados por métodos imunométricos. As respostas entre pacientes e grupo controle foram comparadas pelo teste de Mann-Whitney. Nos grupos G 1 , G 2 e G 3 apenas 4 pacientes responderam com um D LH ³ 7,0 e 2 evoluíram com puberdade precoce verdadeira. A resposta da 17OHP ao ACTH (G 2 e G 3 , n=51) diagnosticou 2 casos de deficiência da 21-hidroxilase, forma não-clássica. Nos outros, as respostas não diferiram do grupo controle. Não houve acúmulo de outros precursores testados pelo ACTH no G 3 . Concluímos que uma minoria de crianças com adrenarca precoce evoluem para puberdade precoce ou têm hiperplasia adrenal congênita na forma não clássica, o que mostra que, após avaliação dos níveis de esteróides basais, o seguimento apenas clínico seria mais prático e econômico, deixando a realização de testes para quando houvesse algum dado inicial ou evolutivo que o indicasse.

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Changes in steroid pattern following acute and chronic adrenocorticotropin administration in premature adrenarche

Cited by 12 publications

References 26 publications

The steroid metabolome of adrenarche

The steroid metabolome of adrenarche

Effects of Long-Term Growth Hormone Therapy on Adrenal Steroidogenesis in Turner Syndrome

Pubarca precoce: estudo retrospectivo clínico e laboratorial

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