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  • 3β-hydroxy-5-androsten-17-one  (1)
  • Androstandiol  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Stellen 5 α-Androstan-3 α, 17 β-diol und 5 α-Androstan-3 α-diol-glukuronid biochemische Marker bei Hirsutismus dar? Eine Untersuchung mittels Gaschromatographie- Massenspektrometrie* (1997)
    Springer
    Monatsschrift Kinderheilkunde 145 (1997), S. 37-43 
    Details
    ISSN: 1433-0474
    Keywords: Schlüsselwörter Hirsutismus ; Androstandiol ; Androstandiolglukuronid ; Gaschromatographie ; Massenspektrometrie ; Key words Hirsutism ; Androstanediol ; Androstanediol glucuronide ; Gaschromatography ; Mass spectrometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Background: It is still controversial, whether the end metabolites of peripheral androgen metabolism, 5 α-androstane-3 α, 17 β-diol and 5 α-androstane-3 α, 17 β-diol glucuronide, represent biochemical markers of hirsutism. Furthermore, discrepant plasma concentrations have been reported in the literature. Method: Using stable isotope dilution/gas chromatography-mass spectrometry, the most specific method in steroid analysis, we investigated healthy females and patients with hirsutism of various etiology. Results: Generally, both androstanediol and androstanediol-glucuronide scattered much in hirsute patients. Patients with adrenal enzyme defects (3 β-hydroxysteroid-dehydrogenasedeficiency, 21-hydroxylase-deficiency) had elevated androstanediol and androstanediol-glucuronide. Hirsute Patients with hyperandrogenaemia but without adrenal enzyme deficiencies had normal androstanediol in 33 % and normal androstanediol-glucuronide in 24 % of cases. 54 % of patients with idiopathic hirsutism had normal androstanediol and 24 % had normal androstanediol-glucuronide. Conclusion: Our results show, that neither androstanediol nor androstanediol-glucuronide are consistently elevated in hirsutism and that both do not discriminate between the various causes of hirsutism.
    Notes: Zusammenfassung Hintergrund: Ob die Endmetaboliten des peripheren Androgenstoffwechsels, 5 α-Androstan-3 α, 17 β-diol und 5 α-Androstan-3 α, 17 β-diol-glukuronid, biochemische Marker bei Hirsutismus darstellen, wird kontrovers diskutiert. Über die Plasmakonzentrationen beider Parameter gibt es ferner erhebliche Diskrepanzen bei den in der Literatur berichteten Werten. Methode: Unter Einsatz von Isotopenverdünnungs-Gaschromatographie-Massenspektrometrie, dem Verfahren mit der höchsten Spezifität in der Steroidanalytik, untersuchten wir gesunde Mädchen und Frauen sowie Patientinnen mit Hirsutismus unterschiedlicher Ätiologie. Ergebnisse: Bei hirsuten Patientinnen streuten beide Parameter stark. Bei Patientinnen mit adrenalen androgenisierenden Enzymdefekten (3 β-Hydroxysteroiddehydrogenasemangel, 21-Hydroxylasemangel) waren sowohl Androstandiol als auch Androstandiolglukuronid erhöht. Hirsute Patientinnen mit Hyperandrogenämie ohne adrenalen Enzymdefekt wiesen in 33 % normales Androstandiol und in 24 % normales Androstandiolglukuronid auf. Patientinnen mit idiopathischem Hirsutismus hatten in 54 % Androstandiol- und in 30 % Androstandiolglukuronidkonzentrationen innerhalb des Streubereichs gesunder Mädchen und Frauen. Schlußfolgerungen: Unsere Ergebnisse zeigen, daß weder Androstandiol noch Androstandiolglukuronid in allen Fällen von Hirsutismus erhöht sind und daß beide Parameter nicht zwischen unterschiedlichen Formen des Hirsutismus diskriminieren.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001120050102
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  • 2
    Electronic Resource
    Electronic Resource
    Urinary excretion of Δ5-pregnenetriol (5-pregnene-3β,17α,20-triol) in healthy children (1980)
    Springer
    European journal of pediatrics 134 (1980), S. 103-107 
    Details
    ISSN: 1432-1076
    Keywords: 3β-hydroxy-5-androsten-17-one ; Dehydroepiandrosterone ; Urine ; Healthy children
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The excretion of Δ5pregnenetriol (Δ5) was determined in 24-h urine samples from 57 children of various ages. The probands were healthy regarding their endocrine states. Six groups of children were selected: Group I: neonates (n=12♂, aged 4 to 24 days), group II: infants (n=11♂, aged 1 to 8 months), group III; small children (n=7♂, 3♀, aged 11/2 to 6 years), group IV: schoolchildren (n=4♂, 5♀, aged 61/2 to 10 years), group V: preadolescents (n=5♂, 4♀, aged 101/2 to 13 years, developmental stages Tanner 2 to 3), group VI: adolescents (n=5♂, 1♀, aged 13–15 years, developmental stages Tanner 3 to 4). The completeness of the 24-h-urine collections was checked by creatinine determinations. The method used for steroid determination consisted of hydrolysis, extraction. Girard-T-reaction, paper chromatography, and photometric end-point determination using the Zimmermann reaction. Dehydroepiandrosterone (DHEA) was determined parallel to Δ5PT. The following results were obtained: $$\begin{gathered} Group I: \hfill \\ \Delta ^5 PT 0.01 - 0.11mg, mean:0.07mg/24h \hfill \\ DHEA 0.04 - 0.12mg, mean:0.07mg/24h \hfill \\ Group II: \hfill \\ \Delta ^5 PT 0.02 - 0.17mg, mean:0.10mg/24h \hfill \\ DHEA 0.01 - 0.10mg, mean:0.05mg/24h \hfill \\ Group III: \hfill \\ \Delta ^5 PT 0.01 - 0.07mg, mean:0.04mg/24h \hfill \\ DHEA 0.03 - 0.09mg, mean:0.05mg/24h \hfill \\ Group IV: \hfill \\ \Delta ^5 PT 0.02 - 0.37mg, mean:0.15mg/24h \hfill \\ DHEA 0.04 - 0.35mg, mean:0.16mg/24h \hfill \\ Group V: \hfill \\ \Delta ^5 PT 0.05 - 0.28 mg, mean:0.12mg/24h \hfill \\ DHEA 0.04 - 0.37mg, mean:0.17mg/24h \hfill \\ Group VI: \hfill \\ \Delta ^5 PT 0.11 - 0.36mg, mean:0.22mg/24h \hfill \\ DHEA 0.12 - 0.42mg, mean:0.22mg/24h \hfill \\ \end{gathered} $$ The excretion of Δ5PT was significantly correlated to the excretion of DHEA (P〈0.001), which can be explained by a common metabolic pathway for both steroids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01846025
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