Urinary Steroids
Urine Tests

Author: Gianpiero Pescarmona
Date: 13/09/2009

Description

Urinary Steroids Profile

Urinary Steroids are measured on the 24h urines. Aim of the test is to provide information about steroid hormones metabolism

The absolute range of single metabolite looks too large, but in some way this hormonal pattern may be representative of people individuality.

In the female, Estradiol (E2) is the major biologically active hormone, whereas it is Testosterone (T) in the male. Compounds in brackets {} are intermediates not assayed in urine. Progesterone(P) is metabolized
to Pregnanediol (PD) in the liver. P is not normally excreted in urine in measurable quantities and Pregnanediol (PD) as measured in urine reflects Progesterone levels both sensitively and accurately.

Age and sex dependance ??

What about the ratios between metabolites or groups of metabolites to identify regulatory steps (enzymes)? See G6PD

KeggHMDB
ANAN
ETET
ADIOLADIOL

Steroids Hormones Details

To access full information on steroid hormones use Full Metabolome Database

Steroids hormones metabolic pathways

Kegg Pathways is as metabolic pathways network allowing fast access to metabolites and enzymes description.

Kegg Pathways-Steroid hormone metabolism - Homo sapiens

Annotated Kegg Pathways-Steroid hormone metabolism

Normal Ranges 2006

Cortisol/cortisone

Cortisol catabolism

5a-Tetrahydrocortisol (HMDB00526) and H4Cortisone/H4Cortisol

Tetrahydrocortisone

Tetrahydrocortisol function

Tetrahydrocortisol

The cortisol metabolite, 20╬▓-dihydrocortisol, has very little glucocorticoid activity, but shows significant angiostatic activity in the CAM comparable to cortisol and Tetrahydrocortisol even more.

Tetrahydrocortisol synthesis depends on the activity of the enzyme 3-alpha hydroxysteroid dehydrogenase that belongs to the Group of xenobiotics inducible CYP450

Inborn errors of adrenal steroidogenesis 2003

11beta-hydroxysteroide dehydrogenases

  • Quinkler M, Zehnder D, Lepenies J, Petrelli MD, Moore JS, Hughes SV, Cockwell P, Hewison M, Stewart PM: Expression of renal 11beta-hydroxysteroid dehydrogenase type 2 is decreased in patients with impaired renal function. Eur J Endocrinol. 2005 Aug;153(2):291-9. [PubMed Link Image]
  • Rosler A, Leiberman E, Rosenmann A, Ben-Uzilio R, Weidenfeld J: Prenatal diagnosis of 11beta-hydroxylase deficiency congenital adrenal hyperplasia. J Clin Endocrinol Metab. 1979 Oct;49(4):546-51. [PubMed Link Image]

Ann Endocrinol (Paris). 2007 Oct;68(5):349-56. Epub 2007 Mar 26.
[11beta-hydroxysteroide dehydrogenases. Recent advances]

[Article in French]

Vantyghem MC, Marcelli-Tourvieille S, Defrance F, Wemeau JL.

Service d'endocrinologie et m├ętabolisme, clinique d'endocrinologie Marc-Linquette, 6, rue du Professeur-Laguesse, CHRU de Lille, 59037 Lille cedex, France. mc-vantyghem@chru-lille.fr

11beta-hydroxysteroide dehydrogenase (11beta-OHSD) enzymes exhibit a regulating action upon cortisol metabolism before access to its receptors. Two types of isoenzymes have been described, type 2 being the most anciently known. Type 2 11beta-OHSD, which changes cortisol into cortisone, is a unidirectional dehydrogenase mainly located in kidney, that protects mineralocorticoid receptors from illicit activation by glucocorticoids. Mutations of the gene coding for this enzyme has been demonstrated in apparent mineralocorticoid excess, which induces hypertension and hypokalemia with low renin and aldosterone levels. Polymorphisms of this gene could modulate essential hypertension and also be responsible for certain forms of acquired apparent mineralocorticoid excess especially after liquorice intoxication, in hypothyroidism, Cushing syndrome, and chronic renal insufficiency. Type 1 11beta-OHSD, which changes cortisone into cortisol, is a reductase, mainly located in liver and adipose tissue. Functional defects of this enzyme have been shown in polycystic ovaries and cortisone reductase deficiency. By contrast, metabolic syndrome, corticoid-induced osteoporosis, and glaucoma are linked to a local over-activity of this enzyme. The understanding of action mechanisms of these two enzymes currently leads to 11beta-OHSD inhibitors development, therefore opening new therapeutic strategies, especially in metabolic syndrome.

What can be expected with ACE inhibitors and similar drugs ??

21-HYDROXYLASE DEFICIENCY

Metabolism Figure
Dignostic Ratios

ET/AN

Inverse correlation with steroid-5-alpha-reductase, the enzyme responsible for the synthesis of
Dihydrotestosterone - DHT and brain neurosteroids

Kegg enzymeKegg pathway
steroid-5-alpha-reductasesteroid-5-alpha-reductase

ET/AN and homosexuality

ET/AN is higher in male homosexuals

  • Androsterone/Etiocholanolone Ratios in Male Homosexuals, 1973
  • A role for 5alpha-reductase activity in the development of male homosexuality? 2004 Ann N Y Acad Sci. 2004 Dec;1032:237-44.
    Higher body hair with lower mesmorphism ratings were observed in Caucasian homosexual men compared with the general male population, reflecting elevated 5alpha-reductase (5alphaR) activity, and higher dihydrotestosterone-to-testosterone (DHT-to-T) ratio, in sharp contrast to 46,XY 5alphaR 2 deficiency subjects, who are often born with ambiguous, or female genitalia, but tend to grow up to be muscular, heterosexual men with very little body hair, or beard. One study also showed them scoring around dull normal IQs. A greater prevalence of liberal body hair growth in men with higher IQs and/or educational levels was also observed in several samples. The exceptions to this statistical trend are too unsettling, however. Nevertheless, the results of a number of published studies, including one showing higher DHT-to-T ratio in homosexual men, done with different objectives over a span of 80 years, together strongly support these findings. Furthermore, in an animal model, "cognitive-enhancing effects" of "5alpha-reduced androgen [metabolites]" were recently demonstrated. ( contradictory )

Urinary steroid measurements in some endocrine and psychiatric diseases. 2005

A deeper insight

1. Mune T, White PC: Apparent mineralocorticoid excess: genotype is correlated with biochemical phenotype. Hypertension. 1996 Jun;27(6):1193-9. [PubMed Link Image]
2. Weykamp CW, Penders TJ, Schmidt NA, Borburgh AJ, van de Calseyde JF, Wolthers BJ: Steroid profile for urine: reference values. Clin Chem. 1989 Dec;35(12):2281-4. [PubMed Link Image]
4. Koren W, Grienspuhn A, Kuznetsov SR, Berezin M, Rosenthal T, Postnov YV: Enhanced Na+/H+ exchange in Cushing's syndrome reflects functional hypermineralocorticoidism. J Hypertens. 1998 Aug;16(8):1187-91. [PubMed Link Image]
7. Rapetti S, Francia G, Iacono C, Martignoni G, Contessi G, Brunelli M, Galvanin F, Serio G: An unusual case of Cushing's syndrome due to ACTH-independent macronodular adrenal hyperplasia. Chir Ital. 2003 Mar-Apr;55(2):235-41. [PubMed Link Image]
8. Melander O, Frandsen E, Groop L, Hulthen UL: No evidence of a relation between 11beta-hydroxysteroid dehydrogenase type 2 activity and salt sensitivity. Am J Hypertens. 2003 Sep;16(9 Pt 1):729-33. [PubMed Link Image]
9. Panin LE, Tuzikov FV, Gimautdinova OI: Tetrahydrocortisol-apolipoprotein A-I complex specifically interacts with eukaryotic DNA and GCC elements of genes. J Steroid Biochem Mol Biol. 2003 Dec;87(4-5):309-18. [PubMed Link Image]
10. Shackleton C, Malunowicz E: Apparent pregnene hydroxylation deficiency (APHD): seeking the parentage of an orphan metabolome. Steroids. 2003 Oct;68(9):707-17. [PubMed Link Image]

Etiocholanolone and fever

Papers Etiocholanolone fever

Pregnenetriol

Analytical Method

additional info from the lab

from other labs...

Urine steroid metabolomics as a biomarker tool for detecting malignancy in adrenal tumors. 2011

Comments
2017-06-20T20:36:36 - Gianpiero Pescarmona

Nomenclatore regionale:

- 90.01.3 = 17CHETOSTEROIDI

- 90.01.4 = 17IDROSSICORTICOIDI

- 90.15.3.1 = CORTISOLO URINARIO

- 90.15.6 = CORTICOSTEROIDI

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