Androsterone steroid profile

Buiarelli et al. (2004) extended the above analytical approach to many more related steroids when they published a method for the direct analysis of 15 urinary anabolic steroids in a single run, namely T, epitestosterone, dehydroepiandrosterone (DHEA), androsterone, etiocholanolone, their sulfates and their glucuronides (Figure 2,2), They extracted 2 mL of human urine by solid-phase extraction with methanol elution and reconstituted the residue in aqueous methanol in the presence of deuterated internal standards (da-epitestosterone glucuronide, [16,16,17-"H3 testosterone sulfate and [16,16,17-2H3]testosterone), then monitored, for example, mJz. 289-97 and 109 for T and epitestosterone, miz 367-97 for their sulfates, and m/z 463-113 and 287 for their glucuronides. The method does not achieve quantitation, but it allows the estimation of ratios, which makes it possible to monitor the urinary steroid profile, which is useful for monitoring the abuse of anabolic steroids. 

Adrenocortical Tumors. Virilization, hypercortisolism, feminization, abdominal pain, palpable abdominal tumor, or combinations of these features are clinical symptoms of adrenocortical tumors. Both types of adrenocortical tumors (carcinoma and adenoma) can produce a wide variety of steroid hormones. This is a consequence of multiple enzyme deficiencies in tumor tissues. The tumor cells are capable of synthesizing large amounts of steroid hormone precursors independent of ACTFI stimulation. Excessively high amounts of DHEA and other 3p hydroxy-5-ene steroids characterize the urinary steroid profile in children with adrenocortical carcinoma, but similar profiles can also be produced by adrenal adenomas. Elevated lip hydroxy-androsterone excretion alone or combined with high excretion of cortisol metabolites or 3p hydroxy-5-ene steroids are characteristic of the urinary steroid profile for adrenocortical adenomas [36,37]. 

The phase-I-metabolism of testosterone leads primarily to 5a-androstan-17P-ol-3-one (dihydrotestosterone), 5a-androstan-3a-ol-17-one (androsterone), and 5P-androstan-3a-ol-17-one (etiocholanolone) (Fig. 3.6,2-4, respectively), which represent important parameters of the so-called urinary steroid profile in sports drug testing (see Chapter 6). 

The quantitative comparisons of steroid urinary profiles may reveal much useful information that is currently sought in modern biomedical research. Thus, while capillary GC/MS techniques have been used to identify the individual urinary metabolites, peak-height comparisons were shown to facilitate characterization of the steroids typical of human newborns [295], studies of various endocrinological disorders [296-299], breast cancer [300] and diabetes mellitus [268], As an example. Figure 3.18 shows a comparison of typical profile differences between normal and diabetic human males [268] briefly, peaks 2 and 3 (androsterone and etiocholano-lone) are depressed in the diabetic, while peaks 48-56 (cortisol metabolites), and peak 66 (a C2j-pentol), are characteristically elevated. 

Figure 1 GC-MS Profile analysis. Total ion chromatogram profiles produced by scanning methoxy-trimethylsilyl derivatives of urinary steroids. (A) Profile from a patient with 11 -hydroxylase deficiency in which the principal steroids are metabolites of IIjS-deoxycortisol (substance S) such as tetrahydrosubstance S (THS) and hexahydrosubstance S epimers (HHS). (B) Profile from the patient s father this profile is essentially normal. Some of the major metabolites are C19 steroids such as androsterone (An), et-iocholanone (Etio), pregnanetriol (PT), and cortisol metabolites (THE, tetrahydrocortisone THF, tetrahydrocortisol and 5a-THF, 5a-tetrahydrocortisol). Peaks 1-3 are internal standards. (Reprinted from Shackleton CHL, Merdinck J, and Lawson AM (1990) In McEwan CN and Larsen BS (eds.) Mass Spectrometry of Biological Materials, pp. 297-377. New York Dekker courtesy of Marcel Dekker Inc.)...

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