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steroid_precursor_and_multisteroid_profiling_in_acc

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Steroid Precursor and Multisteroid Profiling in ACC

Hormonal Evaluation

Steroid precursor and multisteroid profiling in adrenocortical carcinoma (ACC) is the measurement of multiple adrenal steroids or steroid metabolites, usually by mass spectrometry, to detect the disordered steroidogenesis that commonly accompanies malignant adrenocortical tissue.12 Within ACC care it belongs to hormonal evaluation, but it also overlaps with adrenal mass characterization, identification of secretory phenotypes, and biochemical follow-up. Unlike routine endocrine testing, which often emphasizes end-product hormones such as cortisol or aldosterone, multisteroid profiling focuses on precursor-heavy patterns such as excess 11-deoxycortisol, 11-deoxycorticosterone, pregnenolone-derived steroids, and related urinary metabolites.34

ACC may produce broad mixtures of steroid precursors, weakly bioactive intermediates, and mixed hormone excess even when a classic endocrine syndrome is absent.56 This has made steroid profiling of interest as an adjunctive tool for distinguishing ACC from benign adrenocortical adenoma, including some lesions initially labeled nonfunctioning on standard workup.78 Urinary steroid metabolite profiling by gas chromatography–mass spectrometry has the longest clinical literature, while serum and plasma LC-MS/MS panels have been developed as more scalable alternatives.1910

The evidence base is nevertheless constrained by the rarity of ACC and by substantial dependence on retrospective referral-center cohorts, heterogeneous analyte panels, and incomplete assay standardization across laboratories.11110 Available studies generally support steroid profiling as a complementary marker of malignant adrenal biology rather than a definitive diagnostic test. In practice, it may strengthen or lower suspicion for ACC when interpreted with imaging, routine hormonal testing, surgery, and pathology, but it does not establish or exclude carcinoma on its own.812

Diagnostic Context

The biological rationale for multisteroid profiling is that ACC often shows inefficient or incomplete steroid biosynthesis, leading to accumulation of precursor steroids and atypical metabolite patterns rather than isolated elevation of a single end-product hormone.32 Recurrently reported abnormalities include 11-deoxycortisol and tetrahydro-11-deoxycortisol, 11-deoxycorticosterone, pregnanetriol, 5-pregnenetriol, and other 3β-hydroxy-5-ene steroids.131415 As a result, some tumors considered clinically nonfunctioning by conventional testing may still show a detectable malignant steroid fingerprint on broader profiling.166

This approach has been studied mainly in patients with adrenal masses already considered suspicious because of size, CT appearance, mixed hormonal findings, or atypical endocrine presentations.6812 What appears most reliable is recognition of a multisteroid, precursor-dominant pattern rather than reliance on any single analyte alone.14 What is less reliable is interpretation outside the full adrenal-mass workflow, because overlap with adenoma and other adrenal lesions persists. The practical implication is that profiling may refine preoperative suspicion, but it does not replace imaging or histopathology.

Major Biochemical Phenotypes

A commonly described phenotype is occult or mixed steroid excess. ACC may secrete glucocorticoid, androgenic, and precursor steroids simultaneously, sometimes without an overt endocrine syndrome.5146 This pattern helps explain why routine testing directed only at cortisol, aldosterone, or a limited androgen panel may underrecognize malignant secretion when the dominant products are biosynthetic intermediates.211 The reliable conclusion is that biochemical heterogeneity is typical in ACC; the less certain point is how often any specific mixed pattern occurs across unselected populations.

A less common but clinically important phenotype is mineralocorticoid precursor excess, especially 11-deoxycorticosterone-related secretion. Reported patients may present with hypertension, hypokalemia, suppressed renin, and low or non-diagnostic aldosterone, thereby mimicking primary aldosteronism despite a different steroidogenic mechanism.171819 This association is biologically plausible and repeatedly described, but the supporting evidence is dominated by rare cases and small series rather than large comparative cohorts. Clinically, selective measurement of precursor mineralocorticoids may be useful when the phenotype suggests mineralocorticoid excess but aldosterone-based interpretation is discordant.19

Historical reports also describe unusual combinations of early precursors, altered androgen metabolite ratios, and dissociation within the aldosterone pathway, reinforcing the broader principle that ACC-associated steroidogenesis may be abnormal in several directions rather than along a single hormonal axis.20212223 These older data remain useful for mechanism and pattern recognition, although they do not define modern diagnostic thresholds.

Urinary and Blood-Based Profiling

Urinary steroid profiling is the best established modality in ACC, historically by GC-MS and more recently by LC-MS-based platforms.318 Urine testing captures integrated steroid production over time and has repeatedly identified malignant patterns enriched for tetrahydro-11-deoxycortisol, pregnenolone-derived metabolites, and related precursor products.71524 Simplified urinary approaches suggest that a small number of key metabolites may retain practical discriminative value, including strong negative predictive value in low-risk profiles in selected cohorts.24

Serum and plasma steroid profiling by LC-MS/MS has emerged as a more accessible option for centers without specialized urine metabolomics.9410 These studies also suggest that ACC is associated with elevations in several steroid precursors, with 11-deoxycortisol recurring as one of the more informative analytes, although overall model performance varies by cohort and platform.2510 What appears reliable is that blood-based mass spectrometry can detect broader steroid abnormalities than routine single-hormone testing; what remains uncertain is whether blood panels can consistently match the discriminatory performance reported for specialized urinary profiling across institutions.

This difference in specimen type leads to a practical comparison rather than a hierarchy of absolute superiority. Urinary profiling currently has the stronger ACC-specific literature, whereas blood-based panels may be easier to implement in routine endocrine workflows but remain less standardized and potentially more susceptible to non-ACC causes of multisteroid disturbance.11026

Evidence for Distinguishing ACC From Benign Adrenal Tumors

Across reviews and cohort studies, multisteroid patterns generally outperform single steroid measurements for differentiating ACC from adrenocortical adenoma.142 The best results have usually been reported when steroid profiling is combined with tumor size, CT attenuation, or other imaging features rather than interpreted in isolation.11812 This supports a multimodal model in which biochemical profiling contributes incremental information to standard adrenal-mass assessment.

Diagnostic accuracy estimates should still be interpreted cautiously. Many published cohorts are enriched for larger, more hormonally active, or otherwise clinically suspicious tumors, which may inflate apparent performance relative to broader incidentaloma populations.111 The practical implication is comparative: steroid profiling may improve risk stratification beyond routine hormonal workup alone, but surgery, pathology, and established imaging pathways remain the reference standards for definitive diagnosis.

Follow-up and Monitoring

When a tumor shows a clear steroid signature at baseline, limited evidence suggests that abnormal profiles may decline after complete resection and rise again with recurrence or progression.5238 This creates a plausible role for profiling in postoperative surveillance or treatment monitoring, particularly when imaging findings are equivocal or when biochemical recurrence might precede overt radiographic progression.

However, this application is less mature than diagnostic support in an adrenal mass. Optimal timing, analyte selection, and response thresholds are not standardized, and the available evidence remains limited. The reliable point is that serial profiling can reflect tumor-associated steroid production in selected patients; the uncertain point is how broadly this can be generalized across ACC subtypes and treatment settings.

Limitations and Pitfalls

The main limitations are interpretive and methodological rather than procedural. ACC is rare, so much of the literature consists of retrospective series, selected referral populations, and case reports, which limits generalizability.111 Assays also differ in analyte coverage, specimen type, normalization methods, and decision thresholds, making direct comparison between studies difficult and broad implementation challenging.2710

Interpretation depends on clinical context. Age, sex, and physiological variation may influence steroid patterns, supporting the need for context-specific reference frameworks rather than fixed unadjusted cutoffs.2728 In addition, immunoassay-based hormone measurements may be distorted by cross-reactivity with steroid precursors, particularly with marked 11-deoxycortisol excess, which strengthens the rationale for mass spectrometry when unusual steroidogenesis is suspected.292 Overall, the practical implication is that steroid profiling is most informative when performed on validated platforms and interpreted within specialized adrenal care pathways.

Included Articles

  • PMID 226427: This study reports that plasma 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone can be markedly elevated in some functional ACC cases, especially Cushing syndrome due to adrenocortical carcinoma, while adenoma-associated Cushing syndrome remained within the normal range. The findings suggest these steroid measurements may help characterize hormone-producing adrenal disorders, although evidence is limited.30
  • PMID 2141212: In a 24-patient ACC series, urinary steroid profiling frequently showed excess 3β-hydroxy-5-ene steroids and/or cortisol precursor metabolites such as tetrahydro-11-deoxycortisol, including in some tumors without overt endocrine syndromes. Profiles normalized after radical surgery, decreased with chemotherapy response, and rose again with recurrence.5
  • PMID 2794692: This case report highlights that ACC can present as an apparently nonfunctional adrenal tumor when excess deoxycorticosterone causes only mild mineralocorticoid features. Measurement of steroid precursors such as pregnenolone and progesterone, alongside DOC, may help reveal malignant steroidogenesis and distinguish carcinoma from adenoma.31
  • PMID 2822295: This case report describes a mineralocorticoid-secreting ACC presenting like primary hyperaldosteronism, with markedly elevated 11-deoxycorticosterone and corticosterone in addition to aldosterone. The report recommends measuring steroid precursors such as 11-deoxycorticosterone, because abnormal excess may help distinguish carcinoma from a benign aldosterone-producing adenoma.17
  • PMID 3161933: This case report describes a functional ACC causing Cushing’s syndrome with an unusual steroid pattern: markedly elevated urinary 17-ketosteroids driven by etiocholanolone despite normal urinary and plasma DHEA, alongside extreme 11-deoxycortisol excess. The report suggests disordered steroidogenesis with low C17-20 lyase activity and highlights that atypical precursor profiles can still support ACC.32
  • PMID 4017973: In a small series of adrenocortical tumors, urinary steroid profiling by gas chromatography found consistently elevated tetrahydro-11-deoxycortisol and 45-pregnenetriol in all three carcinomas, including a nonfunctional case, suggesting a biochemical clue that may help distinguish ACC from adenoma.13
  • PMID 7209971: A radioimmunoassay method simultaneously measured plasma 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone, finding markedly elevated levels in the single reported patient with adrenocortical carcinoma causing Cushing syndrome, while levels in adenoma-associated Cushing syndrome were usually within the normal range.33
  • PMID 7286345: In two adrenocortical carcinoma cases, broad plasma steroid profiling showed distinct abnormalities despite absent or minimal Cushingoid features: one virilizing, hypertensive case had markedly elevated DOC and 11-deoxycortisol suggesting impaired 11β-hydroxylase activity, while another clinically inactive case showed excess early steroid precursors only.34
  • PMID 8421100: In a small series of adrenal cortical tumors, ACC was associated with undetectable aldosterone despite normal or elevated mineralocorticoid pathway precursors, a pattern not seen in benign lesions. The authors suggest this aldosterone-pathway dissociation may aid biochemical differentiation of malignant from nonmalignant adrenal masses and may track recurrence.23
  • PMID 10915023: Gas chromatography/mass spectrometry urinary steroid profiling showed that ACC had excretory patterns distinct from adrenal adenomas, particularly increased metabolites of 11-deoxycortisol or 3beta-hydroxy-5-ene steroids. The study supports urinary steroid profiling as a potentially useful noninvasive method to help distinguish malignant from benign adrenocortical tumors.3
  • PMID 13762592: This study describes steroid abnormalities in adrenal carcinoma, showing increased urinary etiocholanolone and often elevated etiocholanolone-to-androsterone ratios. In patients with corticoid-producing ACC, etiocholanolone appeared to derive not only from dehydroepiandrosterone but also from other steroid precursors, alongside markedly increased dehydroepiandrosterone secretion.20
  • PMID 13895833: In a patient with metastatic adrenocortical carcinoma, very high urinary pregnanetriol excretion was shown to arise mainly from steroid precursors other than 17-hydroxyprogesterone, likely including 17-hydroxypregnenolone-related pathways. The report details an unusually steroid-rich urinary profile that highlights disordered adrenal steroidogenesis in ACC.21
  • PMID 13960199: In a patient with metastatic adrenal carcinoma, isotope-tracing suggested that urinary pregnanetriol arose predominantly from 17-hydroxypregnenolone rather than 17-hydroxyprogesterone, while both precursors contributed little to 17-ketosteroid production. The study highlights abnormal steroid precursor metabolism that can shape urinary steroid patterns in ACC.22
  • PMID 15816373: This case report highlights that in ACC presenting with hypertension and hypokalemia but normal or low aldosterone and low-normal renin, evaluation of mineralocorticoid precursor steroids can reveal 11-deoxycorticosterone excess. Postoperative normalization of DOC also suggests its utility as a biochemical follow-up marker in such rare functional tumors.18
  • PMID 19481537: This assay study highlights that cortisol immunoassays can be biased in settings with excess steroid precursors, including adrenocortical carcinoma, because 11-deoxycortisol cross-reactivity may falsely elevate measured cortisol. The findings caution that kit-specific reference ranges may not prevent misclassification when unusual steroids are increased.29
  • PMID 19966352: A small retrospective series suggests that urinary steroid profiling by gas chromatography-mass spectrometry may aid ACC diagnosis and follow-up by identifying multiaxial steroid excess, unusual steroid metabolites including pregnenetriols and post-neonatal neonatal steroids, and a high tetrahydro-11-deoxycortisol burden relative to cortisol metabolites.16
  • PMID 21521927: In five ACC cases, urinary steroid profiling by gas chromatography/mass spectrometry showed increased metabolites of steroid precursors, including 17-OH pregnenolone, 17-OH progesterone, DHEA, and 11-deoxycortisol, in all or most tumors. The series suggests precursor-heavy steroid metabolite patterns may support biochemical recognition of ACC, including some clinically nonfunctioning tumors.14
  • PMID 25156173: This case highlights that ACC can rarely present with mineralocorticoid hypertension from excess deoxycorticosterone-pathway precursors despite suppressed renin and aldosterone. Urinary multisteroid profiling by gas chromatography-mass spectrometry identified elevated deoxycortisol, deoxycorticosterone, and corticosterone, prompting adrenal imaging and diagnosis.35
  • PMID 27370636: This study reports that urinary steroid profiling by GC-MS and HPLC can help distinguish adrenocortical carcinoma from adrenocortical adenoma, including in ACC without overt hypercortisolism. Elevated tetrahydro-11-deoxycortisol and DHEA, plus non-classical 5-en-pregnenes and specific metabolite ratios, were highlighted as discriminatory biochemical markers.7
  • PMID 28234802: This review describes urinary steroid metabolite profiling as an emerging noninvasive method to distinguish ACC from benign adrenal tumors. Retrospective cohorts using GC-MS and computational analysis identified a malignant steroid fingerprint, with excess precursor metabolites such as tetrahydro-11-deoxycortisol, and reported diagnostic accuracy above 90% pending prospective validation and scalable tandem mass spectrometry platforms.1
  • PMID 28814383: A 24-hour urine HRAM LC-MS panel quantifying 26 steroid metabolites distinguished ACC from adrenocortical adenoma by showing higher abnormal excretion of multiple steroids, particularly tetrahydro-11-deoxycortisol, pregnanetriol, and 5-pregnenetriol. The study supports multisteroid urinary profiling as a diagnostic aid in adrenal tumor evaluation.15
  • PMID 28904054: This study describes a 13-steroid serum LC-MS/MS panel for evaluating suspected adrenocortical carcinoma and reports that ACC cases showed multiple steroid precursor elevations, with 11-deoxycortisol markedly increased in all cases. The panel differentiated ACC from other adrenal lesions by combining hormone and precursor measurements in one assay.9
  • PMID 29653936: This letter argues that mass spectrometry-based steroid profiling is important for ACC detection, particularly because many patients lack overt endocrine syndromes. It suggests atmospheric pressure photoionization may provide more reliable multisteroid measurement than APCI or ESI and may improve detection of DHEA, a potentially useful marker in pediatric ACC.36
  • PMID 29694956: A pediatric LC-MS/MS study included six treatment-naive ACC cases as a cross-validation group when testing multiples-of-median normalization of multisteroid profiles. The article supports age- and sex-independent steroid data standardization to improve comparability of endocrine profiling, but does not define an ACC-specific diagnostic steroid signature.27
  • PMID 30058921: In adrenal incidentaloma evaluation, ACC may be suggested by a mixed pattern of adrenal hormone excess, especially elevated DHEAS, cortisol, and precursor steroids. Urinary steroid profiling by gas chromatography or mass spectrometry showed promising retrospective accuracy for distinguishing ACC from benign adenoma, but prospective validation is still needed.6
  • PMID 30481155: In a retrospective single-center cohort, plasma LC-MS/MS steroid profiling distinguished ACC from adrenocortical adenoma better than any single steroid, with sex-specific six-steroid logistic models achieving AUCs of 0.95 in men and 0.94 in women. ACC showed higher precursor and sex steroid levels, supporting multisteroid profiling as a useful adjunct in adrenal mass evaluation.4
  • PMID 30893084: This review describes serum steroid profiling by LC-MS/MS as an emerging diagnostic aid for adrenocortical tumors, noting that patients with ACC can show a distinct but heterogeneous steroid fingerprint. A selected serum steroid panel, with 11-deoxycortisol as a key discriminant compound, showed good separation between patients with and without ACC, while further studies are needed for diagnostic and follow-up use.25
  • PMID 31778357: This case report highlights urinary steroid profiling by GC-MS as an adjunct in evaluating adrenal masses when ACC is a concern. It emphasizes that elevated tetrahydro-11-deoxycortisol and related precursor metabolites can suggest malignant steroidogenesis, while also noting uncertainty in oncocytic tumors and the need for further validation.37
  • PMID 32872281: This review argues that mass spectrometry-based steroid profiling can improve hormonal evaluation of suspected ACC by detecting broad panels of steroid precursors and excess secretion with higher specificity than immunoassays, potentially aiding differentiation from nonfunctioning adenomas and supporting follow-up.2
  • PMID 33228607: In cortisol-producing adrenal tumors, inexpensive immunoassay-based serum steroid profiling may help distinguish ACC from cortisol-producing adenoma by showing broadly increased steroid precursors, especially 17-hydroxypregnenolone and 11-deoxycorticosterone, with supportive value from combined DHEAS and androstenedione. In this small cohort, 11-deoxycortisol correlated with ENSAT stage and testosterone correlated with Ki67 index.38
  • PMID 33278379: This review describes how multisteroid profiling by chromatography-mass spectrometry can detect ACC-associated secretion of steroid precursors and metabolites, especially non-bioactive intermediates. Prospective EURINE-ACT data suggest the steroid panel is most useful when combined with tumor size and suspicious imaging rather than used alone.11
  • PMID 34349894: This review highlights urine steroid metabolomics as a prospectively validated diagnostic adjunct for suspected ACC, showing improved accuracy over standard modalities and highest performance when combined with tumor size and CT attenuation. It also emphasizes routine hormonal workup to identify steroid excess patterns, support cortical origin, guide perioperative care, and aid recurrence monitoring.8
  • PMID 35432204: This systematic review of 11-deoxycorticosterone-producing adrenal lesions shows that patients commonly present with hypertension, hypokalemia, suppressed or low-normal aldosterone, and markedly elevated 11-deoxycorticosterone. In hypertensive patients with a primary aldosteronism-like picture but low aldosterone, measuring 11-deoxycorticosterone can help identify this rare ACC-associated secretory phenotype.19
  • PMID 36948238: In adults with adrenal tumors, a simplified LC-MS/MS urinary steroid profile using only 5-pregnenetriol and tetrahydro-11-deoxycortisol classified low-, intermediate-, and high-risk patterns for ACC. Low-risk results showed a 100% negative predictive value for malignancy in both 24-hour and paired spot urine validation cohorts, supporting steroid profiling as a practical adjunct to exclude ACC.24
  • PMID 39231247: In a prospective cohort of 263 patients with adrenal masses, serum 11-deoxycortisol, 17OH-progesterone, and 17OH-pregnenolone measured by LC-MS/MS were higher in ACC than in non-ACC tumors, including functioning adenomas and lesions with unenhanced HU 20 or greater. A machine learning-derived serum steroid score showed moderate discrimination for ACC and may help address limited availability of urine steroid profiling after validation.10
  • PMID 41681699: This review notes that when ACC is suspected, sex steroids and steroid profiling are recommended, and highlights multisteroid profiling by GC-MS or LC-MS/MS as an adjunctive diagnostic approach. In adrenal masses, urinary steroid metabolite panels may help distinguish ACC from benign lesions, especially when combined with tumor size and attenuation features.12
  • PMID 6274897: A 1982 ACTH stimulation study in healthy younger and older adults found age-related differences in adrenal steroid output, with reduced Δ5 steroid responses but preserved or higher Δ4 steroid responses in older individuals.28 While indirect to ACC, this finding adds context for potential age-related variation when interpreting multisteroid profiles.28
  • PMID 36246328: A preliminary veterinary LC-MS/MS study found that serum steroid profiles were broadly similar among dogs with hepatocellular carcinoma, hyperadrenocorticism, and both conditions. Although indirect to ACC, it reinforces that multisteroid abnormalities in blood are not automatically specific for adrenocortical carcinoma and must be interpreted in context.26

References

Footnotes

  1. Diagnosis of a malignant adrenal mass: the role of urinary steroid metabolite profiling.. Curr Opin Endocrinol Diabetes Obes. 2017. PMID: 28234802. Local full text: 28234802.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10

  2. The Potential of Steroid Profiling by Mass Spectrometry in the Management of Adrenocortical Carcinoma.. Biomedicines. 2020. PMID: 32872281. Local full text: 32872281.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6

  3. Urinary steroid profile in adrenocortical tumors.. Biomed Pharmacother. 2000. PMID: 10915023. Local full text: 10915023.md ↩ ↩2 ↩3 ↩4

  4. Plasma steroid metabolome profiling for the diagnosis of adrenocortical carcinoma.. Eur J Endocrinol. 2019. PMID: 30481155. Local full text: 30481155.md ↩ ↩2 ↩3 ↩4 ↩5

  5. Steroid profile in urine: a useful tool in the diagnosis and follow up of adrenocortical carcinoma.. Acta Endocrinol (Copenh). 1990. PMID: 2141212. Local full text: 2141212.md ↩ ↩2 ↩3 ↩4

  6. Advances in our understanding of the prognosis of adrenal incidentaloma.. Expert Rev Endocrinol Metab. 2016. PMID: 30058921. Local full text: 30058921.md ↩ ↩2 ↩3 ↩4 ↩5

  7. Different Types of Urinary Steroid Profiling Obtained by High-Performance Liquid Chromatography and Gas Chromatography-Mass Spectrometry in Patients with Adrenocortical Carcinoma.. Horm Cancer. 2016. PMID: 27370636. Local full text: 27370636.md ↩ ↩2 ↩3

  8. Adrenocortical carcinoma: current state of the art, ongoing controversies, and future directions in diagnosis and treatment.. Ther Adv Chronic Dis. 2021. PMID: 34349894. Local full text: 34349894.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7

  9. A 13-Steroid Serum Panel Based on LC-MS/MS: Use in Detection of Adrenocortical Carcinoma.. Clin Chem. 2017. PMID: 28904054. Local full text: 28904054.md ↩ ↩2 ↩3

  10. Serum Steroid Profiling in the Diagnosis of Adrenocortical Carcinoma: A Prospective Cohort Study.. J Clin Endocrinol Metab. 2025. PMID: 39231247. Local full text: 39231247.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7

  11. Analysis of steroid profiles by mass spectrometry: A new tool for exploring adrenal tumors?. Ann Endocrinol (Paris). 2021. PMID: 33278379. Local full text: 33278379.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6

  12. Clinical Application of Steroid Profiles and Their Interpretation in Adrenal Disorders.. Diagnostics (Basel). 2026. PMID: 41681699. Local full text: 41681699.md ↩ ↩2 ↩3 ↩4

  13. Measurement of urinary steroid profile in patients with adrenal tumor as a screening method for carcinoma.. Endocrinol Jpn. 1985. PMID: 4017973. Local full text: 4017973.md ↩ ↩2

  14. Clinicopathological features, biochemical and molecular markers in 5 patients with adrenocortical carcinoma.. Endocr J. 2011. PMID: 21521927. Local full text: 21521927.md ↩ ↩2 ↩3

  15. High-Resolution, Accurate-Mass (HRAM) Mass Spectrometry Urine Steroid Profiling in the Diagnosis of Adrenal Disorders.. Clin Chem. 2017. PMID: 28814383. Local full text: 28814383.md ↩ ↩2 ↩3

  16. Use of urinary steroid profiling for diagnosing and monitoring adrenocortical tumours.. Hong Kong Med J. 2009. PMID: 19966352. Local full text: 19966352.md ↩ ↩2

  17. Hypermineralocorticoidism due to adrenal carcinoma: plasma corticosteroids and their response to ACTH and angiotensin II.. Clin Endocrinol (Oxf). 1987. PMID: 2822295. Local full text: 2822295.md ↩ ↩2

  18. Adrenocortical carcinoma producing 11-deoxycorticosterone: a rare cause of mineralocorticoid hypertension.. J Endocrinol Invest. 2005. PMID: 15816373. Local full text: 15816373.md ↩ ↩2

  19. 11-Deoxycorticosterone Producing Adrenal Hyperplasia as a Very Unusual Cause of Endocrine Hypertension: Case Report and Systematic Review of the Literature.. Front Endocrinol (Lausanne). 2022. PMID: 35432204. Local full text: 35432204.md ↩ ↩2 ↩3

  20. Precursors of etiocholanolone and androsterone in adrenal carcinoma.. Proc Soc Exp Biol Med. 1961. PMID: 13762592. Local full text: 13762592.md ↩ ↩2

  21. Origin of pregnanetriol in a patient with adrenal carcinoma.. J Clin Endocrinol Metab. 1962. PMID: 13895833. Local full text: 13895833.md ↩ ↩2

  22. Further studies on the origin of pregnanetriol in adrenal carcinoma.. J Clin Endocrinol Metab. 1963. PMID: 13960199. Local full text: 13960199.md ↩ ↩2

  23. Hypoaldosteronism accompanied by normal or elevated mineralocorticosteroid pathway steroid: a marker of adrenal carcinoma.. J Clin Endocrinol Metab. 1993. PMID: 8421100. Local full text: 8421100.md ↩ ↩2 ↩3

  24. Simplified urinary steroid profiling by LC-MS as diagnostic tool for malignancy in adrenocortical tumors.. Clin Chim Acta. 2023. PMID: 36948238. Local full text: 36948238.md ↩ ↩2 ↩3

  25. Serum steroid profiling by mass spectrometry in adrenocortical tumors: diagnostic implications.. Curr Opin Endocrinol Diabetes Obes. 2019. PMID: 30893084. Local full text: 30893084.md ↩ ↩2

  26. Serum steroid profiling of hepatocellular carcinoma associated with hyperadrenocorticism in dogs: A preliminary study.. Front Vet Sci. 2022. PMID: 36246328. Local full text: 36246328.md ↩ ↩2

  27. Multiples of Median-Transformed, Normalized Reference Ranges of Steroid Profiling Data Independent of Age, Sex, and Units.. Horm Res Paediatr. 2018. PMID: 29694956. Local full text: 29694956.md ↩ ↩2 ↩3

  28. Adrenocortical function in old age: response to acute adrenocorticotropin stimulation.. J Clin Endocrinol Metab. 1982. PMID: 6274897. Local full text: 6274897.md ↩ ↩2 ↩3

  29. Cross reactions elicited by serum 17-OH progesterone and 11-desoxycortisol in cortisol assays.. Clin Chim Acta. 2009. PMID: 19481537. Local full text: 19481537.md ↩ ↩2

  30. [In vivo and in vitro studies on 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone in normal subjects and in those with various adrenocortical disorders (author’s transl)].. Nihon Naibunpi Gakkai Zasshi. 1979. PMID: 226427. Local full text: 226427.md ↩

  31. [A case of DOC-producing adrenocortical cancer causing right chest pain].. Nihon Naika Gakkai Zasshi. 1989. PMID: 2794692. Local full text: 2794692.md ↩

  32. Adrenocortical carcinoma with Cushing’s syndrome presenting unusual urinary 17-ketosteroid fractionation.. J Endocrinol Invest. 1985. PMID: 3161933. Local full text: 3161933.md ↩

  33. Plasma concentrations of 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone simultaneously measured in normal subjects and adrenocortical disorders.. Tohoku J Exp Med. 1980. PMID: 7209971. Local full text: 7209971.md ↩

  34. [Plasma steroid hormones in Cushing’s syndrome: their relation to cause and clinical manifestations (author’s transl)].. Nihon Naibunpi Gakkai Zasshi. 1981. PMID: 7286345. Local full text: 7286345.md ↩

  35. An unusual cause of mineralocorticoid hypertension.. Hypertension. 2014. PMID: 25156173. Local full text: 25156173.md ↩

  36. Atmospheric Pressure Chemical Ionization Is a Suboptimal Ionization Source for Steroids.. Clin Chem. 2018. PMID: 29653936. Local full text: 29653936.md ↩

  37. Urinary steroid profiling in diagnostic evaluation of an unusual adrenal mass.. Endocrinol Diabetes Metab Case Rep. 2019. PMID: 31778357. Local full text: 31778357.md ↩

  38. Steroid metabolites for diagnosing and predicting clinicopathological features in cortisol-producing adrenocortical carcinoma.. BMC Endocr Disord. 2020. PMID: 33228607. Local full text: 33228607.md ↩

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