# Glucocorticoid and mineralocorticoid production in hormonally silent adrenocortical tumor tissue in dogs

**Authors:** Kirsten L van Bokhorst, Marit F van den Berg, Hans S Kooistra, Monique E van Wolferen, Elpetra P M Timmermans-Sprang, Andrea Corsini, Stefania Golinelli, Nicole Bechmann, Mirko Peitzsch, Sara Galac

PMC · DOI: 10.1093/jvimsj/aalaf087 · Journal of Veterinary Internal Medicine · 2026-02-02

## TL;DR

This study finds that some hormonally silent adrenal tumors in dogs produce steroid hormones, suggesting they may not be as inactive as previously thought.

## Contribution

The study reveals that hormonally silent adrenocortical tumors in dogs have elevated glucocorticoid and mineralocorticoid precursor concentrations compared to healthy tissue.

## Key findings

- SATs showed higher cortisol and 21-deoxycortisol levels than healthy adrenals.
- SATs had elevated corticosterone and 18-OH-corticosterone compared to normal tissue.
- SATs and cortisol-secreting tumors had similar steroid concentrations.

## Abstract

No consensus exists regarding the monitoring and therapeutic approach to adrenal tumors (ATs) discovered incidentally by diagnostic imaging, when standard endocrine testing yields negative results.

To evaluate tissue concentrations of adrenocortical steroids in hormonally silent adrenocortical tumors (SATs) in dogs.

Fourteen dogs with SATs (12 unilateral, 2 bilateral), 11 dogs with cortisol-secreting adrenocortical tumors (cs-ACTs) and 10 healthy dogs.

Observational study. Diagnosis of SAT was based on finding an AT on diagnostic imaging, negative endocrine function tests, and histopathological and immunohistochemical confirmation. Adrenocortical steroid tissue concentrations were measured by liquid chromatography with tandem mass spectrometry and compared between SATs, cs-ACTs, and normal adrenals (NAs).

Hormonally silent adrenocortical tumors exhibited higher median tissue cortisol (3.62 ng/mg, range 0.05–18.1) and 21-deoxycortisol (0.08 ng/mg, range 0.00–0.44) concentrations than NAs (cortisol 0.38 ng/mg, range 0.01–1.90; 21-deoxycortisol 0.01 ng/mg, range 0.00–0.03; P = .04 and P = .001, respectively), and these concentrations were not significantly different between SATs and cs-ACTs. Furthermore, SATs’ median tissue concentrations of mineralocorticoid precursors corticosterone (2.15 ng/mg, range 0.01–14.1) and 18-OH-corticosterone (0.70 ng/mg, range 0.00–4.89) were higher than in NAs (respectively 0.19 ng/mg [range 0.14–0.54] and 0.05 ng/mg [range 0.01–0.33]; both P = .01) and not different when compared to cs-ACTs.

This study on tissue metabolomics in ATs in dogs demonstrates comparable tissue concentrations of specific glucocorticoids and mineralocorticoids in SATs and cs-ACTs. This implies that some SATs are not hormonally silent, prompting further studies on diagnostics, treatment, and monitoring recommendations.

## Linked entities

- **Chemicals:** cortisol (PubChem CID 5754), 21-deoxycortisol (PubChem CID 92827), corticosterone (PubChem CID 5753)
- **Species:** Canis lupus familiaris (taxon 9615)

## Full-text entities

- **Genes:** TH (tyrosine hydroxylase) [NCBI Gene 403444], CHGA (chromogranin A) [NCBI Gene 607527], REN (renin) [NCBI Gene 403838], PNMT (phenylethanolamine N-methyltransferase) [NCBI Gene 491023], HSD3B2 (hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2) [NCBI Gene 483146] {aka 3b-HSD, HSD3B, HSD3B1}, CYP11A1 (cytochrome P450 family 11 subfamily A member 1) [NCBI Gene 478365], CYP17A1 (cytochrome P450 family 17 subfamily A member 1) [NCBI Gene 477807], ACCS (1-aminocyclopropane-1-carboxylate synthase homolog (inactive)) [NCBI Gene 611393], POMC (proopiomelanocortin) [NCBI Gene 403659] {aka ACTH}, STAR (steroidogenic acute regulatory protein) [NCBI Gene 475588], SYP (synaptophysin) [NCBI Gene 612557]
- **Diseases:** dependent (MESH:D019966), adrenal neoplasia (MESH:D009369), weakness (MESH:D018908), polyuria (MESH:D011141), ATs (MESH:D000310), hyperactivity (MESH:D006948), adrenal disease (MESH:D000307), hypercortisolism (MESH:D003480), ACC (MESH:D018268), alopecia (MESH:D000505), adenoma (MESH:D000236), polyphagia (MESH:D006963), adrenocortical adenoma (MESH:D018246), immune-mediated disease (MESH:C567355), diarrhea (MESH:D003967), endocrine disease (MESH:D004700), polydipsia (MESH:D059606), metastases (MESH:D009362), hypertension (MESH:D006973), back pain (MESH:D001416), adrenal sex steroid producing tumors (MESH:D058533), Pheochromocytoma (MESH:D010673), lower urinary tract disease (MESH:D014570), ACA (MESH:D020243), cs-ACT (MESH:C566879), hemolytic anemia (MESH:D000743), hypokalemia (MESH:D007008), hyperaldosteronism (MESH:D006929), vein (MESH:D000071078), AIs (MESH:C538238)
- **Chemicals:** nitrogen (MESH:D009584), androstenedione (MESH:D000735), Cortisol (MESH:D006854), aldosterone (MESH:D000450), Corticosterone (MESH:D003345), cortisone (MESH:D003348), tricarboxylic acid (MESH:D014233), 17-OH-progesterone (MESH:D019326), 11-deoxycortisol (MESH:D003350), tetrahydro-11-deoxycortisol (MESH:C009412), 11-dehydrocorticosterone (MESH:C003552), progesterone (MESH:D011374), metanephrines (MESH:D008676), 18-Oxo-cortisol (MESH:C038135), E (MESH:D004540), dexamethasone (MESH:D003907), catecholamine (MESH:D002395), 21-deoxycortisol (MESH:C003556), 18-OH-cortisol (-), H (MESH:D006859), creatinine (MESH:D003404), steroid (MESH:D013256), dehydroepiandrosterone (MESH:D003687), 11-deoxycorticosterone (MESH:D003900)
- **Species:** Canis lupus familiaris (dog, subspecies) [taxon 9615], Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12862633/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12862633/full.md

## References

45 references — full list in the complete paper: https://tomesphere.com/paper/PMC12862633/full.md

---
Source: https://tomesphere.com/paper/PMC12862633