Adrenal hyperplasia is diffuse or nodular enlargement of bilateral adrenal glands, developing from excessive hormonal stimulation of the adrenal cortex or, less commonly, the medulla. The most common causes are ACTH-dependent Cushing's disease (pituitary-origin), ectopic ACTH syndrome, congenital adrenal hyperplasia (CAH — 21-hydroxylase deficiency most common), and primary hyperaldosteronism (bilateral idiopathic hyperplasia). On imaging, bilateral adrenal gland thickness increase (limb >10 mm), bilateral diffuse enlargement, or small nodules within adrenal glands are observed. Focal nodular hyperplasia (macronodular hyperplasia) may be confused with unilateral adenoma, but bilateral involvement and multiple nodules support hyperplasia. Diagnosis is based on hormonal evaluation and imaging correlation.
Age Range
20-80
Peak Age
50
Gender
Female predominant
Prevalence
Common
The pathogenesis of adrenal hyperplasia varies according to the underlying etiology. In ACTH-dependent hyperplasia, excessive ACTH secretion from pituitary adenoma (Cushing's disease) or ectopic ACTH sources (small cell lung carcinoma, bronchial carcinoid, thymic carcinoid) stimulates proliferation of zona fasciculata and zona reticularis cells → bilateral diffuse or nodular hyperplasia → excessive cortisol production. Chronic ACTH stimulation increases lipid (cholesterol ester) accumulation in adrenal cortical cells — this intracellular lipid causes opposed-phase signal drop on MRI chemical shift; however, signal drop may be less pronounced than adenoma because lipid content of hyperplastic cells is more variable. In congenital adrenal hyperplasia (CAH), enzyme deficiencies (most commonly 21-hydroxylase) block cortisol synthesis → loss of negative feedback → excessive ACTH from pituitary → adrenal hyperplasia; the androgen pathway remains active → virilization. In ACTH-independent macronodular hyperplasia (AIMAH), aberrant receptor expression (GIP, beta-adrenergic, LH/hCG, serotonin receptors) autonomously stimulates adrenal cells → multiple macronodules (1-5 cm) develop. On imaging, bilateral adrenal enlargement reflects lipid accumulation and vascularity increase in hyperplastic cells.
Diffuse thickening of both adrenal glands (limb >10 mm) with preservation of normal 'Y' or inverted 'V' configuration is the characteristic signature finding for adrenal hyperplasia. This finding reflects the diffuse and uniform effect of widespread cortical stimulation, unlike adenoma (focal mass), carcinoma (large irregular mass), and metastasis (bilateral irregular masses).
On non-contrast CT, diffuse or nodular enlargement is observed in bilateral adrenal glands. Adrenal limb thickness >10 mm (normal <6-8 mm). In diffuse hyperplasia, adrenal gland shape ('Y' or inverted 'V') is preserved but all limbs are thickened. In nodular hyperplasia, multiple small nodules (generally <3 cm) are seen in bilateral adrenal glands. Density is generally low (most cases <10 HU) — reflecting lipid-rich hyperplastic cells. In macronodular hyperplasia (AIMAH), both glands contain multiple large nodules (1-5 cm) and adrenal shape may be distorted.
Report Sentence
Diffuse enlargement is observed in bilateral adrenal glands with adrenal limb thickness bilaterally >10 mm; consistent with adrenal hyperplasia along with low density values.
On chemical shift MRI, variable degree of opposed-phase signal drop is observed in hyperplastic adrenal glands. Signal intensity index (SII) is generally 10-30% and may or may not meet the >20% criterion for adenoma. In diffuse hyperplasia, signal drop is generally bilateral and symmetrically distributed. In nodular hyperplasia, nodules and non-nodular tissue may show different levels of signal drop. In lipid-poor hyperplasia forms, signal drop is minimal or absent.
Report Sentence
Signal drop on opposed-phase chemical shift MRI is observed in bilateral adrenal glands; supporting intracellular lipid content consistent with adrenal hyperplasia.
On contrast-enhanced CT, hyperplastic adrenal glands show mild-to-moderate homogeneous enhancement. Enhancement is slightly more prominent than normal adrenal glands but heterogeneous enhancement is not expected. In nodular hyperplasia, nodules enhance at similar levels to surrounding adrenal parenchyma. In macronodular hyperplasia, slight heterogeneity may be seen in large nodules. Washout analysis can be applied — hyperplastic tissue may show high washout rates similar to adenoma.
Report Sentence
Mild-to-moderate homogeneous enhancement is observed in bilateral hyperplastic adrenal glands; consistent with adrenal hyperplasia.
On T1-weighted images, hyperplastic adrenal glands show isointense or mildly hyperintense signal to liver. Mild T1 hyperintensity is due to intracellular lipid accumulation. In nodular hyperplasia, nodules show homogeneous T1 signal. Hemorrhage or necrosis is not expected and T1 heterogeneity is not typical for adrenal hyperplasia — adenoma or carcinoma should be considered if heterogeneity is present.
Report Sentence
Bilateral adrenal glands demonstrate homogeneous, isointense/mildly hyperintense signal to liver on T1-weighted images; consistent with adrenal hyperplasia.
On T2-weighted images, hyperplastic adrenal glands show isointense or mildly hyperintense signal to spleen. Marked T2 hyperintensity is not expected — high T2 signal should suggest pheochromocytoma or metastasis. Nodules show homogeneous T2 signal. Diffuse hyperplasia also demonstrates bilateral symmetric appearance on T2.
Report Sentence
Bilateral adrenal glands demonstrate homogeneous, isointense/mildly hyperintense signal to spleen on T2-weighted images.
On NP-59 (I-131 6β-iodomethyl-19-norcholesterol) adrenal cortical scintigraphy, bilateral symmetric increased uptake is observed. This finding indicates both adrenal glands have autonomous function and is critically important in differentiating adenoma (unilateral uptake + contralateral suppression) from hyperplasia (bilateral symmetric uptake). NP-59 scintigraphy is particularly decisive in determining etiology of primary hyperaldosteronism (adenoma vs bilateral hyperplasia).
Report Sentence
Bilateral symmetric increased uptake is observed on NP-59 adrenal cortical scintigraphy; consistent with bilateral adrenal hyperplasia and excluding unilateral adenoma.
Criteria
Cushing's disease or ectopic ACTH. Bilateral symmetric diffuse enlargement. Cortisol elevation + non-suppressible dexamethasone test.
Distinct Features
Most common form. Adrenal shape preserved with all limbs thickened. CT density may be low (<10 HU). Pituitary MRI for microadenoma. CT thorax for ectopic source (lung carcinoid).
Criteria
ACTH-independent bilateral macronodular adrenal hyperplasia. Bilateral multiple large nodules (1-5 cm). Aberrant receptor expression. ACTH suppressed, cortisol elevated.
Distinct Features
Adrenal glands can become very large — each may exceed 50 g. Multiple macronodules bilateral. Prominent bilateral enlargement + nodular contour on CT. Each nodule may show different lipid content. Aberrant receptor stimulation tests guide diagnosis.
Criteria
Enzyme deficiency (most commonly 21-hydroxylase). Elevated 17-OH progesterone. Congenital or late-onset. Confirmed by genetic testing.
Distinct Features
Bilateral adrenal enlargement + adrenal rest tumors in testes or ovaries may accompany. In long-term untreated CAH, adrenal glands can become very large — increased risk of myelolipoma. CT bilateral adrenal hyperplasia + testicular US bilateral hypoechoic masses (adrenal rest) is a diagnostic combination.
Distinguishing Feature
Adenoma is usually unilateral focal mass (<4 cm); hyperplasia shows bilateral diffuse enlargement. Adenoma shows >20% signal drop on opposed-phase, hyperplasia variable. NP-59 shows unilateral uptake + contralateral suppression in adenoma, bilateral symmetric in hyperplasia.
Distinguishing Feature
Bilateral adrenal metastasis with known malignancy creates irregularly bordered, heterogeneous masses. No opposed-phase signal drop in metastasis. Metastasis may show high T2 signal. Hyperplasia is smooth-contoured, homogeneous, low-density. Metastasis shows intense FDG uptake on PET-CT, hyperplasia minimal.
Distinguishing Feature
Adrenal lymphoma forms bilateral large homogeneous masses; hyperplasia shows diffuse thickening. B symptoms present in lymphoma. Lymphoma shows low T2 signal, hyperplasia iso-mildly hyperintense. Lymphoma shows no opposed-phase signal drop.
Distinguishing Feature
Granulomatous disease shows rim enhancement, central necrosis, and chronic calcification; hyperplasia shows homogeneous enhancement with no calcification expected. Granulomatous disease with infection history (TB, histoplasmosis). Addison's disease can occur in both but mechanism differs.
Urgency
routineManagement
medicalBiopsy
Not NeededFollow-up
6-monthAdrenal hyperplasia diagnosis is based on hormonal evaluation and imaging correlation; biopsy is generally not needed. Treatment targets the underlying etiology: pituitary adenoma resection in Cushing's disease, primary tumor treatment in ectopic ACTH, medical therapy (spironolactone/eplerenone) in primary hyperaldosteronism (bilateral hyperplasia), glucocorticoid replacement in CAH. Bilateral adrenalectomy may be considered in AIMAH but requires lifelong steroid replacement. Adrenal size may regress with normalization of hormonal levels. Follow-up with hormonal parameters and periodic imaging.
Adrenal hyperplasia is the most common cause of hormonal hypersecretion. In Cushing syndrome, identifying the ACTH source (pituitary vs ectopic) guides treatment. In Conn syndrome, adrenal vein sampling may be needed for lateralization.