Adrenal Calcification: Causes, Diagnosis, and Complications

Calcium deposits in the adrenal glands are often detected incidentally during imaging for unrelated conditions. While they may not always cause symptoms, their presence can indicate underlying pathology requiring further evaluation.

Identifying potential causes and assessing hormonal function are key to determining clinical significance. Diagnostic imaging plays a crucial role in detecting these calcifications, while understanding possible complications helps guide management decisions.

Possible Causes

Adrenal calcification can result from infections, metabolic disorders, hemorrhage, trauma, or congenital abnormalities. Understanding these causes is essential for identifying associated health concerns and determining management strategies.

Infectious Etiologies

Certain infections lead to adrenal calcification, particularly those causing chronic inflammation or tissue destruction. Tuberculosis (TB) is a well-documented cause, often affecting the adrenal glands through hematogenous spread. A study in The Lancet Infectious Diseases (2021) highlighted TB as a significant cause of adrenal insufficiency in endemic regions. Fungal infections, such as histoplasmosis and blastomycosis, can also contribute to calcifications, particularly in immunocompromised individuals. These infections cause granulomatous inflammation, leading to necrosis and subsequent calcification. Bacterial infections, including Neisseria meningitidis in Waterhouse-Friderichsen syndrome, may cause adrenal hemorrhage that later calcifies. Identifying an infectious origin often requires serologic testing, culture analysis, or polymerase chain reaction (PCR) assays.

Metabolic Disorders

Certain metabolic conditions contribute to adrenal calcifications through abnormal calcium deposition or impaired adrenal function. Wolman disease, a rare lysosomal storage disorder, leads to excessive lipid accumulation in the adrenal glands, eventually causing calcification. A 2022 review in Molecular Genetics and Metabolism described how LIPA gene mutations disrupt cholesterol ester metabolism, leading to progressive adrenal involvement. Addison’s disease, particularly when caused by autoimmune destruction, can also result in dystrophic calcifications. Prolonged hypercalcemia from conditions like primary hyperparathyroidism or chronic kidney disease may further contribute to calcium deposition. Evaluating metabolic causes involves assessing serum calcium, parathyroid hormone (PTH) levels, lipid profiles, and genetic testing when hereditary disorders are suspected.

Hemorrhage or Trauma

Adrenal hemorrhage, whether from blunt trauma, anticoagulation therapy, or coagulopathies, can leave residual calcifications. Post-traumatic adrenal calcification has been documented in high-impact injuries, such as motor vehicle accidents, where direct glandular damage leads to hemorrhagic necrosis. A retrospective study in Radiology (2023) found adrenal hemorrhage to be a frequent incidental finding in patients with severe abdominal trauma, with some cases progressing to calcification over months. In neonates, birth-related hypoxia or perinatal stress can trigger adrenal hemorrhage, particularly in preterm infants. Over time, hemorrhagic debris may resolve, leaving calcified remnants detectable on imaging. A history of trauma or anticoagulant use is crucial when evaluating adrenal calcifications of hemorrhagic origin.

Congenital Factors

Certain congenital conditions predispose individuals to adrenal calcifications due to structural abnormalities or genetic mutations affecting adrenal development. Congenital adrenal hyperplasia (CAH), particularly the 21-hydroxylase deficiency variant, has been associated with dystrophic calcifications in longstanding cases. A 2021 study in The Journal of Clinical Endocrinology & Metabolism described how prolonged adrenal hyperplasia and chronic stress on the glands could lead to calcified nodules. Adrenoleukodystrophy, a peroxisomal disorder affecting very-long-chain fatty acid metabolism, may also lead to adrenal calcifications due to progressive glandular dysfunction. Additionally, neuroblastomas, the most common adrenal tumors in pediatric patients, frequently exhibit calcified components on imaging. Identifying congenital contributors involves genetic testing, hormone analysis, and early detection through newborn screening programs.

Clinical Manifestations

Adrenal calcifications can range from asymptomatic incidental findings to significant endocrine dysfunction. Symptoms depend on the underlying cause, the extent of adrenal involvement, and whether hormonal production is affected.

When adrenal insufficiency arises, symptoms often develop gradually. Fatigue, weakness, and unintended weight loss reflect inadequate cortisol levels. Patients may experience gastrointestinal disturbances, including nausea, vomiting, and abdominal pain. Hypotension, particularly orthostatic, is another hallmark feature, as cortisol plays a central role in maintaining vascular tone. In longstanding cases, hyperpigmentation of the skin, especially in areas of friction, may develop due to increased adrenocorticotropic hormone (ACTH) stimulation.

In congenital conditions, symptoms often emerge early in life. Infants with Wolman disease may present with failure to thrive, hepatosplenomegaly, and persistent diarrhea due to systemic lipid accumulation. Children with congenital adrenal hyperplasia may show signs of androgen excess, such as early pubarche or abnormal genital development in severe cases. Neuroblastomas with calcified components may cause palpable abdominal masses, unexplained hypertension, or paraneoplastic syndromes related to catecholamine secretion.

Diagnostic Imaging Tools

Detecting adrenal calcifications often relies on imaging studies performed for unrelated medical concerns. Various imaging modalities, including computed tomography (CT), magnetic resonance imaging (MRI), and ultrasound, provide insights into the size, distribution, and characteristics of calcifications, aiding in differential diagnosis.

CT Scans

Computed tomography is the most sensitive imaging modality for detecting adrenal calcifications due to its high resolution. Non-contrast CT scans effectively identify calcifications as hyperdense foci within the adrenal glands. A 2023 study in European Radiology found that CT imaging detected adrenal calcifications in 94% of cases. CT scans also assess adrenal morphology, identifying masses, hemorrhagic remnants, or glandular atrophy. In adrenal tuberculosis, for example, CT may reveal bilateral gland enlargement with peripheral calcifications. Contrast-enhanced CT further characterizes vascularity and tissue composition, distinguishing benign from malignant processes.

MRI

Magnetic resonance imaging provides superior contrast resolution for assessing adrenal masses, hemorrhagic changes, and lipid-rich lesions. While MRI is less sensitive than CT for detecting calcifications, gradient echo sequences can identify calcified components by demonstrating signal voids. A 2022 review in Radiology: Imaging Cancer emphasized MRI’s role in distinguishing adrenal metastases from benign adenomas. Given its lack of ionizing radiation, MRI is particularly useful in pediatric and pregnant patients.

Ultrasound

Ultrasonography is less commonly used for adrenal imaging in adults due to the retroperitoneal location of the glands, which can be obscured by bowel gas. However, in pediatric patients and neonates, ultrasound is valuable for detecting adrenal hemorrhage and calcifications. High-frequency transducers can identify echogenic foci within the adrenal glands. A 2021 study in Pediatric Radiology highlighted ultrasound’s utility in diagnosing neonatal adrenal hemorrhage, with calcifications appearing as hyperechoic areas. While ultrasound lacks the resolution of CT or MRI, it remains useful in specific clinical scenarios, particularly when radiation exposure is a concern.

Hormonal Function Considerations

The presence of adrenal calcifications raises concerns about adrenal function, as these glands regulate metabolism, electrolyte balance, and stress responses. Assessing glucocorticoid, mineralocorticoid, and catecholamine synthesis is crucial, as disruptions can have significant physiological consequences.

Cortisol production, regulated by the hypothalamic-pituitary-adrenal (HPA) axis, is a primary focus in adrenal health assessment. If calcifications result from infections or autoimmune processes, adrenal tissue destruction can impair cortisol synthesis, leading to fatigue, hypotension, and electrolyte imbalances. Morning serum cortisol levels, ACTH concentrations, and ACTH stimulation tests help evaluate adrenal insufficiency. If adrenal failure is confirmed, glucocorticoid replacement therapy may be necessary.

Aldosterone deficiency can lead to hyponatremia, hyperkalemia, and volume depletion, manifesting as dizziness, salt cravings, and orthostatic hypotension. Plasma renin activity and aldosterone measurements help assess the renin-angiotensin-aldosterone system. In cases of significant mineralocorticoid deficiency, fludrocortisone is often prescribed.

Possible Complications

Adrenal calcifications can lead to progressive adrenal dysfunction, metabolic disturbances, or secondary complications. Extensive glandular damage may impair stress response, increasing the risk of adrenal crises during infections, surgery, or trauma. Without intervention, adrenal crises can cause severe hypotension, electrolyte imbalances, and multi-organ failure.

In cases where calcifications are associated with adrenal masses, further evaluation is necessary to determine malignancy risk. Chronic calcification secondary to hemorrhage or infection may lead to fibrosis and glandular shrinkage, potentially affecting blood flow. Extensive calcifications can, in rare cases, contribute to adrenal gland rupture.

Differential Diagnoses

Distinguishing adrenal calcifications from other pathologies requires careful evaluation of imaging characteristics, clinical history, and laboratory findings. Dystrophic calcifications result from prior tissue damage, while metastatic calcifications arise from systemic calcium-phosphorus imbalances, often seen in chronic kidney disease or hyperparathyroidism.

Adrenal tumors, both benign and malignant, must also be considered. While neuroblastomas frequently exhibit calcifications, pheochromocytomas and adrenal cortical carcinomas may also present with calcified components. Differentiating these entities requires contrast-enhanced CT, MRI, and biochemical testing for catecholamines or adrenal steroid excess. A systematic approach incorporating imaging, endocrine assessment, and clinical correlation is essential for accurate diagnosis and treatment planning.