Adrenal tuberculosis

Last revised by Daniel J Bell on 24 Jul 2023

Tuberculous adrenalitis is the result of adrenal Mycobacterium tuberculosis (TB) infection. Its incidence has decreased in the western world with the declining incidence of tuberculosis.

As the tuberculous infection causes destruction of the adrenal cortex, primary adrenal insufficiency develops. Pathology usually reveals tuberculous granuloma, caseous necrosis, fibrosis, and calcification.

As adrenal involvement progresses, physiological tests for adrenal insufficiency including plasma/urinary cortical measurement and ACTH challenges can raise suspicious for adrenal TB. 

Symptoms of adrenal insufficiency may occur, such as fatigue and abdominal pain. When >90% of the cortex has been destroyed, patients may present with Addisonian crisis, which can be life-threatening.

CT forms the mainstay of evaluation due to its high spatial resolution and availability, but MRI also has a known role in assessing adrenal lesions, particularly in young patients where radiation dose is a concern.

Unenhanced and portal venous phase IV contrast scans are usually performed. A narrow field of view further helps in optimizing spatial resolution in detecting discrete lesions.

  • gland contour:

    • in the early stage there can be mass-like adrenal enlargement

      • smooth adrenal contour is preserved

    • later on adrenal fibrosis and atrophy occurs

      • small adrenals with irregular margins

  • calcification:

    • this is a late feature, often occurring post-treatment

    • it can be punctate, localized, or diffuse

  • gland density:

    • central low density can be seen in early disease

      • due to caseous necrosis

    • with anti-TB treatment the adrenals show homogenous density

  • enhancement:

    • can see areas of relative central hypoenhancement

Imaging features are analogous to CT except for MR limitations in assessing calcified tissue.

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