Adrenal tuberculosis

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

Pathology

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 TbTB. 

Clinical presentation

When up to 90% of the cortex has been destroyed patients can present with a possibly life-threatening Addisonian crisis. Prior to this symptoms of adrenal insufficiency such as fatigue and abdominal pain.

Radiographic features

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

CT

Unenhanced and portal venous phase IV contrast scans are usually performed. A narrow field of view further helps in optimising 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, localised, or diffuse

Gland density

• central low density can be seen in early disease
  • due to caseous necrosis
• with anti-Tb-TB treatment the adrenals show homogenous density

Enhancement

• can see areas of relative central hypoenhancement

MRI

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