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Investigation

Authoring team

Investigations include:

  • biochemistry
    • damage to adrenal cortex results in mineralocorticoid deficiency causing low serum sodium, and raised serum potassium and H+ (1)
    • serum urea and albumin are raised because of dehydration
    • serum renin is raised due to sodium depletion.
    • in secondary hypoadrenalism, electrolytes are usually normal as aldosterone-secreting cells are normal
  • serum cortisol level (ideally between 8-9 am)
    • random measurements have a low sensitivity for Addison's disease due to the pulsatile nature and diurnal variation of cortisol secretion (2)
    • if level of serum cortisol is
      • <100 nanomol/L - adrenal insufficiency is highly likely ( if the patient is not on oral or inhaled steroids)
      • >400 nanomol/L - adrenal insufficiency is unlikely (diagnosis is not excluded if the patient is acutely unwell at the time since cortisol values may increase during illness)
      • between 100 and 400 nanomol/L - refer to a specialist for further investigations e.g. - synacthen test (1)
  • blood glucose may be low - insulin-induced hypoglycaemia

  • possible ECG findings are detailed - click here

Secondary care investigations carried out to confirm the diagnosis and to find the cause nclude:

  • plasma rennin (1)
  • markedly elevated plasma ACTH - greater than 80 ng per litre - with low or normal serum cortisol on presentation or in the morning after omitting replacement therapy is an early indication of primary hypoadrenalism
  • synacthen test:
    • short test may confirm suspected hypoadrenalism
    • depot test may discriminate primary and secondary causes
  • adreno-cortical antibodies - often present in autoimmune adrenalitis - more common in women - 80% - than men - 10%
  • abdominal film - calcified adrenals of tuberculosis
  • chest radiology - tuberculous lesions, areas of malignancy and calcification
  • clinical or serological evidence of other organ specific autoimmune disease

Reference:


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