E-Poster Presentation 63rd Endocrine Society of Australia Annual Scientific Meeting 2020

Mysteriously missing ACTH (#113)

Caroline Bachmeier 1 , Emily Brooks 2 , Jacobus Ungerer 1 , Carel Pretorius 1 , Warrick Inder 2
  1. Department of Chemical Pathology, Pathology Queensland, Brisbane, QLD, Australia
  2. Department of Endocrinology, Princess Alexandra Hospital, Brisbane, QLD , Australia

Abstract

Determining the underlying cause of hypercortisolism requires an accurate measurement of plasma adrenocorticotropic hormone (ACTH). Most laboratories measure ACTH via immunoassays. Interference in immunoassays is rare but well described and if present can lead to false results which can become clinically significant when they lead to invasive testing and inappropriate treatment. We describe the case of a 69-year old man with bilateral adrenal masses and associated mild cushingoid features. Mild biochemical hypercortisolism was accompanied by repeatedly grossly elevated ACTH levels. No ectopic or pituitary source was identified on various imaging modalities. The inconsistency of clinical, imaging and biochemistry findings raised concerns of assay interference. Several laboratory tests to investigate this possibility were performed and indicated that interference in the ACTH assay resulted in falsely elevated ACTH concentrations. The man underwent an adrenalectomy which confirmed an adrenocortical tumour. The erroneous ACTH results could have led to unnecessary and inappropriate further investigations and treatment. Close collaboration of the laboratory and the clinical teams is important to avoid adverse patient outcomes especially if there are inconsistencies in laboratory and clinical findings.

 

Structure of case:

1) Discussion of initial investigations for hypercortisolism and caveats of each test.

2) Discrepancies between imaging findings and biochemistry.

3) What to do if both pituitary MR and adrenal CT show lesions.

4) Laboratory investigations for possible interference.

5) Dynamic tests to differentiate the source of ACTH.