Addison Disease Case Study

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Case Study: Clinical Biochemistry investigation into Addison Disease
Introduction
A fifteen year old male presented to the Emergency Department (ED) with his mother in St. Vincent’s University Hospital (SVUH) on the 8th September 2017 with suspected Addison disease (AD). On initial examination he was found to have severe abdominal pain and prolonged vomiting. Other symptoms could include fatigue, myalgia, weight loss and salt craving (Brooke & Monson, 2017).
Laboratory Investigation and Results
A blood sample was received on this patient into the Biochemistry laboratory in SVUH from ED. A comprehensive metabolic panel was carried out which is shown in Table 1. The sample was analysed on the Roche Cobas 8000 analyser.
Test 08/09/2017 09/09/2017 12/09/2017 22/09/2017 Reference
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(ACTH = adrenocorticotropic hormone.)
Significant low results from the initial sample showed hyponatremia with a sodium level of 103mmol/L, hypochloraemia with a chloride level of 64mmol/L and low total CO2 of 19mmol/L. Hyponatremia is the most common initial laboratory finding as cortisol has weak mineralocorticoid activity and it is also required for free water excretion. A loss of aldosterone activity also leads to natriuresis (Munir & Waseem, 2017).

Significant high results from the initial sample showed hyperkalaemia with a potassium level of 7.5mmol/L, hypercalcemia with a total calcium level of 2.74mmol/L which was also accompanied by an elevated adrenocorticotropic hormone (ACTH) result of 410.6ng/L and plasma renin of
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The result of this was that the cortisol in his serum was elevated as it was synthetic. Therefore he was not diagnosed with AAD by his cortisol

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