Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 15 P255

SFEBES2008 Poster Presentations Pituitary (62 abstracts)

A case of secondary adrenal insufficiency

George Tharakan & Emma Hatfield


Endocrine Unit Department of Investigative Medicine, Charing Cross Hospital, Imperial College Healthcare NHS Trust, London, UK.


A 30-year-old female presented to accident and emergency having been found collapsed. The patient had a reduced Glasgow Coma Scale of 10, was pyrexial, clinically in shock and pale in colour. Initial investigations confirmed hypoglycemia and a metabolic acidosis. A collateral history described a 3 days history of diarrhoea. Her 5-year-old child (who was conceived normally) also had diarrhoea.

The impression was of shock secondary to sepsis and hypovolemia. She was resuscitated successfully with intravenous fluids and antibiotics.

Subsequent history revealed a diagnosis of primary hypothyroidism since 2005. The patient had been non-complaint with thyroxine since November 2006 due to nausea. She was on no other medication (including recreational drugs or topical creams).

A septic screen was negative. Other blood tests were normal except for thyroid function, (TSH 7.99, Free T4 12.8). A short synacthen test demonstrated adrenal insufficiency. Primary adrenal insufficiency was excluded due to repeated low ACTH and negative adrenal antibodies. This was confirmed by a long synacthen test, which demonstrated a late rise in cortisol. The remainder of the pituitary profile and a MRI of the pituitary were normal.

The patient is well on replacement hydrocortisone.

The diagnosis of isolated ACTH deficiency is uncommon. Whilst primary and secondary adrenal failure (SAI) have many similar features, the presence of hypoglycemia and the lack of hyperpigmentation as demonstrated in our patient favour SAI. An episode of infective diarrhoea was the likely precipitant for her acute adrenal failure, and the history of intolerance to thyroxine may be indicative of a relative cortisol deficiency at that time and not true hypothyroidism.

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