Endocrine Abstracts (2005) 9 P213

A case of transient hypopituitarism and hyponatraemia

Y Raste, F Smeeton & D Russell-Jones

Department of Endocrinology, Royal Surrey County Hospital, Guildford, Surrey, UK.

We present the case of a 34 year old man, previously well, who presented with a 4 week history of worsening headaches and confusion.

He was disorientated and confused, but the rest of the examination was largely unremarkable. Admission blood tests revealed him to be profoundly hyponatraemic (serum sodium 100 millimoles per litre, urine sodium 72 millimoles per litre, serum osmolality 202 milliosmoles per kilogram, urinary osmolality 851 millimoles per kilogram).

The patient had an urgent CT brain scan on admission, which was normal. An MRI brain scan showed the pituitary gland to be enlarged with abnormal signal, consistent with acute infarction. The brain parenchyma was also abnormal, consistent with extrapontine demyelination.

Subsequent blood tests suggested the diagnosis of panhypopituitarism (random cortisol 372 nanomoles per litre, prolactin 253 microunits per litre, thyroid stimulating hormone 0.2 microunits per litre, triiodothyronine 1.8 millimoles per litre, thyroxine 5.8 millimoles per litre, luteinising hormone 2 units per litre, follicle stimulating hormone 1.1 units per litre, testosterone less than 3.0 nanomoles per litre). The patient was commenced on replacement hormone therapy. The

hyponatraemia was corrected slowly with fluid restriction.

After initial improvement in symptoms, he re-presented approximately one month later with slurred speech and personality change. On examination, he had cerebellar signs with poor co-ordination and dysarthria. Only his thyroid function was abnormal (thyroid stimulating hormone 0.6 microunits per litre, thyroxine 0.16 millimoles per litre, triiodothyronine 2.8 millimoles per litre); the rest of his pituitary function tests were normal. His thyroxine dose was increased.

A repeat MRI brain scan showed the pituitary to be much smaller than previously. The basal ganglia were also grossly abnormal, again consistent with extrapontine demyelination.

Three months later, this patient made a full recovery. His pituitary function tests remain within normal limits and he no longer requires hormone replacement.

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