A 35-year-old man presented with an apparently short history and clini
cal features of hypopituitarism. The diagnosis was confirmed by the fo
llowing investigations: random plasma cortisol 79 mmol/L (normal = 200
-770 mmol/L), total thyroxine 47 nmol/L (normal = 60-154 nmol/L), plas
ma testosterone 3.5 nmol/L (normal = 9-32 nmol/L), FSH 2.2, LH 2.0 IU/
L (normal = 2-20 IU/L), and no significant rise of cortisol and growth
hormone to insulin hypoglycemia. There was no abnormality of the pitu
itary on CT examination. He had a good response to replacement therapy
but 3 years later ceased all hormone replacement, felt well, and basa
l plasma cortisol, thyroxine, FSH, LH, and testosterone were normal. A
combined pituitary function test 8 years after presentation was norma
l. Fourteen years later he is clinically well with normal basal cortis
ol, thyroxine, TSH, FSH, LH, ACTH, and testosterone; and MRI examinati
on showed that the anterior pituitary gland and stalk were of normal d
imensions but the right two-thirds of the pituitary appeared nonfuncti
onal. It is believed that there has been spontaneous regeneration of a
nterior pituitary tissue after destruction, probably by infarction sev
ere enough to produce panhypopituitarism. The relation of this event t
o a severe illness with headache and prostration 7 years before presen
tation is doubtful because of his fertility during this time.