A 63-year-old female patient was referred to our hospital in February
1994 for a pituitary tumor. On a previous examination, in 1973, she ha
d a goiter, nonspecific symptoms and only an elevated serum T-3. In 19
84 she had become hypothyroid, her goiter had increased, serum T-4 was
69 mol/L, TSH 34.4 mU/L, and TPO antibodies were positive. Hypothyroi
dism due to autoimmune thyroiditis was diagnosed and she received L-T-
4 100 mu g/day. In 1985 and 1986, serum TSH had decreased but remained
slightly elevated, while T-4 was at the upper limits of normal. From
1987 to 1989 her serum TSH rose from 9 to 20 mU/L and remained at that
level for the ensuing 4 years in spite of increasing L-T-4 up to 150
mu g/day. In October 1993, after discontinuing L-T-4 for 6 weeks, TSH
was 23.7 mU/L, T-4 170 nmol/L, I-131 thyroid uptake 52%, and the GT sc
an showed a large pituitary tumor with suprasellar extension. On preop
erative investigation TSH was 40-51 mU/L with no response to TRH or Gn
RH. The alpha-subunit was increased at 6.33 mu g/L with the alpha-TSH/
TSH molar ratio of 1.23. Prolactin was elevated, but plasma cortisol,
FSH, and LH were low. At surgery, we found a large chromophobe adenoma
with few PAS-positive granules and with immunostaining positive for T
SH and prolactin. From the clinical and biological data, we can conclu
de that the patient had probably a TSH-secreting adenoma since the goi
ter was first detected. The development, however, of autoimmune thyroi
ditis with hypothyroidism considerably modified the presentation of th
e disease and may have accelerated the growth of the tumor.