gms | German Medical Science

Pituitary enlargement in hypothyroid patients is usually due to reactive hyperplasia, correlates with TSH circulating levels and disappears with appropriate doses of L-thyroxine. It is a matter of debate whether secondary thyrotroph hyperplasia may lead to adenoma formation. Here, we report on a patient with long standing hypothyroidism, suffering from acute visual loss due to hemorrhage into a large TSH-secreting macroadenoma.

A 38-year-old male, non-compliant patient presented with acute blindness of the right eye and palsy of abducens and oculomotor nerves of the right side after circulatory collapse during thyroid scintigraphy and application of L-thyroxine. Six weeks before a temporal hemianopsia of the left eye had developed. On admission the patient was in an unstable cardiovascular state. Cor bovinum and pretibial myxedema were obvious. Endocrinological investigation showed that hypogonadism and hypocortisolism were present, the level of PRL was low. Basal TSH was > 100 µU/ml (normal range 0.50 – 2.00), fT3 was 2.59 pg/ml (1.80 – 4.60), fT4 0.39 ng/dl (1.00 – 1.80). MRI of the sellar region revealed an intra- and suprasellar pituitary tumor (maximal diameter 48 mm) with infiltration of the right cavernous sinus and elevation and compression of the optic chiasm. A partially necrotic and hemorrhagic adenoma was removed during CT-navigated transsphenoidal surgery. Intraoperatively, the medial wall of the right cavernous sinus was found to be infiltrated by tumor. Early postoperative CT revealed no tumor rest. Histologically, a necrotic and hemorrhagic pituitary adenoma was confirmed. The vital parts showed monomorphic cells. On immunohistochemical study, the tumor was positive for TSH, PRL, and GH. With daily application of L-thyroxin and hydrocortison, the patient recovered within weeks. Three months and two years after surgery, vision of the right eye was normal, on the left side there was a central scotoma and there was complete recovery of Nn. III and VI. On MRI no detectable tumor rest was found. After 2 years, the daily substitution consisted of 30 mg hydrocortison and 175 µg L-thyroxine. Sexual funtion has recovered without testosteron substitution.

Our findings of an invasive tumor suggest that thyrotroph adenomas may result from long-standing primary hypothyroidism as proposed by others (Ghannam NN et al. J Endocrinol Invest 22, 419 – 23, 1999).