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Journal of Clinical Endocrinology & Metabolism Vol. 43, No. 1 137-143
doi:10.1210/jcem-43-1-137
Copyright © 1976 by the Endocrine Society.
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Recurrent Goiter, Hyperthyroidism, Galactorrhea and Amenorrhea due to a Thyrotropin and Prolactin-Producing Pituitary Tumor

K. HORN*, F. ERHARDT*, R. FAHLBUSCH**, C. R. PICKARDT*, K. v. WERDER* and P. C. SCRIBA*

* II. Medizinische Klinik University of Munich, Munich, Germany
** Neurochirurgische Klinik University of Munich, Munich, Germany

Reprint requests to: Dr. Med. Klaus Horn, II. Med. Klinik der Universitaet, 8 Muenchen 2, Ziemssenstrasse 1, FRG.

A 22-year-old woman with recurrent goiter, hyperthyroidism, galactorrhea, and amenorrhea due to a pituitary tumor is described. She had been treated surgically twice for recurrent goiter with tracheal compression. Despite clinical signs of hyperthyroidism and slightly elevated plasma thyroid hormone levels (T4: 11 µg/dl; T3: 189 ng/dl), without thyroid hormone replacement therapy the basal TSH level was elevated up to 23 µU/ml and could not be suppressed by exogenous thyroid hormones: even when the serum thyroid hormone levels were raised into the thyrotoxic range (T4: 16.2 µg/dl T3: 392 ng/dl), the basal TSH fluctuated between 12 and 29 µU/ml. The basal PRL level was elevated up to 6000 µU/ml. The administration of TRH (200 µg iv) led only to small increments of TSH and PRL levels. Bromocriptin (5 mg p.o.) or L-dopa (0.5 g p.o.) suppressed TSH and PRL values significantly. After transsphenoidal hypophysectomy, TSH and PRL were below normal and the patient developed panhypopituitarism. The adenoma showed two cell types which could be identified as lactotrophs and thyrotrophs by electronmicroscopy and immunofluorescence. From these data we conclude that the patient had a pituitary tumor with an overproduction of thyrotropin and prolactin.

Supported by the Deutsche Forschungsgemeinschaft, SFB 51.

This observation was presented in part at the 7th International Thyroid Conference, Boston, 1975.

Received May 19, 1975.




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