Per-Olof Lundberg

Rapid decrease in amino acid metabolism in prolactin-secreting pituitary adenomas after bromocriptine treatment: a PET study.

Four patients with prolactin-secreting pituitary adenomas were examined with positron emission tomography using L-[11C]methionine to monitor the effect of dopamine agonist treatment on the amino acid metabolism in the tumors. Within the first few hours after intramuscular injection of bromocriptine retard (50 mg) the amino acid metabolism decreased by 40%. Two of the patients were reexamined 7 and 9 days later and showed a 70% reduction in the metabolism of the adenomas. This metabolic effect was later accompanied by significant tumor shrinkage in all adenomas. It is suggested that bromocriptine has a general and rapid effect on the protein synthesis of the prolactin-secreting pituitary adenoma cells.

Dopamine Receptors in Pituitary Adenomas and Effect of Bromocriptine Treatment — Evaluation with PET and MRI

Pituitary adenomas are as a rule benign tumors that can originate from immature pituitary stem cells or from one of the more specialized hormone producing cell types. Accordingly, the classification of pituitary adenomas is dominantly based on the type of hormonal activity or lack of such. Hormone serum/plasma levels will often provide an indication of the probable adenoma type. In some cases, however, this information is not sufficient for differentiation, and only fine needle biopsy with cytological evaluation including immunocytochemistry can adequately diagnose the cell types in the tumor. The importance of a proper classification can be illustrated by the different choices of treatment available for the two most common types of pituitary adenomas - prolactinomas and null cell adenomas (hormonally inactive adenomas) (Kovacs et al., 1984). Most of the prolactinomas will respond well to dopamine agonist treatment whereas the null cell adenomas are rarely affected by such treatment. The positive response to dopamine agonist treatment in prolactinomas, a rapid reduction in serum prolactin and tumor shrinkage, has been shown to be dopamine receptor mediated. In the normal pituitary gland the prolactin secreting cells, the lactotrophs, contain dopamine-D2 receptors through which dopamine from the hypothalamus exerts its regulatory inhibitory effect. The exact mechanism behind the dopamine agonist’s effect on prolactinomas is not known.