Masked Hyperprolactinemia in a Case of Aldosterone-Producing Adrenal Adenoma

1 December 1995 | Volume 123 Issue 11 | Pages 893-894

TO THE EDITOR:

A 45-year-old woman was admitted to our hospital for evaluation of hypertension. She had never received a dopamine antagonist, histamine-2-receptor antagonist, or oral contraceptive. Laboratory findings showed hypokalemia (potassium level, 2.6 mEq/L). Endocrine data showed that while the patient was supine, her plasma aldosterone concentration and plasma renin activity were 685 pmol/L and 0.1 µg/L·h, respectively. Her plasma renin activity did not increase after the administration of furosemide (40 mg intravenously) and 2 hours of walking. Her serum prolactin level was 18 µg/L. A computed tomographic scan of the abdomen showed a round and solitary tumor (diameter, 2 cm) in the left adrenal gland. Left adrenalectomy was done in response to a diagnosis of aldosterone-producing adrenal adenoma. Figure 1 shows the patient's clinical course before and after surgery. After the surgery, the patient's plasma aldosterone concentration decreased to the normal level, but her serum prolactin level immediately increased to 130 µg/L. Intravenous injection of 500 µg of thyrotropin-releasing hormone increased her serum prolactin level from 80 to 420 µg/L. Her thyroid function was normal. Magnetic resonance image showed no pituitary adenoma and no lesions in the pituitary stalk or hypothalamus. These findings suggested functional hyperprolactinemia. The serum prolactin level remained elevated for 5 weeks, and spontaneous galactorrhea was observed. After bromocriptine was started, the patient's serum prolactin level decreased, and the galactorrhea disappeared.

View larger version (25K): [in this window] [in a new window]   Figure 1. Clinical course of patient with masked hyperprolactinemia and aldosterone-producing adrenal adenoma. PAC equals plasma aldosterone concentration; PRL equals serum prolactin level.

 

It is well known that prolactin secretion is under tonic dopamine inhibition [1] and that dopamine inhibits aldosterone secretion [2]. Although the endogenous dopaminergic tone in patients with primary aldosteronism remains controversial [3-5], we speculate that primary aldosteronism increased the systemic dopaminergic tone and that the patient's hyperprolactinemia did not become overt until the surgical treatment of her aldosterone-producing adenoma.

Author and Article Information

Top Author & Article Info References

Hamamatsu University School of Medicine; Hamamatsu 431-31; Japan

References

Top Author & Article Info References

1. Macleod MD, Lehmeyer JE. Studies on the mechanism of the dopamine-mediated inhibition of prolactin secretion. Endocrinology. 1974; 94:1077-85.

2. Carey RM, Thorner MO, Ortt EM. Dopaminergic inhibition of metoclopramide-induced aldosterone secretion in man. J Clin Invest. 1980; 66:10-8.

3. Gniadeck TC, Grekin RJ, Gross MD, Villareal JZ. Hyper-responsiveness of aldosterone to metoclopramide in aldosteronism. Clin Endocrinol. 1982; 16:475-81.

4. Jungmann E, Althoff PH, Rosak C, Schwedes U, Schffling K. Endogenous dopaminergic inhibition of aldosterone and prolactin secretion is apparently not increased in primary aldosteronism. Horm Metab Res. 1986; 18:138-40.

5. Demura R, Naruse M, Isawa M, Onoda N, Naruse K, Yamakado M, et al. A patient with a prolactinoma associated with an aldosterone producing adrenal adenoma: differences in dopaminergic regulation of PRL and aldosterone secretion. Endocrinol Jpn. 1992; 39:169-76.

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