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Daughters of Women with Breast Cancer Have Elevated Mean 24-Hour Prolactin (PRL) Levels and a Partial Resistance of PRL to Dopamine Suppression^*

Department of Medicine, The Ohio State University Hospitals Columbus, Ohio 43210

Address requests for reprints to: William B. Malarkey, M.D., The Ohio State University Hospital, 410 West Tenth Avenue, Columbus, Ohio 43210.

Twenty-four-hour luteal phase PRL secretion has been evaluated with a frequent sampling technique in 13 women whose mothers had breast cancer and in 13 age- and weight-matched control subjects. Significantly elevated serum PRL levels were noted throughout the day and night in the young women at risk for breast cancer. Also, 10 of the 13 daughters at risk for breast cancer had mean 24-h PRL levels above the highest mean PRL level of the control population. However, most of the hourly PRL levels in the at risk females were within the range of normal. Serum estradiol, progesterone, testosterone, LH, and FSH levels were not different between the two groups. Although stress cannot be excluded as playing a role in the differences in serum PRL levels, the midprofile plasma cortisol levels were similar between the two groups. Since dopamine is a primary regulator of serum PRL levels, the PRL response of the pituitray lactotrophs of those women at risk for breast cancer was studied with dopamine infusions. A dopamine infusion at a rate of 0.004 µg/kg · min produced an initial suppression of serum PRL levels in the at risk subjects. At 120 min, however, their serum PRL levels returned to basal levels, whereas persistent suppression occurred in the control population. In contrast, a higher dose of dopamine, 0.04 µg/kg ·min, induced a similar degree of PRL suppression in the controls and at risk females. Serum estradiol levels were similar in both groups on the day of each dopamine infusion.

In summary, 1) increased 24-h mean PRL levels have been found in 13 young females whose mothers had breast cancer; 2) in addition, in these women at risk for breast cancer a partial resistance of PRL to dopamine suppression occurred.

^* This work was supported in part by Clinical Research Center Grant RR-34 from the NIH, Bethesda, Maryland; the American Cancer Society, Ohio Division; Grant PDT-32E from the American Cancer Society, New York, New York, and the Mary A. Gertmenian Cancer Research Fund.

Received October 31, 1980.

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