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Persistent Pubertal Macromastia^*

SAMUEL P. MARYNICK, BRUCE C. NISULA, C. PITA, JR. and D.LYNN LORIAUX

Developmental Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institution of Health Bethesda,Maryland 20205

Address requests for reprints to: D. Lynn Loriaux, M.D., Ph.D., Building 10, Room 10B09, National Institutes of Health, Bethesda,Maryland 20205.

Pubertal gynecomastia is a transient phenomenonof several months duration, whereas pubertal macromastia, which can be defined as the development of female-appearing breasts in otherwise normal males at puberty, persists into dulthood. The possibility that abnormalities of sex steroid levels or sex steroid-binding globulin (TeBG) might be involved in the persistence of pubertal macromastia led us to compare the endocrine profiles of nine men with this disorder with those of nine age-matched controls. The patients ranged in age from 15–31 yr, with macromastia being present for 8.7 ± 2.0 yr (mean ± SE). Comparison of the macromastia patients with the controls revealed no differences in plasma testosterone (546 ± 77 vs. 539 ± 86 ng/100 ml), estradiol (44 ± 77 vs. 47 ± 8 pg/ml), TeBGbinding capacity (0.83 ± 0.07 vs. 0.89 ± 0.12 jug/100 ml), TeBGbinding affinity (1.92 ± 0.14 vs. 1.77 ± 0.18 liters/nM), and PRL concentration (11.4 ± 1.8 vs. 12.4 ± 2.7 ng/ml). Also, no differences were found in plasma LH or FSH levels in samples collected every 20 min over an 8-h period (LH, 9.0 ± 0.9 vs. 8.1 ±1.2 mlU/ml; FSH, 7.2 ± 1.0 vs. 6.1 ± 1.1 mlU/ml). The number of LH and FSH secretory spikes occurring during 8 h were not different in the two groups (LH, 2.7 ±0.5 vs. 2.9 ± 0.3; FSH, 2.0 ±0.6 vs. 1.6 ±0.5). LH and FSH increases after 100 jug LRH were similar (LH, 38.3 ± 4.5 vs.31.2 ± 5.8 mlU/ml; FSH, 7.7 ±2.4 vs. 5.1 ±0.7 mlU/ml). The breast tissue histology showed ductular development, fat cells, and fibrous tissue typical of chronic gynecomastia of other causes.

We conclude that the persistence of pubertal macromastia is not associated with demonstrable abnormalities in gonadotropins, PRL, plasma sex steroids, or plasma TeBG.

^* Reported in part at the 34th Annual Meeting of the American Federation for Clinical Research, Washington, D.C., 1977.

Current address: Division of Endocrinology, Department of Internal Medicine, Baylor University, Medical Center, Dallas, Texas 75246.

Received March 5, 1979.

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