Louis J. G. Gooren

in Oxford Textbook of Endocrinology and Diabetes

Second edition

Published on behalf of Oxford University Press

Published in print July 2011 | ISBN: 9780199235292
Published online July 2011 | e-ISBN: 9780199608232 | DOI:

Series: Oxford Textbooks


More Like This

Show all results sharing this subject:

  • Endocrinology and Diabetes


Show Summary Details


Parenchymal and stromal cells with the potential for normal breast development are equally present in prepubertal boys and girls. Men and women do not differ in sensitivity to the hormonal action of sex steroids, and therefore men have the same potential to develop breasts as women. Whether this actually occurs obviously depends on a person’s hormonal milieu. In order to understand the pathophysiology of gynaecomastia it is essential to know that breast tissue is, for its development, under control of both stimulatory hormonal action (oestrogens and progestogens) and inhibitory hormonal action of androgens. Gynaecomastia typically occurs when there is a relative dominance of oestrogenic over androgenic action; many cases of gynaecomastia are not the result of an overproduction of oestrogens per se, but rather due to the failing inhibitory action of androgens (1). In the assessment of gynaecomastia, as much attention must be paid to a potential source of feminizing hormones as to decreased androgen production or interference with the biological action of androgens.

Oestrogens stimulate the proliferation and differentiation of parenchymal ductal elements while progesterone supports alveolar development. The biological actions of oestrogens and progesterone do not appear in cases of growth hormone deficiency. Prolactin stimulates the differentiated ducts to produce milk. Testosterone inhibits the growth and differentiation of breast development, probably through an antioestrogenic action (1).

Whatever the cause, gynaecomastia shows the same histological developmental pattern. At first, there is florid ductal proliferation, with epithelial hyperplasia and increase in stromal and periductal connective tissue, with increased vascularity and periductal oedema. After approximately one year, there is increased stromal hyalinization, dilation of the ducts, and a marked reduction in epithelial proliferation, a ‘burnt-out’ phase of the condition. The result is inactive fibrotic tissue which no longer responds to endocrine therapy.

Gynaecomastia is not an uncommon finding and most cases will not represent a serious medical condition. However, gynaecomastia may signify the presence of a malignancy producing oestrogens, aromatase (the enzyme that converts androgens to oestrogens), or human chorionic gonadotrophin (hCG). Common locations of such tumours are the testis, lungs, liver or the gastrointestinal tract. Consequently, cases of gynaecomastia must be taken seriously and the diagnostic approach must reasonably rule out a malignancy in order to avoid any undue delay in its diagnosis.

Chapter.  3320 words. 

Subjects: Endocrinology and Diabetes

Full text: subscription required

How to subscribe Recommend to my Librarian

Buy this work at Oxford University Press »

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.