An aromatase-producing sex-cord tumor resulting in prepubertal gynecomastia

Article Abstract:

Gynecomastia, the development of large breasts in males, usually occurs in prepubertal children as a result of increased production of estrogen (a female hormone). This results when the activity of aromatase, an enzyme that converts androgens (male hormones) to estrogens, increases, or when levels increase of the steroid molecules from which androgens are formed. An animal model of increased aromatase activity has been described (the Sebright Bantam rooster), and examples of gynecomastia resulting from this cause have been reported in humans. The case report is presented of a four-year-old boy who developed gynecomastia. The boy had Peutz-Jeghers syndrome (an inherited disorder in which polyps form in the intestinal tract) and tumors in both testes. In the initial physical examination, the patient had breasts equivalent in size to that of a girl in early puberty, which grew in the following year to a size consistent with midpuberty. His testes were also of early pubertal size and continued to enlarge in the subsequent nine months. The patient's bone age was 10 years. After removal of both breasts and biopsies of both testicles at the age of five, the patient began treatment with a drug that inhibited aromatase (testolactone). Evaluation of the boy's hormone levels indicated that the most likely cause of his gynecomastia and advanced bone age was increased estrogen production. The testicular biopsies showed the presence of tumors made of ''nests'' of abnormal cells (sex-cord tumors), the most likely source of excessively active aromatase, which catalyzed estrogen production. A discussion of the patient's hormonal status is presented; sex-cord tumors in females with Peutz-Jeghers syndrome are well characterized, perhaps because menstrual disorders are readily called to medical attention. The tumors in this patient were not detectable upon normal examination. (Consumer Summary produced by Reliance Medical Information, Inc.)

Pediatric endocrinology

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Gynecomastia: a continuing diagnostic dilemma

Article Abstract:

Gynecomastia, the development of large breasts in males, can result from a feminizing physiological state. Such a state can be the result of excess formation of estrogen (a female hormone), increases in the ratio of estrogen to androgen (a male hormone), or drugs. Gynecomastia can also develop for reasons unknown, and distinguishing between the two main types (endocrine versus unknown origin) is difficult. This is because estradiol, the hormone that stimulates breast growth, is very potent, and low blood levels are difficult to estimate. The condition may persist even after its cause has been treated, and thus causative factors become difficult to identify. A case report presented in the January 31, 1991 issue of The New England Journal of Medicine illustrates the difficulty of finding the cause of gynecomastia. The four-year-old patient discussed in the case had testicular tumors that secreted estrogen; the diagnosis was suggested after ultrasound studies had been performed, but was not obvious from assaying blood estrogen levels. In fact, hormonal levels are poor diagnostic aids in most cases of gynecomastia. The types of tumors that can result in elevated estrogen levels are tumors of Leydig cells, Sertoli's cells, and, as in the case report, sex-cord tumors. This represents a new type of feminizing tumor. (Consumer Summary produced by Reliance Medical Information, Inc.)

editorial

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A 60-year-old man with persistent gynecomastia after excision of a pituitary adenoma

Article Abstract:

A 60-year-old man was admitted to a hospital because he continued to have gynecomastia after having a pituitary tumor removed. Gynecomastia is an enlargement of the breasts in men. It was originally considered to be a result of the pituitary tumor. His blood level of estradiol was high, as was the level of another hormone called prolactin. His doctors suspected testicular cancer because in men, the testes produce small amounts of estradiol. An ultrasound of his testes showed a mass in the right testicle. The testicle was surgically removed, confirming the presence of a Leydig-cell tumor.

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