Persistent gynecomastia resulting from scalp inunction of estradiol: a model for persistent gynecomastia.
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Alopecia↗
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Gynecomastia after chemotherapy for lymphoma.
Although development of gynecomastia in a patient with cancer may indicate persistence or regrowth of a tumor, we studied three patients with lymphoma in whom development of gynecomastia during or after chemotherapy did not portend a poor outcome. In all patients, serum testosterone levels were normal, serum luteinizing hormone (LH) levels were high-normal or elevated, and serum follicle-stimulating hormone (FSH) levels were clearly elevated. The serum estradiol level of one patient was elevated at the onset of gynecomastia, but it fell to normal as the gynecomastia resolved spontaneously over a three-month period during which the patient received no chemotherapy. In a second patient, gynecomastia resolved over a period of eight months while the patient continued on maintenance chemotherapy, and he remains clinically well in remission 21/2 years after onset of gynecomastia. In the third patient, gynecomastia developed while the patient was in complete remission and off of all therapy, and it remained unchanged for the duration of a 21/2-year remission without therapy. Gynecomastia after chemotherapy for lymphoma is not an ominous prognostic sign and does not necessarily indicate the need for alteration of the treatment regimen.
Adult↗
Endocrine studies in testicular tumor patients with and without gynecomastia: a report of 45 cases.
Prolactin (PRL), human placental lactogen (hPL), the beta-subunit of human chorionic gonadotropin (betahCG), testosterone (T), estrone (E1), and estradiol (E2) were measured in blood samples from 45 patients with testicular tumors, 27 of whom had gynecomastia at some stage of their disease. Forty-two of the 45 patients had at least one abnormal hormone level. The most common abnormality was that of plasma estrone: it was elevated in 32 out of 42 (76%) patients in whom it was measured, suggesting a useful role for E1 as a testicular tumor marker. Prognosis was notably worse in patients with embryonal carcinoma, teratocarcinoma, and choriocarcinoma, in those with gynecomastia and, particularly, galactorrhea. Such patients also had the highest incidence of hormonal abnormalities as well as the most extreme absolute values. Hormonal mechanisms were implicated in the development of gynecomastia and galactorrhea. Prolactin, betahCG, E1, and E2 levels in all permutations correlated significantly among patients with gynecomastia, but not among those without, while estrogen to testosterone ratios were elevated in patients with galactorrhea.
Adolescent↗
Gynecomastia and cannabis smoking. A nonassociation among US Army soldiers.
Eleven patients diagnosed with idiopathic gynecomastia requiring mammoplasty were compared with matched controls to determine if there was an association between cannabis use and gynecomastia. Patients with gynecomastia were not significantly different from controls regarding their history of cannabis use. For those who admitted using cannabis, patients had a higher frequency but a shorter median duration of use than controls; differences were not statistically significant. Our epidemiologic evidence does not support the previously reported relationship between chronic cannabis use and gynecomastia.
Adolescent↗
Gynecomastia and gonadal dysfunction in adolescent boys treated with combination chemotherapy for Hodgkin's disease.
We studied 19 Ugandan boys with Hodgkin's disease who had been treated with mechlorethamine, vincristine, procarbazine and prednisone and who survived at least two years to assess testicular germ-cell depletion in pubescent boys on combination chemotherapy, as had previously been demonstrated in sexually mature men. Nine of 13 pubertal boys (ages 11 to 16) had moderate to severe gynecomastia and germinal aplasia, a 10-fold increase in mean (+/- S.D.) serum follicle-stimulating hormone (34.8 +/- 20.5 mlU per milliliter), a threefold increase in mean luteinizing hormone (17.8 +/- 9.8 mlU per milliliter) and reduced serum testosterone levels. Gynecomastia was not associated with an increase in either serum estradiol or prolactin concentrations. By contrast, six prepubertal boys (three to 10 years of age), similarly treated, showed no change in serum gonadotropins, and gynecomastia did not develop. The data confirm germ-cell depletion after combination chemotherapy and indicate further that Leydig-cell dysfunction, manifested by gynecomastia, may be a consequence of treatment in adolescent boys.
Adolescent↗
Gynecomastia as a physical finding in normal men.
The prevalence of palpable gynecomastia was determined in 306 normal adult men ranging in age from 17-58 yr. Palpable breast tissue was present in 36% and was bilateral in all but 7 subjects. In the great majority of cases, the gynecomastia was 4 cm or less in diameter. A diameter greater than 5 cm was distinctly unusual. With advancing age there was a progressive increase in the prevalence of gynecomastia. This increase was most striking in those over the age of 44 and in the 20- to 24-yr-old group compared to those 19 yr old or less. In those over the age of 44, the prevalence was 57%. These data indicate that palpable gynecomastic is common in normal adult men. This high prevalence must be taken into consideration when attributing gynecomastia to a drug or disease state.
Adolescent↗
Radiography of gynecomastia and other disorders of the male breast.
Mammographic features of 22 pathologically proved cases reflecting disorders of the male breast are described. Two patterns of gynecomastia were observed: a dendritic pattern seen in association with breast enlargement for 6 months or more, and a more florid triangular pattern, seen in association with breast enlargement of recent onset. Male breast carcinoma may be distinguished from gynecomastia by its eccentric location, spiculation, and, in some cases, calcification or involvement of the skin and nipple. Benign conditions simulating carcinoma included a case of drug-induced gynecomastia and a case of inflamed inclusion cyst.
Adult↗
Gynecomastia as a familial incomplete male pseudohermaphroditism type 1: a limited androgen resistance syndrome.
Four postpubertal 46 XY male patients with an inherited form of bilateral gynecomastia were studied to delineate the nature of the disease. Normal serum FSH and moderately elevated serum LH with concomitantly increased circulating levels of testosterone (T) and estradiol (E2) were found persistently in all cases in blood samples drawn at frequent intervals. LRH pituitary stimulation resulted in an exaggerated LH response and a normal FSH response. Chronic administration of T-cyclopentylate failed to decrease serum LH levels. The peripheral conversion rate of androstenedione to estrone was within normal limits. All patients had low ejaculate volumes with relatively normal spermatozoa counts. Testicular biopsies revealed normal Leydig cells and complete spermatogenesis. Urological examination disclosed that the prostate gland was extremely small. The breast tissue demonstrated the presence of tubular structures as well as the specific binding of [3H]T and [3H]dihydrotestosterone (DHT), which was inhibited by nonlabeled T, DHT, E2, and progesterone, but not by cortisol. The pedigree suggested a recessive X-linked inherited trait. A patient with a nonfamilial form of gynecomastia served as a control in all studies. These data were interpreted as demonstrating that this inherited type of gynecomastia represents the mildest expression of the androgen resistance syndromes and, therefore, belongs to the type 1 form of familial incomplete male pseudohermaphroditism.
Adolescent↗
[Irradiation for prevention of gynecomastia prior to estrogen therapy in cases of carcinoma of the prostate (author's transl)].
The most frequent and most unpleasant side-effect of therapy with estrogen hormones in patients with carcinoma of the prostate is the painful gynecomastia. Since 1969, we have been performing the prophylactic irradiation of the mammary glands on 284 patients in order to prevent a hormone-induced gynecomastia. The majority (262 patients) was irradiated with 600 rad surface dose in fractions of 150 rad prior to the hormone therapy. One hundred and two patients, having been treated endocrinologically for 2-75 months, had a follow-up examination. After irradiation, only 19% of the patients did not develop a gynecomastia, and 60% had no mamillary hyperesthesias. Compared to other authors, the therapy was less efficient, the symptoms, however, were discrete. As a consequence, an increase of the radiation dose as well as an alteration of the fractionation must be used.
Aged↗
Surgical correction of massive gynecomastia.
Massive gynecomastia can produce severe psychological problems for the patient. The surgical techniques employed for simple gynecomastia are not effective in correcting the displaced nipple and excess skin. Utilizing a dermal predicle technique, the excess fat and breast tissue have been removed, along with relocation of the nipple. Satisfactory results and acceptable scars have been obtained in four patients.
Adult↗
X-linked hypogonadism, gynecomastia, mental retardation, short stature, and obesity--a new syndrome.
Five male members in four generations of the same family had hypogonadism, gynecomastia, mental retardation, obesity, and short stature. The X-linked mode of inheritance, the distinctive facies, the normal size of the hands and feet, and the true gynecomastia are the main characteristics. Endocrine evaluation and histologic studies of the testes suggest partial hypogonadotropic hypogonadism. This disorder represents a new syndrome distinct from others previously described.
Adult↗
Gynecomastia demonstrated on the bone scan.
Bone scans with 99mtechnetium diphosphonate were performed on 2 patients with gynecomastia induced by diethylstilbestrol therapy for adenocarcinoma of the prostate. Neither patient had evidence of bone metastases but both scans revealed increased isotope concentration over the anterior rib cage at the lateral margin of the chest wall, corresponding in location to the hypertrophic breasts. This observation may be related to similar radionuclide uptake in normal and abnormal female breasts. One should not mistake the finding of gynecomastia for metastases of the ribs.
Adenocarcinoma↗
Surgical correction of nipple hypertrophy in male gynecomastia: case report.
We report a case of nipple hypertrophy in male gynecomastia. By raising 4 small quadrant flaps on the areolar-nipple junction, we were able to do an appropriate core excision of the gynecomastia and hypertrophied nipple--and closure of the flaps produced a small simulated nipple.
Breast↗
[(Gynecomastia as precancerous lesion: aspiration biopsy cytology and its histology)].
In 19 of 39 patients suffering from gynecomastia, between 1967 and 1979 aspiration biopsy cytology and surgery was performed by the author. Atypia and precancerous lesions accompanied by an advanced stage of epithelial proliferation were found in two cases, in two other ones, in addition to the above mentioned lesions, breast cancer was discovered. The myoepithelial elements observed cytologically and histologically are important pathognomonic signs in theses patients. In spite of the few cases, the precancerous nature of gynecomastia, primarily in its proliferative forms, manifests itself.
Adenocarcinoma, Scirrhous↗
Pathophysiology of spironolactone-induced gynecomastia.
Peripheral blood levels of testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone and the metabolic clearance rates of testosterone and estradiol, as well as the peripheral conversion of testosterone into estradiol, were measured in 16 patients with hypertension. Six of these patients were treated with spironolactone and developed gynecomastia. The other 10 patients served as control subjects. The blood testosterone level in the spironolactone-treated group (2.7 +/- 0.5 ng/ml) was significantly less (P less than 0.02) than in the control group (4.4 +/- 0.4 ng/ml). On the other hand, blood estradiol levels in the spironolactone group (30 +/- 4 pg/ml) were significantly greater (P less than 0.01) than in the control group (13 +/- 2 pg/ml). These changes were primarily due to significant increases in the metabolic clearance rate of testosterone (P less than 0.02) and in the rate of peripheral conversion of testosterone into estradiol (P less than 0.001) in the spironolactone-treated group. Thus, spironolactone does alter the peripheral metabolism of testosterone resulting in changes in the ratio of testosterone to estradiol, which could contribute to the production of gynecomastia.
Adult↗
Ultrastructural observations on gynecomastia.
Ten cases of gynecomastia were studied by electron microscopy. The ducts showed proliferation of both epithelial and myoepithelial cells. Intracytoplasmic lumina, previously thought to be a feature of malignant breast lesions, were seen. Squamous metaplasia was observed in some cases. The stroma showed fibroblasts, myofibroblasts, and, occasionally, pericytes. The general morphology of gynecomastia is similar to that of benign lesions of the female breast at the ultrastructural level. The features of the stromal cells reflect the effects of estrogenic stimulation.
Adult↗
Gigantic cystosarcoma phyllodes in a man with gynecomastia.
A 70-year-old man had a breast tumor for 50 years. The tumor, which weighed 8.6 kg, proved to be a malignant cystosarcoma phyllodes. It was successfully removed by a simple mastectomy with low axillary dissection, and a skin graft was performed. The lesion was associated with gynecomastia, and it is believed to have represented a cystosarcomatous transformation of a giant fibroadenoma.
Aged↗
"Masked" 21-hydroxylase deficiency of the adrenal presenting with gynecomastia and bilateral testicular masses.
An infertile 27 year old man with precocious puberty is described. He presented in adulthood with unilateral and then bilateral gynecomastia, and subsequently testicular tumors developed. An early diagnosis of congenital adrenal hyperplasia would have avoided unnecessary surgery. Initial detailed metabolic evaluation led to the erroneous diagnosis of 11-hydroxylase deficiency because of the presence of an unusual steroid (21-desoxycortisol) in serum which was falsely reported as an increased 11-desoxycortisol (compound S). The observed low urinary pregnanetriol measurements would have supported this diagnosis. Subsequent specific measurements of 21-desoxycortisol established its presence in the serum and its major metabolite, tetrahydro-21-desoxycortisol, in the urine. The unique features in this case of 21-hydroxylase deficiency alert the physician to its unusual clinical presentation and the pitfalls that may be encountered when evaluating adrenal steroidogenesis.
Adrenal Glands↗