Gynecomastia. Enzyme-histochemical and histological investigations with a correlation of enzyme activities in gynecomastia and fibro-adenomatosis.
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Acid Phosphatase↗
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Persistent gynecomastia resulting from scalp inunction of estradiol: a model for persistent gynecomastia.
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Alopecia↗
Hormonal studies and physical maturation in adolescent gynecomastia.
As part of a 3-year longitudinal study of lipid and hormonal changes during puberty, 536 boys aged 10 to 15 years were prospectively followed every 6 months to assess development of gynecomastia. The overall prevalence of gynecomastia in the 377 with complete data was 48.5% (51% of white subjects and 46% of black subjects). In the majority of subjects, gynecomastia developed during mid-puberty. Gynecomastia was bilateral in 55% of subjects, on the left side in 19%, and on the right in 26%. Gynecomastia was documented for only one visit in the majority of subjects. When subjects were matched at the onset of gynecomastia for race, visit number, and pubertal rating, there were no significant differences between those with or without gynecomastia in serum estradiol level, testosterone level, estrogen/testosterone, ratio, or dehydroepiandrosterone-sulfate level. However, free testosterone level, weight, and Quetelet index were all significantly lower, and the testosterone-estrogen binding globulin level was significantly greater, in those with gynecomastia. We conclude that approximately half of adolescent boys have transient gynecomastia, usually lasting less than 1 year; those with gynecomastia enter mid-puberty at an earlier age, have a lower Quetelet index, and have lower serum free testosterone levels.
Adolescent↗
Gynecomastia in testicular cancer patients. Prognostic and therapeutic implications.
Eighty-one patients with advanced testicular cancer were evaluated for gynecomastia or severe breast tenderness at diagnosis and after platinum-based chemotherapy. The prognostic significance of gynecomastia in these two settings was explored. At presentation, 10% (8 patients) had gynecomastia or breast tenderness and elevated HCG levels. The likelihood of gynecomastia was greater with increasing HCG level (P = 0.002). However, gynecomastia at presentation was a more powerful independent discriminant of poor survival than the initial HCG level by multivariate analysis (P = 0.004). Fifteen percent (12 patients) developed transient gynecomastia after chemotherapy not attributable to other known causes. HCG levels were normal. Endocrine evaluation typically revealed elevated FSH, LH, and estradiol/testosterone ratios. This may have reflected damage to testicular germinal epithelium. All 12 patients are alive without disease in contrast to the 8 patients who had gynecomastia at diagnosis. Therapy decisions should therefore be based on the time of onset of gynecomastia and in the context of appropriate clinical markers and evaluation.
Adolescent↗
Gynecomastia and cirrhosis of the liver.
Hepatic cirrhosis is frequently listed as a cause of gynecomastia. We found previously that in hospitalized men the prevalence of gynecomastia was correlated with body mass index and with age. The mean body mass index and the prevalence of gynecomastia in the cirrhotic subjects (nonedematous) did not differ from those in the overall population. Because more severely cirrhotic subjects with ascites, peripheral edema, or both usually are thin, we examined 18 more severely cirrhotic subjects and 18 nonobese (mean body mass index, 20.9 +/- 0.6 kg/m2), age-matched control subjects for the prevalence of palpable gynecomastia. Total testosterone, free testosterone, total estrogen, and estradiol concentrations also were measured. Fifty percent of the control subjects had gynecomastia. Breast tissue diameter was correlated with body mass index. The prevalence of gynecomastia in the cirrhotic subjects was 44%. In these subjects no significant correlation was noted between breast tissue diameter and body mass index, presumably because the body mass index was increased owing to fluid retention. The results could not be accounted for based on medications. Serum free testosterone concentrations were lower in the cirrhotic patients than in the controls (0.11 +/- 0.02 vs 0.22 +/- 0.03 nmol/L). The total estrogen-free testosterone ratio was higher in cirrhotic patients (10.3 +/- 2.5 vs 2.6 +/- 0.5), as was the estradiol-free testosterone ratio (2.2 +/- 0.7 vs 0.5 +/- 0.1). These ratios did not differ significantly in cirrhotic subjects with and without gynecomastia. Therefore, these data indicate that factors other than the estrogen-testosterone ratio are playing a role in the development of gynecomastia in both cirrhotic subjects and controls or that breast tissue sensitivity to an elevated estrogen-testosterone ratio is highly varible.
Age Factors↗
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↗
The relationship of concentrations of serum hormones to pubertal gynecomastia.
Pubertal gynecomastia occurred in 20 to 29 boys who were followed for 24 or more months during puberty. Mean concentrations of LH, FSH, prolactin, testosterone, and estrone and estradiol were compared. Although levels did not differ between boys who developed gynecomastia and those who did not, when compared with the stage of puberty, changes were noted between mean concentrations from samples before and when gynecomastia was first noted. A significant increase of estradiol occurred with the onset of gynecomastia, while testosterone levels did not change; thus the testosterone-estradiol ratio decreased. Prolactin concentrations fell significantly with the onset of gynecomastia. These data indicate a difference of hormonal dynamics between boys with and without gynecomastia.
Adolescent↗
Androgenic status of lepromatous leprosy patients with gynecomastia.
The androgenic status of 24 lepromatous leprosy male patients, 12 with and 12 without gynecomastia, was studied in comparison with that of 12 normal healthy males. Plasma testosterone levels were significantly diminished in the gynecomastia group as compared to levels in either of the control groups. The patients without gynecomastia showed values not significantly lower than those of normal males. Histopathologic examination of the leprous testes showed a variable admixture of inflammatory, degenerative anf fibrotic changes which were more severe and more frequent in the patients with gynecomastia than in those without it. Parenchymatous liver function tests showed greater derangement in the gynecomastia group as compared to the controls Histopathology of the liver showed lepromatous infiltration in patients with and without gynecomastia though the changes in liver were minimal in patients who showed total testicular degeneration in the biopsies.
Adolescent↗
[The significance of gynecomastia in general practice].
Gynecomastia in the male is usually due to a change of the estradiol/testosterone ratio in favor of the estrogens. There is usually no need for therapy of the gynecomastia which frequently occurs during puberty and old age. However, it is important not to overlook hormone-secreting tumors, often testicular malignancies, as the underlying cause of gynecomastia. A careful history and clinical investigations including thorough palpation of the testes (sonography) are complemented by a laboratory workup including blood chemistry (liver function) and hormone determinations (estradiol, beta-HCG, FSH, LH, prolactin, testosterone, thyroid hormones). Treatment of gynecomastia includes elimination of the cause of the condition. In cases with fibrous and voluminous gynecomastia breast tissue must be removed surgically. Antiestrogenic treatment with tamoxifen is indicated only in patients with recently developed, tender gynecomastia.
Diagnosis, Differential↗
Breast cancer in a patient with gynecomastia.
A case of breast carcinoma in the midst of florid gynecomastia in a 20-year-old man is reported. Up to now, only two male patients under the age of 21 with breast malignancy have been described in the literature. In contrast, gynecomastia is a more common condition than generally appreciated. The association of gynecomastia, a rather common condition, and cancer of the male breast, a rather uncommon condition, is examined. Mammography is recommended as part of the workup. A new classification of gynecomastia into true, pseudo, and mixed types is suggested. Recommendations for the role of lipoplasty in the treatment of gynecomastia are made.
Adult↗
Gynecomastia and ectopic human chorionic gonadotropin production by transitional cell carcinoma of the bladder.
We report a patient with gynecomastia and ectopic production of human chorionic gonadotropin (HCG) by a transitional cell carcinoma of the bladder. In the present case, serum HCG levels and gynecomastia paralleled the clinical course. On admission, the patient was suffering from invasive transitional cell carcinoma (grade 3) of the bladder with metastasis to the left inguinal lymph nodes, together with gynecomastia. The serum HCG level was also elevated. After anticancer chemotherapy, the apparent bladder lesion and gynecomastia disappeared, and the serum HCG level declined to within normal limits. About 2 months after discharge, when the patient suffered from recurrent invasive tumors of the bladder, gynecomastia reappeared and the serum HCG level again became elevated. beta-HCG was demonstrated in biopsy tissue using the immunoperoxidase technique. The presence of beta-HCG was always focally demonstrated and was shown to be localized in the cytoplasm of the tumor cells.
Carcinoma, Transitional Cell↗
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↗
Male reduction mammoplasty in serious gynecomastias.
This article is a report on long-term followup of a total of 44 serious gynecomastia cases in the stages I-III (according to Deutinger). The treatment consisted of either a semicircular incision and subcutaneous mastectomy or a superiorly or an inferiorly based nipple transposition while performing male reduction mammoplasty. Aesthetically pleasing results could be obtained by a periareolar approach and mastectomy. This inconspicuous procedure is feasible even in massive gynecomastia cases (stage III) or in cases of male breast asymmetry. On the other hand, all cases with breast reduction plasty and nipple transposition resulted in wing-shaped, mainly broad scars, and subjectively unfavorable results. Consequently, we favor the semicircular approach in male reduction mammoplasty in treating serious gynecomastias. With regard to possible male breast cancer etiology, the histological specimen of the mammary gland in gynecomastia is excised prior to any additional liposuction for supplementary body contouring.
Follow-Up Studies↗
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↗
Infantile gynecomastia with bloody nipple discharge.
Gynecomastia and bloody nipple discharge are very rare in childhood. In this report, a case of infantile gynecomastia together with bloody nipple discharge is presented. A hemorrhagic discharge was expressible from the mammary gland. Endocrinologic findings were within the normal limits. Because of persisting bleeding, a subcutaneous mastectomy was performed. The specimen was reported as gynecomastia. This boy is the first reported prepubertal gynecomastia with bloody nipple discharge in the medical literature.
Breast↗
Treatment of gynecomastia with tamoxifen: a double-blind crossover study.
Benign asymptomatic or painful enlargement of the male breast is a common problem, postulated to be due to an increased estrogen/testosterone ration or due to increased estrogenic or decreased androgenic stimulation via estrogen or androgen receptor interactions. Treatment at present consists of analgesic medication or surgery. However, treatment directed against the preponderance of estrogenic stimulation would seem to represent a more specific form of therapy. In the present double-blind crossover study, one-month courses of a placebo or the antiestrogen tamoxifen (10 mg given orally bid) were compared in random order. Seven of ten patients experienced a decrease in the size of their gynecomastia due to tamoxifen (P less than 0.005). Overall, the decrease for gynecomastia for the whole group was significant (P less than 0.01). There was no beneficial effect of placebo (P greater than 0.1). Additionally, all four patients with painful gynecomastia experienced symptomatic relief. There was no toxicity. The reduction of breast size was partial and may indicate the need for a longer course of therapy. A followup examination was performed in eight out of ten patients nine months to one year after discontinuing placebo and tamoxifen. There were no significant changes from the end of the initial study period except for one tamoxifen responder who developed a recurrence of breast tenderness after six months, and one nonresponder who demonstrated an increase in breast size and a new onset of tenderness after ten months. Therefore, antiestrogenic treatment with tamoxifen may represent a safe and effective mode of treatment for selected cases of cosmetically disturbing or painful gynecomastia.
Administration, Oral↗
Elevated serum estradiol associated with increased androstenedione-testosterone ratio in adolescent males with varicocele and gynecomastia.
OBJECTIVE: To investigate the testicular function in adolescents with pubertal gynecomastia associated with varicocele before and after varicocelectomy. DESIGN AND PATIENTS: We have studied six male adolescents 15 to 19 years of age with bilateral gynecomastia. They were selected among other adolescents with gynecomastia because of the presence of visible varicoceles. All of them had normal physical examination and secondary sexual characteristics. This was prospective study of 3 months' duration. All the patients that were included finished the study. SETTING: All the patients were evaluated in the Endocrine Clinic of Winthrop-University Hospital, a tertiary care unit. INTERVENTION: Serum testosterone (T), androstenedione (A), and estradiol (E2) responses to the administration of human chorionic gonadotropin (hCG) 2,000 IU for 3 consecutive days before and 3 months after varicocelectomy were determined. RESULTS: Varicocelectomy did not cause any significant changes in the basal (pre-hCG) levels of the steroid. However, the increase in T levels achieved with hCG was significantly (P less than 0.005) higher after varicocelectomy (before T, 925 +/- 212 ng%; after T, 1,649 +/- 406 ng%). Simultaneously, the stimulated levels of E2 and A were significantly lower (P less than 0.005) after varicocelectomy (E2, 62 +/- 12 pg/mL; A, 326 ng% +/- 80 ng%) than before (E2, 106 +/- 13 pg/mL; A, 580 ng% +/- 95 ng%). CONCLUSION: The reciprocal effect on the levels of T and its immediate precursor, A, suggests an impairment of the 17-ketoreductase enzyme activity. The increased levels of E2 after hCG and its normalization after varicocelectomy suggests that varicoceles may play a pathogenetic role in the development of 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↗