Cases reported "Gynecomastia"

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1/9. 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.
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2/9. The endocrinopathy of poems syndrome.

    We describe the clinical features and post mortem findings in a patient with poems syndrome (P--polyneuropathy, O--organomegaly, E--endocrinopathy, M--M protein, S--skin changes), with particular emphasis on the evolution of the endocrinopathy over a three year period. In addition to gynaecomastia this case exhibited primary hypothyroidism and primary and secondary adrenal and gonadal failure. The widespread nature of the endocrine changes suggests that a circulating substance interferes with the action of trophic hormones, possibly by inhibiting second messenger production.
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3/9. Ectopic production of human chorionic gonadotropin by poorly differentiated transitional cell tumors of the urinary tract.

    We performed a 5-year histopathological review of 41 consecutive cases of transitional cell carcinoma. Of these cases 8 were positive for human chorionic gonadotropin immunoperoxidase tissue staining. All tumors were grade III and stages ranged from A to D. Three patients presented with gynecomastia as the clinical manifestation of elevated serum levels of beta-human chorionic gonadotropin. These findings document the association of this phenomenon with lesions of an aggressive nature. As with the loss of cell surface antigens, the appearance of human chorionic gonadotropin within the tumor cells may be further evidence of dedifferentiation. Human chorionic gonadotropin production may be a potential marker to gauge tumor response to chemotherapy and, perhaps, a predictor of future aggressiveness and over-all progression.
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4/9. cimetidine blocks testosterone synthesis.

    Although an assortment of endocrine dysfunctions are reported in men treated with cimetidine hydrochloride, gonadotropin and sex steroid levels are usually normal. A 66-year-old man with previously normal sexual function presented with breast tenderness and sexual dysfunction after receiving cimetidine. His plasma testosterone level was low, and elevated gonadotropin levels suggested a primary testicular disorder. His sexual dysfunction improved and his plasma testosterone level rose to normal after cimetidine therapy was discontinued. Readministration of cimetidine therapy resulted in the prompt recurrence of his sexual problems and low testosterone level. A reversible defect in 17-beta-hydroxysteroid dehydrogenase is the mechanism postulated to have caused his low testosterone level. While the frequency of this abnormality is uncertain, its reversible nature and the wide use of cimetidine make it an important cause of sexual dysfunction in men.
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5/9. Familial gynecomastia without hypogonadism.

    A family, six members of which had gynecomastia without hypogonadism, is presented. Endocrine studies failed to show the specific nature of breast enlargement in the patients. Chromosomal studies using peripheral leukocytes resulted in normal findings. In one of the patients, chromosomal studies were done using breast tissue and fascia, and again no abnormalities could be detected. The mode of inheritance may be autosoma dominant with sex limitations; however, X-linked inheritance cannot be ruled out.
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6/9. breast lumps in men: four case reports and a literature review.

    Four cases of men who consulted their family physicians because of breast lumps are reported. Their final diagnoses were as follows: intraductal carcinoma, gynecomastia, seminoma, and lipoma. A review of the literature revealed a lack of data on the prevalence of breast lumps among male adults, considerable ambiguity in clinical definitions of the term "gynecomastia," and a general uncertainty about the prevalence of malignancy in such lesions. Further epidemiologic studies are needed to determine the true prevalence and nature of breast lumps in men.
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7/9. Leydig-cell tumor of the testis with gynecomastia and elevated estrogen levels.

    A normally-virilized 24-year-old white man who had gynecomastia was found to have a Leydig-cell tumor of the testis, without demonstrable metastases. Hormonal evaluation revealed negative serum and urine tests for human chorionic gonadotropin, and normal steroid excretion. Prior to orchiectomy, serum estradiol was elevated and serum testosterone depressed; postoperatively these values reverted to normal. Attempts to quantitative the estradiol content of the tumor failed to show a significant increase over normal testicular tissue, however. Histologically, the tumor showed classic Reinke crystalloids, the nature of which remains undefined. Electron-microscopic studies showed these crystals to have a regular hexagonal pattern.
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8/9. Pituitary adenoma and bilateral male breast cancer: an unusual association.

    An unusual case is presented of bilateral breast cancer in a male patient with a long history of endocrine dysfunction due to a prolactinoma. The role of abnormal endocrine function in the development of male breast cancer is reviewed. The strongest association between aberrant endocrine function and male breast cancer occurs in patients with Klinefelter's syndrome, who have an approximate 3% lifetime risk of developing breast cancer. Retrospective case-control studies indicate that both estrogen excess and androgen deficiency may be involved in male breast cancer. Clinical studies of estrogen, androgen, and prolactin levels in male breast cancer patients have yielded conflicting results, and the precise nature of the hormonal mechanisms involved in the development of male breast cancer remains to be defined.
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9/9. Apocrine cells in a fine needle aspirate of gynecomastia. A case report.

    BACKGROUND: Apocrine cells are a common finding in female mammary cysts, while only rare cases of apocrine metaplasia in gynecomastia have been found in surgical specimens. CASE: A 65-year-old male presented with painful, monolateral gynecomastia. Fine needle aspiration biopsy showed sheets of large, eosinophilic epithelial cells. On immunocytochemistry these cells were positive for apocrine marker GCDFP-15. The patient had ischemic heart disease and was under treatment with spironolactone. CONCLUSION: Apocrine cysts in gynecomastia are rare histologic findings, and this is the first case diagnosed by fine needle aspiration. The finding of apocrine cells confirms the nonneoplastic nature of the lesion, avoiding surgical excision.
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