Cases reported "Gynecomastia"

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11/280. serum inhibin B concentration in a prepubertal boy with gynecomastia and peutz-jeghers syndrome.

    gynecomastia in boys with peutz-jeghers syndrome and Sertoli cell tumors of gonadal origin results from increased estrogen production due to increased aromatase activity within the testicular tumor. We present a prepubertal boy with peutz-jeghers syndrome, gynecomastia and bilateral neoplastic Sertoli cell proliferation in whom the only abnormal hormonal profile was increased concentration of inhibin B and Pro-alpha C in serum. ( info)

12/280. trisomy 4 in a case of gynecomastia.

    gynecomastia is an anomaly associated with alterations in the levels of hormones, especially estrogens. Sufferers of gynecomastia present a high risk of developing carcinomas. Only two cytogenetic descriptions of this type of mammary proliferation are available. In the present study, we analyzed chromosomally a sample of breast tissue from a patient with gynecomastia following short-term culture. The only clonal chromosomal alteration encountered was trisomy of chromosome 4. This alteration has not been described previously for samples of gynecomastia or breast cancer in males. We believe that the alterations in hormone levels in the male breast tissue that lead to this type of cellular proliferation induce the formation of chromosomal abnormalities, making the cells more susceptible to becoming malignant. ( info)

13/280. Gynaecomastia as a presenting feature of thyrotoxicosis.

    The association between gynaecomastia and thyrotoxicosis is well recognised. However, the reported frequency of the association is variable, partly depending upon the defining criteria used. Here we report two patients with thyrotoxicosis in whom gynaecomastia was the presenting feature. Both patients had other contributing factors, which are assumed to have predisposed to gynaecomastia. In both patients, the gynaecomastia resolved with successful treatment of the thyrotoxicosis. When gynaecomastia is a presenting, or prominent feature of thyrotoxicosis, the possibility of additional underlying pathology should be considered. ( info)

14/280. Prepubertal gynecomastia: indirect exposure to estrogen cream.

    OBJECTIVE: To describe the clinical course of 3 prepubertal boys who presented with gynecomastia resulting from indirect exposure to a custom-compounded preparation of estrogen cream used by each child's mother. METHODOLOGY: Each child was initially referred to the Children's Medical Center of Dallas' endocrinology Center and followed for over 1 year. RESULTS: All 3 boys presented with gynecomastia and elevated estradiol levels. Two had accelerated growth and advanced bone ages. Within 4 months after each child's mother discontinued use of the topical estrogen preparation, each child's gynecomastia regressed and estradiol levels returned to normal. CONCLUSION: Indirect exposure to excessive amounts of topical estrogen may cause gynecomastia, rapid changes in growth, and advanced bone age in prepubertal children. Because custom-compounded topical estrogen preparations are not regulated by the food and Drug Administration and may contain high concentrations of estrogen, we recommend that women requiring estrogen use an alternate form of estrogen delivery if they are in frequent close contact with children. ( info)

15/280. Cytologic atypia in a 53-year-old man with finasteride-induced gynecomastia.

    finasteride has been associated with the development of gynecomastia. Although cytoplasmic vacuolization has been noted in prostatic epithelium in men taking this drug, we found no documentation of the cytologic changes in finasteride-associated gynecomastia. We present the case of a 53-year-old man who developed unilateral gynecomastia following finasteride therapy for alopecia. A fine-needle aspiration biopsy of the mass was diagnosed as adenocarcinoma on the basis of nuclear atypia and particularly because of cytoplasmic vacuolization. Subsequent excisional biopsy revealed benign gynecomastia with no evidence of malignant change. The ductal epithelium did exhibit cytoplasmic vacuolization similar to that described in the prostate following finasteride therapy. We believe this is the first reported case documenting the cytologic changes seen in gynecomastia secondary to finasteride therapy. Cytoplasmic vacuolization in this setting should not be considered evidence of malignancy in men with gynecomastia. As with gynecomastia in general, extreme caution should be used before rendering a cytologic diagnosis of malignancy. ( info)

16/280. Preserved male fertility despite decreased androgen sensitivity caused by a mutation in the ligand-binding domain of the androgen receptor gene.

    Mutations in the androgen receptor gene are considered as incompatible with preservation of fertility and have been suggested as a cause of male infertility. Two adult brothers, referred because of gynecomastia and hormonal levels in serum indicating androgen insensitivity (high sex hormone-binding globulin, and LH levels, despite extremely high testosterone concentration), turned out to be relatives to a third young man, referred independently of the two others and exhibiting identical clinical and hormonal stigmata. In all three men, we found a C-->A substitution at position 2470 (exon 7) in the androgen receptor gene, leading to a Gln824Lys mutation in the ligand-binding domain of the receptor. Exploring the family history revealed that their grandfathers, on their mothers' side, were brothers; and the Gln824Lys mutation was also found in the one of them who was still alive. Binding studies with the mutant receptor in transfected COS-7 cells, with mibolerone as ligand, exhibited equal Kd (0.7 vs. 1.0 nmol/ L), IC50 (0.8 vs. 1.1 nmol/L), and maximum binding (7.1 vs. 8.9 fmol/ 10(6) cells), as compared with the wild-type (WT) receptor. In a chloramphenicol acetyl transferase trans-activation assay, the activity of the mutant receptor was identical to that of the WT, when the synthetic androgen R1881 was'used as a ligand; but with dihydrotestosterone, in concentrations up to 10 nmol/L, the activity of Gln824Lys mutated receptor was 10-62% of the WT variant. Thus, Gln824Lys mutation was found, both in vivo and in vitro, to cause slight impairment of receptor function but was compatible with preservation of male fertility. The patients inherited the mutation from their grandfathers through their mothers, and one of the young men possessing the mutation has fathered a daughter. ( info)

17/280. Response to LH-RH and HCG in two brothers with the Reifenstein syndrome.

    Two brothers with Reifenstein syndrome underwent LH-RH and HCG tests at various ages ranging from 13 to 17 years. We found that at age 13 the plasma LH and FSH response to one LH-RH injection was normal. After the age of 14, the basal plasma concentration of LH and FSH and their response to LH-RH became elevated. Concomitantly the plasma testosterone levels rose to abnormal levels. These findings are compatible with progressive development of primary gonadal dysfunction and with peripheral insensitivity to testosterone. ( info)

18/280. Clinicopathological studies of a patient with adult T-cell leukemia and pseudogynecomasty.

    We present a rare case of adult T cell leukemia/lymphoma (ATL) in which leukemic T cells expressed CD4 and CD25 surface antigens and infiltrated mammary glands during clinical course of the disease. A 40-year-old male was admitted with long-standing skin lesions and leukocytosis. Peripheral blood lymphocytes were highly pleomorphic and presented CD2, CD4, CD25, CD38 membrane surface antigens. The patient proved to be seropositive for human T-cell lymphotropic virus type I (HTLV-I) antibodies. Monoclonal expansion of lymphoid cells integrated with HTLV-I genome was observed, and the diagnosis of ATL chronic type was made. He underwent a chemotherapy regimen, and skin lesions and leukocytosis improved markedly. He progressed with an indolent clinical course of ATL, when he was admitted with bilateral hyperplasia of breast, recurrent skin lesions, and leukocytosis. breast biopsy revealed bilateral gynecomasty, extensive leukemic infiltration of typical ATL cells in the mammary glands, and the presence of mammary epithelial cells productively infected with HTLV-I. This is the first report describing invasion of the mammary tissue with HTLV-I-transformed T-cells and HTLV-I-associated breast disease. ( info)

19/280. Bilateral galactocele in a male infant: a rare cause of gynecomastia in childhood.

    A galactocele is a rare benign breast lesion usually occurring in females during or following lactation. These lesions are a rare cause of breast enlargement in infants and children. In this article we present a 10 month-old boy who was admitted with a two-month history of bilateral progressive breast enlargement, and diagnosed as having galactocele. Our purpose was to emphasize the importance of galactocele as a benign condition in the differential diagnosis of gynecomastia in childhood. ( info)

20/280. Estrogen secreting adrenal adenocarcinoma in an 18-month-old boy: aromatase activity, protein expression, mRNA and utilization of gonadal type promoter.

    We examined clinical, endocrinological and molecular biological aspects of an estrogen-secreting adrenal carcinoma in an 18-month-old male to clarify the pathogenesis of this condition. An 18-month-old boy was referred for evaluation of progressive bilateral gynecomastia and appearance of pubic hair. The patient had elevated plasma estradiol (349 pg/ml) and testosterone (260 ng/dl) levels that completely suppressed FSH and LH levels, and was subsequently diagnosed with an adrenal tumor on the right side. After removal of a 300-g adenocarcinoma, gynecomastia regressed and essentially normal hormone levels were restored. aromatase activity in the tumor tissue determined by the 3H-water method was 71.0-104.4 pmol/min/mg protein. High levels of aromatase protein and mRNA in the tumor tissue were also demonstrated, while neither aromatase activity nor protein was detected in normal adrenal glands. To investigate the regulation of aromatase expression in the adrenal carcinoma, we examined the usage of alternate promoters responsible for aromatase gene transcription. In the present case, the amounts of aromatase mRNA utilizing gonadal types of exon 1c (1.3) and 1d (II) were significantly higher than those that using other exon 1s. This result suggested that the utilization of a gonadal-type exon 1 might be involved in the over-production of aromatase in estrogen-secreting adrenal carcinoma. ( info)
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