Cases reported "Gynecomastia"

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1/8. The role of lipoaspiration in defeminization of klinefelter syndrome: a case report.

    klinefelter syndrome is the most frequent sex chromosome anomaly. Affected men characteristically present a tall stature, eunuchoid contours with feminine fat distribution, gynecomastia, hypogonadism, infertility, and behavioral and psychiatric disorders. diagnosis is confirmed by karyotype, which demonstrates an extra x chromosome. Treatment is mainly directed toward appropriate defeminization. Current treatment consists of testosterone replacement therapy and surgical correction of gynecomastia.
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2/8. Familial adrenal feminization probably due to increased steroid aromatization.

    5/10 members of a North African family (father, 2 male and 2 female siblings) had gynaecomastia, early growth and short final stature. The 8-year-old propositus had advanced bone age, facial acne, gynaecomastia, pubic hair and prepubertal testicular volume. Basal oestrone (E1) was elevated (670 pmol/l) and increased with adrenocorticotropic hormone (ACTH; 826 pmol/l). After human chorionic gonadotropin stimulation testosterone (T) responded normally whereas E1 and oestradiol (E2) remained unchanged. ACTH-dependent adrenal feminization was confirmed by a transient reduction of breast tissue following dexamethasone or cypropterone acetate treatment. testolactone increased T/E2 (from 5.6 to 20.3) and A/E1 (from 3.4 to 31.4) ratios and temporarily reduced the breast tissue. In conclusion, this is a familial type of adrenal feminization with increased adrenal androgen aromatization. This is the first time that male-to-male and male-to-female transmission has been reported.
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3/8. Immune complex disease and gynecomastia.

    A man with arthritis, gynecomastia and a rash histologically showing leukocytoclastic vasculitis, dermatitis herpetiformis and immunoglobulin g deposits at the dermoepidermal junction is reported. In contrast to cases of systemic lupus erythematosus (SLE) associated with vesiculobullous eruptions and similar histological features, our patient had neither bullae nor serological evidence of SLE. Conversely, no men already reported had evidence of feminization. Thus, our case appears to be unique.
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4/8. Familial male pseudohermaphroditism with gynaecomastia due to 17 beta-hydroxysteroid dehydrogenase deficiency. A report of 3 cases.

    Three sisters with male pseudohermaphroditism due to 17 beta-hydroxysteroid dehydrogenase deficiency are described. On the basis of a 46 XY karyotype and female phenotype all subjects were thought to have the testicular feminization syndrome. At puberty the two older patients developed signs of virilization and gynaecomastia. In these patients the plasma androstenedione level was 4-5 times higher than normal, whilst the plasma testosterone level was low compared to the normal range and, under basal conditions, their plasma androstenedione to testosterone ratio was 20-25 times higher than normal. Interestingly, in the third, prepubertal case, the basal androstenedione to testosterone ratio was normal but became six times higher than normal after hCG stimulation. These data support the diagnosis of male pseudohermaphroditism due to 17 beta-hydroxysteroid dehydrogenase deficiency and underline the diagnostic value of the hCG stimulation test prepubertally.
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keywords = feminization
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5/8. Clinical and endocrinological characterization of two subjects with Reifenstein syndrome associated with qualitative abnormalities of the androgen receptor.

    The androgen receptor in fibroblasts cultured from a biopsy of scrotal skin from 1 subject with Reifenstein syndrome has been found to be normal in amount and to bind dihydrotestosterone with normal affinity but to be qualitatively abnormal as evident by thermolability and instability upon ultracentrifugation. The family study of this subject and endocrine studies document androgen resistance in the index patient and his affected uncle. These findings provide evidence for X-linkage of this disorder, and suggest that the mutations that give rise to this phenotype are probably allelic to the mutations of the androgen receptor that cause testicular feminization.
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6/8. feminization in hepatocellular carcinoma corrected by chemotherapy: a case report.

    A 17-year-old boy with metastatic hepatocellular carcinoma and feminization became asymptomatic after administration of antineoplastic agents. serum estradiol level, urine estrogens, and tumor estrogen receptors were changed after the treatment. achievement of partial remission resulted in normalization of the serum sex hormone profile and disappearance of the feminization in spite of the presence of residual tumor. Thus, serum hormone levels alone cannot be used as tumor markers for control of therapy. This suggests that chemotherapy may have altered the biological behavior of the tumor, which resulted in loss of its ability to synthesize estrogen estrogen receptors.
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ranking = 0.4
keywords = feminization
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7/8. The aromatase excess syndrome is associated with feminization of both sexes and autosomal dominant transmission of aberrant P450 aromatase gene transcription.

    Increased extraglandular aromatization has been reported as the cause of familial gynecomastia. We studied a kindred with aromatase excess inherited in an autosomal dominant manner, in which affected males had heterosexual precocity and/or gynecomastia, and affected females had isosexual precocity and/or macromastia. The propositus was a 9-yr-old boy with gynecomastia. His 7.5-yr-old sister had precocious puberty, and their father and paternal grandmother had peripubertal gynecomastia and macromastia, respectively. serum concentrations of gonadal and adrenal steroid hormones were determined before and after the administration of corticotropin and/or hCG. aromatase activity was determined by [3H]delta4-androstenedione to [3H]estrone conversion by cultured skin fibroblasts and/or Epstein-Barr virus-transformed lymphocytes and was detected by immunohistochemistry and/or Western analysis. Linkage was examined with a polymorphism of the aromatase (P450arom) gene. The P450arom messenger ribonucleic acid was analyzed by rapid amplification of complementary dna (cDNA) ends, ribonuclease protection assay, and RT-PCR. hCG testing demonstrated a high rate of conversion of delta4-androstenedione to estrone and of testosterone to estradiol in the propositus and his father. Treatment of the propositus and his sister was initiated with an aromatase inhibitor (testolactone) and a GnRH analog, which successfully delayed skeletal and pubertal development in both children. Markedly increased aromatase activity was found in the patients' fibroblasts and Epstein-Barr virus-transformed lymphocytes. The P450arom polymorphism segregated with the disease in the family. A new 5'-splice variant was present in the patients' P450arom messenger ribonucleic acid, thus identifying yet another first exon of this gene, which appears to be aberrantly expressed in this family. In conclusion, a family with the aromatase excess syndrome is described, in which the condition was inherited in an autosomal dominant manner, led to feminizing manifestations in both sexes, and was associated with the aberrant utilization of a novel transcript of the P450arom gene.
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ranking = 0.8
keywords = feminization
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8/8. Bilateral sertoli cell tumor of testes with feminizing and masculinizing activity occurring in a child.

    A case of an unusual, histologically atypical, bilateral sertoli cell tumor of testis, in association with masculinization and feminization effects, that occurring in a 5-year-old boy, is presented. Although Sertoli cell tumors are not infrequent, this case is morphologically and endocrinologically unique.
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ranking = 0.2
keywords = feminization
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