Disease relevance of Gynecomastia

• If a late-onset form exists, hypogonadism and gynecomastia caused by decreased testosterone production and increased estrogen production, respectively, would be expected as the major clinical manifestations in men [1].
• Other risk factors significantly associated with breast cancer among men were drug treatment associated with prolactin elevations, radiation treatment, family history of breast cancer among first-degree relatives, a history of gynecomastia, gonadal injury, and treatment for inguinal hernias [2].
• Clomiphene citrate therapy was initiated in a male with Laennec's cirrhosis complicated by gynecomastia, testicular atrophy, impotence, and loss of libido [3].
• We also report for the first time the detection of MMTV-like sequences in 62% (8 of 13) of male breast cancer samples and 19% (10 of 52) of male gynecomastia samples screened [4].
• The data show that AROM+ mouse model is a novel tool to further analyze the use of P450arom inhibitors in the treatment of the dysfunctions in males associated with misbalanced estrogen to androgen ratio, such as pituitary adenoma, testicular dysfunction, and gynecomastia [5].

Psychiatry related information on Gynecomastia

• However, it is not selective for the aldosterone receptor, and side effects include gynecomastia, erectile dysfunction and menstrual irregularity [6].
• A 53-year-old man with a short stocky build, mild mental retardation, gynecomastia and hypogonadism was found to have a small ring Y chromosome unassociated with mosaicism [7].

High impact information on Gynecomastia

• An aromatase-producing sex-cord tumor resulting in prepubertal gynecomastia [8].
• Gynecomastia during omeprazole therapy [9].
• Cimetidine, a histamine H2-receptor antagonist widely used to treat peptic ulceration, is known to cause gynecomastia and sexual dysfunction in some men [10].
• Amiodarone-induced gynecomastia [11].
• Tamoxifen for gynecomastia induced by anabolic steroids [12]?

Chemical compound and disease context of Gynecomastia

• Gynecomastia from exposure to vaginal estrogen cream [13].
• 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 [14].
• Letter: Methadone-associated gynecomastia [15].
• Metronidazole-induced gynecomastia [16].
• Reversible gynecomastia associated with sulindac therapy [17].

Biological context of Gynecomastia

• The complete form of androgen insensitivity syndrome is characterized by 46, XY karyotype, external female phenotype, intra-abdominal testes, absence of uterus and ovaries, blindly ending vagina, and gynecomastia [18].
• Phenotypically, he exhibited signs of long-standing estrogen excess, such as feminine body build, gynecomastia, and varicose veins [19].
• This ratio is controlled in vertebrates by aromatase; its gene expression can be inhibited in different ways, and this is crucial for the treatment of estrogen-dependent diseases such as breast cancer, or gynecomastia in males for instance [20].
• In this series diabetes or glucose impairment was more common than previously reported and, like gynecomastia, did not correlate with size of triplet repeats, severity or patterns of neurologic involvement [21].

Anatomical context of Gynecomastia

• More severely affected individuals also develop gynecomastia associated with enhanced estradiol secretion by the testis [22].
• Progesterone enhances estrogen's stimulation of mammary gland growth, and our findings suggest that progesterone may play a role in the gynecomastia that occurs in men with hyperthyroidism [23].
• Increased aromatase activity in pubic skin fibroblasts from patients with isolated gynecomastia [24].
• Using reverse transcriptase in situ PCR, RNA transcripts from the env gene were also detected within cancerous epithelial cells of 78% of DNA-positive tumors, 80% of gynecomastia samples, and 0% of normal tissues screened [25].
• From the results of this study we conclude that both ovarian and testicular components of the gonads of these two individuals were endocrinologically active, and that their gynecomastia likely developed as a consequence of gonadal estradiol secretion [26].

Gene context of Gynecomastia

• The mean percentage of ER-, PR-, and AR-positive cells were significantly higher in gynecomastia than in carcinoma [27].
• Studies on the interactions between drugs and estrogen: analytical method for prediction system of gynecomastia induced by drugs on the inhibitory metabolism of estradiol using Escherichia coli coexpressing human CYP3A4 with human NADPH-cytochrome P450 reductase [28].
• Differential expressions of BRCA1 and BRCA2 in infantile gynecomastia [29].
• Relatively strong aromatase immunoreactivity was observed in all cases of carcinoma, but in only 11 of 30 cases (37%) of gynecomastia [27].
• Prolactin responses to provocative thyrotropin releasing hormone (TRH) stimulation were evaluated in 20 cirrhotic men with gynecomastia [30].

Analytical, diagnostic and therapeutic context of Gynecomastia

• Throughout puberty, ratios of delta 4-androstenedione to estrone (E1) and estradiol (E2) were significantly lower in the gynecomastia group than in the control group [31].
• Prophylactic breast irradiation with a single dose of electron beam radiotherapy (10 Gy) significantly reduces the incidence of bicalutamide-induced gynecomastia [32].
• In patients with advanced forms of prostate cancer bilateral orchiectomy was associated with the lowest incidence of gynecomastia, followed by nonsteroidal antiandrogen therapy, diethylstilbestrol and estrogen in rank order [33].
• 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 [34].
• We have studied the expression of C3, C4, factor B, and HLA-DRalpha mRNA by in situ hybridization in gestational mammary gland specimens and compared these findings to those in breast tissue affected with an inflammatory process, lactating adenoma or idiopathic gynecomastia [35].

References