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, 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. Physiologic gynecomastia is common in newborns, adolescents, and older men. It is self-limited, but can be treated to minimize emotional distress and physical discomfort. Nonphysiologic gynecomastia may be caused by chronic conditions e.
Discontinuing use of contributing medications and treating underlying disease are the mainstay of treatment. Medications, such as estrogen receptor modulators, and surgery have a role in treating gynecomastia in select patients. Treatment should be pursued early and should be directed by the patient. Although the adult male breast contains minimal amounts of adipose and glandular tissue, there is potential for proliferation if estrogen or progesterone levels increase.
Gynecomastia, which can be physiologic or nonphysiologic, occurs when the estrogen-to-testosterone ratio in men is disrupted, leading to proliferation of glandular breast tissue. Enlarge Print. Discontinuing use of spironolactone Aldactone often results in regression of breast tissue within three months. Routine testicular ultrasonography should be considered in men with gynecomastia to detect nonpalpable testicular tumors that were missed on clinical examination.
Mammography and breast ultrasonography should be performed in men if the physical examination raises suspicion for breast cancer. Tamoxifen and raloxifene Evista are effective for preventing and treating gynecomastia in men being treated for prostate cancer. Physiologic gynecomastia has a trimodal age distribution, with incidence peaking in newborns, adolescents, and men older than 50 years. Up to 90 percent of newborn boys have palpable breast tissue secondary to transplacental transfer of maternal estrogens.
Children with symptoms that persist after their first birthday should be examined further; they may be at risk of persistent pubertal gynecomastia. One-half of adolescent males will experience gynecomastia, with typical onset at 13 to 14 years of age, or Tanner stage 3 or 4. Although adolescent physiologic gynecomastia often resolves spontaneously, intervention may be warranted to ameliorate emotional distress. Decreasing free testosterone levels may contribute to a final peak in gynecomastia incidence in men older than 50 years.
Although older men are less likely to present for evaluation of gynecomastia than adolescents, a study of hospitalized men estimates that approximately 65 percent of men between 50 and 80 years of age experience some degree of gynecomastia.
Nonphysiologic gynecomastia can occur at any age as a result of a number of medical conditions, medication use, or substance use. Common causes of nonphysiologic gynecomastia are listed in Table 1. Androgen insensitivity syndrome. Congenital anorchia. Klinefelter syndrome.
Testicular torsion. Testicular trauma. Viral orchitis. Adrenal tumors. Gastric carcinoma producing hCG. Large cell lung cancer producing hCG.
Pituitary tumors. Renal cell carcinoma producing hCG. Testicular tumors, particularly Leydig or Sertoli cell tumors. Secondary hypogonadism. Kallmann syndrome. Familial gynecomastia. Human immunodeficiency virus. Malnutrition and disorders of impaired absorption e. Gynecomastia—a difficult diagnostic problem. Endokrynol Pol. Adolescent physiologic gynecomastia should resolve within six months to two years after onset. If symptoms persist after two years or past 17 years of age, further evaluation is indicated.
Use of medications or substances associated with gynecomastia or other underlying illness may be a factor. If no other etiology can be found and if the patient desires treatment, supplementation with testosterone, use of estrogen receptor—modifying agents, or referral for surgery to improve cosmesis is warranted.
After persistent pubertal gynecomastia, medication use and substance use are the most common causes of nonphysiologic gynecomastia. Agents associated with gynecomastia are listed in Table 2. Increases sex hormone—binding globulin concentration. Information from references 7 , and 9 through Additionally, lavender, tea tree oil, dong quai, and Tribulus terrestris an ingredient in performance-enhancing supplements have been linked to gynecomastia.
Anabolic steroid use often causes irreversible gynecomastia. The injection of exogenous testosterone inhibits natural production of testosterone, which cannot recover rapidly enough between steroid-injecting cycles to prevent estrogen predominance. Attempts to prevent gynecomastia with the use of concomitant tamoxifen or other aromatase inhibitors may result in irreversible adverse effects. Liver injury may impair hepatic degradation of estrogens and increase levels of sex hormone—binding globulin that contribute to increased peripheral estrogens.
Patients with alcohol-related liver disease are at particular risk of gynecomastia because phytoestrogens in alcohol and the direct inhibition of testosterone production by ethanol further disrupt the estrogen-to-testosterone ratio. Gynecomastia may be the only presenting symptom in men with primary hypogonadism.
For example, one-half of men with Klinefelter syndrome have gynecomastia. Although testicular tumors are rare, approximately 10 percent of persons with testicular tumors present with gynecomastia alone. Adrenal tumors may secrete estrogen and estrogen precursors, causing a similar disruption in the estrogen-to-testosterone ratio. These tumors can be detected by elevated serum dehydroepiandrosterone sulfate levels or increased urinary ketosteroid levels.
Similarly, the presence of human chorionic gonadotropin hCG in serum can be used to detect hCG-secreting tumors that may include testicular germ cell, liver, gastric, or bronchogenic carcinomas.
All of these tumors require surgical excision. Gynecomastia occurs in 10 to 40 percent of men with hyperthyroidism, although it is rarely the only symptom at presentation. Hormonal dysfunction is common in men with renal failure because of overall suppression of testosterone production and direct testicular damage secondary to uremia.
Conditions that impair absorption, such as ulcerative colitis and cystic fibrosis, may result in gynecomastia. Refeeding after prolonged malnutrition can also trigger breast tissue proliferation. Although malnutrition suppresses hormone production, refeeding helps resume production. However, the liver lags in recovery and cannot fully degrade estrogens. Although obesity causes pseudogynecomastia a proliferation of adipose rather than glandular tissue , elevated weight is also associated with true gynecomastia.
New research suggests that leptin and aromatase activity associated with obesity contribute to increased circulating estrogens, causing gynecomastia. Other rare causes of gynecomastia include exposure to phthalates and lead, emotional stress, and repetitive mechanical stress causing unilateral symptoms.
Oestrogen stimulates breast tissue growth whilst androgens inhibit it. The important factor is the ratio of active androgens to oestrogens. Therefore, it may be caused by :.
Once this ratio falls, breast tissue is stimulated to grow. This leads to proliferation of breast ducts and fibroblastic stroma. If the stimulus to proliferation continues then the ducts and fibroblastic stroma are replaced by fibrosis and gynaecomastia becomes well established and irreversible. These should be performed on a clinical basis, ie according to the history and examination.
For example, if the patient is on gynaecomastia-inducing medication then these tests may not be necessary. Blood tests are not indicated in those with fatty breast enlargement, physiological pubertal or senile changes, an identified drug cause, or a clinically apparent cancer. In these cases, imaging and needle core biopsy will usually be required [ 4 ].
Refer to a local 'one-stop' breast clinic if there is any doubt or suspicion of a sinister cause. Eur J Breast Health. J Clin Endocrinol Metabol. Measurement of androgen and estrogen receptors in breast tissue from subjects with anabolic steroid-dependent gynecomastia. Life Sci. Adolescent gynecomastia: not only an obesity issue. Ann Plast Surg. A physiologic role for testosterone in limiting estrogenic stimulation of the breast. Pearlman G, Carlson HE. Gynecomastia: an update.
The Endocrinologist. Endocrinology of gynaecomastia. Ann Clin Biochem. Gynecomastia: pathophysiology, evaluation, and management. Mayo Clin Proc. Plasma phthalate levels in pubertal gynecomastia. Evaluation of anti-androgenic activity of di- 2-ethylhexyl phthalate. Agency for Toxic Substances and Disease Registry. Toxicological profile for di- 2-ethylhexyl -phthalate. Epidemic of gynecomastia among illegal Haitian entrants.
Public Health Rep. Epidemic of gynecomastia among haitian refugees: exposure to an environmental antiandrogen. Endocr Pract. Luteinizing hormone and human chorionic gonadotropin decrease type 25 alpha-reductase and androgen receptor protein levels in women's skin. Progesterone stimulates mammary gland ductal morphogenesis by synergizing with and enhancing insulin-like growth factor-I action. Progesterone, prolactin, and gynaecomastia in men with liver disease.
High serum progesterone in hyperthyroid men with Graves' disease. Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study.
J Clin Pathol. Correll CU. Effect of hyperprolactinemia during development in children and adolescents. J Clin Psychiatry. Coexpression and cross-regulation of the prolactin and sex steroid hormone receptors in breast cancer. Ruan W, Kleinberg DL. Insulin-like growth factor I is essential for terminal end bud formation and ductal morphogenesis during mammary development. Mazur T, Clopper RR. Pubertal disorders. Psychology and clinical management. Endocrinol Metab Clin North Am.
Longitudinal effects of aging on serum total and free testosterone levels in healthy men. Baltimore Longitudinal Study of Aging. Serum levels of free and bound testosterone in hyperthyroidism. Clin Endocrinol Oxf. Klinefelter's syndrome. Deciduoid-like stromal cells in a diabetic patient with bilateral gynecomastia: a potential diagnostic pitfall. Virchows Arch ; 6 Gynecomastia in HIV-infected patients receiving antiretroviral therapy. Goldman RD. Drug-induced gynecomastia in children and adolescents.
Can Fam Physician. Holzbeierlein JM. Managing complications of androgen deprivation therapy for prostate cancer.
Urol Clin North Am. Marijuana: interaction with the estrogen receptor. J Pharmacol Exp Ther. Basaria S. Androgen abuse in athletes: detection and consequences.
The role of mammography in male patients with breast symptoms. Sonographic features of gynecomastia.
J Ultrasound Med. Male gynecomastia and risk for malignant tumours--a cohort study. BMC Cancer. Male breast cancer.
Multidisciplinary meeting on male breast cancer: summary and research recommendations. J Clin Oncol. Review article: epidemiology of male breast cancer. A meta-analysis of published case-control studies and discussion of selected aetiologic factors.
Int J Cancer. Prevalence of Klinefelter's syndrome in male breast cancer patients. Anticancer Res. Classification and management of gynecomastia: defining the role of ultrasound-assisted liposuction. Plast Reconstr Surg. Ratnam BV. A new classification and treatment protocol for gynecomastia.
Aesthet Surg J. Classification and surgical correction of gynecomastia. Cordova A, Moschella F. Algorithm for clinical evaluation and surgical treatment of gynaecomastia. J Plast Reconstr Aesthet Surg. Hammond DC. Surgical correction of gynecomastia.
0コメント