Mais conteúdo relacionado




  2. Gynecomastia : - Benign enlargement of male breast caused by proliferation of glandular breast tissue Pseudogynecomastia : - Excess of skin and/or adipose tissue in the male breasts without the growth of true glandular breast tissue - Commonly associated with obesity and can be ruled out by physical exam
  3. Gynecomastia is the most common benign disorder of the male breast tissue and affects 35 percent of men, being most prevalent between the ages of 50 and 69.
  4. CAUSES : Altered ratio of estrogens to androgens mediated by an increase in estrogen action, a decrease in androgen action, or a combination of these two factors. Physiologic Non - Physiologic
  5. Physiologic
  6. Newborns • At birth or in the first weeks of life • Estrogens produced by the placenta are transferred into the baby‘s circulation, thereby leading to temporary gynecomastia in the baby • Usually resolves after two or three weeks Adolescents • Hormonal imbalance (elevated ratio of estrogen to androgen) during early puberty, either due to decreased androgen production from the adrenals and/or increased conversion of androgens to estrogens • As early as age 10 and peaks at ages 13 and 14 • Usually resolves spontaneously within 1 to 3 years as pubertal progression increases testosterone levels and cause regression of breast tissue Older adults • Declining testosterone levels and an increase in the level of subcutaneous fatty tissue seen as part of the normal aging process can lead to gynecomastia in older males. • Increased fatty tissue, a major site of aromatase activity, leads to increased conversion of androgenic hormones such as testosterone to estrogens.
  7. Non - Physiologic
  8. DRUGS : • Cimetidine • Ketoconazole • Gonadotropin-releasing hormone analogues • Human growth hormone • 5α-reductase inhibitors such as finasteride and dutasteride • Certain oestrogens used for prostate cancer • Antiandrogens such as bicalutamide, flutamide and spironolactone • Calcium channel blockers such as verapamil, amlodipine, and nifedipine • Risperidone, olanzapine, anabolic steroids • Alcohol, opioids, efavirenz, alkylating agents • Omeprazole
  9. Refeeding gynecomastia • Malnutrition and significant loss of body fat suppress gonadotropin secretion, leading to hypogonadism. • This is reversible when adequate nutrition resumes, where the return of gonadotropin secretion and gonadal function cause a transient imbalance of oestrogen and androgen that mimics puberty, resulting in transient gynecomastia. • This phenomenon, also known as refeeding gynecomastia, was first observed when men returning home from prison camps during World War II developed gynecomastia after resuming a normal diet • Similar to pubertal gynecomastia, refeeding gynecomastia resolves on its own in 1–2 years
  10. Chronic disease • Renal failure patients, Chronic kidney disease undergoing dialysis Resolves spontaneously within 1–2 years. • Liver failure or cirrhosis, Alcoholic liver disease, Ethanol • Conditions that can cause malabsorption such as cystic fibrosis or ulcerative colitis • Inherited disorders such as spinal and bulbar muscular atrophy and the very rare aromatase excess syndrome.
  11. Hypogonadism • Gynecomastia can be caused by absolute deficiency in androgen production due to primary or secondary hypogonadism. • Primary hypogonadism results when there is damage to the testes (due to radiation, chemotherapy, infections, trauma, etc.), leading to impaired androgen production. It can also be caused by chromosomal abnormality seen in Klinefelter syndrome, which is associated with gynecomastia in about 80% of cases. • Secondary hypogonadism results when there is damage to the hypothalamus or pituitary (due to radiation, chemotherapy, infection, trauma, etc.), and similarly lead to impaired androgen production. The net effect is reduced androgen production while serum estrogen levels (from peripheral aromatization of androgens) remain unaffected. The lack of androgen-mediated inhibition of breast tissue proliferation combined with relative estrogen excess result in gynecomastia.
  12. Tumors • Leydig cell tumors, Sertoli cell tumors (such as in Peutz–Jeghers syndrome) and hCG-secreting choriocarcinoma • Other tumors such as adrenal tumors, pituitary gland tumors (such as a prolactinoma), or lung cancer • Individuals with prostate cancer who are treated with androgen deprivation therapy
  13. PATHOPHYSIOLOGY Estrogen excess Androgen deficiency Increased levels of sex hormone-binding globulin Androgen resistance Medications •Tumors (Testicular, Choriocarcinoma, Adrenal, Pituitary gland, Lung) •Peutz-Jeghers syndrome •Aromatase excess syndrome •Obesity •Aging •Primary hypogonadism (Klinefelter's syndrome) •Secondary hypogonadism •Hyperthyroidism (Gra ve's disease) •Cirrhosis •Androgen insensitivity syndromes •Oral contraceptives •Calcium channel blockers •Cimetidine •Ketoconazole •Gonadotropin- releasing hormone analogues •Human growth hormone •Human chorionic gonadotropin •5α-reductase inhibitors •Antiantrogens
  14. • History and physical examination Palpation of breast Penile size and development Testicular development Masses that raise suspicion for testicular cancer Development of secondary sex characteristics such as the amount and distribution of pubic and underarm • Diagnosis A review of the medications  To rule out Liver disease : Aspartate transaminase and alanine transaminase  To rule out renal damage : Serum creatinine  To rule out hyperthyroidism : Thyroid-stimulating hormone levels Total and free levels of testosterone, luteinizing hormone, follicle stimulating hormone, estradiol, serum beta human chorionic gonadotropin (β-hCG), and prolactin If this evaluation does not reveal the cause of gynecomastia, then it is considered to be idiopathic gynecomastia (of unclear cause).
  15. Differential diagnosis : Pseudogynecomastia Breast cancer Mastitis Lipoma Sebaceous cyst Dermoid cyst Hematoma Metastasis Ductal ectasia Fat necrosis Hamartoma
  16. IMAGING :  Mammography : Point to malignancy would be painless, non moveable (fixed), irregularly shaped, and skin changes  Ultrasound : If a tumor of the adrenal glands or the testes is suspected
  17.  Histology : FNAC • Proliferation and lengthening of the ducts • An increase in connective tissue • An increase in inflammation and swelling surrounding the ducts • An increase in fibroblasts in the connective tissue Chronic gynecomastia • Increased connective tissue fibrosis • An increase in the number of ducts • Less inflammation than in the acute stage of gynecomastia • Increased subareolar fat • Hyalinization of the stroma
  18. SIMON CLASSIFICATION OF GYNECOMASTIA Grade I: Minor enlargement, no skin excess Grade II: Moderate enlargement, no skin excess Grade III: Moderate enlargement, skin excess Grade IV: Marked enlargement, skin excess
  19. TREATMENT : If the gynecomastia doesn't resolve on its own in 2 years, then medical treatment is necessary. Medications : • Selective estrogen receptor modulators (SERMs) such as Tamoxifen, Raloxifene, and Clomifene • Aromatase inhibitors (AIs) such as Anastrozole Surgery : • Most effective known treatment for gynecomastia. • Surgical treatment should be considered if the gynecomastia persists for more than 12 months, causes distress (i.e. physical discomfort or psychological distress), and is in the fibrotic stage. • In adolescent males, it is recommended that surgery is postponed until puberty is completed (penile and testicular development should reach Tanner scale Stage V)
  20. Surgical approaches  Subcutaneous mastectomy  Liposuction-assisted mastectomy  Laser-assisted liposuction  Laser-lipolysis without liposuction
  21. Complications of mastectomy : • Hematoma • Surgical wound infection • Breast asymmetry • Changes in sensation in the breast • Necrosis of the areola or nipple • Seroma • Noticeable or painful scars • Contour deformities