GYNECOMASTIA
PRESENTOR : DR IJAN DHAMALA
MODERATOR : DR SUDHIR KUMAR SINGH

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

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.

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

Physiologic

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.

Non - Physiologic

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

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

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.

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.

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

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

• 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).

Differential diagnosis :
Pseudogynecomastia
Breast cancer
Mastitis
Lipoma
Sebaceous cyst
Dermoid cyst
Hematoma
Metastasis
Ductal ectasia
Fat necrosis
Hamartoma

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

 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

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

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)

Surgical approaches
 Subcutaneous mastectomy
 Liposuction-assisted mastectomy
 Laser-assisted liposuction
 Laser-lipolysis without liposuction

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

THANK YOU