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
Increased levels of sex
Estrogen excess Androgen deficiency hormone-binding Androgen resistance Medications
globulin

•Oral contraceptives
•Calcium channel
blockers
•Tumors (Testicular,
Choriocarcinoma, •Cimetidine
Adrenal, Pituitary •Ketoconazole
•Primary
gland, Lung) hypogonadism •Gonadotropin-
•Hyperthyroidism (Gra releasing hormone
•Peutz-Jeghers (Klinefelter's
ve's disease) •Androgen insensitivity analogues
syndrome syndrome) syndromes
•Cirrhosis •Human growth
•Aromatase excess •Secondary hormone
syndrome hypogonadism
•Human chorionic
•Obesity gonadotropin
•Aging
•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