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    Gynecomastia

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    Tania Davis
    1. Gynecomastia is a common condition in adolescent males characterized by benign breast enlargement due to a proliferation of glandular breast tissue. 2. It occurs in approximately 65% of males during puberty due to an imbalance of rising estrogen levels and rising but slower testosterone levels. 3. Evaluation involves differentiating gynecomastia from pseudogynecomastia caused by fat tissue or muscle prominence, and considering underlying causes like certain drugs, medical conditions, or tumors if it is unilateral or persistent.

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    Gynecomastia

    Uploaded by

    Tania Davis
    105 views30 pages
    1. Gynecomastia is a common condition in adolescent males characterized by benign breast enlargement due to a proliferation of glandular breast tissue. 2. It occurs in approximately 65% of males during puberty due to an imbalance of rising estrogen levels and rising but slower testosterone levels. 3. Evaluation involves differentiating gynecomastia from pseudogynecomastia caused by fat tissue or muscle prominence, and considering underlying causes like certain drugs, medical conditions, or tumors if it is unilateral or persistent.

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    1. Gynecomastia is a common condition in adolescent males characterized by benign breast enlargement due to a proliferation of glandular breast tissue. 2. It occurs in approximately 65% of males during puberty due to an imbalance of rising estrogen levels and rising but slower testosterone levels. 3. Evaluation involves differentiating gynecomastia from pseudogynecomastia caused by fat tissue or muscle prominence, and considering underlying causes like certain drugs, medical conditions, or tumors if it is unilateral or persistent.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    105 views30 pages

    Gynecomastia

    Uploaded by

    Tania Davis
    1. Gynecomastia is a common condition in adolescent males characterized by benign breast enlargement due to a proliferation of glandular breast tissue. 2. It occurs in approximately 65% of males during puberty due to an imbalance of rising estrogen levels and rising but slower testosterone levels. 3. Evaluation involves differentiating gynecomastia from pseudogynecomastia caused by fat tissue or muscle prominence, and considering underlying causes like certain drugs, medical conditions, or tumors if it is unilateral or persistent.

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    © All Rights Reserved
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    Download as ppt, pdf, or txt
    of 30

    Primary Care of Adolescents

    University of South Florida


    College of Nursing
    Tampa, FL

    Increase in glandular and stromal tissue of the

    male breast
    Usually benign & transient
    Can be due to serious underlying disorders
    Can persist long enough that the adolescent
    seeks treatment
    True gynecomastia must be distinguished
    from fatty tissue overlying the pectoral
    muscles

    Occurs in 19.6% of 10.5 year-old males


    Peak incidence 64.6% at age 14 and then less

    common
    Mean age at onset is 13 years, 2 months
    4% will have severe gynecomastia aka type III

    gynecomastia
    >4 cm in diameter or approximately equal to the
    midpubertal female breast that persists into adulthood
    IN ONE STUDY:
    17% of males 19 and younger & 33% of 20 24 year

    olds had palpable breast tissue at least 2 cm in


    diameter

    1.2 years after a boy

    reaches stage 2
    genital development
    and 0.4 years after
    reaching stage 2
    pubic hair

    STAGE AT ONSET
    G1
    20%
    G2
    50%
    G3
    20%
    G4
    10%

    Breast tissue at birth is similar in males &

    females
    Responds similarly to estrogens during childhood
    At puberty, breast tissue of boys demonstrates
    both ductal & periductal mesenchymal tissue
    proliferation
    Involutes & atrophies as testicular androgens

    increase to adult levels


    IN FEMALES, under the influence of increasing

    levels of both estrogen & progesterone, breast


    tissue continues to develop

    THE
    BALANCE
    BETWEEN
    ESTROGEN &
    TESTOSTERO
    NE LEVELS
    DETERMINES
    THE EXTENT
    OF BREAST
    DEVELOPME
    NT IN MALES

    ANDROGENS
    Stimulate breast tissue

    development
    Increase can lead to
    gynecomastia
    Estradiol levels increase
    4 5 times in puberty
    PEAK ESTRADIOL
    LEVELS MAY BE
    REACHED BEFORE
    TESTOSTERONE LEVELS
    PEAK

    Antagonize breast

    tissue development
    Testosterone levels
    increase 30 40 times
    Testes produce only
    20% of circulating
    estrogens
    Remainder produced
    at extraglandular sites
    by AROMATIZATION

    STEROIDGEN
    ESIS
    Aromatase
    (estrogen
    synthetase)
    plays a key role
    in estrogen
    production in
    men ~
    enzymatically
    produces
    estrogen in
    extraglandular
    tissues

    Increases in
    extraglandu
    lar tissue
    (as in
    obesity)
    result in
    significant
    elevations
    of
    circulating
    estrogens

    MEDICATIONS
    Kleinfelter's

    Spironolactone

    syndrome
    Thyrotoxicosis
    Cirrhosis
    Adrenal neoplasms
    Testicular neoplasms

    Ketoconazole
    Exogenous intake of

    estrogens (oral or
    topical)
    Drug use (increases
    fetal aromatase)

    1. INCREASE IN ESTRADIOL SECRETION FROM


    TESTES
    Leydig cell tumors, adrenal tumors

    2. EXCESSIVE EXTRAGLANDULAR
    CONVERSION OF ANDROGENS TO
    ESTROGENS BY AROMATASE
    Overproduction of adrenal precursors
    Enhancement of extraglandular aromatase activity
    Disease states ~ hyperthyroidism, liver disease
    Increased body fat ~ obesity
    Medication or drug use
    Idiopathic (persistence of a fetal form of aromatase)

    3 INCREASE IN BIOAVAILABILITY OF
    ESTROGENS
    Decrease in amount of estrogen bound to sex
    hormone binding globulin (SHBG)
    Use of spironolactone or ketoconazole

    4 EXOGENOUS INTAKE OF ESTROGENS


    Oral or topical

    1. IMPAIRMENT OF TESTICULAR
    PRODUCTION IN LEYDIG CELLS
    Primary hypogonadism (anorchia, Klinefelter syndrome)
    Secondary hypogonadism through disorders of the
    hypothalamus or pituitary
    Congenital enzyme defects
    Drug-induced inhibition of enzymes needed in
    testosterone synthesis (spironolactone, ketoconazole)
    Chronic stimulation of Leydig cells by high levels of hCG
    can lead to a reduction in testosterone biosynthesis
    Hyperestrogenic states leading to suppression of LH and
    testosterone secretion

    3. INCREASED HEPATIC CLEARANCE OF


    ANDROGENS
    4. INCREASE IN SHBG LEADING TO A
    DECREASE IN FREE TESTOSTERONE

    1. ANDROGEN-RECEPTOR DEFICIENCY
    STATES ANDROGEN INSENSITIVITY
    SYNDROMES
    2. DRUG INTERFERENCE WITH ANDROGEN
    RECEPTORS
    Spironolactone, flutamide, cimetidine

    3. DRUGS THAT MIMIC ESTROGENS &


    STIMULATE ESTROGEN-RECEPTOR SITES
    Digoxin and phytoestrogens in some
    marijuana preparations

    1. Forms ~ Type I, Type II, Type III


    Type I ~ one or more subareolar nodules, freely

    moveable

    FIRM, RUBBERY CONSISTENCY, TENDER ON PALPATION


    OR WITH CONTACT OF CLOTHES, ETC.

    Type II ~ breast nodules beneath areola but also

    extending beyond the areolar perimeter (SAA)


    Type III ~ resembles breast development of SMR 3 in
    girls

    CONSISTENCY SIMILAR TO FEMALE BREAST

    2. Occurs Bilaterally in 77 95% of cases, with

    concurrent or sequential involvement of both breasts


    3. Physical Exam (see above)

    SUBAREOL
    AR
    NODULE
    BENEATH
    THE
    AREOLA OF
    THE NIPPLE

    1. Physiological ~ pubertal gynecomastia


    2. Medication or drug use
    3. Underlying medical disorders
    4. Pseudogynecomastia ~ caused by adipose

    tissue in some obese males or prominent


    musculature in some physically fit
    adolescent boys
    5. Breast mass ~ secondary to cancer, dermoid
    cyst, lipoma, hematoma, or neurofibroma

    Controversy as to which meds cause

    gynecomastia
    MORE THAN 300 REPORTED

    Sufficient evidence exists to implicate calcium

    channel blockers, chemotherapeutic agents,


    H2-receptor blockers, ketoconazole,
    spironolactone
    Committee on Safety of Medicines in the UK

    Renal failure and

    dialysis
    Recovery from
    malnutrition
    Primary gonadal failure:
    Klinefelter syndrome,
    Reifenstein syndrome
    Secondary
    hypogonadism
    Hyperthyroidism
    Liver disease: cirrhosis,
    hepatoma

    Neoplasms
    Testicular
    Adrenal
    Ectopic hCG

    production

    Lung, liver & kidney

    cancers

    Enzyme defects in

    testosterone
    biosynthesis
    Excessive
    extraglandular
    aromatase activity

    History ~ screen for medications & drug use

    and clues suggesting systemic illness


    Physical exam
    Differentiation of gynecomastia vs. pseudo-

    gynecomastia vs. musculature vs. excessive


    adipose tissue
    Findings suggestive of hypogonadism,
    hyperthyroidism or hypothyroidism
    Testicular mass or atrophy
    Findings suggestive of liver disease

    Place teen in supine position, with hands behind

    his head; examiner places the thumb and


    forefinger at opposing margins of the breast
    IN GYNECOMASTIA, as fingers are brought
    together, rubbery or firm breast tissue can be
    felt and is freely moveable; occasionally a
    tender disk of tissue concentric to the areola is
    found
    IN PSEUDOGYNECOMASTIA, no discrete mass is
    felt

    Breast enlargement in adolescents with the


    following:
    1.Unilateral or bilateral, subareolar, rubbery or
    firm mass
    2.Not using any medications or drugs
    associated with gynecomastia
    3.Normal testicular examination
    4.Lack any evidence of renal, hepatic, thyroid,
    or other endocrine disease

    R/O renal, hepatic, thyroid disorders


    If an endocrine disorder is suspected order

    hCG, LH, serum testosterone and


    estradiol/estrone sulphate
    Can help in differentiating the cause of

    nonpubertal gynecomastia

    1.

    Elevated hCG ~ order testicular U/S


    1.
    2.

    2.

    Mass found ~ testicular germ cell tumor


    Normal: extragonadal germ cell tumor or hCG-secreting
    neoplasm likely ~ obtain CXR and abdominal CT

    Decreased testosterone with

    Elevated LH ~ primary hypogonadism including


    Klinefelter syndrome and testicular atrophy cause by
    mumps orchitis
    Normal or low LH ~ order serum prolactin
    Elevated prolactin ~ probably prolactin-secreting
    pituitary tumor
    Obtain MRI of hypothalamic-pituitary axis

    Normal prolactin ~ secondary hypogonadism

    3. Elevated testosterone & LH ~ measure T4 and

    TSH

    Elevated T4, low TSH ~ HYPERTHYROIDISM


    Normal T4, TSH ~ ANDROGEN RESISTANCE

    4. Elevated estradiol with normal LH ~ obtain

    testicular U/S

    Mass found ~ Leydig or Sertoli cell tumor


    Normal ~ obtain adrenal CT or MRI

    Mass found ~ adrenal neoplasm


    No mass ~ increased extraglandular aromatase activity

    5. Normal concentrations of hCG, LH, testosterone

    and estradiol ~ IDIOPATHIC GYNECOMASTIA

    Treat underlying cause


    Discontinue implicated medications
    Pubertal gynecomastia ~ reassurance, will

    likely improve or resolve within 6 12 months


    Medication intervention
    Surgical intervention ~ in older adolescents
    with moderate to severe gynecomastia
    associated with psychological complications, or
    in older patients in which gynecomastia is
    unlikely to resolve spontaneously, surgical
    treatment is preferable
    ULTRASONIC LIPOSUCTION

    Testosterone, dihydrotestosterone, androgenic

    progesterone (danazol), antiestrogens (clomiphene,


    tamoxifen & raloxifene), and aromatase inhibitors
    (testolactone, anastrozole, letrozole & formestane)
    NOT APPROVED BY THE FDA FOR THE TREATMENT

    OF GYNECOMASTIA, STUDIES LIMITED


    Should be reserved for individuals who have more

    than mild to moderate gynecomastia and in those


    who have significant concern about the condition
    Tamoxifen 10 20 mg twice daily for 3 months

    Prepubertal gynecomastia usually resolves in

    12 18 months
    In 27% of affected adolescents, the condition
    lasts for greater than 1 year and in 7.7% for
    greater than 2 years
    A small percentage of cases will persist into
    adulthood

    There has been NO


    proven
    relationship
    between
    gynecomastia and
    the development
    of breast cancer
    in males

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