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    Gynecomastia Gynecomastia Presentation Transcript

    • Gynecomastia September 29, 2004 Isabel Tejeda, MD
    • Case Presentation
      • ID/CC: 20 yo Latino male in general good health with 2yrs of unilateral tender, enlarged left breast.
    • History of Present Illness
      • Noticed enlarged left breast with increasing tenderness and size 2yrs ago
      • Dull pain to touch and with movement
      • Denies nipple discharge/galactorrhea
      • Denies SOB/CP
      • Denies history of trauma
      • Cannot remember when physical changes of puberty began
    • Past Medical History
      • Hx of physical and verbal abuse by father
      • Hx of depression and suicidal attempt with pills, last attempt one year ago, no current SI
      • +PPD, -CXR, hx INH tx years ago
    • Medications
      • None
      • NDKA
    • Family History
      • Father: Alcoholic
      • Mother: Anxiety, Depression, GERD
      • Sister: In good health
      • Cousin w/ cervical cancer
    • Social History
      • Returned to US 4 months ago with pregnant wife
      • Living with relatives
      • Works in construction
    • Health Related Habits
      • Denies current and prior use of Alcohol, Tobacco, Drugs
    • Physical Exam
      • VS: BP116/59 HR59 RR16 Weight 139lbs
      • Gen: Thin, flat affect, NAD, well dressed, answering questions appropriately, emotionally labile during interview
      • HEENT: WNL
      • CVS: RRR S1S2 no murmers
      • Lungs: CTA
      • Breasts: Visually enlarged left breast. Enlarged breast tissue 4cm with rubbery amorphous mass above nipple, no discrete masses. +TTP. No skin discolorations, dimpling, nipple retraction or discharge.
      • GU: Normal male genitalia. Bilateral descended testes, non-tender, no masses palpated
      • Neuro: A&O x 4, CN II-XII intact, good strength
    • Questions?
      • What is the work-up for unilateral, tender, persistent gynecomastia in a 20yo male?
      • Do I need to worry about breast cancer or other pathologic conditions?
      • What treatments exist?
    • Definition of Gynecomastia
      • True Gynecomastia: presence of a rubbery or firm mass extending concentrically and symmetrically from the nipple. Usually bilateral but can be unilateral.
      • Pseudogynecomastia: fat deposition without glandular proliferation, on exam fingers will not meet any resistance until they reach the nipple
      • Breast cancer: hard or firm eccentric in location from the nipple, and may be associated with skin dimpling, nipple retraction or discharge, and axillary lymphadenopathy
    • Prevalence
      • Gynecomastia has three peaks.
      • 1. Infancy: 60-90% transient due to high maternal estrogen. Normally regresses over 2-3 week period.
      • 2. Adolescence: 4-69% with wide variation due to examiner observation. Onset 10-12y/o and peaks 13-14y/o. Normally regresses w/in 18mo and persistence uncommon after 17y/o.
      • 3. Older men: 24-65% with highest prevalence in the 50-80y/o.
    • Etiologies in patients seeking help for Gynecomastia
      • Drugs: 10-25%
      • No detectable abnormality: 25%
      • Persistent pubertal gynecomastia: 25%
      • Cirrhosis or malnutrition: 8%
      • Primary hypogonadism: 8%
      • Testicular tumors: 3%
      • Secondary Hypogonadism: 2%
      • Hyperthyroidism: 1.5%
      • Chronic renal insufficiency: 1%
    • Pathophysiologic Causes for Gynecomastia
      • The basic mechanisms of gynecomastia include a decrease in androgen production, an increase in estrogen production, or increased availability of estrogen precursors for peripheral conversion to estrogen.
      • Androgen receptor blockade and increased binding of androgen to sex-hormone binding globulin (SHBG).
      • Estrogen-like or antiandrogen effects of Drugs
    • Absolute increase in free estrogen
      • Direct secretion from:
        • Maternal-placental-fetal unit
        • Testes
        • Adrenal glands
      • Extraglandular aromatization of precursors by adipose, liver, skin, muscle, kidney and bone.
      • Displacement from sex hormone-binding globulin as SHBG has higher affinity for androgens than estrogens.
      • Enhanced sensitivity of breast tissue to circulating estrogen via increased aromatization
      • Exogenous estrogen admininstration, ex. drugs
    • Decreased endogenous free androgens
      • Decreased secretion by testes and adrenals
      • Increased metabolism via aromatization
      • Increased binding to sex hormone-binding globulin
      • Congenital defects in androgen receptor structure or function
      • Displacement of androgens from receptor
    • Specific Pathogeneses
      • Puberty
        • No difference serum measurements of testosterone, estradiol, estrone, or gonadotropins.
        • Boys who develop gynecomastia have an transient increase in estradiol concentration at onset of puberty
        • During puberty, the serum estradiol concentrations rise to adult levels before the testosterone concentration.
      • Adult men
        • Multifactorial including increase body fat, decrease in testosterone by testes and increase in LH, and likely polypharmacy.
    • Specific Pathogeneses
      • Drugs
        • May increase estrogens or act as antiandrogens by binding receptors and displacing androgens.
        • Others increase aromatization of testosterone to estradiol, decrease testosterone production, displace testosterone from SHBG, thereby increasing its metabolic clearance .
      • Cirrhosis
        • Increase androstenedione and its conversion to estrone and estradiol.
        • Elevated SHBG levels, reducing free testosterone
      • Malnutrition
        • Decrease androgen with normal estrogen production.
        • Refeeding mimics normal puberty hormone pattern.
    • Specific Pathogeneses
      • Male hypogonadism
        • Primary hypogonadism can be associated with Klinefelter’s or enzymatic defect in the testosterone biosynthetic pathway, or testicular trauma, infection, infiltrative disorders, vascular insufficiency or aging.
        • Net effect is decrease in testosterone with increase in estradiol.
        • Secondary hypogonadism due to hypothalamic or pituitary abnormality result in low testosterone and increase in estrogen precursors .
      • Testicular neoplasm
        • Germ cell tumor may present with gynecomastia (2.5-6% of patients) which is a poor prognosis.
        • Leydig cell tumor may present with gynecomastia (20-30%)
        • These neoplasms produce estrogen/androgen inbalances.
    • Specific Pathogeneses
      • Hyperthyroidism due to Graves’ disease
        • As many as 25-40% have gynecomastia due to increase of SHBG and enhanced aromatization
      • Chronic renal failure and dialysis
        • 50% develop gynecomastia due to Leydig cell dysfxn resulting in low testosterone
      • Feminizing adrenocortical tumors
        • Rare malignant tumors that have gynecomastia( 98%), palpable tumor(58%), and testicular atrophy(50%).
    • Specific Pathogeneses
      • Ectopic production hCG
        • Precocious puberty in boys with hepatoblastomas
        • In adults, large cell CA of lung, gastric CA, renal cell Ca, and occasionally hepatomas.
      • True Hermaphroditism
        • Harbor both testicular and ovarian tissue. Increased estrogen activity can suppress testosterone production by testes.
      • Androgen Insensitivity Syndromes
        • Defects or absence of androgen receptors in target tissue
      • Excessive extraglandular aromatase activity
        • X-linked recessive or sex-limited autosomal trait have many fold increase in extraglandular conversion of plasma androstenedione to estrone.
    • Work-up
      • History
        • Onset
        • Bilateral/unilateral
        • Pain
        • Change in size
        • Nipple discharge
        • Drugs/medications
        • PMH
        • Family history
    • Work-up
      • Complete Physical Exam and ROS
        • Look for signs and sx of liver and kidney disease
        • Evaluate for hyperthyroidism, eg. Weight loss, tachycardia, goiter, tremor, or exophthalmos.
        • Seek for signs and sx that may suggest hypogonadism, eg. Impotence, decreased libido, strenght, and change in testicular size.
        • Check for abdominal mass and testicular mass.
        • Careful breast exam.
    • Work-up
      • Labs if gynecomastia of recent onset, persistent, or painful/tender and has no clear physiologic etiology.
        • BMP, LFT’s, TSH, LH, FSH, hCG, Prolactin, Estradiol, Testosterone, Androstenedione
      • Imaging? US and mammogram for any eccentric or discrete mass.
    • Treatment Options
      • Watchful Waiting
      • Medications
      • Surgery
    • Treatments
      • Watchful waiting
        • In healthy adolescent with normal PE and genital exam, reevaluate in 6 months
        • Gynecomastia attributed to a medication should be stopped and patient reassessed after stopping medication
        • Regression will occur in 85% of patients with gynecomastia due to various causes
    • Treatments
      • Medications
        • May be indicated in patients with persistent gynecomastia, eg. Later puberty with severe pain, tenderness, psychosocial issues of embarrasment.
        • Consider that current medications have only been studied in small sizes that have been unblinded and uncontrolled.
        • Three types of medical therapy
          • Androgens, antiestrogens and aromatase inhibitors
          • None are FDA approved for gynecomastia
    • Androgens
      • Testosterone
        • Has not been shown to be more effective than placebo and can be aromatized exogenously.
        • However, has been shown to reduce the prevalence of gynecomastia in patients with cirrhosis
      • Dihydrotestosterone (nonaromatizable androgen)
        • One report noted decrease in breast volume in 75% of patients and resolution in 25%. No noted side effects and there was a decrease in tenderness within 1-2 weeks
      • Danazol
        • In a single placebo-controlled study, 23% of patients had complete resolution vs 12% in the placebo group. Danzol appeared safe and well tolerated but does have well known SE: edema, wght gain, acne, nausea and muscle cramps.
    • Antiestrogens
      • Clomiphen
        • Response rates of 36-95% have been reported, however two major studies of pubertal gynecomastia found that fewer than one half of patients had more than 20% decrease in breast volume or were satisfied with the results.
      • Tamoxifen
        • Two randomized double-blinded studies with a total of 16 patients using Tamoxifen 10mg po bid showed a statistically significant reduction in pain and breast size however none had complete remission. Patients received treatment for upto 4 months with out major side effects, except for occassional epigastric distress and nausea.
    • Surgery
      • Should be considered in patients who do not respond to medical therapy or who have long standing gynecomastia.
      • Options Include
        • Liposuction
        • Direct surgical excision, or both
      • Complications
        • Permanent numbness, compromise of blood supply, irregular contour, hematoma, seroma, wound infection.
    • Back to Case Presentation
      • Labs: Normal
      • Referral to breast clinic: Scheduled mammogram and advised to return if increase in breast size, pain, or discrete mass.
    • References
      • Up To Date, Vol 12 No.2
      • The effect of tamoxifen on sex hormone binding globulin in adolescents with pubertal gynecomastia. J Pediatr Endocrinol Metab . 2004 Aug;17(8);1115-9 [abstract]
      • Sonography of pediatric male breast masses: gynecomastia and beyond. Pediatr Radiol. 2004 Sep 17 [abstract]
      • Tamaxifen treatment for pubertal gynecomastia. Int J Adolesc Med Health. 2003 Oct-Dec;15(4):359-63 [abstract]
      • Management of physiological gynaecomastia with tamoxifen. Breast. 2004 Feb;13(1);61-5.