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Gynaecomastia
evaluation and
management
Dr sumer yadav
Definition
Gynaecomastia is an enlargement
of the male breast, secondary to
proliferation of both epithelial and
stromal components .
Gynaecomastia term is derived
from Greek words gynae (female)
and mastos(breast). Enlargement
of the male breast looking like
women breast
Prevalence
• Gynaecomestia is a common
condition . In various studies its
prevalence is found to be about
36% in healthy young adult males ,
57% in healthy old males.
• The neonatal period - In neonates it is
estimated that 60 to 90% of infants have
transient gynaecomastia due to
transplacental transfer of maternal
estrogens……...
........This stimulus for breast
growth ceases as the estrogens
are cleared from the neonatal
circulation and the breast tissue
gradually regresses over a 2 to 3
week period . It usually
regresses completely by the end
of first year.
Puberty
• Transient gynaecomastia may occur
in up to 60% boys. It may first appear
at as early as 10 years of age, with a
peak onset between 13 to 14 years,
followed by an involution that is
generally complete by 16 to 17 years
In old age
• The incidence of gynaecomastia
increase in advancing age , with the
highest prevalence found at the age of
50 to 80 years range. Ageing is
associated with progressive testicular
dysfunction with reduction in serum
testosterone level and, in some cases,
elevated Luteinising hormone (LH).
Pathophysiology
• Gynaecomastia results from an
altered estrogen – androgen balance ,
in favor of estrogen, or increase
breast sensitivity to a normal
circulating estrogen level. The
imbalance is between the stimulatory
effect of estrogen and the inhibitory
effect of androgen.
Estrogens induced ductal
epithelial hyperplasia , ductal
elongation and branching,
proliferation of the periductal
fibroblasts, and an increase in
vascularity . The histologic
picture is similar in male and
female breast tissue after
exposure to estrogen.
• Estrogen production in males is
mainly from the peripheral conversion
of androgens ( testosterone and
androstenedione ) through the action
of the enzyme aromatase, mainly in
muscles, skin and adipose tissue in
the form of estrone and estradiol.
• The normal production ratio of
testosterone to estrogen in males is
approximately 100:1. But in ciculation
it is 300:1.
Histopathology
• Characteristic findings include
proliferation of ductules and stroma
(consisting of connective tissue
elements such as fibroblasts, collagen
and myofibroblasts) and occasional
acini. Gynaecomastia of short duration
consists of a prominent ductular
component with loose stroma. Long
standing gynaecomastia consists of
dense stroma with few ductules.
Causes
Physiological Gynaecomastia
• New born
• Adolescence
• Aging
 Pathological Gynaecomastia
 Deficient production or action of
testosterone
• Congenital anorchia
• Androgen resistance (testicular
feminization and reifenstein syndrome
…..
• Klinefeltar syndrome
• Viral orchitis
• Trauma
• Castration
• Neurological and granulomatous
diseases
• Renal failure
….
Increase estrogen production
 Increased estrogen secretion
• Testicular tumor
• True hermaphroditism
• Carcinoma of the lungs and other tumor
producing HCG
……….
…....
 Increase substrate for extra glandular
aromatase
• Adrenal disease
• Liver disease (cirrhosis of the liver)
• Malnutrition
• Hyperthyroidism
 Increase in extra glandular aromatase
………
 Drugs
• Estrogens
• Drugs that enhances estrogen secretions
( gonadotropins , clomiphen )
• Inhibitors of testosterone synthesis or
action
I. Ketoconazole
II. Metronidazole
III. Alkylating agent
IV. Cisplatin
V. Spironolactone
VI. Cimetidine
VII. Flutamide
• Unknown mechanism
 Busulfan
 Isoniazide
 Methyldopa
 Tricyclic antidepressant
 Penicillamine
 Diazepam
 Omeprazole
 Growth hormone
 Calcium channel blocker
 Metoclopramide
 Angiotensin converting
enzyme inhibitors
 Heroin
 Marijuana
• Idiopathic
• Most patients of gynaecomastia are
asymptomatic
• It may be an incidental finding during routine
physical examination
• The main presenting symptom in patient with
recent onset of gynaecomastia is usually
breast or nipple pain and tenderness and
those who present late usually complain of
breast enlargement
Clinical features and
diagnostic evaluation
Physical examination
• Perform a thorough examination of breast ,
noting their size and consistency. Also
determine the presence of any nipple
discharge or axillary lymphadinopathy.
• Differentiate between the true
gynaecomastia and pseudo gynaecomastia
/ lipomastia.
• Gynaecomastia can be detected when the
size of glandular tissue exceeds 0.5 cm in
diameter. ………..
……
• Examination of the testicles , noting there
size and consistency. Carefully look for
any nodules or asymmetry
• Note signs of feminization, including
typical body hair distribution and
eunuchoid habitus
• Check for any stigmata of chronic liver
diseases , thyroid disease or renal
disease
Simon’s classification of
gynaecomastia
Group 1
• Minor but visible breast enlargement without
skin redundancy
Group 2A
• Moderate breast enlargement without skin
redundancy
Group 2B
• Moderate breast enlargement with minor skin
redundancy
Group 3
• Gross breast enlargement with skin redundancy
that looks like a pendulous female breast
Investigations
• Patients with physiological
gynaecomastia do not require further
evaluation
• Further evaluation is necessary in
patients with the following
I. Breast size greater then 5 cm
(macromastia)
II. A lump that is tender , of recent onset ,
progressive or of unknown duration
III. Sign of malignancy
Serum chemistry
 LFT
 Thyroid function test
 Renal function test
 Total or free testosterone level ,
serum prolactine , LH , oestradiol ,
dehydroepiandrostenone sulphate
levels to evaluate a patient with
possible feminization syndrome
 Urinary 17 ketosteroid
 Beta HCG
Imaging Studies
 USG breast
 Mammography
 Testicular ultra sonography and
thermography
 CT Scan for adrenal gland
 MRI for pituitary gland
Differential Diagnosis
• Pseudo gynaecomastia
• Breast cancer
• Dermoid cyst
• Haematoma
• Lipoma
• Lymphangioma
• Neurofibroma
Treatment
• Generally no treatment is required for
physiological gynaecomastia
• A major factor that should influence the
initial choice of therapy is the duration of
gynaecomastia
• If the patient is at the pubertal age, and
has an otherwise normal general physical
and testicular examination , he probably
has transient or persistent gynaecomastia
….….…
Reexamination at six month intervals
should determine whether the
condition is transient or persistent .
At this time , medical or surgical
therapy should be considered. If the
patient is on a drug causing
gynaecomastia , this should be
stopped or changed to another
medication if possible , and
reexamine the patient after one
month .
If the drug was the cause ,
then reduction in breast pain
and tenderness should occur
during that time . Similarly ,
breast enlargement following
cytotoxic chemotherapy may
also resolve spontaneously.
Treatment of hyperthyroidism and
surgical removal of testicular ,
adrenal , or other causative
tumor may lead to regression in
patients with hypogonadism ,
treatment with testosterone may
produce regression by providing
androgen and suppressing LH
stimulated oestradiol secretion.
Medical treatment
• As gynaecomastia has high frequency
of spontaneous regression , the
decision of when to treat is often
difficult. Trials of medical therapy should
be limited to only six months , due to
limited experience and unknown long
term side effects of the drugs . When
gynaecomastia has been present for
more then 2 years , medical therapy is
unlikely to be effective , and surgery
may be the only useful treatment
• Options include androgens
(testosterone , danazole) , anti
estrogen( clomiphene , tamoxifen) and
aromatase inhibitors
• Androgen
 Testosterone – it is a male sex
hormone given in dose of 200 to 300
mg IM
 Danazole – it is synthetic steroid analog
with strong antigonadotropic activity
(inhibits LH and FSH) and weak
androgenic action doses are 200 mg bd
for 3 months. It is the only drug liscenced
for the treatment of gynaecomastia in UK.
• Antiestrogen
 Clomiphene citrate – it stimulates
release of pitutory gonadotropin 50 to 100
mg QID for 6 months.
 Tamoxifen – compititive binds to estrogen
receptor , producing a nuclear complex
that inhibits estrogen effects. Dose 10 to
20 mg BD
• Aromatase inhibitors
 Testolactone – it is synthetic peripheral
aromatase inhibitors . It blocks production
of estradiol and estrone from testosterone.
Dose 150 mg TDS for 6 months
Surgery
Surgical treatment is indicated in patients
in whom the gynaecomastia causes
distress and psychological trauma , when
there is no underlying treatable condition
and when hormonal treatment is failed,
then operative treatment is indicated
Surgical treatment includes
• Open subcutaneous mastectomy
• Endoscopic assisted subcutaneous
mastectomy
• Liposuction assisted mastectomy
• Ultra sound assisted liposuction
• Open subcutaneous mastectomy –
this is most commonly performed
procedure in gynaecomastia. This is
carried out through circumareolarincision
between 3 and 9 o clock position. The
length of incision varies
• Endoscopic assisted subcutaneous
mastectomy – with this technique it is
possible to excise the glandular breast
tissue through very small distant incision.
Thus avoiding breast and areolar scar
• Liposuction assisted mastectomy
– this is most popular method used to
correct pseudo gynaecomastia.
Advantage compared to the open
subcutaneous mastectomy includes
reduced risk of nipple / aerioral
ischemia , reduced chance of nipple
distortion , lower risk of saucer
deformity and reduced risk of
hemorrhage and hematoma.
• This technique is not
recommended for glandular
gynaecomastia. The Incesion is 3
to 4 mm in length, it can be made
in axillary folds or inframammary
fold or periareolar . Post operative
compression garments are
applied for at least two weeks .
• Ultrasound assisted
liposuction – this permits
emulsification and cavitations of
glandular tissue which can then be
followed by standard liposuction to
remove excess fat in liquefied tissue
Complication of
surgery
• Bleeding and hematoma
• Seroma
• Nipple , areola related complications –
inversions, distortion and alteration of
symmetry and necrosis
• Scar related complications includes
painful hypertrophid or keloid scar
• Breast asymmetry
• Contour irregularity
• Infection
Prevention
Two situations exist in which
gynaecomastia can be
prevented. The first is by avoiding
drugs that can cause
gynaecomastia.
The second
area of prevention applies to
patients with prostate cancer who
are about to receive estrogen or
anti androgen therapy.
Studies have shown that
prophylactic breast irradiation
(with low dose of 900 red) is
effective in preventing
gynaecomastia in patients with
prostate cancer.
Prognosis
Regardless of he etiology of
gynaecomastia the pronosis is
excellent. Studies have shown that
90% of physiological
gynaecomastia involutes
spontaneously within 2 years.
In drug induced gynaecomastia,
withdrawal of the medication leads
to regression in 60% of the patient
• If the gynaecomastia is of long
duration it is unlikely to regress
spontaneously.
THANKSTHANKS

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gyencomastia

  • 3. Gynaecomastia is an enlargement of the male breast, secondary to proliferation of both epithelial and stromal components . Gynaecomastia term is derived from Greek words gynae (female) and mastos(breast). Enlargement of the male breast looking like women breast
  • 4. Prevalence • Gynaecomestia is a common condition . In various studies its prevalence is found to be about 36% in healthy young adult males , 57% in healthy old males. • The neonatal period - In neonates it is estimated that 60 to 90% of infants have transient gynaecomastia due to transplacental transfer of maternal estrogens……...
  • 5. ........This stimulus for breast growth ceases as the estrogens are cleared from the neonatal circulation and the breast tissue gradually regresses over a 2 to 3 week period . It usually regresses completely by the end of first year.
  • 6. Puberty • Transient gynaecomastia may occur in up to 60% boys. It may first appear at as early as 10 years of age, with a peak onset between 13 to 14 years, followed by an involution that is generally complete by 16 to 17 years
  • 7. In old age • The incidence of gynaecomastia increase in advancing age , with the highest prevalence found at the age of 50 to 80 years range. Ageing is associated with progressive testicular dysfunction with reduction in serum testosterone level and, in some cases, elevated Luteinising hormone (LH).
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  • 10. Pathophysiology • Gynaecomastia results from an altered estrogen – androgen balance , in favor of estrogen, or increase breast sensitivity to a normal circulating estrogen level. The imbalance is between the stimulatory effect of estrogen and the inhibitory effect of androgen.
  • 11. Estrogens induced ductal epithelial hyperplasia , ductal elongation and branching, proliferation of the periductal fibroblasts, and an increase in vascularity . The histologic picture is similar in male and female breast tissue after exposure to estrogen.
  • 12. • Estrogen production in males is mainly from the peripheral conversion of androgens ( testosterone and androstenedione ) through the action of the enzyme aromatase, mainly in muscles, skin and adipose tissue in the form of estrone and estradiol. • The normal production ratio of testosterone to estrogen in males is approximately 100:1. But in ciculation it is 300:1.
  • 13. Histopathology • Characteristic findings include proliferation of ductules and stroma (consisting of connective tissue elements such as fibroblasts, collagen and myofibroblasts) and occasional acini. Gynaecomastia of short duration consists of a prominent ductular component with loose stroma. Long standing gynaecomastia consists of dense stroma with few ductules.
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  • 16. Causes Physiological Gynaecomastia • New born • Adolescence • Aging  Pathological Gynaecomastia  Deficient production or action of testosterone • Congenital anorchia • Androgen resistance (testicular feminization and reifenstein syndrome
  • 17. ….. • Klinefeltar syndrome • Viral orchitis • Trauma • Castration • Neurological and granulomatous diseases • Renal failure
  • 18. …. Increase estrogen production  Increased estrogen secretion • Testicular tumor • True hermaphroditism • Carcinoma of the lungs and other tumor producing HCG ……….
  • 19. …....  Increase substrate for extra glandular aromatase • Adrenal disease • Liver disease (cirrhosis of the liver) • Malnutrition • Hyperthyroidism  Increase in extra glandular aromatase ………
  • 20.  Drugs • Estrogens • Drugs that enhances estrogen secretions ( gonadotropins , clomiphen ) • Inhibitors of testosterone synthesis or action I. Ketoconazole II. Metronidazole III. Alkylating agent IV. Cisplatin V. Spironolactone VI. Cimetidine VII. Flutamide
  • 21. • Unknown mechanism  Busulfan  Isoniazide  Methyldopa  Tricyclic antidepressant  Penicillamine  Diazepam  Omeprazole  Growth hormone
  • 22.  Calcium channel blocker  Metoclopramide  Angiotensin converting enzyme inhibitors  Heroin  Marijuana • Idiopathic
  • 23.
  • 24. • Most patients of gynaecomastia are asymptomatic • It may be an incidental finding during routine physical examination • The main presenting symptom in patient with recent onset of gynaecomastia is usually breast or nipple pain and tenderness and those who present late usually complain of breast enlargement Clinical features and diagnostic evaluation
  • 25. Physical examination • Perform a thorough examination of breast , noting their size and consistency. Also determine the presence of any nipple discharge or axillary lymphadinopathy. • Differentiate between the true gynaecomastia and pseudo gynaecomastia / lipomastia. • Gynaecomastia can be detected when the size of glandular tissue exceeds 0.5 cm in diameter. ………..
  • 26. …… • Examination of the testicles , noting there size and consistency. Carefully look for any nodules or asymmetry • Note signs of feminization, including typical body hair distribution and eunuchoid habitus • Check for any stigmata of chronic liver diseases , thyroid disease or renal disease
  • 27. Simon’s classification of gynaecomastia Group 1 • Minor but visible breast enlargement without skin redundancy Group 2A • Moderate breast enlargement without skin redundancy Group 2B • Moderate breast enlargement with minor skin redundancy Group 3 • Gross breast enlargement with skin redundancy that looks like a pendulous female breast
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  • 31. Investigations • Patients with physiological gynaecomastia do not require further evaluation • Further evaluation is necessary in patients with the following I. Breast size greater then 5 cm (macromastia) II. A lump that is tender , of recent onset , progressive or of unknown duration III. Sign of malignancy
  • 32. Serum chemistry  LFT  Thyroid function test  Renal function test  Total or free testosterone level , serum prolactine , LH , oestradiol , dehydroepiandrostenone sulphate levels to evaluate a patient with possible feminization syndrome  Urinary 17 ketosteroid  Beta HCG
  • 33. Imaging Studies  USG breast  Mammography  Testicular ultra sonography and thermography  CT Scan for adrenal gland  MRI for pituitary gland
  • 34. Differential Diagnosis • Pseudo gynaecomastia • Breast cancer • Dermoid cyst • Haematoma • Lipoma • Lymphangioma • Neurofibroma
  • 35. Treatment • Generally no treatment is required for physiological gynaecomastia • A major factor that should influence the initial choice of therapy is the duration of gynaecomastia • If the patient is at the pubertal age, and has an otherwise normal general physical and testicular examination , he probably has transient or persistent gynaecomastia ….….…
  • 36. Reexamination at six month intervals should determine whether the condition is transient or persistent . At this time , medical or surgical therapy should be considered. If the patient is on a drug causing gynaecomastia , this should be stopped or changed to another medication if possible , and reexamine the patient after one month .
  • 37. If the drug was the cause , then reduction in breast pain and tenderness should occur during that time . Similarly , breast enlargement following cytotoxic chemotherapy may also resolve spontaneously.
  • 38. Treatment of hyperthyroidism and surgical removal of testicular , adrenal , or other causative tumor may lead to regression in patients with hypogonadism , treatment with testosterone may produce regression by providing androgen and suppressing LH stimulated oestradiol secretion.
  • 39. Medical treatment • As gynaecomastia has high frequency of spontaneous regression , the decision of when to treat is often difficult. Trials of medical therapy should be limited to only six months , due to limited experience and unknown long term side effects of the drugs . When gynaecomastia has been present for more then 2 years , medical therapy is unlikely to be effective , and surgery may be the only useful treatment
  • 40. • Options include androgens (testosterone , danazole) , anti estrogen( clomiphene , tamoxifen) and aromatase inhibitors • Androgen  Testosterone – it is a male sex hormone given in dose of 200 to 300 mg IM
  • 41.  Danazole – it is synthetic steroid analog with strong antigonadotropic activity (inhibits LH and FSH) and weak androgenic action doses are 200 mg bd for 3 months. It is the only drug liscenced for the treatment of gynaecomastia in UK. • Antiestrogen  Clomiphene citrate – it stimulates release of pitutory gonadotropin 50 to 100 mg QID for 6 months.
  • 42.  Tamoxifen – compititive binds to estrogen receptor , producing a nuclear complex that inhibits estrogen effects. Dose 10 to 20 mg BD • Aromatase inhibitors  Testolactone – it is synthetic peripheral aromatase inhibitors . It blocks production of estradiol and estrone from testosterone. Dose 150 mg TDS for 6 months
  • 43. Surgery Surgical treatment is indicated in patients in whom the gynaecomastia causes distress and psychological trauma , when there is no underlying treatable condition and when hormonal treatment is failed, then operative treatment is indicated Surgical treatment includes • Open subcutaneous mastectomy • Endoscopic assisted subcutaneous mastectomy • Liposuction assisted mastectomy • Ultra sound assisted liposuction
  • 44. • Open subcutaneous mastectomy – this is most commonly performed procedure in gynaecomastia. This is carried out through circumareolarincision between 3 and 9 o clock position. The length of incision varies • Endoscopic assisted subcutaneous mastectomy – with this technique it is possible to excise the glandular breast tissue through very small distant incision. Thus avoiding breast and areolar scar
  • 45.
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  • 53.
  • 54. • Liposuction assisted mastectomy – this is most popular method used to correct pseudo gynaecomastia. Advantage compared to the open subcutaneous mastectomy includes reduced risk of nipple / aerioral ischemia , reduced chance of nipple distortion , lower risk of saucer deformity and reduced risk of hemorrhage and hematoma.
  • 55. • This technique is not recommended for glandular gynaecomastia. The Incesion is 3 to 4 mm in length, it can be made in axillary folds or inframammary fold or periareolar . Post operative compression garments are applied for at least two weeks .
  • 56. • Ultrasound assisted liposuction – this permits emulsification and cavitations of glandular tissue which can then be followed by standard liposuction to remove excess fat in liquefied tissue
  • 57. Complication of surgery • Bleeding and hematoma • Seroma • Nipple , areola related complications – inversions, distortion and alteration of symmetry and necrosis • Scar related complications includes painful hypertrophid or keloid scar • Breast asymmetry • Contour irregularity • Infection
  • 58. Prevention Two situations exist in which gynaecomastia can be prevented. The first is by avoiding drugs that can cause gynaecomastia. The second area of prevention applies to patients with prostate cancer who are about to receive estrogen or anti androgen therapy.
  • 59. Studies have shown that prophylactic breast irradiation (with low dose of 900 red) is effective in preventing gynaecomastia in patients with prostate cancer.
  • 60. Prognosis Regardless of he etiology of gynaecomastia the pronosis is excellent. Studies have shown that 90% of physiological gynaecomastia involutes spontaneously within 2 years. In drug induced gynaecomastia, withdrawal of the medication leads to regression in 60% of the patient
  • 61. • If the gynaecomastia is of long duration it is unlikely to regress spontaneously.