Download Case 029: Breasts like his wife`s. 1. What is this patient`s condition?

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Case 029: Breasts like his wife’s.
Authors:
David C Chung MD, FRCPC
Thomas YK Chan MD, PhD, FRCP
Affiliation:
The Chinese University of Hong Kong
A 61 year old former bank manager came to the Clinic complaining of enlargement
of his breasts. He has always been in good health, was not on any medications, but
has gained 10 kg in weight since retirement a year ago. He noticed that both his
breasts were becoming fuller, like those of his wife, and wanted to know if that was
abnormal.
Physical examination revealed an obese patient of stated age. His vital signs were:
oral temperature 36.8 oC, BP 144/88 mmHg, pulse rate 72/min and regular,
respiratory rate 12/min. Besides symmetrical fullness of both breasts, examination of
the systems revealed no abnormalities.
1. What is this patient’s condition?
This male patient had female-like breasts. The condition is called gynecomastia.
Gynecomastia has to be differentiated from pseudo-gynecomastia. While
gynecomastia is the development of 5 cm or more of true glandular tissue in the
breast of a male patient, pseudo-gynecomastia is simply the accumulation of fatty
tissue in the breast of an obese male patient.
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2. How to distinguish gynecomastia from pseudo-gynecomastia?
Gynecomastia can be distinguished from pseudo-gynecomastia by careful
examination of the breasts. Glandular tissue hypertrophy in gynecomastia may
be unilateral, asymmetrical, or symmetrical while distribution of adipose tissue is
always symmetrical. Glandular tissue feels rubbery firm and is subareolar;
adipose tissue is soft and lacks substance. If in doubt, mammography can be
used to distinguish gynecomastia from pseudo-gynecomastia.
When examining a person presenting with gynecomastia, it is important also to
look for other features of feminization (e.g. loss of facial hair) and examine his
testes. Testes with a long diameter of less than 3 cm suggest hypogonadism; the
presence of a testicular mass suggests the presence of a functioning tumor
(Leydig cell or Sertoli cell tumor).
3. What medical conditions are associated with gynecomastia?
Gynecomastia is a surprisingly common condition seen in 50% of pubertal boys
and 30 – 50% of post-pubertal men. Conditions that are associated with
gynecomastia include:
Idiopathic
o As many as 25% of patients have idiopathic gynecomastia.
Physiologic
o New born.
o Puberty.
o Aging (andropause).
Pathologic
o Drug induced. A large number of drugs have been reported to cause
gynecomastia. A partial list includes ACE inhibitors, amiodarone, antiandrogens, calcium channel blockers, cancer chemotherapy agents,
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clomiphene, digitalis compounds, estrogen and its precursors, H2-receptor
antagonists, HIV antiretroviral drugs (efavirenz, didanosine), isoniazid,
ketoconazole, marijuana and substances of abuse (alcohol, amphetamine,
heroin, methadone), methyldopa, metoclopramide, metronidazole,
penicillamine, phenothiazines, phenytoin, reserpine, spironolactone, sulindac,
theophylline, and anti-depressants.
o Liver cirrhosis.
o Renal failure and dialysis.
o Cushing’s syndrome.
o Hyperthyroidism.
o Primary gonadal failure from testicular torsion and trauma, castration, viral
orchitis, granulomatous disease of the testes.
o Estrogen producing tumors (testicular tumor, bronchial carcinoma).
o Prolactinemia (pituitary tumor).
o Re-feeding after starvation.
o Klinefelter’s syndrome.
4. What is the pathologic basis of developing gynecomastia?
The development of gynecomastia is related to an increase in the ratio of free
circulating estrogens to androgens (bound hormones are not active):
Pathophysiology
Examples of disease conditions
estrogen production
Testicular tumor, bronchial carcinoma
estrogen clearance
Liver disease
androgen to estrogen conversion
Liver disease, hyperthyroidism, obesity
androgen production
Aging, liver disease, hypogonadism
binding of androgen by globulin
Liver disease, hyperthyroidism
Gonadal suppression
Prolactinoma and hyper-prolactinemia
One or more of above
Drugs
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5. How to distinguish gynecomastia from male breast cancer?
Although male breast cancer is rare, all male patients presenting with breast
enlargement should be assessed with this entity in mind. A breast malignancy is
usually unilaterally and the lump eccentric rather than subareolar. Consistency is
firm to hard and its shape irregular. It may be fixed to underlying tissue and to
skin, causing skin dimpling. A heightened degree of suspicion is required to make
the diagnosis. Mammography is helpful and biopsy for a morphologic diagnosis is
often required.
6. What laboratory investigations should be ordered in patients with
gynecomastia?
Laboratory investigations should be guided by a detailed medical history,
including history of self-medication, and complete general physical examination.
General investigations should include complete blood counts, renal function tests,
liver function tests, and thyroid function test to screen for dysfunction in these
systems and chest x-ray to rule out metastatic carcinoma and bronchial
carcinoma with inappropriate hormone secretion.
When indicated, specific investigations can include:
o Plasma testosterone.
o Plasma testosterone in conjunction with luteinizing hormone (LH) and
follicular stimulating hormone (FSH). This helps to differentiate primary
hypogonadism (failure at the testicular level) from secondary hypogonadism
(failure at the hypothalamic-pituitary level). Plasma testosterone is low while
LH and FSH levels are raised in primary hypogonadism; low level of
testosterone is associated with low, sometimes normal, levels of LH and FSH
in secondary hypogonadism.
o Plasma estradiol.
o Plasma β-human chorionic gonadotropin (marker of testicular and lung or liver
malignancies).
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o Plasma α-fetal protein (marker of testicular and other tumors).
o CT scan of head to rule out pituitary tumor.
o Basal plasma prolactin level assay if prolactinoma is suspected.
o Karyotype analysis for Klinefelter’s syndrome.
7. What is the treatment for gynecomastia?
For post-pubertal gynecomastia, a diligent search should be mounted to discover
the underlying cause and treatment should be directed at the cause. If
gynecomastia is drug-induced, the offending drug should be removed or
supplanted if at all possible. The condition will regress within a month after
discontinuation of the offending drug.
Gynecomastia in the adolescent deserves more attention.
o Most gynecomastia in adolescent boys appears approximately 6 months after
the onset of puberty.
o Most will resolve spontaneously in 6 months to 2 years.
o Gynecomastia that is troubled by persistent pain may be treated with a 3 – 9
month course of an estrogen receptor modulator (raloxifene or tamoxifen).
Aromatase inhibitors (letriozole, anastrozole, exemestane) are less effective
and can prevent epiphyseal fusion.
o Subcutaneous mastectomy or endoscopically assisted liposuction should be
reserved for patients with persistent and embarrassing disease.
Patient’s progress
Further questioning and examination revealed no clues pointing to systemic or
testicular disease. He denied taking any medications, either prescribed or bought
over the counter. His blood counts, renal function, liver function, thyroid function,
ECG, chest x-ray, were normal. Testosterone and estradiol levels were within
normal limits. There was no indication to pursuit further investigation. It was
explained to him and his wife that gynecomastia was not uncommon among
geriatric patients, particularly when associated with weight gain, and the cause
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was unclear. The patient was not particularly bothered by his condition. He did
not want aggressive therapy, therefore, he was advised to increase his daily
exercise level and readjust his diet so as to maintain his body weight at preretirement level. He was also advised to report to the Clinic immediately for any
adverse developments but otherwise return for follow-up in 6 months.
Further readings
Fitzgerald PA. 26 – Endocrinology. In Tierney LM et al (editors): Current Medical
Diagnosis and Treatment, 45th edition. McGraw-Hill, 2006.
Modest GA. Chapter 22 – Gynecomastia. In Noble: Textbook of Primary Care
Medicine, 3rd edition. Mosby, 2001.