The nurse is assessing a patient who has gynecomastia which is a sign of gynecomastia

Journal Article

Harold E. Carlson

1Department of Medicine, Endocrinology Division, Stony Brook University, Stony Brook, New York 11794-8154

*Address all correspondence and requests for reprints to: Harold E. Carlson, M.D., Department of Medicine, Endocrinology Division, HSC T15-060, Stony Brook University, Stony Brook, New York 11794-8154.

Search for other works by this author on:

Published:

01 January 2011

• 
  PDF
• Split View
• • Article contents
  • Figures & tables
  • Video
  • Audio
  • Supplementary Data
• • Email
  • Twitter
  • Facebook
  • More

Close

Navbar Search Filter Microsite Search Term Search

Accreditation and Credit Designation Statements

The Endocrine Society is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The Endocrine Society has achieved Accreditation with Commendation.

The Endocrine Society designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Learning Objectives

Upon completion of this educational activity, participants should be able to

cuss the hormonal pathogenesis of gynecomastia.

Appropriately evaluate and recommend therapy for patients with gynecomastia.

Target Audience

This continuing medical education activity should be of substantial interest to endocrinologists.

Disclosure Policy

Authors, editors, and Endocrine Society staff involved in planning this CME activity are required to disclose to learners any relevant financial relationship(s) that have occurred within the last 12 months with any commercial interest(s) whose products or services are discussed in the CME content. The Endocrine Society has reviewed all disclosures and resolved or managed all identified conflicts of interest, as applicable.

The following individual reported relevant financial relationships:

Harold E. Carlson, M.D., has received a consulting fee from Eli Lilly and Company.

Disclosures for JCEM Editors are found at http://www.endo-society.org/journals/Other/faculty_jcem.cfm.

The following individual reported NO relevant financial relationships:

Leonard Wartofsky, M.D., reported no relevant financial relationships.

Endocrine Society staff associated with the development of content for this activity reported no relevant financial relationships.

Acknowledgement of Commercial Support

This activity is not supported by grants, other funds, or in-kind contributions from commercial supporters.

Privacy and Confidentiality Statement

The Endocrine Society will record learner’s personal information as provided on CME evaluations to allow for issuance and tracking of CME certificates. No individual performance data or any other personal information collected from evaluations will be shared with third parties.

Method of Participation

This Journal CME activity is available in print and online as full text HTML and as a PDF that can be viewed and/or printed using Adobe Acrobat Reader. To receive CME credit, participants should review the learning objectives and disclosure information; read the article and reflect on its content; then go to http://jcem.endojournals.org and find the article, click on CME for Readers, and follow the instructions to access and complete the post-activity test questions and evaluation. The estimated time to complete this activity, including review of material, is 1 hour. If you have questions about this CME activity, please direct them to .

Activity release date: January 2011

Activity expiration date: January 2012

A 39-yr-old man was referred because of bilateral tender breast enlargement noted 2 months ago, without bleeding or nipple discharge. He was in generally good health until 7 months ago, when he was diagnosed with Hodgkin’s lymphoma. He completed chemotherapy with a combination of cytotoxic agents 3 months ago. He is a nonsmoker and drinks 12 ounces of beer two to three times per week. He has two children, ages 7 and 10 yr. His libido and erectile function are normal. There is no family history of breast or testicular cancer.

On physical examination, he was not obese, with a body mass index of 26.0 kg/m2. Vital signs were normal, as was the examination of the eyes, thyroid, heart, lungs, abdomen, and extremities. Both breasts were enlarged, with palpable, rubbery glandular tissue centered beneath the areolae measuring approximately 3 cm in diameter bilaterally; the breast tissue was moderately tender. There was no skin or nipple retraction and no ulceration. Both testes were descended and were low-normal in size and consistency; the penis was normal. His beard and body hair were normal.

Laboratory studies showed normal renal, hepatic, and thyroid function. Serum β-human chorionic gonadotropin (hCG) was less than 5 mIU/ml (normal). Total serum testosterone, drawn at 0800 h, was 340 ng/dl (normal, 241–827 ng/dl), estradiol was 54 pg/ml (normal, <29 pg/ml), LH was 38 mIU/ml (normal, 1.5–9.3 mIU/ml), FSH was 56 mIU/ml (normal, 1.6–8.0 mIU/ml), and prolactin was 9 ng/ml (normal, 2–18 ng/ml).

Background

Gynecomastia is defined as the presence of palpable breast tissue in males and is common in normal individuals, particularly in the newborn period, at puberty, and in the elderly. Around 60% of all boys develop transient pubertal breast enlargement (1), and 30–70% of adult men have palpable breast tissue, with the higher prevalence being seen in older men and those with concurrent medical illnesses (2–4).

Histologically, the primary feature of gynecomastia is ductular proliferation in a background stroma of fibrous connective tissue (2, 5); about half of all men demonstrate histological evidence of gynecomastia at autopsy (6). Most often, gynecomastia is bilateral, but it may sometimes be unilateral or asymmetric. With the passage of time, the connective tissue component of gynecomastia tends to become denser and more fibrotic (5).

Receptors for androgens, estrogens, progesterone, and prolactin are found in the male breast (7, 8). It has been shown that estrogens stimulate breast tissue proliferation, whereas androgens inhibit this process (9–11). It is believed that most cases of gynecomastia are caused by an imbalance of these two influences, with estrogen-induced stimulation predominating (12, 13). Such an imbalance may occur with increased estrogen action on the breast, decreased androgen action, or a combination of the two. This may be due to an increase in circulating or tissue levels of estrogen, a decrease in circulating or tissue levels of androgen, increased responsiveness of the breast to estrogen (e.g. increased numbers of estrogen receptors), or decreased breast responsiveness to androgens (e.g. androgen insensitivity due to receptor mutations or drugs). More than one of these derangements may be present in a single patient; for example, the increased prevalence of gynecomastia in older men may be related to increased adiposity with age (14) [adipose tissue is a major site of aromatization of androgens to estrogens (15)], decreased serum free testosterone due to aging [with decreased testosterone production as well as increased binding of testosterone to SHBG (16)], and greater use of medications that may alter androgen or estrogen concentrations or action.

Although prolactin receptors are present in the male breast (8), hyperprolactinemia may lead to gynecomastia through its effects on the hypothalamus to cause central hypogonadism. Prolactin has also been reported to decrease androgen receptors and increase estrogen and progesterone receptors in breast cancer cells (17, 18); if a similar effect were to occur in the male breast, gynecomastia might result. The role of prolactin, progesterone, and circulating or locally produced growth factors [e.g. IGF-I, epidermal growth factor (EGF), etc.] is unclear at present.

Table 1 summarizes the major known causes of gynecomastia. It is important to keep these factors in mind because they will help guide the choice of therapy and may, in some instances, require treatment independent of their role in causing breast enlargement. A more detailed discussion of these individual causes can be found in recent reviews of the topic (13, 19).

TABLE 1.

Causes of gynecomastia

TABLE 1.

Causes of gynecomastia

Evaluation

Several questions need to be answered in evaluating every male patient with breast enlargement:

1. 1.

   Is the breast enlargement of recent onset or associated with pain or tenderness?

2. 2.

   Is the breast enlargement due to increased glandular tissue or is it only adipose tissue (pseudogynecomastia)?

3. 3.

   Are there findings suggestive of breast cancer?

4. 4.

   Is there evidence of a testicular tumor, which might lead to gynecomastia by producing estrogen or stimulating its production?

5. 5.

   Can a cause for the breast enlargement be identified?

6. 6.

   Is the patient troubled by the breast enlargement?

Gynecomastia is common in normal men and may frequently be noted on routine physical examination. A healthy man with long-standing stable gynecomastia and a negative history and physical examination generally does not need further evaluation. The presence of new-onset breast pain, tenderness, or enlargement suggests a more recent, ongoing process and should prompt further testing to detect underlying systemic or endocrine problems.

A detailed history should be obtained, including the duration of the gynecomastia, the presence of breast pain or tenderness, systemic disease (e.g. chronic liver or renal disease; hyperthyroidism; hypogonadism; prostate, testicular, or other cancer), recent weight gain or loss, use of medication or recreational drugs, exposure to other chemicals, fertility and sexual function. A thorough medication history is particularly important and should include the use of nonprescription medications, anabolic steroids, and dietary supplements (Table 2). A family history of gynecomastia would suggest the possibility of an androgen resistance syndrome, familial aromatase excess, or estrogen-producing Sertoli cell tumors [as may occur in Peutz-Jeghers syndrome or in the Carney complex (20, 21)]. A family history of BRCA2-positive breast cancer significantly increases the lifetime risk of male breast cancer to 8–10% in carriers of the mutation (22).

TABLE 2.

Drugs commonly implicated in gynecomastia

TABLE 2.

Drugs commonly implicated in gynecomastia

The physical examination should note features of virilization (voice, facial and body hair, skeletal muscle bulk), testicular size and/or masses, penile size and development, signs of chronic liver or kidney disease, and evidence of hyperthyroidism. The breasts should be carefully examined to differentiate true gynecomastia with palpable glandular tissue from pseudogynecomastia, in which only adipose tissue can be felt; I have found it useful to examine the patient’s breasts in both the supine and seated position, using a pincer movement with the thumb and forefinger to delineate the presence and size of glandular elements, comparing the subareolar area to a nearby fold of adipose tissue. Attention should be paid to the symmetry and smoothness of the glandular tissue; unusual firmness, asymmetry, or an eccentric location (not centered beneath the areola), fixation to the skin or chest wall, nipple retraction, bleeding or nipple discharge, ulceration, or associated lymphadenopathy should all suggest the possibility of breast carcinoma (23) and should lead to biopsy or excision.

Routine biochemical testing should evaluate thyroid, liver, and kidney function, along with measurements of serum testosterone (total and/or bioavailable), estradiol, LH, FSH, prolactin, and β-hCG.

In two reported series of men with gynecomastia, the cause was determined to be physiological (i.e. puberty or associated with aging) or idiopathic in more than 50% of the patients (24, 25).

Therapy

Asymptomatic men with long-standing breast enlargement do not require treatment; reassurance is often all that is required. In those with symptoms (pain, tenderness, embarrassment, or excessive worry), treatment is guided by the cause and by the patient’s goals (relief of discomfort, restoration of normal appearance, reassurance regarding cancer or treatment of an underlying illness).

In men with an identifiable underlying disorder (e.g. hyperthyroidism, testicular tumor), treatment of that disorder will often ameliorate the breast enlargement and symptoms, at least partially. Similarly, if the gynecomastia is believed to be due to a medication or recreational drug, withdrawal of that agent should lead to at least some improvement over a period of a few months. If the breast enlargement has been present for more than 1 yr, complete regression is less likely, due to the predominance of dense fibrous tissue (13, 19). Teenage boys with pubertal gynecomastia can usually be observed, with the expectation that the gynecomastia will spontaneously resolve over 1–2 yr in most cases (26). Gynecomastia related to dialysis or refeeding is also generally self-limited, and reassurance may be sufficient treatment (27, 28).

In some men with hypogonadism of short duration, testosterone replacement may lead to the resolution or improvement of associated gynecomastia (29, 30). However, because testosterone can be aromatized to estradiol, it may worsen the breast enlargement in some cases, and the patient should be warned of this possibility.

Antiestrogens have been increasingly used in recent years to decrease the stimulatory effect of estrogens on the male breast. Tamoxifen and raloxifene, which block the estrogen receptor, and aromatase inhibitors such as anastrozole have all been used with varying degrees of success in the treatment of gynecomastia. Although studies of their effects have been limited, there appears to be reasonable evidence supporting the utility of tamoxifen (31–35) and some evidence that raloxifene is approximately as useful as tamoxifen (35). Neither tamoxifen nor raloxifene has been associated with significant side effects in the majority of patients (31–35). Tamoxifen has been used in doses of 10–20 mg/d and raloxifene at a dose of 60 mg/d for 3–9 months. In contrast, anastrozole was no better than placebo in a randomized, double-blind trial in patients with pubertal gynecomastia (36). Anastrozole was successfully used to reduce the estrogen excess and breast enlargement in a patient with familial aromatase excess (37), a patient with a feminizing Sertoli cell tumor (38), and two hypogonadal men with gynecomastia induced by testosterone therapy (39). It should be noted that none of these drugs have been approved for the treatment of gynecomastia.

For men with gynecomastia due to androgen deprivation therapy for prostate cancer, prophylactic radiation therapy directed at the breast has been somewhat successful in preventing new-onset gynecomastia (40–42). Tamoxifen has also been used successfully in this situation (43) and appears to be superior to both radiotherapy (44) and anastrozole (45, 46). Daily administration of tamoxifen was shown to be more efficacious than weekly dosing (47).

Surgery to remove the breast tissue has been widely used in the treatment of gynecomastia. It should probably be performed by highly experienced surgeons to achieve the best cosmetic result. Excision with or without liposuction has been successfully used (48, 49). Surgical treatment of pubertal gynecomastia should generally be postponed until the completion of puberty to minimize the possibility of postoperative regrowth of breast tissue.

Figure 1 illustrates a suggested scheme for the evaluation and treatment of gynecomastia.

Fig. 1.

Suggested algorithm for the management of gynecomastia. H&P, History and physical examination; Rx, therapy; Wt, weight. [Reprinted from H. S. Narula and H. E. Carlson: Endocrinol Metab Clin North Am 36:497–519, 2007 (13 ), with permission from Elsevier.]

Controversies and Areas of Uncertainty

Several parts of the evaluation process remain controversial. Some authors have recommended performing mammography and/or breast ultrasound in all cases (50–52); in agreement with others (24, 53–58), my own practice has been to use these imaging tools only when there are physical findings that raise a suspicion of breast cancer or a BRCA-2 mutation is suspected or known to be present. Although the sensitivity and specificity of mammography are both greater than 90% in the diagnosis of male breast cancer, the much higher prevalence of gynecomastia compared with breast cancer leads to a positive predictive value of only 55% (59). For breast sonography, the positive predictive value was reported as only 17% (60). Therefore, universal application of imaging seems unlikely to be cost-effective. In one study of male breast mammography, all of the men diagnosed with breast cancer also had physical findings that were suspicious for malignancy (55).

Some authors have felt that the routine laboratory evaluation of all men with gynecomastia to detect underlying disease is also not cost-effective, citing reports that only a small number of patients have unsuspected relevant laboratory findings and suggesting more selective laboratory testing, guided by the individual patient’s medical history and examination (53, 57). It is certainly true that asymptomatic men with incidentally discovered palpable breast tissue generally need only a careful history and physical examination and do not usually benefit from laboratory testing. Factors that bear on this question include the potential seriousness of a positive laboratory finding (e.g. detection of a malignant tumor secreting hCG), the cost of the laboratory test, and the likelihood of the underlying disease being present in a man with no symptoms or signs other than gynecomastia (e.g. hypogonadism, chronic hepatic disease or renal insufficiency, hyperthyroidism, Leydig cell tumor). The perceived need to practice defensive medicine undoubtedly contributes, as well. Unfortunately, there is no consensus on this matter. The issue may particularly arise in older men, in whom palpable breast tissue is a common incidental finding. Although hypogonadism is also common in this age group, it is not clear whether serum testosterone should be measured in all such individuals if they are truly asymptomatic (i.e. no local breast symptoms and no symptoms of hypogonadism). There would appear to be little clear benefit from testosterone treatment in the absence of symptoms, so I do not routinely obtain screening laboratory tests in such patients.

In the realm of therapy, medical treatment has its own controversies. The overall response rate to tamoxifen has varied from 50–80%, although reported side effects have been few (31–35). It has not yet been clearly established whether tamoxifen and raloxifene are of equal benefit, although it seems reasonably clear that both are more effective than aromatase inhibitors (36, 45, 46). Surgical therapy is generally agreed to be the most effective means of restoring the normal contour of the breast, but many different techniques and approaches are in current use and are likely to be influenced by the degree of breast enlargement as well as the proportion of glandular and fibrous tissue vs. adipose tissue present (61, 62). In addition, not all patients treated surgically are pleased with the results (63).

Returning to the Case

Our patient developed tender bilateral breast enlargement in the setting of recent cytotoxic chemotherapy for lymphoma. Although his prior fertility history was normal, his total serum testosterone was in the low-normal range, with elevated serum LH, FSH, and estradiol but normal serum prolactin and negative β-hCG. There was no evidence of thyroid, renal, or hepatic disease. His compensated primary hypogonadism was most likely a consequence of his cancer chemotherapy. Stimulation of Leydig cells by LH (or hCG) increases aromatase activity and estradiol secretion (64). Literature reports suggest that many (although not all) such patients with chemotherapy-induced gynecomastia will have spontaneous recovery of Leydig cell function over several months, with gradual improvement or disappearance of the breast enlargement and tenderness (30, 65–67). Alternatively, he could be offered testosterone supplementation or tamoxifen therapy, with a good chance that his gynecomastia would decrease in size and tenderness because his breast enlargement had been present for only a few months. Finally, surgery would probably be the most certain way to cure this man’s gynecomastia. After an extensive discussion of all these options, he chose to forego active treatment, opting for continued observation. Over the next 6 months, his serum testosterone LH and FSH returned to mid-normal, and his breasts were no longer tender or enlarged.

This patient is in many ways typical of the sort of patient seen by endocrinologists for gynecomastia. Although his history suggested the ultimate cause, it was important to rule out other underlying diseases and neoplasms and then to offer the patient the appropriate therapeutic modalities from which to choose.

Conclusions

Patients with asymptomatic palpable breast tissue need only a careful history and physical examination; most of these patients have either persistent pubertal gynecomastia or age-related gynecomastia. Patients with symptomatic gynecomastia need, in addition to a careful history and physical examination, appropriate screening laboratory tests to detect underlying disorders and guide therapy. Most such cases have a benign etiology or are idiopathic. Underlying causes should be corrected, when possible; medical therapy or surgery can be offered to patients with persistent symptoms.

Disclosure Summary: The author has previously consulted for Eli Lilly, Inc.

Abbreviations:

 

• hCG,

  Human chorionic gonadotropin.

1

Nydick

M

1961

Gynecomastia in adolescent boys.

JAMA

178

:

449

–

454

2

Bannayan

GA

1972

Gynecomastia: clinicopathologic study of 351 cases.

Am J Clin Pathol

57

:

431

–

437

3

Nuttall

FQ

1979

Gynecomastia as a physical finding in normal men.

J Clin Endocrinol Metab

48

:

338

–

340

4

Carlson

HE

1980

Gynecomastia.

N Engl J Med

303

:

795

–

799

5

Nicolis

GL

1971

A study of the histopathology of human gynecomastia.

J Clin Endocrinol Metab

32

:

173

–

178

6

Williams

MJ

1963

Gynecomastia: its incidence, recognition and host characterization in 447 autopsy cases.

Am J Med

34

:

103

–

112

7

Gill

S

2001

Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study.

J Clin Pathol

54

:

956

–

960

8

Ferreira

M

2008

Prolactin receptor expression in gynaecomastia and male breast carcinoma.

Histopathology

53

:

56

–

61

9

Dimitrikakis

C

2002

Androgens and mammary growth and neoplasia

.

Fertil Steril

77

(

Suppl 4

):

S26

–

S33

10

Kanhai

RC

2000

Short-term and long-term histologic effects of castration and estrogen treatment on breast tissue of 14 male-to-female transsexuals in comparison with two chemically castrated men.

Am J Surg Pathol

24

:

74

–

80

11

Burgess

HE

1993

An immunohistochemical study of the long-term effects of androgen administration on female-to-male transsexual breast: a comparison with normal female breast and male breast showing gynecomastia.

J Pathol

170

:

37

–

43

12

Mathur

R

1997

Gynecomastia: pathomechanisms and treatment strategies.

Horm Res

48

:

95

–

102

13

Narula

HS

2007

Gynecomastia.

Endocrinol Metab Clin North Am

36

:

497

–

519

14

Niewoehner

CB

1984

Gynecomastia in a hospitalized male population.

Am J Med

77

:

633

–

638

15

Santen

RJ

2009

History of aromatase: saga of an important biological mediator and therapeutic target.

Endocr Rev

30

:

343

–

375

16

Kaufman

JM

2005

The decline of androgen levels in elderly men and its clinical and therapeutic implications.

Endocr Rev

26

:

833

–

876

17

Ormandy

CJ

1997

Coexpression and cross-regulation of the prolactin and sex steroid hormone receptors in breast cancer.

J Clin Endocrinol Metab

82

:

3692

–

3699

18

Gutzman

JH

2004

Endogenous human prolactin and not exogenous human prolactin induces estrogen receptor α and prolactin receptor expression and increases estrogen responsiveness in breast cancer cells.

J Steroid Biochem Mol Biol

88

:

69

–

77

19

Braunstein

GD

2007

Gynecomastia.

N Engl J Med

357

:

1229

–

1237

20

Young

S

1995

Feminizing Sertoli cell tumors in boys with Peutz-Jeghers syndrome.

Am J Surg Pathol

19

:

50

–

58

21

Stratakis

CA

2001

Clinical and molecular features of the Carney complex: diagnostic criteria and recommendations for patient evaluation.

J Clin Endocrinol Metab

86

:

4041

–

4046

22

Evans

DG

2010

Risk of breast cancer in male BRCA2 carriers.

J Med Genet doi

:

10.1136/jmg.2009.075176

23

Mathew

J

2008

Primary breast cancer in men: clinical, imaging, and pathologic findings in 57 patients.

AJR Am J Roentgenol

191

:

1631

–

1639

24

Bowers

SP

1998

Cost-effective management of gynecomastia.

Am J Surg

176

:

638

–

641

25

Ersöz

H

2002

Causes of gynaecomastia in young adult males and factors associated with idiopathic gynaecomastia.

Int J Androl

25

:

312

–

316

26

Biro

FM

1990

Hormonal studies and physical maturation in adolescent gynecomastia.

J Pediatr

116

:

450

–

455

27

Schmitt

GW

1968

Transient gynecomastia in chronic renal failure during chronic intermittent hemodialysis.

Ann Intern Med

69

:

73

–

79

28

Jacobs

EC

1948

Gynecomastia following severe starvation.

Ann Intern Med

28

:

792

–

797

29

Friedman

NM

1980

Leydig cell dysfunction and gynaecomastia in adult males treated with alkylating agents.

Clin Endocrinol (Oxf)

12

:

553

–

556

30

Harris

E

2001

Gynaecomastia with hypergonadotrophic hypogonadism and Leydig cell insufficiency in recipients of high-dose chemotherapy or chemoradiotherapy.

Bone Marrow Transplant

28

:

1141

–

1144

31

Parker

LN

1986

Treatment of gynecomastia with tamoxifen: a double-blind crossover study.

Metabolism

35

:

705

–

708

32

Khan

HN

2004

Management of physiological gynaecomastia with tamoxifen.

Breast

13

:

61

–

65

33

Hanavadi

S

2006

The role of tamoxifen in the management of gynaecomastia.

Breast

15

:

276

–

280

34

Caocci

G

2008

Gynecomastia in a male after dasatinib treatment for chronic myeloid leukemia.

Leukemia

22

:

2127

–

2128

35

Lawrence

SE

2004

Beneficial effects of raloxifene and tamoxifen in the treatment of pubertal gynecomastia.

J Pediatr

145

:

71

–

76

36

Plourde

PV

2004

Safety and efficacy of anastrozole for the treatment of pubertal gynecomastia: a randomized, double-blind, placebo-controlled trial.

J Clin Endocrinol Metab

89

:

4428

–

4433

37

Binder

G

2005

Dominant transmission of prepubertal gynecomastia due to serum estrone excess: hormonal, biochemical and genetic analysis in a large kindred.

J Clin Endocrinol Metab

90

:

484

–

492

38

Lefevre

H

2006

Prepubertal gynecomastia in Peutz-Jeghers syndrome: incomplete penetrance in a familial case and management with an aromatase inhibitor.

Eur J Endocrinol

154

:

221

–

227

39

Rhoden

EL

2004

Treatment of testosterone-induced gynecomastia with the aromatase inhibitor, anastrozole.

Int J Impot Res

16

:

95

–

97

40

Dobs

A

2005

Incidence and management of gynecomastia in men treated for prostate cancer.

J Urol

174

:

1737

–

1742

41

Dicker

AP

2003

The safety and tolerability of low-dose irradiation for the management of gynaecomastia caused by antiandrogen monotherapy.

Lancet Oncol

4

:

30

–

36

42

Tyrrell

CJ

2004

Prophylactic breast irradiation with a single dose of electron beam radiotherapy (10 Gy) significantly reduces the incidence of bicalutamide-induced gynecomastia.

Int J Radiat Oncol Biol Phys

60

:

476

–

483

43

Fradet

Y

2007

Tamoxifen as prophylaxis for prevention of gynaecomastia and breast pain associated with bicalutamide 150 mg monotherapy in patients with prostate cancer: a randomized, placebo-controlled, dose-response study.

Eur Urol

52

:

106

–

114

44

Perdonà

S

2005

Efficacy of tamoxifen and radiotherapy for prevention and treatment of gynaecomastia and breast pain caused by bicalutamide in prostate cancer: a randomized controlled trial.

Lancet Oncol

6

:

295

–

300

45

Saltzstein

D

2005

Prevention and management of bicalutamide-induced gynecomastia and breast pain: randomized endocrinologic and clinical studies with tamoxifen and anastrozole.

Prostate Cancer Prostatic Dis

8

:

75

–

83

46

Boccardo

F

2005

Evaluation of tamoxifen and anastrozole in the prevention of gynecomastia and breast pain induced by bicalutamide monotherapy of prostate cancer.

J Clin Oncol

23

:

808

–

815

47

Bedognetti

D

2010

An open, randomized, multicentre, phase 3 trial comparing the efficacy of two tamoxifen schedules in preventing gynaecomastia induced by bicalutamide monotherapy in prostate cancer patients.

Eur Urol

57

:

238

–

245

48

Handschin

AE

2008

Surgical management of gynecomastia—a 10-year analysis.

World J Surg

32

:

38

–

44

49

Hammond

DC

2009

Surgical correction of gynecomastia

.

Plast Reconstr Surg

124

(

1 Suppl

):

61e

–

68e

50

Vetto

J

1998

Accurate and cost-effective evaluation of breast masses in males.

Am J Surg

175

:

383

–

387

51

Cordova

A

2008

Algorithm for clinical evaluation and surgical treatment of gynaecomastia.

J Plast Reconstr Aesthet Surg

61

:

41

–

49

52

Devalia

HL

2009

Current concepts in gynaecomastia.

Surgeon

7

:

114

–

119

53

Neuman

JF

1997

Evaluation and treatment of gynecomastia.

AM Fam Physician

55

:

1835

–

1844

54

Hanavadi

S

2006

Is mammography overused in male patients?

Breast

15

:

123

–

126

55

Hines

SL

2007

The role of mammography in male patients with breast symptoms.

Mayo Clin Proc

82

:

297

–

300

56

Hines

SL

2008

Evaluation of breast masses in older men.

Geriatrics

63

:

19

–

24

57

Niewoehner

CB

2008

Gynaecomastia and breast cancer in men.

BMJ

336

:

709

–

713

58

Johnson

RE

2009

Gynecomastia: pathophysiology, evaluation, and management.

Mayo Clin Proc

84

:

1010

–

1015

59

Evans

GF

2001

The diagnostic accuracy of mammography in the evaluation of male breast disease.

Am J Surg

181

:

96

–

100

60

Patterson

SK

2006

Outcome of men presenting with clinical breast problems: the role of mammography and ultrasound.

Breast J

12

:

418

–

423

61

Gikas

P

2007

Management of gynecomastia: an update.

Int J Clin Pract

61

:

1209

–

1215

62

Ratnam

BV

2009

A new classification and treatment protocol for gynecomastia.

Aesthet Surg J

29

:

26

–

31

63

Ridha

H

2009

How happy are patients with their gynaecomastia reduction surgery?

J Plast Reconstr Aesthet Surg

62

:

1473

–

1478

64

Forest

MG

1979

Kinetics of human chorionic gonadotropin-induced steroidogenic response of the human testis. II. Plasma 17α-hydroxyprogesterone, Δ4-androstenedione, estrone, and 17β-estradiol: evidence for the action of human chorionic gonadotropin on intermediate enzymes implicated in steroid biosynthesis.

J Clin Endocrinol Metab

49

:

284

–

291

65

Turner

AR

1982

Gynecomastia after cytotoxic therapy for metastatic testicular cancer.

Arch Intern Med

142

:

896

–

897

66

Saeter

G

1987

Gynaecomastia following cytotoxic therapy for testicular cancer.

Br J Urol

59

:

348

–

352

67

Aki

FT

1996

Gynecomastia as a complication of chemotherapy for testicular germ cell tumors.

Urology

48

:

944

–

946

Copyright © 2011 by The Endocrine Society

Copyright © 2011 by The Endocrine Society

Which assessment finding would the nurse identify as gynecomastia?

What does gynaecomastia feel like?

Is gynecomastia a sign of cancer?

What is gynecomastia select all that apply?