Thursday, July 31, 2008

Gynecomastia -- a repost

 Updated 3/2017-- photos and all links (except those to my own posts) removed as many are no longer active and it was easier than checking each one.

This is a repost from last August with a few additions.
Gynecomastia is defined as benign, excess breast tissue development in male individuals. Recent studies have reported an overall incidence of 32 - 36 %, and up to 64.6 % in adolescent boys. The incidence of bilateral involvement also varies in the literature from 25 -75 percent of patients. The underlying cause seems to be an increase in the ratio of estrogen to androgen activity. 
In general physiologic gynecomastia can be observed in three peaks during life.
  1. The neonatal period: 60-90% of infants have transient gynecomastia due to transplacental transfer of maternal estrogens.
  2. Puberty: 48-64% of boys at puberty have gynecomastia. Usually peak age of onset is between 13 and 14 years, followed by a decline in late teenage years.
  3. Late in life: The highest prevalence of gynecomastia is seen among men aged 50-80 years.
Pathologic gynecomastia occurs as a result of various metabolic disorders (alcoholic cirrhosis), endocrine disorders (hyperthyroidism, adrenal cortical hyperplasia), acquired hypogonadal states (orchitis, testicular trauma), congenital hypogonadal states (Klinefelter syndrome, congenital anorchia), and increased estrogen states (bronchogenic carcinoma, testicular tumors). (Table 1--MedScape article)
Pharmacologic gynecomastia occurs by several mechanisms, including increased direct estrogenic activity, increased secretion of estrogen, decreased testosterone synthesis, and decreased androgen sensitivity. There are also many drugs with poorly understood mechanisms that are associated with gynecomastia. (Table 2--MedScape article)
Clinical evaluation of patients with gynecomastia is very important. However, further work-up is rarely indicated.
History should include age, duration and onset of breast enlargement, symptoms of pain or tenderness, medications and recreational drug use, and psychological and social effects. A review of systems that covers all the above mentioned causes should be obtained.
Physical examination of the breasts should involve assessment for glandular or fat predominance (by the pinch test), degree of glandular ptosis, skin excess, nodules/masses, and nipple abnormalities or discharge. Glandular or parenchymal tissue is characterized by rubbery breast tissue that is mobile and extends from a subareolar, centric position. Breast cancer accounts for 0.2% of all malignancies in men and generally presents as a unilateral firm mass, often eccentric in location rather than centered beneath the areola. This should be remembered if any suspicious nodules or masses are found. These may have abnormal firmness, overlying skin ulceration, eccentric location, or abnormal nipple discharge.
The normal male breast is typically flat with some fullness around the nipple-areola complex. The nipple-areola complex is normally 2 - 4 cm in diameter (average, 2.8 cm) and located over the fourth intercostal space. Nipple to sternal notch distance is, on average, 20 cm. A muscular male chest may exhibit superior fullness with a transition to a flat inferior chest near the inframammary fold. Completion of the physical examination should in particular assess for testicular enlargement/atrophy and asymmetry, thyromegaly, hepatomegaly, pulmonary abnormalities, and abdominal masses. Additional diagnostic testing should be individualized to address abnormalities identified in the history or physical examination.
The majority of patients with gynecomastia require no treatment other than removal of the precipitating cause. If it is drug-induced, it may regress if the offending medication is stopped. Treatment of hyperthyroidism, correction of hypogonadism and surgical removal of testicular, adrenal or other causative tumors can also lead to regression.
Treatment for gynecomastia is indicated in cases where it produces significant pain, embarrassment or emotional discomfort and therefore interfering with the patient's life. A patient should consider proceeding with surgical management once diagnosis of gynecomastia is established of nonphysiologic causes or of duration greater than approximately 12 months, because hypertrophic breast tissue beyond this stage usually becomes irreversibly fibrotic.
Classification of gynecomastia as defined by Rod Rohrich, MD & others is based on the amount and character of breast hypertrophy and the degree of ptosis.
Grade I patients --minimal hypertrophy (less than 250 gm of breast tissue).
  • Grade IA--primarily fatty breast tissue. Suction-assisted lipectomy can be used with great success.
  • Grade IB--primarily fibrous breast tissue
Grade II patients -- moderate hypertrophy (between 250 and 500 gm of breast tissue).
  • Grade IIA--primarily fatty breast tissue. Suction-assisted lipectomy can be used with great success.
  • Grade IIB--primarily fibrous breast tissue
Grade III --severe hypertrophy (more than 500 gm of breast tissue), grade 1 ptosis
Grade IV --severe hypertrophy (more than 500 gm of breast
tissue), grade 2 or 3 ptosis
Ultrasound-assisted liposuction is effective in all grades of gynecomastia. Usually, no further treatment is needed in grade I or II gynecomastia. Often, single ultrasound-assisted liposuction treatment is all that is necessary for grades III and IV, especially in those with mild ptosis and good skin quality. Often the glandular tissue will need direct excision which can be done through a small peri-areolar incision. If removal of redundant skin and/or resistant lipodystrophy is still required after ultrasound-assisted liposuction, a staged excision is delayed for 6 to 9 months to allow for maximal skin retraction and healing, thus potentially allowing down staging of the magnitude of the excisional technique (and therefore minimizing scarring)

Classification and Management of Gynecomastia: Defining the Role of Ultrasound-Assisted Liposuction.; Plastic & Reconstructive Surgery. 111(2):909-923, February 2003; Rohrich, Rod J. M.D.; Ha, Richard Y. M.D.; Kenkel, Jeffrey M. M.D.; Adams, William P. Jr., M.D.
Breast Cancer in a Patient with Gynecomastia; Plastic & Reconstructive Surgery. 84(6):976-979, December 1989; Fodor, Peter Bela M.D.
Management of Gynaecomastia: An Update ; Int J Clin Pract. 2007; 61(7):1209-1215.; P. Gikas, MD; Kefah Mokbel, MS, FRCS (also a MedScape article)
Gynecomastia--eMedicine article, June 9, 2006; Ali Fawzi, MD
Additional References & Info
Gynecomastia, eMedicine Article, Nov 15, 2006; Mark R Allee MD and Mary Zoe Baker MD
This is a very nice youtube video (some of it is graphic)

1 comment:

MomTFH said...

Great clinical post.

I wanted to add a case study, so people can include this is their history questions. My ex husband suffered gynecomastia. At the time, he and his doctor had no idea why it happened - we were leaning towards a psychosomatic reaction to my breastfeeding our new son.

Several years later, I read that topically applied tea tree oil, (Melaleuca alternifolia) can cause gynecomastia. My ex husband was using tea tree oil liberally on a fungal infection at the time, and he got gynecomastia very quickly. It did go away when he stopped using it. We just didn't make the connection at the time.