1. Dr Ayed Alanezi Senior spescialist Pediatric endocrine
Gynecomastia
Dr Ayed Alanezi
Senior spescialist
Pediatric endocrine

2. Definition
Gynecomastia is defined as the presence of palpable breast tissue in males
It is common in normal individuals
Particularly in the newborn period, at puberty, and in the elderly

3. Gynaecomastia Term is derived from Greek words:
Gynae (female) mastos(breast)

6. Lobes of female breast
A healthy female breast is made up of 12–20 sections called lobe

7. Male breast Nipple Rudimentary blind ducts
Extending to short distance rarely beyond the boundary of the areola
Without lobule formation
Fat
Fibrous tissue

8. Gynecomastia
The benign proliferation of glandular breast tissue in males.

9. Gynecomastia
Glandular tissue is symmetrically distributed around the areolar-nipple complex
No terminal alveolar development

10. Gynecomastia
It can generally be detected when the glandular tissue is >0.5 cm (0.2 inches) in diameter
May be tender to palpation early in the course.
bilateral

11. Pseudogynaecomastia
Breast prominence due solely to Fat deposition without glandular proliferation
on exam fingers will not meet any resistance until they reach the nipple

12. Pathogenesis of gynecomastia

13. Hormones that affect the breast
Estrogens
Prolactin
Androgens

14. Hormones that affect the breast
Estrogens
Ductal hyperplasia, elongation and branching
Fibroblast proliferation
Increase in vascularity

15. Hormones that affect the breast
Source of Estrogens
Peripheral conversion of androgens
Aromatase enzyme
Present in muscles, skin and adipose tissue

16. Hormones that affect the breast
Prolactin: 
Decrease androgen receptors
Increase estrogen and progesterone receptors

17. Hormones that affect the breast
Androgens: Inhibit breast prolofiration

18. Physiological gynecomastia
Neonate
Puberty
Old age

19. The neonatal period
In neonates, 60 to 90% have transient gynaecomastia
Due to transplacental transfer of maternal estrogens
Breast tissue gradually regresses over a 2 to 3 week period.
It usually regresses completely by the end of first year.

20. Puberty Transient gynaecomastia may occur in up to 60%
With a peak onset between 13 to 14 years
Followed by an involution that is generally complete by 16 to 17 years

21. Pathological gynecomastia
Occurrence outside the neonatal or pubertal age groups
Rapid progression
Enlargement >4 cm (1.6 inches) in diameter
Persistence for more than 2 years or after age 17 years

22. Etiologies of gynecomastia
Idiopathic : 25%
Physiologic gynecomastia : 25%
Medication or substance use: 10-25%
Cirrhosis: 8%
Hypogonadism: 10%
Tumors: 3%
Hyperthyroidism: 1.5%
Chronic renal insufficiency: 1%

24. Management
The majority of cases of physiologic pubertal gynecomastia resolve spontaneously within a year of onset
Most patients can be managed with reassurance and observation.
Adjunctive psychotherapy may be beneficial for adolescents with psychosocial consequences

25. Pharmacologic therapy
The US Food and Drug Administration (FDA) has not approved any drug for this indication.
Accepted indications:
physiologic gynecomastia > 4 cm in diameter
rapidly progressive
Associated with embarrassment that interferes with normal daily activities

26. Pharmacologic therapy
Anti-estrogens
Tamoxifen
raloxifene
Aromatase inhibitors
block the estrogen receptor:

27. Pharmacologic therapy
Neither tamoxifen nor raloxifene has been associated
with significant side effects in the majority of patients.
Tamoxifen has been used in doses of 10–20 mg/d
Raloxifene at a dose of 60 mg/d for 3–9 months.

28. Aromatase inhibitors
Anastrozole was successfully used to reduce the estrogen excess and breast enlargement in a patient with
Familial aromatase excess
Patient with a feminizing Sertoli cell tumor
Hypogonadal men with gynecomastia induced by testosterone therapy.

30. Thank you

31. Approach to gynecomastia
Breast enlargement 
The size, timing of onset, and duration of breast enlargement
Breast size ≥4 cm and rapid progression may indicate greater hormone imbalance and a pathologic cause.
Beyond the neonatal period,

32. Approach to gynecomastia
Pubertal status and age
pubertal gynecomastia is most common during mid-puberty
prepubertal gynecomastia is always pathologic
Associated symptoms
Mild pain
galactorrhea
Beyond the neonatal period,

33. Approach to gynecomastia
Review of systems
Family history 
Medications
Psychosocial effects 
•Hypogonadism
•Hyperthyroidism
•Liver disease
•Renal disease

34. Complete Physical Exam
Body mass index (BMI)
Sexual maturity rating, Testes and Genitalia
Careful breast exam
Stigmata of liver and kidney disease
Evaluate for hyperthyroidism

35. Laboratory tests RFT LFT TSH LH, FSH, Estradiol, Testosterone HCG
Prolactin
Androstenedione, DHEAs

36. Imaging
US and mammogram for any eccentric or discrete mass

37. APPROACH TO DIAGNOSIS
Laboratory and imaging studies usually are not necessary in adolescents with clinical features typical of physiologic gynecomastia

38. Etiologies of pathological gynecomastia
Idiopathic : 25%
Physiologic gynecomastia : 25%
Medication or substance use: 10-25%
Cirrhosis: 8%
Primary hypogonadism: 8%
Secondary Hypogonadism: 2%
Tumors: 3%
Hyperthyroidism: 1.5%
Chronic renal insufficiency: 1%
An increase in aromatase activity
Increase in the sex hormone–binding globulin concentration

39. Etiologies of pathological gynecomastia
Idiopathic : 25%
Physiologic gynecomastia : 25%
Medication or substance use: 10-25%
Cirrhosis: 8%
Primary hypogonadism: 8%
Secondary Hypogonadism: 2%
Tumors: 3%
Hyperthyroidism: 1.5%
Chronic renal insufficiency: 1%
Medications used in disease management
Declining nutrition
Chronic illness

40. Etiologies of pathological gynecomastia
Idiopathic : 25%
Physiologic gynecomastia : 25%
Medication or substance use: 10-25%
Cirrhosis: 8%
Increase in the sex hormone–binding globulin concentration
Reduced clearance of estrogens
Primary hypogonadism: 8%
Secondary Hypogonadism: 2%
Tumors: 3%
Hyperthyroidism: 1.5%
Chronic renal insufficiency: 1% )

41. Etiologies of pathological gynecomastia
Idiopathic : 25%
Physiologic gynecomastia : 25%
Medication or substance use: 10-25%
Cirrhosis: 8%
Primary hypogonadism: 8%
Secondary Hypogonadism: 2%
Tumors: 3%
Hyperthyroidism: 1.5%
Chronic renal insufficiency: 1%
Klinefelter syndrome
Cryptorchidism
Anorchia
Enzyme defects of testosterone production
Infections
Trauma

43. Approach to gynecomastia
Review of systems
Family history 
Medications
Psychosocial effects 
•Hypogonadism
•Hyperthyroidism
•Liver disease
•Renal disease

44. Etiologies of pathological gynecomastia
Idiopathic : 25%
Physiologic gynecomastia : 25%
Medication or substance use: 10-25%
Cirrhosis: 8%
Primary hypogonadism: 8%
Secondary Hypogonadism: 2%
Tumors: 3%
Hyperthyroidism: 1.5%
Chronic renal insufficiency: 1%
Testicular Leydig-cell or Sertoli-cell tumor.
(hCG)–secreting tumor
Adrenal tumor
Androstenedione
DHEAs

45. Etiologies of pathological gynecomastia
Idiopathic : 25%
Physiologic gynecomastia : 25%
Medication or substance use: 10-25%
Cirrhosis: 8%
Primary hypogonadism: 8%
Secondary Hypogonadism: 2%
Tumors: 3%
Hyperthyroidism: 1.5%
Chronic renal insufficiency: 1%
Congenital
Gonadotropin-releasing hormone deficiency
Acquired
Pituitary tumor (hyperprolactinemia)