Clinical_Rounds_in_Endocrinology_Volume_II_-_Pediatric_Endocrinology

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  1. What are the common drugs associated with gynecomastia?


The drugs which commonly cause gynecomastia and the implicated mecha-
nisms are summarized in the table given below.

Mechanism Drugs
Estrogen-like activity Digoxin, isoniazid
Increased substrate for aromatization Androgens, hCG
Decreased estradiol metabolism Cimetidine
Increased free estradiol (decreased binding of
estradiol with SHBG)

Spironolactone, ketoconazole

Decreased androgen production Spironolactone, ketoconazole, antiretroviral
therapy
Androgen receptor blocker Flutamide, cyproterone, cimetidine
Induction of aromatase activity GH, thyroxine, hCG


  1. What are the available treatment options for the management of
    gynecomastia?
    All patients with painful or rapidly progressive gynecomastia and those hav-
    ing cosmetic concerns should be treated. The treatment of gynecomastia
    depends on the underlying etiology. Discontinuation of the offending drug,
    if possible, usually results in regression of gynecomastia within a few weeks
    to months. Patients with gynecomastia due to hyperthyroidism respond to
    antithyroid drugs, and those with gynecomastia due to hypogonadism
    respond to androgen therapy; however, testosterone therapy itself can induce/
    worsen gynecomastia. Patients with estrogen-/hCG-secreting tumors should
    be managed surgically. Obese subjects should be encouraged for weight loss.
    If there is no reversible cause for gynecomastia or if gynecomastia has not
    responded to these measures, medical/surgical therapy should be
    considered.

  2. What are the drugs available to treat gynecomastia?


Patients with recent-onset gynecomastia respond better to medical therapy
than those with long-standing gynecomastia (>1–2 years), as long-standing
gynecomastia is associated with stromal fibrosis. Selective estrogen receptor
modulators (SERMs) like tamoxifen and raloxifene have been shown to be
effective in approximately 90 % of patients, irrespective of etiology of gyne-
comastia. Tamoxifen is commonly used at doses of 10–20 mg daily for a
period of 3–9 months. Aromatase inhibitors like anastrozole and testolactone
are less effective than SERMs; however, they are likely to be more effective
in testosterone- induced gynecomastia and in those with aromatase excess
states. Non-aromatizable androgen like dihydrotestosterone (e.g., DHT topi-
cal gel) has also been tried in the management of gynecomastia. Surgical
therapy should be considered in those with long-standing gynecomastia,

7 Delayed Puberty

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