ETIOPATHOGENESIS AND TREATMENT PRINCIPLES OF GYNECOMASTIA

Аннотация

Gynecomastia (GM) is characterized by enlargement of the male breast, caused by glandular proliferation and fat deposition. GM is common and occurs in adolescents, adults and in old age. The aim of this review is to discuss the pathophysiology, etiology, evaluation and therapy of GM. A hormonal imbalance between estrogens and androgens is the key hallmark of GM generation. The etiology of GM is attributable to physiological factors, endocrine tumors or dysfunctions, non-endocrine diseases, drug use or idiopathic causes. Clinical evaluation must address diagnostic confirmation, search for an etiological factor and classify GM into severity grades to guide the treatment. A proposal for tailored therapy is presented. Weight loss, reassurance, pharmacotherapy with tamoxifen and surgical correction are the therapeutic options. For long-standing GM, the best results are generally achieved through surgery, combining liposuction and mammary adenectomy. Keywords: adolescent, gynecomastia, breast, surgery, IGF-1, aromatase. ЭТИОПАТОГЕНЕЗ, КЛИНИКА И ПРИНЦИПЫ ЛЕЧЕНИЯ ГИНЕКОМАСТИИ Аннотация. Гинекомастия (ГМ) характеризуется увеличением мужской груди, вызванным разрастанием железистой ткани и отложением жира. ГМ является распространённым явлением и встречается у подростков, взрослых и пожилых людей. Цель этого обзора — обсудить патофизиологию, этиологию, диагностику и терапию ГМ. Гормональный дисбаланс между эстрогенами и андрогенами является ключевым признаком возникновения ГМ. Этиология ГМ может быть связана с физиологическими факторами, эндокринными опухолями или нарушениями, неэндокринными заболеваниями, употреблением препаратов или идиопатическими причинами. Клиническая оценка должна включать подтверждение диагноза, поиск этиологического фактора и классификацию ГМ по степеням тяжести для выбора подходящего лечения. Представлено предложение по индивидуализированному лечению. Терапевтические варианты включают снижение массы тела, успокоение пациента, фармакотерапию с использованием тамоксифена и хирургическую коррекцию. Для длительно существующей ГМ наилучшие результаты обычно достигаются с помощью хирургии, сочетая липосакцию и аденэктомию молочной железы. Ключевые слова: Подросток, Гинекомастия, Грудь, Хирургия, Инсулиноподобный фактор роста 1 (ИФР-1). 1782 ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 4 Gynecomastia is a relatively common disorder. Its causes range from benign physiological processes to rare neoplasms. To diagnose the etiology of the gynecomastia, the clinician must understand the hormonal factors involved in breast development. Parallel to female breast development, estrogen, growth hormone (GH), and IGF-1 are required for breast growth in males. Since a balance exists between estrogen and androgens in males, any disease state or medication that increases circulating estrogens or decreases circulating androgens, causing an elevation in the estrogen to androgen ratio, can induce gynecomastia. Due to the diversity of possible etiologies, including a neoplasm, performing a careful history and physical is imperative. Once gynecomastia has been diagnosed, treatment of the underlying cause is warranted. If no underlying cause is discovered, then close observation is appropriate. If the gynecomastia is severe and of recent onset, medical therapy can be attempted, and if ineffective, glandular tissue can be removed surgically. Etiological factors of Gynecomastia 1. Physiological causes:  Neonatal gynecomastia – due to transplacental maternal estrogens.  Pubertal gynecomastia – common and usually transient, caused by temporary hormonal imbalance.  Aging – decreased testosterone production and increased peripheral conversion of androgens to estrogens. 2. Pathological causes: a. Endocrine Disorders  Primary hypogonadism (e.g., Klinefelter syndrome, testicular failure)  Secondary hypogonadism (e.g., pituitary tumors)  Hyperthyroidism – increases sex hormone-binding globulin (SHBG) and alters estrogen/testosterone ratio.  Adrenal tumors or Leydig/Sertoli cell tumors b. Systemic diseases  Liver disease (e.g., cirrhosis) – impaired metabolism of estrogens.  Chronic kidney disease – associated with hormonal imbalances and sometimes medications used in dialysis. 3. Drug-induced:  Anti-androgens: flutamide, spironolactone, bicalutamide.  Estrogens or estrogen-like compounds.  Anabolic steroids (especially during withdrawal). 1783 ResearchBib IF - 11.01, ISSN: 3030-3753, Volume 2 Issue 4  Medications: Cimetidine, Ketoconazole, Digoxin, Calcium channel blockers (e.g., verapamil), Antipsychotics (e.g., risperidone), Antidepressants (e.g., tricyclics), Chemotherapy agents 4. Idiopathic: In many cases, especially in pubertal males, no definitive cause is found. 5. Obesity Increased peripheral aromatization of androgens to estrogens in adipose tissue. Physiologic gynecomastia: Gynecomastia, breast development in males, can occur normally during three phases of life. The first occurs shortly after