Gynecomastia is a benign proliferation of glandular breast tissue in males. It results from an imbalance of estrogen and androgen levels. Common causes include physiological changes during puberty or aging, as well as medical conditions or medications that influence hormone levels. Evaluation involves medical history, physical exam, and hormone level testing. Mild or temporary cases may resolve on their own or with tamoxifen treatment, while surgery is recommended for chronic or severe gynecomastia.
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
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Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
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Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
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RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
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2. DEFINITION
❖ Gynecomastia:
A benign proliferation of the glandular tissue of the male
breast, is diagnosed as a palpable mass of at least 0.5 cm in
diameter (usually underlying and within the area under the
nipple).
❖ Pseudo-gynecomastia:
Enlargement of the male breast, as a result of increased fat
deposition also called as Adipomastia or Lipomastia.
3. • Rubbery-to-
firm,
• Discrete ,
• Finely Lobular,
• Freely mobile
disc of tissue,
• That extend
concentrically
from under the
nipple & areola.
• Soft
• Non-discrete
• Irregularly
lobular
• Similarly to
subcutaneous
fat in abdomen
4. PREVALENCE
❖ Asymptomatic palpable breast tissue is common in normal males, particularly in the neonate(60%–90%),
at puberty(60%–70%), and with increasing age (20%–65%, >50 years).
❖ Because of this high prevalence, gynecomastia is considered a relatively normal finding during these
periods of life. (so called physiologic at these ages)
8. ❖ Gynecomastia results from an imbalance between the stimulatory effect of estrogen and the inhibitory effect of
androgen on breast development.
❖ The imbalance is commonly caused by ;
✓Increased production of estrogen,
✓Decreased production of testosterone, or
✓Increased conversion of androgens to estrogens in peripheral tissue.
9. CLINICAL MANIFESTATION
❖ Gynecomastia usually manifests as a palpable, discrete button of tissue radiating from beneath the nipple and
areola.
❖ Gynecomastia feels “gritty” when the breast is pinched between the thumb and forefinger.
❖ Fatty tissue (Pseudo-gynecomastia), unlike gynecomastia, will not cause resistance until the nipple is reached.
(Difference in clinical examination).
11. Histopathological Classification
❖ Three histologic patternsof gynecomastia have been recognized.
• Floridpattern: consists of an increase in the number of buddingducts,
• Fibroustype: has dilated ducts, minimal duct epithelial proliferation,no periductaledema, and a
virtually acellularfibrous stroma.
• Intermediatepattern contains features of both types.
❖ Florid patternresponse well to medical treatment, while fibrous type needs surgical management.
12. CAUSES OF GYNECOMASTIA (FREQUENCY %)
(A) Physiological : (25%)
▪ Neonatal gynecomastia results from placental transfer of estrogen.
▪ During early puberty, production of estrogens begins earlier than testosterone production, thus causing an
imbalance in the ratio of estrogens to androgens. Its usually regresses within 1 to 2 years. (can persist in 25%
cases)
▪ With aging, testosterone production decreases, and peripheral androgen to estrogen conversion often increases
because of an age-related increase in adipose tissue.
(B) Idiopathic : (25%)
13. (C) ESTROGEN EXCESS :
In post-pubertal boys and adult men, the testes secrete 6-10 µg of estradiol and 2.5 µg of estrone per day. Since this only
comprises a small fraction of estrogens in the circulation (i.e. 15% of estradiol and 5% of estrone), the remainder of
estrogen in men is derived from the extraglandular aromatization of testosterone and androstenedione to estradiol and
estrone.
18. EVALUATION
(A) HISTORY
Age
Duration of the gynaecomastia
Presence of pain.
Use of drugs including recreation drugs e.g. Alcohol
Presence of symptoms suggestive of pathological cause.
Symptoms of hypogonadism - reduced libido, erectile dysfunction.
Systemic disease: Hepatic, Renal, Endocrine disease. (Thyrotoxicosis, Cushing syndrome).
Family history of breast malignancy.
19. ❖ Breast :
▪ The examination is performed by having the
patient lie on his back with his hands behind his
head. The examiner then places his or her thumb
and forefinger on each side of the breast and
slowly brings them together.
▪ Gynecomastia is appreciated as a concentric,
rubbery-to-firm disk of tissue, often mobile,
located directly beneath the areolar area.
▪ Pseudogynecomastia presents no discrete mass
▪ Other masses due to disorders such as cancer tend
to be eccentrically positioned (insert)
(B) PHYSICAL EXAMINATION
20. ❖ Testicularpalpation:
• Exclude tumour.
• Assess testicular size—?atrophy
❖ 2° sex characteristics.
❖ Look for evidence of systemic disease e.g.
• Chronic liver or renal disease,
• Thyrotoxicosis ,
• Cushing's syndrome.
22. (D) ADDITIONAL INVESTIGATIONS
➢ If testiculartumour is suspected, e.g. raised estradiol/hCG: testicular USG.
➢ If adrenal tumour is suspected, e.g. markedly raised estradiol:abdominal CT or MRI scan.
➢ If breast malignancyis suspected: mammography; FNAC/tissue biopsy.
➢ If lung cancer is suspected, e.g. raised hCG: chest radiograph.
➢ Other investigations, dependingon clinical suspicion, e.g. renal or thyroid function.
23.
24.
25.
26. MANAGEMENT
(A)MedicalTreatment:
The underlying disease should be treated.
Offending drugs should be discontinued.
ER antagonists (tamoxifen, 10 to 20 mg daily, or raloxifene, 60 mg daily) are effective in treating pubertal and
adult gynecomastia and preventing gynecomastia induced by androgen deprivation therapy.
Aromatese inhibitors ( anastrazole) are not effective (reason not clear).
Medical therapy is ineffective for chronic, fibrous gynecomastia.
27. (B) Surgery :
With long standing gynecomastia (more than 1 year): surgical reduction mammoplasty
(i.e. removal of breast tissue with or without periareolar adipose tissue) is necessary if
breast enlargement is severe, painful, socially embarrassing or disfiguring.
(C) Radiation therapy :
Low-dosage external beam radiation therapy (900 cGy or less) is effective, but less
effective than tamoxifen, for prevention of gynecomastia due to anti-androgen
monotherapyfor prostatecancer.
28. COURSE AND PROGNOSIS
➢ Pubertal gynecomastiausuallyregresses spontaneouslywithin 1 or 2 years.
➢ Patients who develop drug-induced gynecomastia generally have complete or near-complete
regression of the breast changes if the offending drug is discontinuedduring the early, florid stage.
➢ Once gynecomastia from any cause has reached the fibrotic stage, little or no spontaneous
regression occurs, and medical therapyis ineffective.