1 Dr Mahmoud AlBalas Consultant Breast Oncoplastic Reconstructive and Aesthetic Surgery Assistant Professor of Surgery Hashemite University Introduction Fibroadenoma Intraductal Papilloma ID: 907886
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Slide1
Benign Breast Tumors
12/7/2021
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Dr. Mahmoud Al-Balas
Consultant Breast Oncoplastic, Reconstructive and Aesthetic Surgery
Assistant Professor of Surgery – Hashemite University
Slide2Introduction
FibroadenomaIntraductal Papilloma
LipomaHamartomaGranular Cell Tumor
Radial Scar
Gynecomastia
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Slide3Fibroadenoma
Benign Tumor
Incidence: 8-10% (1955) BUT recent studies estimate it as high as 25% in Asymptomatic Women.Any age; mainly 20-30 yrs. OldComposed of epithelial and stromal elements.
Arise form TDLU
Might arise from bcl-2 positive mesenchymal cells similar to solitary fibrous tumors.
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Slide4Fibroadenoma
PathogenesisUnknown
Hormonal stimulation (increased estrogen sensitivity, OCP in young age)EBV in immunosuppressed women
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Slide5Fibroadenoma
Clinical Presentation:
Most are asymptomaticIf symptomatic: Firm, movable mass. Painless BUT may be associated with discomfort when large or in pressure area (i.e. wire of female brassiere)
Multiple, bilateral in 20% of cases
Medical attention ? Pain – Rapid growth – Cosmetic effect – Fear of malignancy
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Slide6Fibroadenoma
Radiologic Findings:
Ultrasound: Usually the first radiologic modality of diagnosis. Round, oval, or lobular well circumscribed hypoechoic mass.
Mammogram:
Female > 35 years old
Personal or Family history of BC.
Clinically suspicious lesion
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Slide7Fibroadenoma
Pathologic Classification
Size: < 5 cm> or equal 5 cm (Giant fibroadenoma or Juvenile giant fibroadenoma in young age)
Microscopic architecture of ductal elements:
Pericanalicular.
Intracanalicular.
Simple Vs. Complex (i.e. with hyperplasia, metaplasia or sclerosing adenosis)Rare types:Tubular (pure) adenoma
prominent adenosis with very little stroma
Lactational adenoma lactational changes in secretory glands in fibroadenoma of pregnant or breast feeding women.
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Slide8Fibroadenoma
Management
: Follow up if < 2.5 cm , low growth, no personal or family history of BC
Excision
High growth rate
Fibroepithelial lesion
Complex lesions (i.e. may have slightly higher risk for BC)Patient desire, pain, cosmeticsOlder women
FH of BC
Surgical excision vs. US-Guided vacuum-assisted biopsy device (i.e. ling term data for recurrence not yet available)
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Slide912/7/2021
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Breast Mass
Physical Examination
Ultrasound
FNA / CNB
Compatible with FA
Excise
FU Q6 months
Until age 35
FU until complete regression
Age 35
Yes
NO
Enlarged
Regression
No change
Management of Fibroadenoma in women younger than 35 years old
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Breast Mass
Physical Examination
Ultrasound
Mammography
FNA / CNB
Compatible with FA
Excise
FU 6-12 months
Routine follow up
Incomplete regression
Yes
NO
Enlarged
Complete regression
Management of Fibroadenoma in women older than 35 years old
Slide11Intraductal Papilloma
Benign rare neoplasms.Incidence 2-3% of population.
Usually age 30-55Develop within the mammary ductTypically small (few mm) and may grow to several centimeters.
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Slide12Pathology
Composed of breast epithelium supported by underlying stroma and a branching fibrovascular core.
May be associated with ductal epithelial hyperplasia, ADH or DCIS. Atypical features associated with Intraductal papilloma carry higher risk of malignancy.
Upgrading rate for CIS or IC was variable reported 0-29%
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Slide13Intraductal Papilloma
Classification:
Solitary or Multiple ( papillomatosis)Central (subareolar) or peripheral.Clinical presentation:
Central:
Spontaneous nipple discharge, serous, greenish or bloody (30%)
Mass (rare)
Peripheral:More frequently are asymptomaticIncidentally discovered on imaging studies.
Higher association with malignancy (specially when multiple and Atypia is found)
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Slide14Intraductal Papilloma
Imaging
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Imaging Modality
Central Intraductal Papilloma
Peripheral
Intraductal Papilloma
Mammography
Frequently Occult
Architectural distortion
Nodular densities
Mass +/-
calcifications
Calcifications alone
Ultrasound
Intraductal mass
Complex
cystic lesion with dilated duct
Ductogram
Completely obstructed duct
Duct expansion and distortion
Intraductal filling defects
Wall irregularity
Slide15Intraductal Papilloma
Treatment: Surgical excision
Low risk lesions for upgrading:No microcalcificationsAbsence of atypiaMicroscopic size lesions
Sufficient amount of tissue on core biopsy.
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Slide16Lipoma
Most common soft tissue tumor of the body (2.1/1000).Benign tumors of bland appearing adipose tissue.
Reported in every area of the body. Breast Lipoma incidence is unknown (Lanng, 2004 ~ 4.6%)
Reported in Males & Females.
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Slide17Lipoma
Clinical Presentation:Painless, semi-firm, mobile mass, well circumscribed, variable in size.
Giant lipoma if at lest 10 cm.Work-up:
Triple Assessment
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Slide18Lipoma
Radiologic findings:Mammogram
:A mass with a density similar to normal surrounding breast. Very thin surrounding capsule.Benign appearing microcalcifications within the mass (i.e. may represent fat necrosis)
Ultrasound
:
Isoechoic / hyperechoic mass
Thin echogenic capsuleNo posterior acoustic shadow
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Slide19Lipoma
Pathology:
Gross smooth, fatty mass, encapsulated +/- lobulationsHistologically mature adipocytes with capsule.
Management:
Observation
Liposuction for small lipomas
Surgical excision
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Slide20Hamartoma
Definition
:Rare breast tumors of breast tissue with stromal tissue and fat without structural organization. First described as mastoma (Prym
, 1928)
Females and Males.
Incidence is unknownReported among young as well as elderly.
Clinical Presentation:Asymptomatic – well circumscribed – mobile – soft – non tender mass.
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Slide21Hamartoma
RadiologyDifficult to distinguish from other benign breast lesions.
Mammogram~ Breast-in-Breast pattern (similar density to surroundings)
Architectural distortion
Asymmetric mass with mixed densities and pseudocapsule
Well circumscribe nodule
UltrasoundHypoechoic homogenous mass with distinct borders
No acoustic shadow
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Slide22Hamartoma
Pathology
Gross Appearance:Smooth, lobulated massVariable amount of fat and fibrous tissue on cross sectioning.Associated pathological changes:
Apocrine metaplasia
Usual papillary hyperplasia
Stromal hyperplasia
CystsAdenosis
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Hamartoma Classification
Characteristics
Adenolipoma
Disorganized being glandular, adipose and stromal tissue
Pseudocapsule
(compressed tissue at border)
Chondrolipoma
Benign
hyaline cartilage with breast lobules and adipose tissue
Myoid
Hamartoma
Smooth muscle component with breast
component
Slide23Hamartoma
Management
FNA has little role in precise diagnosisComplete surgical excision is curative
No need to obtain margins beyond hamartoma
Recurrence is rare; due to incomplete excision
Pure forms are not associated with increased risk of breast cancer
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Slide24Granular Cell Tumor
Rare , Benign
Occur in both Men and WomenAge range 19-70 years (i.e. most frequent in 40 – 50 years)Neural origin (i.e. Schwann cells)
First descried by
Arbiskosov
in 1926 as a Tongue mass tumor.Can arise in any organ in the body (i.e. Skin, Oral cavity, Digestive tract)
5-8% of GCTs occur in breast. Most commonly observed in African American women.
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Slide25GCTs
Clinical Presentation:Any quadrant of the breast (i.e. mostly in medial aspect due to their perineural origin along the path of supraclavicular nerve)
Can present as malignant massHard – Non tender – Mobile mass
Rarely
Skin changes, nipple retraction, breast edema
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Slide26GCTs
Radiologic Findings variable presentation (benign or malignant features)
Mammogram
Smooth, rounded or lobulated Benign appearance
Speculated malignant appearance
US
Hypoechoic (homo-/heterogenous) with posterior acoustic shadow
Anechoic mass
MRI also variable appearance (not specific for diagnosis)
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Slide27GCTs
PathologyGross appearance:
Variable size (few centimeters up to 6 cm)Smooth surfaceOccasionally lobulated and hard
Microscopic features (i.e. similar to
Schwann
cells)
Non encapsulatedPolygonal cells (in groups, sheets or nests)Eosinophilic cytoplasmBland nuclei
Positive cytoplasmic and nuclear staining for S-100
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Slide28GCTs (Malignant variant)
Rare ; 1-2% of all GCTsSuggestive criteriaSize > 5cm
Areas of necrosis within the tumorHigh mitotic activityNuclear pleomorphism
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Slide29GCTs
Management
Needle Biopsy establish the diagnosisLocal excision is recommended to exclude coexisting malignant pathologyNo increase risk for BC in future
Recurrence is very low even in close or positive margins
No role for radiotherapy or for chemotherapy
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Slide30Radial Scar
Benign breast lesion.
Unknown originDescribed by prof. Hamperl in 1975Many other terms used to describe it (e.g. rosette-like lesion, proliferative centers, borderline breast tumors, non-encapsulated sclerosing lesion, etc.)
Lesion characteristics:
Hyalinized sclerotic center containing abundant elastic and elastoid masses.
Lesions radiate into periphery and enclosing lobuli.
Lobuli reveal epithelial proliferation range from simple hyperplasia with epithelial villi to other forms of rare true papilloma
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Slide31Radial Scar
Terms correspond to the pathological size: Lesion with size < 9 mm
Radial ScarLesion size > 9 mm Complex sclerosing adenosis
True prevalence is unknown (Asymptomatic)
Estimated incidence from postmortem studies range between 7-28%
Estimated detection rate with mammogram is 0.03-0.09%
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Slide32Radial Scar
Clinical PresentationFrequently Asymptomatic; incidental mammographic finding
Painless firm breast mass (large lesions) … role out carcinoma (Triple assessment)Any site of the breast can be involved.
No chest wall fixation or skin involvement is reported.
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Slide33Radial Scar
Imaging
Mammogram (Tabar and Dean criteria); classical featuresArchitectural distortion with central lucency
Radiating long and thin spicules that vary in appearance on different projections.
Absence of microcalcifications
No clinically palpable mass
Not all present with above features; some may lack central lucency and other may have microcalcifications
Mammographic resemblance to carcinoma necessitate the need for the biopsy
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Slide34Radial Scar
US1/3 of cases are not visible on US.Hypoechoic mass or parenchymal distortion
No additional information that can differentiate from carcinoma. MRINot all mammographic detected scars are visible on MRI.
Promising tool to differentiate from carcinoma.
High negative predictive value for high risk lesions including radial scars specifically.
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Slide35Radial Scar
Gross Pathology
Gross similar to carcinoma
Firm lesion – pale core – irregular edges –yellow streaks infiltrate adjacent normal breast tissue.
Microcysts surrounding radial scars can be seen (not typical for carcinoma)
Histology
Fibroelastotic core with entrapped ducts and radiating ducts and lobules at varying degree of proliferation.
Calcification can be seen.
Associated lesion can be seen also (atypical lesions, LN, in-situ or invasive carcinoma)
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Slide36Radial Scar
DDX
Postoperative changesFat necrosisCarcinoma; specially
Tubular
carcinoma (the need for immunohistochemical differentiation)
Note
the risk of develop subsequent carcinoma in patient with previously diagnosed radial scar is controversial (from no risk to increased risk theories)
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Slide37Radial Scars
Management
Surgical ExcisionDue to possible presence of associated lesions or upstage to in-situ or invasive carcinomaUpstage rate 0-32%
Observation (a trend by some professionals)
Completely excised microscopic scars
No atypia
No enhancing MRI lesions
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Slide38Gynecomastia
Being male breast enlargement
Unilateral or bilateralPainless or tender (secondary to glandular proliferation and fat deposition)Psychological impact.
3 distinct peaks
High prevalence
Neonatal; observed in 75%
Adolescence; 4-69%Old age; 55%
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Slide39Gynecomastia
Etiology / PathophysiologyImbalance of estrogen and androgen levels in male breast tissue
Male breast tissue has:Estrogen receptors
mediate glandular proliferation
Androgen receptors
inhibit glandular proliferation
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Slide40Gynecomastia
Pathophysiology
Increased
Estrogen Level / Effect
Decreased Androgen Level / Effect
Increased
production (adrenals, testes)
Decreased production
by testes
Increased peripheral aromatization
Altered androgen metabolism
Exposure to estrogen like substances
Androgen receptor defects
Medications
(more release of estrogen than androgen from sex hormone binding globulin)
Medications shift androgen from their receptors
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Slide41Gynecomastia
Neonatal gynecomastia:
Placental transfer of maternal estrogen into fetal circulationTransient processResolve spontaneously
Adolescent gynecomastia:
Peak age 13 – 14
Peripheral aromatization of circulation androgen
Transient process; resolves with 1-3 years8% of cases continue into adulthoodReassurance and surveillance
Impact: psychological (embarrassment) and fear of malignancy
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Slide42Gynecomastia
Adult gynecomastia:
IdiopathicPhysiologicalAlso called senile gynecomastia
Due to decreased levels of circulating androgens either to decreased production or increased peripheral conversion to estrogen
Medication related
Chronic diseases (liver failure, renal failure, testicular tumors, adrenocortical tumors, pituitary adenoma, hypogonadism, hyperthyroidism, obesity, ectopic hormone release, etc.)
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Slide43Gynecomastia
Clinical valuation and Workup
Clinical history and Physical examAssessment of regional lymph nodesDistinguishing clinical feature is
concentric enlargement
Frequently bilateral
Pseudogynecomastia Excess fat deposition without concomitant ductal proliferationSoft bilaterally enlarged breast
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Etiology
%
Idiopathic
25%
Acute / persistent in puberty
25%
Medications
10-20%
Cirrhosis / Malnutrition
8%
Hypogonadism
8%
Renal diseases
1%
Testicular tumors
3%
Slide44Gynecomastia
Alarming featuresUnilateralEccentric growth pattern
Skin or nipple changesNipple dischargelymphadenopathyFamily history of breast cancer
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Mammogram in male BC
Sensitivity
92%
Specificity
90%
Laboratory Work up
LFT
KFT
TSH
Prolactin
Beta-HCG
LH
Testosterone
Slide45Gynecomastia
Gynecomastia
Stages
Nodular Pattern
Recent
onset < 1 year
Fan shaped subareolar density
Appear as hypoechoic subareolar
mass with fat tissue surrounding
Reversible stage / no fibrosis established
Dendritic Pattern
In more chronic stage
Flame
(or cone) shaped density infiltrate deeper, surround fat
Irreversible fibrosis
Diffuse
glandular pattern
US
/ Mammogram similar to female breast
In patient treated with high doses of estrogen
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Slide46Gynecomastia
Pathology
Florid phase
(reversible)
In 1
st
year of onset
Proliferation
of ductal epithelium and stromal elements
Periductal inflammation and edema
No fibrosis
Non surgical treatment might be successful
Fibrotic phase
(irreversible)
Start after 6 months
Minimal
ductal proliferation
Hyalinized periductal tissue
Only
surgical treatment
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Slide47Gynecomastia
ManagementLook for possible underlying cause.
SurgeryMainstay of treatment in long standing casesSubcutaneous mastectomy
Liposuction
Prophylaxis strategy in high risk patients (e.g. prostate cancer)
Radiotherapy
Tamoxifen ?! Not yet FDA approved
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Slide48The End
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