Specialist Breast Oncoplastic and Reconstructive Surgery Assistant Professor of Surgery The Hashemite University 1272021 Dr Mahmoud AlBalas MBBS MSc 1 introduction The vast majority of the lesions that occur in the breast are benign ID: 907875
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Slide1
Benign Breast Diseases
Dr. Mahmoud Al-Balas, MBBS, MScSpecialist Breast Oncoplastic and Reconstructive SurgeryAssistant Professor of Surgery – The Hashemite University
12/7/2021
Dr. Mahmoud Al-Balas, MBBS, MSc
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Slide2introduction
The vast majority of the lesions that occur in the breast are benign. The term “benign breast diseases” encompasses a heterogeneous group of lesions that may present a wide range of symptoms or may be detected as incidental microscopic findings.The incidence of benign breast lesions begins to rise during the 2
nd decade of life and peaks in the 4th-5th
decades
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Slide3Targets of management
Distinguish benign lesions from in situ and invasive breast cancerAssess a patient’s risk of developing breast cancerAvoid unnecessary surgical procedures
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Slide4Classification
Category
Pathology / Disease
Developmental Abnormalities
Ectopic breast (mammary heterotopia)
Underdevelopment of the breast (hypoplasia)
Amastia
(complete absence of both breast and nipple)
Amazia
(presence of only nipple without breast tissue )
Nipple (
polythelia
), areola, glandular tissue (polymastia)Congenital Ulnar-mammary syndrome Poland’s syndrome Turner’s syndrome Congenital adrenal hyperplasiaAcquired hypoplasia (iatrogenic) Trauma RadiotherapyInflammatory and related lesionsMastitisMammary Duct EctasiaFat NecrosisAcute mastitsGranulomatous mastitisForeign body reactionsZuska’s diseaseFibrocycstic ChangesBreast CystsAdenosis
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Slide5Developmental Abnormalities
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Slide6Ectopic breast (mammary heterotopia)
Described as both supernumerary and aberrant breast tissueThe most common congenital abnormality of the breast.Location
mostly along the milk line; the most frequent sites are the chest wall, vulva, and axilla (i.e. most frequent site).Can be seen in other areas (knee, thigh, buttock, face, ear, neck)
It may vary in its components of nipple (polythelia), areola, and glandular tissue (
polymastia
).
Absence of nipple makes the diagnosis of an accessory breast tissue difficult.
The accessory breast tissue responds in the same way as normal breast tissue to physiological influences
More common among Asians, especially Japanese
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Slide7Clinical significance
Recognition of ectopic breast tissue is important because it can develop a variety of benign and malignant lesions encountered in the normal breast. It has been reported that ectopic breast tissue is more prone to malignant change and that ectopic breast cancer occurs at an earlier age; however, it is rareExcessive breast growth (macromastia) can be seen in pregnancy as well as during adolescence.
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Slide8Underdevelopment of the breast (hypoplasia)
CongenitalUsually associated with genetic disordersUlnar-mammary syndromePoland’s syndrome
Turner’s syndromeCongenital adrenal hyperplasiaPoland’s syndrome has been reported to be associated with breast cancer most often.
Some recent studies suggesting the association of ulnar-mammary syndrome and BCAcquired
Usually Iatrogenic
Most commonly subsequent to trauma or radiotherapy
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Slide9http://pip-uk.org/wp-content/uploads/poland_syndrome_visual.png
http://plasticsurgeonforkids.com/wp-content/uploads/Mob-Poland.jpg
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Slide10Inflammatory and Related Lesions
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Slide11Acute mastitis
Puerperal or lactation mastitisDefined as cellulitis of the interlobular connective tissue within the mammary gland, which can result in abscess formation and septicemia.Usually occurs during the first 3 months postpartum as a result of breast feedingOccur in 2% to 24% of breastfeeding women from several weeks to up to 1 year after delivery in women who continue to breastfeed
10% develop a breast abscess
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Slide12Risk factors
Improper nursing techniqueMilk stasis and cracks or fissures of the nippleMay facilitate entrance of microorganisms through the skinStress and sleep deprivationLower the mother’s immune status and inhibit milk flow, thus causing engorgement
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Slide13Causative agents
S. aureus most common pathogenCoagulase-negative staphylococciβ-hemolytic streptococci
Other Streptococcus
faecalis, Escherichia coli
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Slide14Presentation
Pain – swelling – induration - redness – hotness – dischargeEarly diagnosis and early management of mastitis is of valueThe duration of symptoms before starting treatment is found to be the only independent risk factor for abscess development
https://www.babycentre.co.uk/a251/mastitis
http://www.mayoclinic.org/diseases-conditions/mastitis/multimedia/mastitis/img-20008120
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Slide15Management
Breast emptying with frequent nursing or manual pumping and Empiric antibiotic therapyLittle consensus on the type or duration of antibiotic therapy and when to begin antibioticsAbscess drainageI&D
US guided aspiration
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Slide16Breast feeding during mastitis ?
Continue breastfeedingIncreasing the frequency of feedsManually emptying the breast between feeds.Initiate feeds on the unaffected breast and change the infant's position at different feeds.
Continued breastfeeding is not harmful to the infant
Weaning / decrease feeding have an increased risk of developing a breast abscess.
https://bebefeliz.com/files/2011/09/mastitis.jpg
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Slide17Analgesics (e.g. ibuprofen or acetaminophen)
Increased fluid intake and adequate nutrition should be encouraged. Either cold or warm compresses may be used for comfortWarm compresses may aid in breast drainage
Wear some type of non-constricting breast support
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Slide18Outpatient treatment
Dicloxacillin 500 mg PO QID / 10-14 daysCephalexin 500 mg PO QID /10-14 daysAmoxicillin-clavulanate 500 mg PO TID or 875 mg PO BID for 10-14 days If beta-lactam allergy:
Clarithromycin 500 mg PO BID for 10-14 days (or see following section) If suspected community-acquired methicillin-resistant Staphylococcus aureus
(CA-MRSA) infection:Clindamycin 300 mg PO TID for 10-14 days
Doxycycline 100 mg PO BID for 10-14 days (pregnancy Category D and secreted in breast milk; do not use in pregnancy or if breastfeeding)
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Slide19Inpatient treatment
Nafcillin 2 g IV q4h or Oxacillin 2 g IV q4h If beta-lactam allergy or MRSA suspicion:
Clindamycin 600 mg IV q8h or Vancomycin 15 mg/kg IV q12h
For rare strains or refractory cases:Tigecycline 100-mg IV infusion, then 50-mg IV infusion q12h for 5-14 days (pregnancy Category D and unknown if secreted in breast milk; do not use in pregnancy or if breastfeeding)
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Slide20Clinical hints
Patients with recurrent mastitisRule out abscess with ultrasonography.Consider choosing an antibiotic to cover (MRSA): clindamycin, trimethoprim-sulfamethoxazole, or vancomycin.
Patients with nonpuerperal mastitisConsider the possibility of cancer.A ruptured cyst may be associated with inflammation.
The mastitis may be self-limited, and antibiotics therefore of questionable benefit.
If antibiotic treatment is needed, provide it as for lactating women
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Slide21Granulomatous mastitis
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Slide22Granulomatous mastitis
A rare benign inflammatory breast disease of variable etiologiesInfectious etiology (e.g. TB)Foreign materialSystemic autoimmune diseases (e.g. sarcoidosis and Wegener’s granulomatosis)Idiopathic
Identification of the etiology requires microbiologic and immunologic testing in addition to histopathologic evaluation
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Slide23Idiopathic granulomatous mastitis
A non-caseating granulomatous lesions without an identifiable cause.Diagnosis by excluding other possible causesCause is unknown; may be attributed to a localized autoimmune response to retained and extravasated fat- and protein-rich secretions in the duct
Histologicallychronic non-
caseating granulomatous inflammation typically limited to lobuli.
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Slide24Granulomatous Lobular Mastitis
Sarcoidosis
Centered on lobules
Widespread distribution
Granulomas may not be well formed
Well formed tight granulomas
Associated inflammtion may be extensive
Frequently lacks extensive accompanying inflammation (naked granulomas)
May have associated fat necrosis and abscess
Necrosis and abscess rare
Granulomatous Lobular Mastitis
Mammary Duct
Ectasia
Centered on lobules Centered on ducts Granulomatous inflammation May have giant cells but usually lacks formed granulomas Nearly all cases postpartumMay occur without associated pregnancy Granulomatous Lobular Mastitis Puerperal Mastitis No infectious organisms Bacterial infection Mean interval two years from delivery Recent delivery 12/7/202124Dr. Mahmoud Al-Balas, MBBS, MSc
Slide25Microscopic findings of idiopathic granulomatous mastitis. 2A Empty spaces of varying sizes surrounded by granulomatous inflammation and micro-abscess formation (H & E, 40×) 2B
Epithelioid granuloma admixed with polymorphonuclear cells and multinucleated giant cells
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Slide26Presentation
Ill defined painful mass in the breastCan involve any quadrantBilateral involvement is rareSkin thickness, sinus and abscess formationAxillary lymphadenopathy
Nipple retractionMay be mistaken with breast carcinoma
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Slide27Treatment
Complete surgical excision whenever possible plus steroid therapy.Spontaneous resolution occurPrognosis 5-50% of the cases have
PersistenceRecurrenceComplications (e.g. abscess formation, fistulae, and chronic suppuration)
long-term follow up is necessary in these patients
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Slide28Steroid treatment
* 30 mg/day oral prednisoloneTopical prednacinolone (bid); four times per week** 40–60 mg/day prednisolone for 1 month. Then tapered to 30 mg/alternate day over a period of 1–2 months, and after 6 months the dosage was 10–15 mg/alternate day. The maintenance dosage of prednisolone was 5–7.5 mg/alternate day. Steroid was stopped after 1.5–2 years
PPIsAntibiotics (i.e. empirically)
* Topical Steroids to Treat Granulomatous Mastitis: A Case Report.
Korean J Intern Med
. 2011 Sep; 26(3): 356–359
**
Combined Long-Term Steroid and Immunosuppressive Treatment Regimen in Granulomatous Mastitis.
Breast Care (Basel)
. 2012 Aug; 7(4): 297–301.
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Slide29Foreign Body
Silicone and paraffin, following breast augmentation or reconstruction with implantsSilicone granulomas (siliconomas)After direct injection of silicone into the breast tissue or after extracapsular rupture of an implantSecondary fibrosis and contracturePainful hard mass
Histopathology F.B with granulomatous reaction and multinucleated giant cells
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Slide3012/7/2021
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Dr. Mahmoud Al-Balas, MBBS, MSc
Recurring subareolar abscess
(Zuska’s disease)
Slide31Recurring subareolar abscess
(Zuska’s disease)Rare, benign bacterial infection of the breast90% of patients are smoker
A triad of:Draining cutaneous fistula from the subareolar tissueChronic thick, pasty discharge from the nipple
History of multiple, recurrent mammary abscesses
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Slide32Pathology
Squamous metaplasia of one or more lactiferous ducts in their passage through the nipple (i.e. probably induced by smoking)Keratin plugs obstruct and dilate the proximal duct, which then becomes infected and ruptures. Abscess formation beneath the nipple, and fistula opens at the margin of the areola for drainage.
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Slide33Treatment
Surgical drainage the acute inflammation resolvesComplete excision of the affected duct and sinus tract
(fistulectomy [Hadfield operation]) Smoking cessation
Abscesses may recur when the process develops in another duct
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Slide34Mammary Duct Ectasia
Also called periductal mastitisDistinctive clinical entity that can mimic invasive carcinoma clinically. Age: middle-aged to elderly parous womenPresentation:
Nipple discharge (bloody, serous, creamy white, yellow)Palpable subareolar massNoncyclical mastalgiaNipple inversion or retraction.
The pathogenesis and the etiology of the disease are still being debated.Smoking has been implicated as an etiologic factor in mammary duct ectasia. More association with young smokers
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Slide35Pathologic findings
Dilatation of major ducts in the subareolar region.Accumulation of eosinophilic, granular secretions and foamy histiocytes within the duct epithelium and the lumen.The inspissated luminal secretions may undergo calcificationsUsually an asymptomatic lesion and is detected mammographically because of microcalcifications.
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Slide36https://mammography.files.wordpress.com/2014/01/screen-shot-2014-01-23-at-10-26-53-am.png
https://images.radiopaedia.org/images/3101295/c4562b72050968bdac2e4023935350_thumb.jpeg
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Slide37Management
There is no evidence in the literature indicating that mammary duct ectasia is associated with an increased risk for breast cancer.CNB if clinical presentation and mammographic findings are suggestive for malignancy
Generally does not require surgery and should be managed conservativelySurgical excision of the main duct
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Slide38Fat necrosis
Is a benign nonsuppurative inflammatory process of adipose tissue. Causes:Secondary to traumaAccidental
SurgicalRadiation therapyAssociated with breast pathologyCarcinoma
Lesion with suppurative or necrotic degeneration (e.g. mammary duct ectasia, fibrocystic disease with large cyst formation)
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Slide39Clinically
Ill-defined or spiculated dense massSkin retractionEcchymosisErythemaSkin thickness
Radiologic workup for evaluation and to distinguish it from a malignant lesionMammogram
ill-defined and irregular, spiculated mass-like area +/- calcificationsMore defined with time (oil cyst)US
hypoechoic mass with well-defined margins +/- mural nodule(s)
http://breast-cancer.ca/necrofat/
http://image.slidesharecdn.com/breastpathology-1-120708034042-phpapp01/95/breast-pathology-1-59-728.jpg
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Slide40Histologically
:Anuclear fat cells often surrounded by histiocytic giant cells and foamy phagocytic histiocytesManagement:
Conservative management
Excisional biopsy is required if carcinoma cannot be excluded preoperatively
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Slide41Fibrocystic Changes
The most frequent benign disorder of the breast.Generally affect premenopausal women between 20 and 50 years of ageObserved clinically in up to 50% and histologically in 90% of women
May be multifocal and bilateral. The most common presenting symptoms are breast pain and tender nodularities in breasts.
The exact pathogenesis of the entity is not clearHormonal imbalance, particularly estrogen predominance over progesterone
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Slide42FCC:
Dupont and Page Classification
Nonproliferative lesions
Cysts
Papillary apocrine changes
Epithelial-related calcifications
Mild epithelial hyperplasia
Ductal ectasia
Nonsclerosing adenosis
Periductal fibrosis
70% of cases
No increase in risk of BC
Proliferative lesions without atypia
Moderate or florid ductal hyperplasia of the usual type
Sclerosing adenosis
Radial scar
Intraductal papilloma or papillomatosisBC RR increase 1.3-1.9 timesProliferative lesions with atypia (atypical hyperplasia)Atypical ductal hyperplasia (ADH)Atypical lobular hyperplasia (ALH)BC RR increase 3.9-13 times> 80% of patients with atypical hyperplasia do not develop invasive cancer during their lifetimes12/7/2021Dr. Mahmoud Al-Balas, MBBS, MSc42
Slide43Determinants of breast cancer risk after the diagnosis of benign breast disease
Histologic featuresAge at biopsyIn comparison to women > 55 years old, the risk for breast cancer in young women with a diagnosis of atypical epithelial proliferation is twice.Degree of family history of BC
Strong family history may increase breast cancer risk even in patients with nonproliferative lesions
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Slide44Breast Cysts
Fluid-filled, round or ovoid structures1/3 of women between 35 and 50 years oldClassificationSizeSubclinical (microcysts)
majority of casesPalpable (gross) cysts 20%–25% of cases, generally are simple cysts
StructureSimple cysts
Complex / atypical cysts
5-5.5% of all breast US examinations
Internal echoes – thin septations – thickened/irregular wall – absent posterior enhancement
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Slide45http://www.celebritydiagnosis.com/wp-content/uploads/2014/10/simple-breast-cyst.jpg
http://www.ultrasoundpaedia.com/uploads/53003/ufiles/breast/breast%20pathology/breast-cysts-complex-v-simple.jpghttp://images.radiopaedia.org/images/2868244/91a37d5c3b7352aa4d8331e29e49a2.png
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Slide46http://blog.myesr.org/wp_live_esr11_23zcq/wp-content/uploads/2013/06/Fig.-5.jpg
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Slide47Clinical significance and management
Gross simple cysts are not associated with increased risk of malignancyRoutine follow upMalignancy rate of complex cysts 0.3%Follow up with imaging studiesComplex cysts with intracystic mass/nodule are suspicious for malignancy
CNB or surgical biopsy
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Slide48Epithelial Hyperplasia
Epithelial hyperplasia is one of the most challenging FCCs to diagnose properly. The most common form of proliferative breast diseaseClassified into:
Ductal Lesions
Lobular Lesions
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Slide49Ductal hyperplasia
Increase the number of cell layers lining of breast ducts > 2 layers More frequently diagnosed with the use of mammogram and detection of microcalcificationsUsual (simple) ducal hyperplasiaMild hyperplasia
3-4 cell layers, no luminal distentionModerate hyperplasia > 4 cell layers thickness, bridging of luminal space
Florid hyperplasia distended and possible obliterated lumen
Atypical Hyperplasia
Uniform population of cells
Mimic low grade DCIS
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Slide50Usual Ductal Hyperplasia (UDH)
Atypical Ductal Hyperplasia (ADH)
30% of breast biopsies
10% of breast biopsies
Late premenopausal age
Late premenopausal age
No Atypia
Atypia
RR for BC increase slightly (1.5-2X)
RR increase by (4-5X) over 10-15 years
Represent low grade intraductal carcinoma in 1-3 ducts, size less than or equal 2 mm
For ADH; risk of cancer decreases after 15 years
Premenopausal with ADH have higher risk for developing BC than postmenopausal women.
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Slide51Lobular hyperplasia
A description include ALH and cLCISBoth ALH and LCIS have very similar histologic features, except for extent & degree of proliferationConsidered as risk factors for BC (not precursors)Rarely clinically detected
Diagnosed during breast biopsies (i.e. 0.5-4% of all benign breast biopsies)More common in premenopausal womenMulticentric (85%) and bilateral in (30-67%)
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Slide52Histopathology
Intra-acinar proliferation of small, uniform, non cohesive cells. Negative for E-cadherin in 85% of cases.
ALH
cLCIS
Extent
of proliferation
Proliferation not occluding the lumen
Lumen is occluded
Risk of BC
RR 4-5 X
RR 8-10 X
Site of BC
Ipsilateral : contralateral =
3:1
Risk is equal in both breasts
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Slide53Management
ALHSystemic follow-up and appropriate risk assessmentcLCISWLE to role out synchronous DCIS or invasive carcinomaUpgrade rate 3-30%
Negative margins are required for pLCISLRR risk 6% with positive margins and 1-2% in negative marginsOther options
ChemopreventionBilateral risk reducing mastectomy preserved for patients with additional risk of BC
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Slide54Columnar Cell Lesions
Columnar Cell Changes
Columnar Cell Hyperplasia
Flat Epithelial Atypia
In 40 % of NCB for microcalcifications
1-2% of NCB for microcalcifications
44 – 51 years old women
44 – 51 years old women
Low risk for BC
Risk lower than ADH
Enlarged TDLU and dilated acini
CCC/CCH + Atypia
1-2 layers of columnar typical epithelial cells
> 2 layers of columnar typical epithelial cells
30% of cases have worse lesion on excision
Close surveillance and follo
w upSurgical excision Role out DCIS / IDC12/7/2021Dr. Mahmoud Al-Balas, MBBS, MSc54
Slide55Radial Scar and Sclerosing lesions
Radial Scar (RS)
Microglandular Adenosis (MGA)
Sclerosing Adenosis (SA)
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Adenosis
a proliferative lesion characterized by an increased number or size of glandular components, mostly lobular units.
Slide56Sclerosing adenosis
Benign lobulocentric lesion (disordered acinar, myoepithelial, and connective tissue elements)Can mimic invasive carcinoma both grossly and microscopically
May manifest as a palpable mass or as a suspicious finding at mammography.
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Slide57Strongly associated with various proliferative lesions
Epithelial hyperplasiaIntraductal or sclerosing papillomaComplex sclerosing lesionCalcificationApocrine changesIt can coexist with both invasive and in situ cancers
SA is a risk factor for invasive breast cancer apart from its association with other proliferative lesions of the breast
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Slide58Microglandular adenosis
Proliferation of round, small glands distributed irregularly within dense fibrous and/or adipose tissue. Histologic features Glandular structures have open lumina with eosinophilic material inside Lack the outer myoepithelial layer seen in other types of adenosis (most important)
Hard to differentiate microglandular adenosis from tubular carcinoma (TC)MGA stain positive for laminin or type IV collagen
Benign, some evidence of the potential to become invasive carcinoma.
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Slide59MGA has a tendency to recur if not completely excised
Variants of MGA (rare)Apocrine adenosisTubular adenosis
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Slide61Radial Scar
is a rosette-like proliferative breast lesiona mimicker of scirrhous breast carcinoma25% of cases radial scars can be palpable30% of cases, a radial scar is associated with DCIS and tubular carcinoma of the breast
Gross description25% are palpable
Mimic carcinoma
Histopathologic features
The characteristic stellate histologic appearance of an RS is the result of ducts and lobules radiating outward from a central fibroelastic core
Duct and lobules display variable epithelial hyperplasia, adenosis, duct ectasia, and papillomatosis
https://upload.wikimedia.org/wikipedia/commons/thumb/1/13/Radial_scar.jpg/230px-Radial_scar.jpg
http://www.breastpathology.info/Images/Benign/Radial_scar/RS_DCISai_700.jpg
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Slide62http://blog.myesr.org/wp_live_esr11_23zcq/wp-content/uploads/2013/06/Fig.-31.jpg
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Slide64SA
RS
MGA
Pre- & Peri- menopausal
Any age
45-55 years
Benign
Incidence: 4% - 28%
Multiple 67%
Bilateral 43%
Benign
Rare
No increase in BC risk
Size:
<
1 cm
RS > 1 cm complex sclerosing lesionRR of BC increase by 2XMultiple/larger RS associated with higher risk of BCBenignFrequently associated with invasive carcinomaFollow-upCase dependentCNBSurgical excisionSurgical excision12/7/2021Dr. Mahmoud Al-Balas, MBBS, MSc64
Slide65Intraductal papilloma
Benign tumor of the epithelium of mammary ducts
Multiple branching papillae lined by epithelium and myoepithelium within one or more dilated ducts.
Shows predilection for extreme ends of the ductal system: lactiferous sinuses and terminal ductules
May be associated with hyperplasia (usual
or atypical ) or metaplasia (apocrine or squamous)
Types:
Central single papilloma
Multiple papillomas (papillomatosis)
Juvenile papillomatosis
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Slide66Solitary intraductal papilloma (SIP)
Multiple
intraductal papilloma (MIP)
Age
50-60 years
Young
age
More likely bilateral
location
MC
subareolar
MC
peripheral
Subareolar
At least 5 clearly separate papillomas within localized
breast segment
RR for BC2XSignificant correlation between ADH within SIP and BC risk3XPrognosisADH or DCIS confined to SIP have no prognostic significance or impactTreatmentExcisional biopsyFollow upExcisional biopsyFollow up12/7/2021Dr. Mahmoud Al-Balas, MBBS, MSc66
Slide67Juvenile papillomatosis
Severe ductal papillomatosis in women < 30 years old8 cases have been reported in maleAssociate with high risk of BCLong term follow up for patient and family
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Slide68Proliferative stromal lesions
Diabetic Fibrous Mastopathy
Pseudoangiomatous Stromal Hyperplasia of the Breast
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Slide69Diabetic Fibrous Mastopathy
Uncommon form of lymphocytic mastitis and stromal fibrosis. It occurs both in premenopausal women and (rarely) in men with long-standing type 1 IDDM with severe diabetic microvascular complications.
Clinical presentationSolitary or multiple ill-defined, painless massImmobile, discrete lesions in one or both breasts that raise the suspicion of carcinoma.
MMX & US
highly suspicious for breast cancer
CNB is always essential for definitive diagnosis
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Slide70Pathologic characteristic
Dense keloid-like fibrosisPeriductal, lobular, or perivascular lymphocytic infiltration (predominantly B cells)Lobular atrophyEpithelioid fibroblasts embedded in dense fibrous stroma.
The pathogenesis is unknownMay be secondary to immune reaction to the abnormal accumulation of altered ECM in the breastECM is a manifestation of the effects of hyperglycemia on connective tissue
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Slide71Management
Routine annual follow-up is recommendedCNB to role out suspicious carcinomaCore needle biopsy may be useful in the diagnosis of recurrent lesions on follow-up
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Slide72Pseudoangiomatous stromal hyperplasia of the breast (PASH)
Benign myofibroblastic proliferation of nonspecialized mammary stroma. Ranges from incidental, microscopic foci to clinically and mammographically evident breast massesMale and female
Cause unknown
Small percentage of PASH are positive for ER or PR
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Slide73Well-circumscribed, dense, rubbery mass mimicking a fibroadenoma or a phyllodes tumor.
MMx and US features nonspecificCNB is necessary to exclude a malignancyGross descriptiona well-demarcated mass with a smooth external surface.
The cut surface consists of homogeneous white and rubbery tissue.
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Slide74Histologically
A complex network of anastomosing slit-like spaces within a densely collagenous stromaMay confused with mammary angiosarcoma (i.e. immunohistochemical vascular markers are used for distinction)Spindle cells in PASH are strongly positive for vimentin and CD34 and negative for cytokeratin and factor VIII.
Management WLEGood prognosis
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Slide75Resources
Benign breast diseases: Classification, Diagnosis, and management. The Oncologist 2006; 11:435-449http://emedicine.medscape.com/article/2028354-overviewhttp://www.glowm.com/section_view/heading/Puerperal%20Mastitis/item/142
https://bmcsurg.biomedcentral.com/articles/10.1186/1471-2482-14-66https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192210/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515783/https://radiopaedia.org/articles/fat-necrosis-breast-2
Lobular neoplasia: morphology, biological potential and management in core biopsies. Frances P
O’malley
. Modern Pathology 2010, 23, S14-S2
Breast Disease, Diagnosis and Pathology volume 1. Adnan Aydiner
https://radiopaedia.org/articles/radial-scar
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