MICROCALCIFICATION IN BENIGN BREAST DISEASE

Report
Dr Azar Naimi MD.ACP
Poursina research Lab
Hormoz Island
Type I: calcium
oxalate
dihydrate
crystals
(Weddelite) are
birefringent,
predominantly
in benign
lesions. In
ducts.
Type II: calcium
phosphates
largely in the
form of
hydroxyapatite
are not
birefringent: in
benign and
malignant
lesions. In ducts
and stroma.
Hormoz Island
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What should we do if we receive a kind of
specimen, excised for non palpable lesion with
microcalcification?
For first step, radiography of the intact
specimen is an essential part of the processing
of these specimens. This is to ensure that the
lesion is contained the calcification.
A specimen X-ray should be sent to the
pathologist along with the specimen.
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If the mammographic abnormality reveals
microcalcification, the pathologist should make
every effort to identify them in histologic
sections.
If X-ray of the sliced tissue specimen is
available, all abnormal areas seen should be
submitted and labelled on the radiograph.
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If these are not identified in the sections the
following steps should be followed:
The microcalcification may represent calcium
oxalate crystals. These requires polarization lenses
to visualize.
X-ray of the paraffin blocks and any remaining wet
tissue, if any. Multiple level sections can be made
of the blocks containing the calcification.
Calcification can be leached out by acidic fixatives
or shattered out by the microtome blade. The PH
of the fixative should be checked regularly.
Hormoz Island
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If radiology is looking for a calcs, then report a
specific pathologic identity that would be
compatible with calcs.
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Sclerosing adenosis
Radial scar
Columnar cell change
Intraductal papilloma
ALH
Mucocele like lesions
Apocrine metaplasia
Old fibroadenoma
Old fat necrosis
Calcification associated with lactational change
Ductectasia
Hormoz Island
Sclerosing adenosis
Microcalcifications are
present in > 50% of cases
and may be prominent
Calcs usually numerous,
fine textured and located
within sclerosed acinar
lumens
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Hormone imbalance and dysregulation of ER
may play a role in development of SA
Most common in peri menopausal women
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Most common presentation: Finding during
screening mammography
Less commonly presents as a palpable mass
Classified as proliferative disease without
atypia
MAMMOGRAM
MICROCALCIFICATION
Lobulocentric proliferation of acini around a
central duct with stromal sclerosis and
compression of lumens
 Arises within terminal duct lobular unit
Must be at least 2x larger than average lobule
 2 cell layers may be best appreciated at
periphery
 May be difficult to see if center of lesion is
sampled in a core needle biopsy
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Most common benign lesion mistaken for
invasive carcinoma
More difficult to diagnose on core needle
biopsy when borders and lobulocentric pattern
may not be evaluable
1.5-2x increased relative risk for development
of invasive carcinoma or 5-7% actual lifetime
risk
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Consider surgical consultation about excisional
biopsy: No, unless radiographically discordant
Persian Golf
Radial scar
Typically, these
lesions are identified
as 'distortions of
architecture'/'stellat
e lesions' on
mammograms
If calcs are seen,
which is not
uncommon, they are
an added extra
rather than the
main imaging diagno
stic feature
RADIAL SCAR
Calcs are normally
luminal, fine textured
and associated with the
various pathological
processes seen as part of
these lesions e.g.
sclerosing
adenosis within the lesion
columnar cell change
usual type epithelial
hyperplasia
MAMMOGRAM
GROSS APPEARANCE
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Complex sclerosing lesion (CSL) is less specific
term. Sometimes defined as a RSL > 1 cm in
size
Most RSLs are microscopic findings
Larger RSLs may present as mammographic
density or even palpable mass
Both in situ and invasive carcinomas have
been reported in association with RSL(>2 cm)
RADIAL SCAR
Central nidus, varying
degrees of fibrosis and
fibroelastosis in stellate
or radial configuration
o Associated
proliferative epithelial
component
o Varying degrees of
proliferative epithelial
changes
o Smaller ducts can
become entrapped in
dense fibrous stroma
within central fibrotic
region
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RSL is histologic risk factor for subsequent
development of breast carcinoma
Presence of epithelial atypia, increased size,
and multiple lesions are likely associated with
increased risk for development of malignancy
Studies to identify myoepithelial cells may be
helpful in difficult case.
However, results of myoepithelial cell studies
to rule out malignancy must be interpreted
with caution
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Few small-series studies have shown that 40%
of patients with radial scar on CNB had
carcinoma (DCIS or invasive) at excision; and
22% reported ADH on follow-up excision
Should be excised
Columnar Cell
Change
Frequently
accompanied by
microcalcification
Calcs often fine may be luminal,
intra-epithelial or in
adjacent stroma
Oxalate calcs
uncommon
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Cells line dilated terminal ductal lobular units
(TDLUs)
Cystic spaces frequently contain luminal
secretions and flocculent material
Molecular studies show genetic changes similar
to those found in low-grade DCIS and invasive
cancer
Morphologic spectrum based on presence and
degree of epithelial atypia
COLUMNAR CELL CHANGE WITH
INTRA-EPITHELIAL CALC
COLUMNAR CELL CHANGE
WITH PERIDUCTAL CALCS
What does this mean?
 Flat epithelial atypia
 “older term” clinging carcinoma
 FEA(Flat Epithelial Atypia) represents columnar cell
lesion with varying degrees of cytologic atypia
 Intraductal alteration of the epithelial cells of 1-5 layers
of “low grade” nuclei
 Frequently coexists with lobular neoplasia and/or
tubular carcinoma
 If FEA is encountered on excision:
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Perform multiple levels to look for architectural
changes of ADH or low-grade DCIS
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Submit all tissue for microscopic examination
FEA found on needle core biopsy:
• Surgical excision is recommended
• Diagnosis is upgraded to more serious lesion in
20-30% of cases CCC found on needle core biopsy
(without atypia)
• Most likely incidental finding as result of
microcalcifications
• Can be followed as long as there are no other
worrisome clinical or mammographic findings
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Hormoz Island
Intraductal
papilloma
Benign epithelial
proliferative lesions
characterized by
papillary ingrowths into
major ducts (LDP) or
smaller
ducts (SDP)
Presentation of LDP:
 Nipple discharge present in 80% of cases:
unilateral and spontaneous
• Sanguinous or serosanguinous: 70%
• Bloody (less common): May be due to papilloma
twisting on stalk and infarction
 Palpable subareolar mass
Presentation of SDP
 Finding on screening mammography
 Incidental finding in a biopsy for another lesion
 Usually does not cause discharge or a palpable
mass
Arborizing fronds of tissue with welldeveloped central fibrovascular core
Lined by epithelial cells, myoepithelial cell layer
 Presence of myoepithelial cells and their
distribution in lesion is helpful diagnostic
feature
 May require use of myoepithelial markers to
aid in the diagnostic evaluation in problematic
cases
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Intra ductal
papilloma
Calcification common
Fine luminal calcs
and/or coarser calcs
seen at periphery
associated with sclerosis
in and around the
papilloma
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Mild increased risk of subsequent carcinoma:
1.5-2.0x relative risk or - 5-7% lifetime risk
Risk similar to that for moderate or florid
ductal epithelial hyperplasia
Surgical consultation for lesions> 10 mm.
In core needle biopsies:
 Management of lesions diagnosed as benign
papillomas on core needle biopsy is controversial
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Risk of carcinoma on excision of benign papillomas is
very low
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When cases are carefully selected and there is good
radiologic/pathologic correlation, carcinomas on
excision are absent or rare « 5%)
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However, distinction between benign papillomas and
atypical papillomas can be difficult, and some
authorities recommend excision of all papillary lesions
on core needle biopsy
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Papillomas with atypia should be excised as 20-60% of
cases will reveal carcinoma on excision
Atypical Lobular
Hyperplasia
ALH is composed of
a monomorphic
proliferation of
discohesive
polygonal or
cuboidal cells that
are small and
round. In lobules,
these cells begin to
fill acinar spaces,
but few are widely
distendedrciJ.
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ALH is an incidental finding in breast biopsies
performed for other indications
Calcifications often present in areas adjacent to
ALH
The hallmark feature of ALH, LCIS, and
invasive lobular carcinoma is loss of E-cadherin
expression
ALH is cytologically identical to lobular
carcinoma in situ (LClS) but is more limited in
extent
ALH is associated with a 4-5x increased relative
risk or a 13-17% lifetime risk of developing
invasive carcinoma
 In some studies, a strong family history of breast
cancer doubles risk of invasive carcinoma to 8x
 Ductal involvement by ALH (pagetoid extension)
is associated with 8x risk or a 26% lifetime risk
• LClS has a l0x increased relative risk or a lifetime
riskof - 30%
• Carcinomas that occur in women after a diagnosis
of LN average> 10 years to diagnosis
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ALH may be found as an incidental finding in
a core needle biopsy
• If there is no other reason for excision, the value
of excision based solely on presence of ALH is
unclear
 Likelihood of cancer on excision is higher in the
following settings:
• Radiologic lesion is a mass or highly suspicious
calcifications (linear &/or branching)
• ALH shows atypical features, such as higher
nuclear grade, or is associated with calcifications
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What is the recommendation?
Surgical consultation
Up to 20% upgraded at lumpectomy
Hormoz Beach
Mucocele like
lesions
Uncommon
breast lesion,
composed of
mucin containing
cysts that may
rupture
MLL is usually asymptomatic
Screening mammograms may show mass or
calcifications
 Range from benign to ADH or DCIS to
mucinous carcinoma
 30% of mucocele-like lesions were identified as
mucinous carcinoma on surgical excision
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Data are limited, and excision is recommended
whenever an atypical mucocele-like lesion or
acellular stromal mucin identified on CNB
Sunset in Hormoz

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