CASE REPORT

A Case of a Bilateral Inflammatory Breast Cancer:

A Case Report
James Kurtz, DO, Deepa Halaharvi, DO, Shakir Sarwar, MD and
Mark Cripe, DO
Ohio Health Breast and Cancer Services, Grant Medical Center, Columbus, Ohio

n Abstract: Cases of bilateral inflammatory breast cancer (IBC) are extremely rare. Our search criteria only found one
other record of metachronous bilateral IBC (1). We present the case of a patient who was treated for IBC with neoadjuvant
chemotherapy, modified radical mastectomy (MRM), and whole breast radiation. Less than 1 year later, the patient had a
recurrence of IBC on the left chest wall with in the radiated field, as well as a new IBC on the contralateral side. Bilateral
IBC is extremely rare. This entity can present challenges for the standard treatment of IBC with neoadjuvant chemotherapy,
MRM, and whole breast radiation (2). Our case study shows the importance of scheduled routine imaging, screening with
physical examination after IBC management, and good patient compliance in this aggressive disease (3). n
Key Words: contralateral inflammatory breast cancer, inflammatory breast cancer, locally advanced breast cancer

C ases of bilateral inflammatory breast cancer (IBC)

are extremely rare. Our search criteria only
found one other record of metachronous bilateral IBC
(1). We present the case of a patient who was treated
for IBC with neoadjuvant chemotherapy, modified
radical mastectomy (MRM), and whole breast radia-
tion. Less than 1 year later, the patient had a recur-
rence of IBC on the left chest wall with in the
radiated field, as well as a new IBC on the contralat-
eral side.
CASE REPORT
A 55-year-old woman with a medical history of
drug and alcohol abuse presented to the emergency
department with 2- to 3-week history of swollen,
painful, and inflamed left breast on February 2012.
Initially, she was treated with antibiotics (Bactrim)
for a presumed diagnosis of mastitis. Two weeks
later, she presented to our breast health clinic where
she was a found to have a 3-cm palpable mass at 5
o’ clock of her left breast as well as left axillary lym-
Address correspondence and reprint requests to: James Kurtz, DO,
Doctor’s Hospital - General Surgery, 5100 W. Broad St., Columbus, OH
43228, USA, or e-mail: James.kurtz@ohiohealth.com
DOI: 10.1111/tbj.12578
© 2016 Wiley Periodicals, Inc., 1075-122X/16
The Breast Journal, Volume 22 Number 3, 2016 342–346
phadenopathy. Imaging (diagnostic mammogram and
ultrasound) revealed an ill-defined lobular 3.2 9 2.3
9 2 cm hypoechoic mass at 4 o’ clock 3 cm from
the nipple. There was also an enlarged axillary lymph
node that measured 2.9 9 1.2 9 2.7 cm. A left
breast core needle biopsy confirmed Infiltrating Duc-
tal Carcinoma, grade 3, Stage IIIC. Left breast skin
biopsy was negative for carcinoma but showed
dilated lymphatics. Receptors were negative for estro-
gen and progesterone but positive for HER-2 neu. A
metastatic survey was negative, including computed
tomography (CT) scan of chest, abdomen, and pelvis;
positron emission tomography (PET) scan; and a
bone scan. After multi-disciplinary review of her
imaging and pathology, she underwent neoadjuvant
chemotherapy with four cycles of Adriamycin and
Cytoxan followed by weekly Taxol changed to
Abraxane secondary to side effects and she was also
placed on Herceptin. Postneoadjuvant chemotherapy,
clinically she did have partial clinical response with
resolution of left breast mass and decrease in size of
the left axillary lymph nodes. A left MRM was per-
formed on October 2012. Pathology confirmed a par-
tial response with residual cancer, 2.4-cm invasive
ductal carcinoma, grade 3 with lymphovascular inva-
sion throughout breast and in superficial dermal lym-
phatics. She had 12 of 19 positive lymph nodes with
extracapsular extension. Her closest margin was pos-

terior at 6 mm. Pathologist noted that there was very
little treatment effect identified in the tumor. She
received chest wall and nodal radiation in November
2012. Surveillance PET/CT scan was performed
6 months after surgery and was negative for metasta-
sis. The PET scan in this series did show some
increased uptake on the inferior portion of the right
scapula that seemed to correlate with a healing frac-
ture on CT. It is unclear whether this was pathologic
or not (Figs 1–3).
Figure 1. Mammogram (mediolateral oblique view) of left breast
showing skin thickening and enlarged lymph nodes and normal
mammogram (mediolateral oblique view) of right breast (February
2012).
A Bilateral Inflammatory Breast Cancer • 343
Eleven months after the left MRM, the patient pre-
sented to the hospital with 3 weeks of contralateral
breast pain, swelling, and redness, as well as left chest
wall nodules on the previous mastectomy site and pal-
pable contralateral axillary lymphadenopathy. She
denied symptoms of metastatic disease such as chronic
cough, back pain, headaches, double, or blurred
vision. She was afebrile and without leukocytosis at
this time. On physical examination, she had peau d’
orange skin changes, a 6 cm 9 5 cm mass at central
breast at 12 o’ clock position, an inverted nipple, and
palpable axillary lymph nodes on the right. The
incision on the left chest wall was well healed, but
nodularity was noted on the left chest wall, without
Figure 2. Mammogram (mediolateral view and craniocaudal view)
of the right breast showing diffuse thickening of the skin and lym-
phadenopathy (September 2013).
344 • kurtz et al.
Figure 3. Nodules noted on left chest wall (site of previous modi-
fied radical mastectomy) and note the erythema, peau d’ orange,
and inverted nipple of right breast.
left axillary lymphadenopathy. Both an ultrasound
and diagnostic mammogram were interpreted as
suspicious for neoplastic versus inflammatory process
on the right. MRI of the brain was negative for metas-
tasis and PET-CT did not show any systemic disease.
A punch biopsy was performed of the left chest wall
nodules as well as a right breast core needle biopsy. A
left chest wall biopsy showed carcinoma in the dermal
lymphatics with slightly positive estrogen receptor,
negative progesterone receptor, and positive her-2 neu
receptor. Right breast biopsy was positive for invasive
ductal carcinoma with extensive angiolymphatic inva-
sion, estrogen receptor and progesterone receptor neg-
ative, and her-2 neu positive. After rediscussion at the
multi-disciplinary tumor board, she was started on
Taxotere, Herceptin, and Perjeta combination. She is
also going to in-house rehabilitation program for her
drug and alcohol addiction, and she has showed good
compliance.
CONCLUSIONS
Bilateral IBC is extremely rare. This entity can pre-
sent challenges for the standard treatment of IBC with
neoadjuvant chemotherapy, MRM, and whole breast
radiation (2). Our case study shows the importance of
scheduled routine imaging, screening with physical
examination after IBC management, and good patient
compliance in this aggressive disease (3).
DISCUSSION
Inflammatory breast cancer was first introduced by
Lee and Tannenbaum in 1924 (4). IBC represents the
most aggressive presentation of breast cancer. Inci-
dence in the United States ranges from 1% to 5% (5).
Swollen, red, hot without fever, peau d’ orange are
pathognomonic of this disease. This can be confused
with mastitis (6). Although the diagnosis is clinical,
tumor emboli in dermal lymphatics seen on pathologic
examination support the diagnosis of IBC (7). AJCC
staging is T4NxMx- stage IIIC and is characterized by
rapid metastasis and poor survival (8). The treatment
of IBC uniformly consists of neoadjuvant chemother-
apy followed by MRM, radiation, and endocrine ther-
apy (if appropriate) (9–11). IBC is commonly estrogen
and progesterone receptor negative and her-2 neu
amplified (12). Parton et al. found that 33–52% of
IBC shows strong HER-2 positivity (12). Despite the
advances in breast cancer treatment, we have not
made great strides in survival of patients with IBC.
According to a recent publication based on eight stud-
ies, the 5-year overall survival and disease-free
survival are 46% and 40%, respectively (13). The
introduction of trastuzumab for treatment in her-2
neu oncogene-positive breast disease has resulted in
improved outcomes in this population (14). Earlier
age at diagnosis, hormone receptor negative status,
and a later stage at diagnosis have all been linked to
higher risk of contralateral breast cancer. Risk of con-
tralateral breast cancer following IBC has been
reported in only one study, with higher risk noted for
patients within the first 2 years after diagnosis (15).
According to Surveillance, Epidemiology, and End
Results (SEER) rules, metachronous cancers occurring
two or more months after initial cancer diagnosis are
considered independent primaries unless the medical
records indicate that the tumor is recurrent or meta-
static disease (16). Others have determined that
2 years after initial cancer diagnosis is the most
appropriate single cutoff to separate probable recur-
rent or metastatic disease (those diagnosed within
2 years of the first cancer) from probable independent
primaries (those diagnosed two or more years after
cancer diagnosis) (15). Concordance status between
primary and contralateral disease according to prog-
nostic factors, such as hormone receptor status, has
also been used to determine the relationship between
primary and contralateral disease (17).

We report a recurrent and metastatic IBC after
neoadjuvant treatment, MRM, and radiation of the
first IBC. Schairer et al. calculated absolute risk of
contralateral breast cancer following IBC according
to age at diagnosis, interval since the primary tumor,
and type of contralateral breast cancer using data
from the population-based registries in the National
cancer Institute’s SEER program (18). They found
the absolute risk of contralateral breast cancer fol-
lowing IBC increased rapidly in the first 5 years after
diagnosis, while that of non-IBC increased more
gradually over time. The absolute risk of contralat-
eral IBC after first IBC diagnosis in a patient over
50 years of age is 0.9% and 1.1% at 2 and 5 years,
respectively (18).
There are only two other accounts of bilateral IBC
reported in case reports or published literature. Our
case is unique in that the patient developed a recurrent
ipsilateral as well as metastatic contralateral IBC 19
months after the treatment of the first IBC. As previ-
ously stated, the cancers in the contralateral breast
diagnosed within 2 years of first cancer diagnosis are
most likely recurrent/metastatic disease and those diag-
nosed after 2 years are most likely independent second
primaries. Our patient developed recurrence in the left
chest wall after receiving neoadjuvant chemotherapy,
surgery, radiation, Herceptin, and endocrine therapy.
A potential reason our patient may have had IBC
spread from left side to right side could be due to new
connections made secondary to obstruction of lym-
phatics in the left axilla as she had MRM a year prior.
There may be new lymphatic connections that cross
the median plane to the contralateral breast in absence
of proper lymphatic flow to the axilla. There was over-
all concordance on estrogen receptor, progesterone
receptor, and her-2 neu receptor as well as the histol-
ogy of the contralateral IBC without any evidence of
DCIS. These facts support the idea that the contralat-
eral IBC is from local metastasis instead of a new pri-
mary tumor. Harris et al. demonstrated that the
prognostic factors for patients with IBC include lymph
node involvement, extent of involvement of the breast,
and response to chemotherapy (19). Our patient had
extensive lymph node involvement (12/19 lymph
nodes), and there was a 2.4-cm residual cancer in the
left breast at MRM after neoadjuvant chemotherapy.
Studies also have shown that the response to
chemotherapy is an important predictor of outcome.
Our patient had poor response to chemotherapy in
which higher rate of recurrence is to be expected. Also
A Bilateral Inflammatory Breast Cancer • 345
her lack of compliance aids to her developing recur-
rence, yet contralateral IBC is unexpected.
Biomarkers for early detection and targeted therapies
based on an understanding of the genomic profiling of
IBC might help us to understand why it is so aggressive
and also may improve the clinical management of this
disease and improve survival among patients (20). This
case report shows the importance of vigilant screening
of the mastectomy site as well as the opposite breast fol-
lowing the diagnosis of IBC.
In conclusion, IBC remains a therapeutic challenge
despite advances in systemic therapy, and further stud-
ies are required to identify more active biological
agents for this aggressive disease. Patient compliance
combined with aggressive surveillance is important in
identifying recurrent disease.
REFERENCES
1. Masannat YA. Case report of bilateral inflammatory breast
cancer. Eur J Cancer Care 2010;19:558–60.
2. DeVita V, Lawrence T, Rosenberg S. Cancer: Principles &
Practices of Oncology. Philadelphia, PA: Lippincott Williams &
Wilkins, 2011:1438–9.
3. Dawood S, Ueno NT, Valero V, et al. Differences in survival
among women with stage III inflammatory and noninflammatory
locally advanced breast cancer appear early: a large population-
based study. Cancer 2011;1:1819–26.
4. Lee BJ, Tannenbaum NE. Inflammatory Carcinoma of
the Breast: a report of twenty-eight cases from the breast clinic
of Memorial Hospital. Surg Gynecol Obstet 1924;39:580–95.
5. Levine PH, Stenhorn SC, Ries LG, Aron JL. Inflammatory
breast cancer: the experience of the surveillance, Epidemiology and
End Results (SEER) program. J Natl Cancer Inst 1985;74:291–7.
6. Uematsu Takayoshi. MRI findings of inflammatory breast
cancer, locally advanced breast cancer, and acute mastitis: T2-
weighted images can increase the specificity of inflammatory breast
cancer. Breast Cancer 2012;19:289–94.
7. Anderson WF, Schairer C, Chen BE, Hance KW, Levine PH.
Epidemiology of inflammatory breast cancer. Breast Dis 2005-
2006;22:9–23.
8. Compton CC, Byrd DR, Garcia-Aguilar J, Kurtzman SH,
Olawaiye A, Washington MK. AJCC Cancer Staging Atlas: a Com-
panion to the Seventh Editions 419 of AJCC Cancer Staging Manual
and Handbook. New York: Springer-Verlag, 2012:423.
9. National Comprehensive Cancer Network. NCCN Guideline
update: Breast Cancer Version 3.2014. Fort Washington, PA: Jour-
nal of the National Comprehensive Cancer Network, 2014:MS62–5.
10. Singletary SE. Surgical management of inflammatory breast
cancer. Semin Oncol 2008;35:72–7.
11. Dawood S, Merajver SD, Viens P, et al. International expert
panel on inflammatory breast cancer: consensus statement for stan-
dardized diagnosis and treatment. Ann Oncol 2011;22:515–23.
12. Parton M, Dowsett M, Ashley S, Hills M, Lowe F, Smith
IE. High incidence of HER-2 positivity in inflammatory breast can-
cer. Breast 2004;000:97–103.
13. Rehman S, Reddy C, Tendulkar RD. Modern outcomes of
inflammatory breast cancer. Int J Radiat Oncol Biol Phys
2012;84:619–24.
346 • kurtz et al.
14. Dawood S, Ueno NT, Cristofanilli M. The medical treat-
ment of inflammatory breast cancer. Semin Oncol 2008;35:64–71.
15. Rubino C, Arriagada R, Delaloge S, Le MG. Relation of risk
of contralateral breast cancer to the interval since the first primary
tumor. Br J Cancer 2010;102:213–9.
16. Curtis RE, Freedman DM, Ron E, et al. New Malignancies
among Cancer Survivors: SEER Cancer Registries, 1973-2000. Bethesda
MD: National Cancer Institute, 2006. NIH Publ. No. 05-5302.
17. Swain SM, Wilson JW, Mamounas EP, et al. Estrogen recep-
tor status of primary breast cancer is predictive of estrogen receptor
status of contralateral breast cancer. J Natl Cancer Inst
2004;96:516–23.
18. Schairer C, Brown LM, Mai PL. Inflammatory breast cancer:
high risk of contralateral breast cancer compared to comparably
staged non-inflammatory breast cancer. Breast Cancer Res Treat
2011;129:117–24.
19. Harris EER, Schultz D, Bertsch H, Fox K, Glick J, Solin
L. Ten year outcome after combined modality therapy for inflam-
matory breast cancer. Int J Radiat Oncol Biol Phys
2003;55:1200–8.
20. Nguyen D, Sam K, Tsimelzon A, et al. Molecular hetero-
geneity of inflammatory breast cancer: a hyperproliferative
phenotype. Clin Cancer Res 2006;12:5047–54.