Case Report

J Oncol Pharm Practice

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Docetaxel-induced cardiac-respiratory ! The Author(s) 2017

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arrest in a patient with chronic DOI: 10.1177/1078155217714860
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atrial fibrillation

Mostaqul Huq, Tracie M Balvanz and Scott Mambourg

Abstract
Docetaxel has been approved by the Food and Drug Administration for the treatment of many cancer types, including
breast cancer, head and neck cancer, lung cancer, and prostate cancer. Many severe to life-threatening side effects
(Grades 35) of docetaxel have been reported in clinical trials, case reports, and Food and Drug Administration
Adverse Events Reporting System. These include anaphylactic reactions, febrile neutropenia, fluid retention, acute
respiratory distress, pleural effusion, pneumonia, and peripheral neuropathy. There were fewer cardiac toxicities
reported for docetaxel as compared to paclitaxel, which were less severe. In this report, we present a clinical case of
docetaxel-induced cardiac-respiratory arrest in a 62-year-old Hispanic male patient with stable chronic atrial fibrillation,
who has been recently diagnosed with metastatic prostate cancer. The cardiac event developed within 15 min of
docetaxel infusion during the second cycle of chemotherapy despite using recommended premedication with
corticosteroids.

Keywords
Docetaxel, cardiac arrest, medication safety

Date received: 5 December 2016; revised: 20 April 2017; accepted: 22 April 2017

Introduction
Further, a European Organisation for Research and
Docetaxel (DT) is a semisynthetic derivative of taxanes Treatment of Cancer (EORTC) Early Clinical Trials
currently approved by the Food and Drug Group reported 26% of AHR incidence with DT, of
Administration (FDA) for the treatment of breast which only 0.5% of patients had to discontinue ther-
cancer, non-small cell lung cancer, hormone-refractory apy.6 A typical AHR of DT is associated with ushing,
prostate cancer, gastric adenocarcinoma, and mild or acute rash, pruritus, fever, dyspnea, constrictive
squamous cell carcinoma of the head and neck.1 chest, epigastric or back pain.1,2 Most of the hypersen-
Myelosuppression, hypersensitivity reactions, cumula- sitivity reactions to DT occur during the rst two
tive uid retention, and neurotoxicity are frequently cycles and always within minutes after the start of the
reported toxicities related to DT. Other common toxi- infusion.3 Premedication with corticosteroids is recom-
cities include skin reactions (erythema, desquamation, mended to reduce the severity of DT-related hypersen-
and nail changes), nausea/vomiting, mucositis, general sitivity reactions.1
alopecia, and diarrhea.1,2 Fewer cardiac toxicities have
been reported related to DT, which were non-fatal and
primarily related to hypersensitivity reaction.3,4 The Pharmacy Services, VA Sierra Nevada Health Care System,
US Department of Veterans Affairs, Reno, NV, USA
incidence of acute hypersensitivity reactions (AHR)
related to DT varies among studies, showing 13% in Corresponding author:
Mostaqul Huq, Clinical Pharmacy Specialist, Research and Oncology,
phase I and 31% in phase II trials without using VA Sierra Nevada Health Care System, Pharmacy Services (119),
any premedication. Only 7% of them appeared to be 975 Kirman Ave, Reno, NV 89502, USA.
severe (Grade 35), but none were cardiac related.4,5 Email: mostaqul.huq@va.gov
2 Journal of Oncology Pharmacy Practice 0(0)

We have conducted a Medline database search on Table 1. Patients current medication profile.
PubMed for case reports on DT using the search term
Drug and directions Indications
Docetaxel and Case Report. This revealed several
case reports of rare non-fatal side eects including Albuterol/ipratropium 100/20 mg inhaler COPD
acute respiratory distress, pneumonitis, pleural eu- One inhalation QID PRN
sion, hyper-eosinophilia, sclerosing cholaginitis, myo- Atorvastatin 40 mg PO HS Hyperlipidemia
sitis, diuse pneumopathy, subungual hemorrhage, Carvedilol 6.25 mg PO BID A-fib, CHF
glaucoma, polyneuropathy, venous thrombosis, Cholecalciferol 2000 IU PO daily Vitamin D
inappropriate antidiuretic hormone secretion, hepato- Cyanocobalamin 1000 mg PO daily Anemia
cellular necrosis, scleroderma, and gastrointestinal Dabigatran Etexilate 150 mg PO BID A-fib
pneumatosis. In addition, several articles that summar-
Docetaxel 100 mg IV over 60 min Q2W Prostate cancer
ized the FDA reports of adverse drug reactions (ADRs)
Furosemide 20 mg PO Daily HTN/CHF
showed more fatalities associated with DT as compared
to paclitaxel (54% vs. 29%, p < 0.001) despite both Leuprolide (Eligard ) 45 mg SC Q6M Prostate cancer
being in the same drug class.1 Cardiotoxicities such as Latanoprost 0.05% eye drops 1 drop OU HS Glaucoma
supraventricular rhythm disturbances and cardiac func- Metformin 500 mg PO BID T2DM
tion abnormalities have been reported as relatively Prochlorperazine 10 mg PO TID PRN Nausea/vomiting
infrequent side eects of paclitaxel, but not with DT. Trazodone 50 mg PO HS Insomnia
Routine cardiac monitoring is not recommend for
A-fib: atrial fibrillation; BID: twice daily; CHF: congestive heart failure;
either drug.3,4 A case report showed cardiac conduction COPD: chronic obstructive pulmonary disease; HS: at bedtime;
abnormalities after neoadjuvant chemotherapy with HTN hypertension; OU: both eyes; PO: per oral; PRN: as needed;
doxorubicin and DT for primary breast carcinoma, Q6M: every six months; Q2W: every two weeks; QID: four times
but not with DT alone.7 Currently, there are no cardiac daily; SC: subcutaneously; T2DM: type 2 diabetes mellitus.
toxicity warnings or precautionary statements in the
prescribing information for DT. Here, we present a
clinical case of DT-related cardiac-respiratory arrest, The second cycle (Day 14) was held for a week due to
which developed during the second cycle of DT infu- mild symptoms of upper respiratory tract infection. A
sion in a 62-year-old Hispanic male patient recently week later (Day 21), the patient returned to the clinic to
diagnosed with metastatic prostate cancer. resume the second cycle of DT treatment. The patient
presented with some complaints of weakness and fati-
gue (ECOG score 3). The pre-treatment vitals were rec-
Case orded as height 1.83 m, weight 145 kg, blood pressure
A 62-year-old Hispanic male patient was recently diag- (BP) 111/68, heart rate (HR) 72, respiratory rate (RR)
nosed with metastatic prostate cancer and prescribed 22, body mass index (BMI) 43.4, oxygen saturation
hormone blockade therapy with gonadotropin-releas- (SaO2) 91%. The pre-treatment laboratory values
ing hormone (GnRH) analogue (i.e. leuprolide injec- were within normal limits except low hemoglobin
tion, 45 mg subcutaneously every six months). The (9.3 mg/dL), low RBC (3.5 million/mL) counts, and ele-
patient was subsequently prescribed DT (50 mg/m2 vated level of alkaline phosphatase (450 IU/L) (Table
every two weeks) by the oncologist. The pertinent med- 2). The patient was pre-medicated with IV dexametha-
ical history of the patient includes type 2 diabetes mel- sone (12 mg in 50 mL 0.9% NS over 15 min) and a
litus (T2DM), chronic obstructive pulmonary disease single dose of oral ondansetron 24 mg. Approximately
(COPD), myocardial infarction (MI), hyperlipidemia, 1 h after premedications, DT (100 mg in 250 mL 0.9%
hypertension (HTN), congestive heart failure (CHF), NS over 60 min) IV infusion was started. However,
and chronic atrial brillation (A-b). All chronic within 15 min of beginning the DT infusion, the
comorbid conditions were medically managed and patent underwent cardiac-respiratory arrest with no
clinically stable. The current medication prole is signs of pulse or breathing. The IV infusion was imme-
shown in Table 1. Three months after the diagnosis diately stopped and CPR was started. The patient
of prostate cancer, the patient returned to the clinic returned to spontaneous circulation after three cycles
for the rst cycle of IV chemotherapy with DT of CPR. Post CPR vitals revealed: HR 98, BP 173/106,
(50 mg/m2, every two weeks) 100 mg in 250 mL 0.9% and SaO2 98%. Upon regaining consciousness, the
NS over 60 min. The patient was pre-medicated with IV patient stated that he had been experiencing mild diz-
dexamethasone (12 mg in 50 mL 0.9% NS) over 15 min ziness and nausea before sudden collapse. The patient
and IV ondansetron (16 mg in 50 mL 0.9% NS) over was immediately transferred to emergency department
15 min to prevent DT-related infusion reaction and (ED). Upon arrival to ED, the vitals were recorded as
chemotherapy induced nausea/vomiting, respectively. temperature (Temp) 96.5 F, BP 108/68, HR 87, RR 32,
Huq et al. 3

Table 2. The patients vitals and laboratory data.

Patients historical presentations

Day1 Day 14 Day 21 Day 21 Day 22 Day 24

Parameters Cycle 1 Hold Cycle 2 ED InPat DC Normal value Unit

Height 1.83 1.83 1.83 1.83 1.83 1.93 n/a m

Weight 142.3 145 145 147 n/a n/a n/a kg
BMI 42.5 43.4 43.4 n/a n/a n/a 18.525 kg/m2
BP 105 89 111 108 116 126 120 mmHg
/50 /60 /68 /68 /64 /94 /80
HR 91 76 72 87 95 97 60100 bpm
RR 18 20 22 32 18 18 1216 /min
SaO2 (%) 98 93 91 99 92 91 95100 %

Temp (F) 97.8 97.8 97.9 96.5 97.8 96.6 97.899 F
WBC 6.3 3.5 4.6 6.5 7.2 5.7 410.8 K/mL
RBC 3.1 3.5 3.5 3.5 3.8 3.7 4.76.1 M/mL
Hemoglobin 8.4 9.1 9.3 9.2 9.9 9.6 1418 g/dL
Hematocrit 26 29 30 32 34 33 3851 %
Neutrophil 79.7 36 64.6 76.5 85 27.4 5169 %
ANC 5.0 1.3 3.0 5.5 6.2 n/a 27.5 K/mL
Lymphocytes 11.3 51.1 26 8.7 9.3 62.1 2338 %
Eosinophil 0.2 0.1 0.2 0.0 0.0 0.0 05 %
Monocytes 8.5 12.0 8.4 3.5 2.8 9.2 412 %
Basophil 0.3 0.7 0.8 0.0 0.3 0.3 01 %
Platelet 249 193 176 145 179 n/a 130400 K/mL

Na+ 136 139 n/a 141 139 139 136146 mmol/L

K+ 4.0 3.7 n/a 4.2 4.5 3.8 3.65.3 mmol/L
Ca 9.2 8.6 n/a 8.7 8.8 n/a 8.810.3 mg/dL
Mg n/a n/a n/a n/a 2.0 n/a 1.62.5 mg/dL
Glucose 120 131 n/a 144 222 107 70109 mg/dL
Chloride 99 108 n/a 110 104 102 102114 mmol/L
CO2 26 26 n/a 24 27 28 2432 mmol/L
BUN 14 8 n/a 14 16 14 825 mg/dL
SCr 0.6 0.5 0.6 0.53 0.6 0.6 0.71.3 mg/dL
CrCl 140 168 140 159 140 140 > 60 mL/min
AST 26 9 n/a 12 12 <5 1333 IU/L
ALT 20 7 n/a 7 7 9 731 IU/L
Alk 608 400 450 516 534 461 37108 IU/L
T. bilirubin 1.1 0.7 n/a 1.2 1.1 n/a 0.41.3 mg/dL
Albumin 3.0 3.2 n/a 3.5 3.5 3.2 3.54.7 g/dL
Values shown in bold indicate abnormal lab results.
Alk: alkaline phosphatase; ANC: absolute neutrophil counts; AST: aspartate aminotransferase; ALT: alanine aminotransferase; BMI: body-mass index;
BP: blood pressure; BUN: blood urea nitrogen; CrCl: creatinine clearance; DC: discharged; ED: emergency department; InPat: inpatient; HR: heart rate;
RR: respiratory rate; SCr: serum creatinine; SO2: oxygen saturation; T. bilirubin: total bilirubin.

and SaO2 99%. The subsequent vitals were shown as Table 2. The EKG recorded upon arrival to the ED
BP 126/68, HR 84, RR 23, SaO2 97% 1 h after, and BP showed a QTc interval of 523 ms with an ejection frac-
127/78, HR 81, RR 25, SaO2 97% 2 h after, respect- tion of 65% (data not shown), indicating a case of atrial
ively, suggesting mild tachycardia and tachypnea. The brillation with possible right ventricular hypertrophy.
historical presentation of patients vitals is shown in All other elements in the EKG were within normal
4 Journal of Oncology Pharmacy Practice 0(0)

limits including HR 88, normal sinus rhythm, no arrest during the second cycle within 15 min of DT infu-
change in ST/T segments, and no signs of cardiac ische- sion. The timing of the cardiac event is comparable to
mia. Further, cardiac enzymes were negative. The the likelihood pattern of DT-related infusion reactions
patient was transferred to inpatient care on the same during the rst two cycles. The patient also recalled
day with continuous tele-monitoring and oxygen ther- experiencing dizziness and nausea before sudden col-
apy via mask delivery. The patients home medications lapse, suggesting that the incident was related to DT.
(Table 1) were instituted during inpatient stay. The It has been recommended to observe hypersensitivity,
patient ultimately survived and was discharged from especially with the rst two infusions of DT.5 DT
the hospital under stable condition on Day 3. Upon should be discontinued and re-challenge should be
discharge from hospital, the patient was evaluated by avoided for severe reactions.
cardiologist, showing an EKG report comparable to In this case report, the patient has a chronic history
the baseline (data not shown). Patient is currently of A-b, which has been stable and medically managed
under oncology palliative care. with beta-blocker and dabigatran for nearly two years.
The patient has multiple comorbid conditions including
COPD, past MI, and CHF. The historical data of
Discussion patients labs and vitals suggest the presence of mild
In clinical settings, IV infusion of DT is given with a anemia, hypotension, and tachycardia. The DT-related
usual dose between 40 mg/m2 and 160 mg/m2 in NS infusion reactions might have posed an additional
over 60120 min.8 Several infusion-related anaphylactic burden to existing cardiovascular problems that led to
reactions has been reported with DT during clinical sudden cardiac arrest in this patient. Further, the
trials. The overall incidence is approximately 25%. patient had history of near-syncope and occasional
Premedication with corticosteroids are recommended bouts of hypotension. Therefore, it is possible that
to reduce the severity of anaphylaxis and uid reten- patient might have experienced cardiac syncope
tion. These reactions typically occur within minutes or before cardiac arrest. In clinical trials and/or post-mar-
hours of drug administration. Approximately 2% of keting data/case reports of DT, decreased left ventricu-
patients will experience potentially life-threatening lar ejection fraction by 10% (8%), hypotension (3%),
reactions even with premedication. A typical AHR of and pulmonary reaction (41%) have been reported. In
DT is associated with ushing, mild or acute rash, prur- less than 1% patients, DT also showed acute respira-
itus, fever, dyspnea, constrictive chest, epigastric or tory distress, atrial brillation, atrial utter, cardiac
back pain.2 Severe hypersensitivity reactions, character- arrhythmia, sinus tachycardia, cardiac tamponade,
ized by generalized rash/erythema, hypotension, chest pain, and chest tightness.8 For this patient, the
bronchospasms, or rare anaphylaxis may occur, which EKG report, immediately after the onset of the event,
could be fatal. This has occurred even in patients showed an ejection fraction of 60% and a QTc interval
receiving a three-day corticosteroid premedication.1,2 of 523 ms (reference < 430 ms), which could be prob-
Hypersensitivity reactions require immediate discon- lematic for patients with chronic A-b. Furthermore,
tinuation of the DT infusion and administration of any cardiac side eects of DT mentioned above in a
appropriate therapy. The exact mechanism of hyper- patient with chronic A-b could possibly exacerbate
sensitivity to taxanes is less well dened. Symptoms the pre-existing cardiac conditions. Chronic A-b is
associated with standard infusion reactions and hyper- also a risk factor for heart failure, which can lead to
sensitivity/allergic reactions have been attributed cardiac arrest. This patient has a history of CHF, and
mainly to cytokine release and mast cell/basophil acti- currently on furosemide 20 mg oral daily and carvedilol
vation.9 Most of the hypersensitivity reactions to DT 6.25 mg oral twice daily. The patient consistently pre-
have been reported to occur during the rst two cycles sented elevated B-type natriuretic peptide (BNP) level
within minutes after the start of the infusion.5 In this (data not shown) with the most recent level of 245 pg/
report, the patient was pre medicated with IV dexa- mL (normal range: 1100). Therefore, a mild-to-mod-
methasone 12 mg and IV ondansetron 16 mg prior to erate severe infusion-related reaction of DT could cause
cycle 1; and IV dexamethasone 12 mg and oral ondan- a huge burden in this patient with multiple cardiac
setron 24 mg prior to cycle 2. It is important to note abnormalities, leading to sudden cardiac arrest. We
that prescribing information for DT suggests a three- applied the Naranjo algorithm system to dene the
day oral premedication (Days 1, 0, +1) with cortico- probability of this ADR.10 According to the Naranjo
steroids. However, in our practice setting, all patients algorithm, the probability of ADRs is dened as def-
on DT receive premedication with IV corticosteroids inite (score > 9), probable (score 58), pos-
(dexamethasone 12 mg) only on the day of infusion sible (score 14), and doubtful (score 0).10 The
without any problem. The patient safely completed ADR in the case report was classied as possible
the rst cycle of DT infusion, but underwent cardiac with a score of 4 based on Naranjo algorithm.
Huq et al. 5

Therefore, it could be argued that this adverse reaction and bradyarrhythmias), clinically relevant QT pro-
is not the direct result of DT-related infusion, rather longation may occur, resulting in Torsade de
related to patients pre-existing cardiac condition or pointes.12 DT is not considered as a QT prolonging
exacerbation of pre-existing condition. It is important agent. The patients electrolytes were within normal
to note that one of the major limitations for most algo- limit and the dose of ondansetron was clinically con-
rithms used for dening the probability of ADRs is that sidered safe. Taken together, it is doubtful that
without re-challenge of the oending agent, it is dicult ondansetron alone or in conjunction with DT had a
for causality to be graded more than possible.11 Re- concerted eect on pre-existing condition that led to
challenging a patient with an oending agent that cardiac arrest.
resulted in a life-threatening condition is a tough deci- Further, the patient was pre medicated with
sion or a question of ethical consideration. The patient immediate-release oral ondansetron 24 mg tablet, but
received rst dose of DT safely. The patients under- not the oral disintegration tablet (ODT) form. The
lying cardiac condition was stable before initiating the fatal cardiac event occurred approximately 1 h after
second dose of DT infusion as evident from the oral administration of ondansetron 24 mg. Based on
patients vitals and ECOG performance status. This the pharmacokinetic parameters of oral ondansetron
suggests that pre-existing cardiac condition or exacer- (tmax 2 h, Cmax 94 ng/mL, bioavailability 60%,
bation of pre-existing condition alone is not directly and t1/2 4.5 h),13 only about 50% (12.6 mg) of its
associated with the cause or the severity of this adverse administered dose was estimated to be systemically
reaction. It is more likely related to DT infusion during absorbed, which is lower than safe IV dose of ondanse-
cycle 2. tron 16 mg. The event was captured within 15 min of
We have conducted a comprehensive medication DT infusion during cycle 2. This allowed infusion of
review for the patient to assess whether DT alone or only one-fourth (25 mg) of 100 mg total dose (50 mg/
any other medication had a concerted eect on this m2) of DT. Clinically, DT up to 160 mg/m2 has been
cardiovascular event. Based on the review, we have used safely. The doses administered for both drugs were
found that all 5-HT3 antagonists including ondansetron signicantly lower than clinically safe target dose.
has warnings against dose-dependent QTc prolonga- During cycle 1, they did not cause any problem even
tion. QTc prolongation can cause Torsade de pointes, with their full dose. Therefore, it is quite unlikely that a
which can lead to sudden cardiac arrest.12 The patient lower dose of either agent or both caused exacerbation
was pre medicated with IV ondansetron 16 mg before of underlying cardiac conditions.
the rst dose of DT and an oral dose of ondansetron Additionally, both ondansetron and DT are major
24 mg before the second dose of DT infusions. Further, substrates for CYP3A4. Ondansetron is a minor sub-
the patient medical record showed previous exposure to strate for CYP1A2, CYP2C9, CYP2D6, CYP2E1 and a
ondansetron to a maximum daily dose of 16 mg within weak inhibitor of CYP1A2 and CYP2C9.8,12 The half-
the past six months. Patients underlying cardiac con- life of DT is approximately 11 h.8 Pre medication with
dition (A-b) was medically managed and stable before oral ondansetron 1 h prior to DT infusion for 15 min
initiating chemotherapy, and pre-medication with allowed only one-fourth of DT (25 mg out of 100 mg)
ondansetron during cycle 1 as well as prior exposures and about one-half of ondansetron dose (12.6 mg out of
to both oral and IV ondansetron were performed safely 24 mg) systemically absorbed. During this short span of
without exacerbation of underlying cardiac conditions. time, it is unlikely to encounter a signicant shift in
Therefore, it is less likely that ondansetron alone caused predicted pharmacokinetic or pharmacodynamic
the exacerbation of pre-existing cardiac condition drugdrug interactions between the two agents that
during cycle 2 of DT infusion that led to cardiac led to this severe ADR. The FDA reports of ADRs
arrest. It is more likely to be related to the pre-dispos- also showed more fatalities associated with DT as com-
ing risk of DT-related infusion reaction during cycle 2. pared to paclitaxel.1 There is also a black box warning
A single dose IV ondansetron >16 mg or oral ondanse- against more DT-related fatalities in patients who have
tron >24 mg is not recommended to prevent QT pro- abnormal liver function.8 The patients alkaline phos-
longation, which usually occurs 1 to 2 h after IV phatase levels are consistently high despite normal ALT
administration. IV formulations of 5-HT3 antagonists and AST. This suggests that high alkaline phosphatase
are more associated with EKG interval changes rela- level is related to bone metastasis of the prostate
tive to oral formulations.12 In most patients, EKG cancer, ruling out the possibility that this cardiac fatal-
changes were considered not clinically relevant. ity is related to hepatic function. Considering all factors
However, in conjunction with other agents that pro- discussed above, this fatal cardiac event in a patient
long the QTc interval or in patients with cardiovas- with chronic atrial brillation is more associated with
cular abnormalities or other risk factors for QT DT-related infusion than other related contributing
prolongation (electrolyte abnormalities, heart failure, factors.
6 Journal of Oncology Pharmacy Practice 0(0)

this article: The project was supported from the internal

Conclusion resources.
Cardiac toxicities have not been reported during the
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