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Respiratory Medicine Case Reports
journal homepage: www.elsevier.com/locate/rmcr
Case report
Acute eosinophilic pneumonia following electronic cigarette use
Zhaohui L. Artera,∗ , Amanda Wigginsa, Caleb Hudspatha,
Adam Kislinga, David C. Hostlerb,
Jordanna M. Hostlerb
a Internal Medicine Department, Tripler Army Medical Center,
Honolulu, HI, USA
b Pulmonology Department, Tripler Army Medical Center,
Honolulu, HI, USA
A R T I C L E I N F O
Keywords:
Vaping
Electronic cigarette use
Acute eosinophilic pneumonia
A B S T R A C T
Electronic cigarette (e-cigarette) use, or vaping, is gaining
widespread popularity among adults aged 18–35.
Vaping is commercially promoted as a safer alternative to
traditional cigarette smoking. Previous studies have

reported a close relationship between conventional cigarette
smoking and acute eosinophilic pneumonia (AEP),
but only one case report to date associates vaping with AEP in a
male patient. We present the first case of AEP
involving a young female after use of e-cigarettes. Clinicians
should consider AEP when evaluating young pa-
tients with hypoxic respiratory failure and a recent history of e-
cigarette use. This case highlights the need for
more research into the relationship between e-cigarettes and
AEP.
1. Introduction
E-cigarettes are battery-operated devices that heat liquid
nicotine,
producing an aerosol or vapor, which the user then inhales [1].
E-ci-
garettes were first developed in 2003, entered the United States
in 2006
[2], and have been promoted as a safe and effective alternative
to
traditional cigarettes [3]. In spite of their rapid rise in
popularity and
worldwide sales, the effects of e-cigarettes use on short and
long-term
health are poorly understood. This case describes a young,
healthy fe-
male who developed hypoxic respiratory failure from acute
eosinophilic
pneumonia (AEP) after using e-cigarettes.
2. Case report
A previously healthy 18-year-old female presented to the
Emergency Room after one day of fever, nonproductive cough,
diffi-

culty breathing, and pleuritic chest pain. Two months prior to
pre-
sentation she started vaping using a “Baby Smok Beast Mod”
device
with 6% nicotine fluid 5 times per day for 30 minutes. She
denied
traditional cigarette smoking, drug use, exposure to pulmonary
irri-
tants, recent respiratory illness or history of deployment to the
Middle
East. Initial vitals were remarkable for oxygen saturation of
88% on
room air, temperature of 102.4 °F, heart rate of 122 beats/min,
re-
spiratory rate of 22 breaths/min, and blood pressure of 104/68
mm Hg.
On physical exam, she was found to be in mild distress with
tachy-
cardia, tachypnea and facial flushing. There was neither
accessory
muscle use nor chest wall tenderness, and her lungs were clear
to
auscultation bilaterally. There was no lower extremity edema or
calf
tenderness. Laboratory tests revealed significant leukocytosis of
19.6 × 109/L with 91.2% granulocytes and 0.5% eosinophils.
Initial
chest x-ray demonstrated right lower lung airspace
consolidation con-
sistent with a pneumonia. Intravenous azithromycin was
initiated and
she was admitted to the hospital for further monitoring.
Overnight, she
developed moderate distress with worsening tachycardia,
dyspnea, and

hypoxemia. Increasing levels of oxygen by nasal cannula were
required
to maintain her oxygen saturation above 92%, meanwhile her re-
spiratory rate increased to 30 breaths/min. Repeat examination
re-
vealed bibasilar inspiratory crackles. D-dimer was elevated to
0.79
mcg/ml. Repeat chest radiograph demonstrated increasing
airspace
opacities. A computed tomography pulmonary angiogram
(CTPA) was
completed due to concern for pulmonary embolism (PE). The
CTPA
excluded PE, but found diffuse ground-glass patchy airspace
disease
and coalescing nodules (Fig. 1).
Due to worsening respiratory failure overnight, the patient was
transferred to the Intensive Care Unit (ICU) for closer
monitoring and
respiratory support. Bronchoscopy with bronchial alveolar
lavage (BAL)
was performed, revealing 26% eosinophils in the lavage fluid.
Sputum
and BAL cultures were negative for viral, fungal, and bacterial
patho-
gens. No other infectious etiologies to include TB, legionella,
strongy-
loides, coccidioides, or histoplasma were found. Given her
acute onset
of symptoms, negative alternative workup, and significant BAL
eosi-
nophilia the diagnosis of AEP was made. She was started on
methyl-
prednisolone 125mg intravenous every 6 hours. After two days
she

showed significant improvement and was switched to
prednisone 60mg
https://doi.org/10.1016/j.rmcr.2019.100825
Received 18 January 2019; Received in revised form 9 March
2019; Accepted 17 March 2019
∗ Corresponding author.
E-mail address: [email protected] (Z.L. Arter).
Respiratory Medicine Case Reports 27 (2019) 100825
2213-0071/ © 2019 Published by Elsevier Ltd. This is an open
access article under the CC BY-NC-ND license
(http://creativecommons.org/licenses/BY-NC-ND/4.0/).
T
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00825&domain=pdf
oral once daily. She fully recovered 6 days after starting
steroids, and
was discharged home on oral prednisone with subsequent
tapering. On
discharge, her vital signs and physical exam were within normal
limits.
A repeat chest x-ray performed on the day of discharge showed
sig-

nificant improvement of the airspace opacities bilaterally (Fig.
2).
3. Discussion
Since its original description in 1989 [4], fewer than two
hundred
AEP cases have been reported; there is a 2:1 male
predominance. AEP is
a challenging diagnosis to make since patients frequently appear
to
have a rapidly progressive infectious process with chest
radiographs
mimicking bacterial pneumonia. A diagnosis of AEP is based
upon
identification of characteristic symptoms, a detailed patient
history, a
thorough clinical evaluation, and eosinophilia on BAL [5,6].
Previous
studies have reported a close relationship between conventional
ci-
garette smoking and AEP [7–9]. The mechanism by which
cigarette
smoking induces AEP is suspected to be a strong inflammatory
stimulus
that recruits macrophages and neutrophils to lung tissue. This
induces
pro-inflammatory cytokines, such as interleukin (IL)- 5, IL-6,
IL-7, and
tumor necrosis factor, which may be the inciting event causing
eosi-
nophil-rich exudate within the alveoli [10,11].
E-cigarettes are gaining widespread popularity over the past few
years with 10.8 million adult users in the United States as of

2016 [12].
Recent studies have shown that the mechanism of inflammation
and
cytokine stimulation in e-cigarette users is similar to cigarette
smokers,
including elevation of IL-6 and IL-8 [13,14]. This raises
concerns that e-
cigarettes may induce AEP and other lung diseases, as their use
pro-
motes pulmonary inflammation by a mechanism similar to
traditional
cigarette smoking. Due to the wide variety of vaping devices
and fluid
brands (and constituent chemical compounds), more research is
re-
quired to determine the exact cause of e-cigarette induced AEP.
Physicians should consider AEP in previously healthy patients
with
hypoxic respiratory failure who have a history of recent e-
cigarette use.
Previous AEP cases have been associated with traditional
cigarettes [7],
pulmonary irritants [15], or military service in the Middle East
[16]. As
E-cigarette use becomes more prevalent, it may become a more
common trigger of AEP. In this case of clear association, the
patient had
no other traditional exposures which could cause AEP, leaving
e-ci-
garettes as the most likely causative irritant. One prior case of
e-ci-
garette-associated AEP was reported in a male patient in 2014
[17]; this
is the first case of AEP involving a female after use of e-
cigarettes. Al-

though most cases of AEP are diagnosed in the male population,
further
research may suggest whether AEP is more common in males
due to
confounding factors such as job preference and smoking
prevalence, or
organic factors.
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for harm and ben-
efit, Addiction 109 (11) (2014) 1801–1810.
[3] O. Rom, A. Pecorelli, G. Valacchi, A.Z. Reznick, Are E-
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(2015) 65–74.
[4] J.N. Allen, E.R. Pacht, J.E. Gadek, W.B. Davis, Acute
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569–574.
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[6] F. Philit, B. Etienne-Mastroianni, A. Parrot, C. Guerin, D.
Robert, J.F. Cordier,
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Care Med. 166 (9) (2002) 1235–1239.
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[8] H. Uchiyama, T. Suda, Y. Nakamura, et al., Alterations in
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(2008) 1174–1180.
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[13] C.A. Lerner, I.K. Sundar, H. Yao, et al., Vapors produced
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[14] Q. Wu, D. Jiang, M. Minor, H.W. Chu, Electronic cigarette
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Fig. 1. Computed tomography pulmonary angiogram showing
diffuse ground-
glass patchy airspace disease.
Fig. 2. Chest radiography before and after steroids treatment.
Top left and
right: Chest PA and lateral upright series before treatment. Note
made of bi-
basilar airspace opacities. Bottom left and right: Chest PA and
lateral upright
series after treatment. Significant interval decreased patchy
airspace disease
within the bilateral lungs.
Z.L. Arter, et al. Respiratory Medicine Case Reports 27 (2019)
100825
2
http://refhub.elsevier.com/S2213-0071(19)30026-7/sref1

9 (9) (2014) e108342.
[15] W.N. Rom, M. Weiden, R. Garcia, et al., Acute
eosinophilic pneumonia in a New
York City firefighter exposed to World Trade Center dust, Am.
J. Respir. Crit. Care
Med. 166 (2002) 797.
[16] A.F. Shorr, S.L. Scoville, S.B. Cersovsky, et al., Acute
eosinophilic pneumonia
among US Military personnel deployed in or near Iraq, J. Am.
Med. Assoc. 292
(2004) 2997.
[17] D. Thota, E. Latham, Case report of electronic cigarettes
possibly associated with
eosinophilic pneumonitis in a previously healthy active-duty
sailor, J. Emerg. Med.
47 (1) (2014) 15–17.
Z.L. Arter, et al. Respiratory Medicine Case Reports 27 (2019)
100825
3

http://refhub.elsevier.com/S2213-0071(19)30026-7/sref17Acute
eosinophilic pneumonia following electronic cigarette
useIntroductionCase reportDiscussionReferences
https://doi.org/10.1177/2333794X19833725
Global Pediatric Health
Volume 6: 1 –3
© The Author(s) 2019
Article reuse guidelines:
sagepub.com/journals-permissions
DOI: 10.1177/2333794X19833725
journals.sagepub.com/home/gph
Creative Commons Non Commercial CC BY-NC: This article is
distributed under the terms of the Creative Commons
Attribution-NonCommercial 4.0 License
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permits non-
commercial use, reproduction and distribution of the work
without further permission provided the original work is
attributed as specified
on the SAGE and Open Access pages
(https://us.sagepub.com/en-us/nam/open-access-at-sage).
Case Report and Literature Review
Introduction
Pulmonary cystic fibrosis (CF) is not a rare disease, but it
is a potentially life-threatening disease in children. The
most common cause is a genetic mutation on chromo-

some 7. Clinical symptoms may be aggravated by respi-
ratory tract infections. This study describes the case of a
15-year-old boy who suffered from a recurrent cough and
expectoration over a 10-year period, the underlying
cause of whose symptoms clearly being pulmonary CF,
as confirmed through genetic and sweat testing.
Case Presentation
On February 20, 2017, a 15-year-old boy with a 10-year
history of recurrent cough and expectoration was pre-
sented. A definitive diagnosis of pulmonary CF was
made through genetic testing (mutation on p.G970D)
and sweat testing at the Beijing Children’s Hospital in
2012. Additionally, a definitive diagnosis of hepatic cir-
rhosis was also made at the Beijing Children’s Hospital
6 years previously. The first episode of hematemesis
occurred in June 2017, which improved after an antibi-
otic’s regimen and hemostasis treatment.
Six days earlier, the patient’s parents reported he had
begun coughing again, accompanied by sticky white and
yellow sputum, chest pain and distress, nausea without
dyspnea, hemoptysis, and so on, and presented a fever,
which reached a maximum of 38.0°C. Chest and upper
abdomen computed tomography scans revealed double-
lung emphysema and mild bronchiectasis complicated by
multiple liver conditions including hepatic cirrhosis,
833725GPHXXX10.1177/2333794X19833725Global Pediatric
HealthHuang et al
case-report2019
1The Third Affiliated Hospital of Zunyi Medical College,
Zunyi, China

Corresponding Author:
Daishun Liu, Zunyi 563000, China.
Email: [email protected]
Recurrent Cough and Expectoration for
10 Years: A Case Report
Ting Huang, MD1 , Caihong Li, MD1, and Daishun Liu, PhD1
Abstract
Rationale. Most cases of cystic fibrosis occur in Europe, with
only a few occurring in Asia. Pulmonary cystic fibrosis
is not a rare disease, but in children it is a potentially life-
threatening condition. Children suffering from pulmonary
cystic fibrosis rarely survive to adulthood, and responses to
treatment are generally poor. The most common
cause of cystic fibrosis is a genetic mutation on chromosome 7.
Patient concerns. A 15-year-old boy with healthy
parents suffered from a recurrent cough and expectoration for
nearly 10 years. Six years previously, a definitive
diagnosis of pulmonary cystic fibrosis and hepatic cirrhosis was
made at the Beijing Children’s Hospital. The first
occurrence of hematemesis occurred 1 year ago. The main
symptoms, which caused this period of hospitalization,
were cough, expectoration, and hematemesis. Diagnoses. The
underlying cause was finally determined to be the
cystic fibrosis transmembrane conductance regulator gene
(p.G970D). After genetic and sweat testing performed
at the Beijing Children’s Hospital in 2012, a definitive
diagnosis of cystic fibrosis was made. Interventions. The patient
was administered hemostatic treatment, antibiotics, and cough
relief and sputum reduction therapy. Outcomes. The
patient’s condition rapidly improved and continued to remain
stable, though future relapse is possible following
respiratory tract infections. Lessons. This case indicates that in
the case of any child that presents a recurrent

cryptogenic cough and expectoration, whether accompanied by
hematemesis or not, pulmonary cystic fibrosis
should be considered. In order to determine underlying causes
and prepare for cystic fibrosis transmembrane
conductance regulator modulator therapy, genetic and sweat
testing are recommended to be conducted if available.
Keywords
pulmonary cystic fibrosis, hematemesis, cystic fibrosis
transmembrane conductance regulator
Received August 14, 2018. Received revised December 18,
2018. Accepted for publication December 31, 2018.
https://us.sagepub.com/en-us/journals-permissions
https://journals.sagepub.com/home/gph
mailto:[email protected]
2 Global Pediatric Health
collateral circulation formation, and a slight amount of
ascites. Examinations carried out on February 20, 2018,
indicated the following abnormalities: blood count (white
blood cell count = 10.3 × 109/L, hemoglobin = 131 g/L,
platelet = 130 × 109/L), liver functionality (total biliru-
bin = 136.9 µmol/L, aspartate transaminase = 76.9 U/L,
alanine transaminase = 63.5 U/L), levels of prothrombin
time (18.1 seconds), and activated partial thromboplastin
time (48.6 seconds). Other biochemical tests, including
C-reactive protein, were normal, and the serum G test was
positive (135.50 pg/mL). Pathogens including methicillin-
resistant Staphylococcus aureus, Pesudomonas pyocya-
neum, gram-positive cocci, fungi, and Mycoplasma
pneumonia immunoglobulin M were all detected from the
sputum culture, gram stain, serum G test, and respiratory

tract profile (immunoglobulin M), while tuberculosis was
absent from the sputum culture and tuberculin skin test.
The patient was diagnosed with bronchiectasis, compli-
cated by infection, CF lung, esophagogastric vein ligation
(postoperative), hepatic cirrhosis decompensation, chronic
disease-related malnutrition, hyperbilirubinemia, multi-
ple organ failure (heart, liver, lung), and acquired coagu-
lation dysfunction. These symptoms resolved after
administering antibiotics and nutritional supplementa-
tion. However, after a transfusion of approximately 250
mL of fresh blood on March 6, 2018, the patient suffered
a sudden episode of hematemesis, accompanied by dizzi-
ness, weakness, palpitations without fever, tachypnea,
and loss of consciousness. On admission the patient was
treated by hemostasis under endoscopic and other sup-
portive agents. The patient’s symptoms rapidly improved,
and he was soon discharged.
Figures 1 and 2 show respectively double-lung
emphysema, minor bronchiectasis complicated by infec-
tion, and diffuse liver diseases.
Discussion
CF is a genetic multi-organ disease predominantly char-
acterized by pulmonary involvement, typically resulting
in respiratory failure and premature death.1 Most patients
with pulmonary CF die from related complications, such
as respiratory failure or pulmonale.2 Recent advances in
genetic functions research and genetic testing have made
it possible to make accurate early diagnoses of suspected
CF and mutation-specific therapies, and the prospect of
truly personalized medicine enable patients to enjoy a
high quality of life, even into adulthood.
Pulmonary CF is characterized by inflammation and

reshaping of the airways in addition to mucus accumula-
tion, leading to respiratory symptoms such as coughing,
expectoration, chest distress, and shortness of breath. In
severe cases, respiratory failure and pulmonary heart
disease will follow.3,4 Diagnostic confirmation should
be focused on positive observation of suggestive clinical
features in both children and adults, but may also be
accomplished through positive sweat testing or review
of family history in the case of asymptomatic infants.1,5
The objective of CF treatment is to prevent respiratory
tract infection, reduce the quantity and viscosity of lung
mucus, improve breathing function, and maintain ade-
quate nutrition. When available, some patients may also
be treated using CF transmembrane conductance regula-
tors. Though cited as the most promising approach,
genetic-level treatment is currently lacking.
Four years ago, at age 11, the patient was accurately
diagnosed with pulmonary CF and hepatic cirrhosis, in
addition to other complications, which severely affected
his quality of life. If this diagnosis were to have been
made when he primarily presented a recurrent and unex-
plained cough, and if given appropriate treatment, his
Figure 1. Chest computed tomography. Figure 2. CT
examination for liver.
Huang et al 3
quality of life and life expectancy might be much better.
This case serves as a reminder that children with recur-
rent coughs and multiple organ damage should be iden-
tified with CF.

Author Contributions
TH: Contributed to conception and design; contributed to
acquisition; drafted manuscript; critically revised manuscript;
gave final approval; agrees to be accountable for all aspects of
work ensuring integrity and accuracy.
CL: Contributed to design; contributed to analysis; critically
revised manuscript; gave final approval; agrees to be account-
able for all aspects of work ensuring integrity and accuracy.
DL: Contributed to conception; contributed to analysis and
interpretation; critically revised manuscript; gave final
approval;
agrees to be accountable for all aspects of work ensuring integ-
rity and accuracy.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
article.
Funding
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
Ethical Approval
Ethical approval was obtained from the local ethics committee.
Informed Consent
Informed consent was obtained for this study.
ORCID iD

Ting Huang https://orcid.org/0000-0002-6277-6619
References
1. Castellani C, Duff AJA, Bell SC, et al. ECFS best prac-
tice guidelines: the 2018 revision. J Cyst Fibros. 2018;17:
153-178.
2. Burgel PR, Bellis G, Olesen HV, et al. Future trends in
cystic fibrosis demography in 34 European countries. Eur
Respir J. 2015;46:133-141.
3. Jiang K, Jiao S, Vitko M, et al. The impact of cystic fibro-
sis transmembrane regulator disruption on cardiac func-
tion and stress response. J Cyst Fibros. 2016;15:34-42.
4. Sander DB, Fink A, Mayer-Hamblett N, et al. Early
life growth trajectories in cystic fibrosis are associ-
ated with pulmonary function at age 6 years. J Pediatr.
2015;167:1081-1088.e1.
5. Farrell PM, White TB, Ren CL, et al. Diagnosis of cys-
tic fibrosis: consensus guidelines from the cystic fibrosis
foundation. J Pediatr. 2017;181S:S4-15.
https://orcid.org/0000-0002-6277-6619

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