Histiocytic pleural effusion: the strong clue to malignancy

Abstract

Background
There have been many studies on the clinical characteristics of neutrophilic, lymphocytic, and/or eosinophilic pleural effusion. While caring for patients with pleural effusion, we found that histiocytic pleural effusion (HisPE) was not uncommon. However, few studies have explored HisPE. The purpose of the present study was to determine the clinical characteristics and etiologies of HisPE.

Methods
In this retrospective study, HisPE was defined as pleural fluid white blood cells comprised of ≥ 50% histiocytes. Using a clinical data warehouse, patients with HisPE among all patients aged >18 years who underwent thoracentesis and pleural fluid analysis between January 2010 and December 2019 at Ulsan University Hospital were enrolled. A total of 295 (9.0%) of 3279 patients who underwent thoracentesis were identified as HisPE patients. Among them, 201 with exudative HisPE were included. Clinical characteristics and etiologies were extracted from medical records and analyzed.

Results
Among the 201 patients with exudative HisPE, the major causes were malignant pleural effusion ( n = 102 [50.7%]), parapneumonic effusion ( n = 9 [4.5%]), and tuberculous pleurisy ( n = 9 [4.5%]). In the 102 patients with malignant pleural effusion, the main types of cancer were lung ( n = 42 [41.2%]), breast ( n = 16 [15.7%]), and stomach cancer ( n = 11 [10.8%]). Among lung cancers, adenocarcinoma ( n = 34 [81.0%]) was the most common histology.

Conclusions
The leading cause of exudative HisPE was malignancy, particularly lung cancer. Physicians should consider the possibility of malignant disease if histiocytes are predominantly present in pleural effusion.

Full text

R E S E A R C H Open Access
Histiocytic pleural effusion: the strong clue
to malignancy
Ganghee Chae
1†
, Jae-Bum Jun
2†
, Hwa Sik Jung
3
, Chui Yong Park
1
, Jin Hyoung Kim
4
, Byung Ju Kang
4
,
Hyeon Hui Kang
4
, Seung Won Ra
4
, Kwang Won Seo
4
, Yangjin Jegal
4
, Jong Joon Ahn
4
, Sang Hyuk Park
5
and
Taehoon Lee
4*
Abstract
Background: There have been many studies on the clinical characteristics of neutrophilic, lymphocytic, and/or
eosinophilic pleural effusion. While caring for patients with pleural effusion, we found that histiocytic pleural
effusion (HisPE) was not uncommon. However, few studies have explored HisPE. The purpose of the present study
was to determine the clinical characteristics and etiologies of HisPE.
Methods: In this retrospective study, HisPE was defined as pleural fluid white blood cells comprised of ≥50%
histiocytes. Using a clinical data warehouse, patients with HisPE among all patients aged >18 years who underwent
thoracentesis and pleural fluid analysis between January 2010 and December 2019 at Ulsan University Hospital were
enrolled. A total of 295 (9.0%) of 3279 patients who underwent thoracentesis were identified as HisPE patients.
Among them, 201 with exudative HisPE were included. Clinical characteristics and etiologies were extracted from
medical records and analyzed.
Results: Among the 201 patients with exudative HisPE, the major causes were malignant pleural effusion (n= 102
[50.7%]), parapneumonic effusion (n= 9 [4.5%]), and tuberculous pleurisy (n= 9 [4.5%]). In the 102 patients with
malignant pleural effusion, the main types of cancer were lung (n= 42 [41.2%]), breast (n= 16 [15.7%]), and
stomach cancer (n= 11 [10.8%]). Among lung cancers, adenocarcinoma (n= 34 [81.0%]) was the most common
histology.
Conclusions: The leading cause of exudative HisPE was malignancy, particularly lung cancer. Physicians should
consider the possibility of malignant disease if histiocytes are predominantly present in pleural effusion.
Keywords: Histiocytes, Thoracentesis, Pleural effusion, Exudate, Malignancy
Background
The pleural space typically contains only a few milliliters
of pleural fluid, which is not visible on imaging studies.
Thus, the detection of fluid in the pleural space on im-
aging studies is abnormal. Many conditions are associated
with pleural fluid accumulation, and the most useful
method for the differential diagnosis of pleural effusion
(PE) is a diagnostic thoracentesis [1,2]. Via diagnostic
thoracentesis, PE can be categorized as transudate or ex-
udate according to Light’s criteria [3]. Transudative PE is
a secondary manifestation of extrapulmonary systemic dis-
eases that induce volume overload; therefore, further
pleural fluid examination is generally not needed. In con-
trast, exudative PE is predominantly caused by a primary
disease of the lung or pleura and requires further diagnos-
tic investigations. Among them, the differential count of
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data made available in this article, unless otherwise stated in a credit line to the data.
* Correspondence: tleepulalg@uuh.ulsan.kr
†
Ganghee Chae and Jae-Bum Jun contributed equally to this manuscript as
the first authors.
4
Division of Pulmonary and Critical Care Medicine, Department of Internal
Medicine, Ulsan University Hospital, University of Ulsan College of Medicine,
877 Bangeojinsunhwando-ro, Dong-gu, Ulsan 44033, Korea
Full list of author information is available at the end of the article
Chae et al. World Journal of Surgical Oncology (2021) 19:180
https://doi.org/10.1186/s12957-021-02296-1
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

pleural fluid white blood cells (WBCs) aids differentiation
of the causal diseases. Pleural fluid WBCs include neutro-
phils, lymphocytes, eosinophils, and other mononuclear
cells such as histiocytes [2,4,5].
The characteristics and causes of neutrophilic,
lymphocytic, and eosinophilic PE are relatively well-
established [4–6]. However, although histiocytic pleural
effusion (HisPE) is not uncommon in clinical practice,
few studies have explored HisPE. Therefore, the aim of
the present study was to determine the clinical charac-
teristics and etiologies of HisPE.
Methods
Study design and population
This was a retrospective cross-sectional study. All patients
aged >18 years who underwent thoracentesis and pleural
fluid analysis between January 2010 and December 2019
at Ulsan University Hospital were initially collected (n=
3279). We defined HisPE as when histiocytes comprised
≥50% of the differential count of pleural fluid WBCs; using
this definition, 295 (9.0%) of 3279 patients were identified
as HisPE patients. Among the 295 patients with HisPE,
Light’s criteria were used to exclude patients with transu-
dative HisPE (n= 90). Those with missing data (n=4)
were also excluded. Accordingly, 201 exudative HisPE pa-
tients were enrolled and analyzed.
Data collection
Initial patient data were collected from a clinical data-
base platform in conjunction with the electronic medical
records at Ulsan University Hospital (Ulsan University
Hospital Information of Clinical Ecosystem [uICE]). The
collected data included age, sex, smoking status, pleural
fluid differential cell count of WBCs, red blood cell
(RBC) count, adenosine dehydrogenase (ADA), protein
and lactate dehydrogenase (LDH), and serum protein
and LDH.
In order to determine the final diagnosis (i.e., causes of
HisPE), a detailed chart review of individual patients was
conducted. The following criteria were used for the
causes of HisPE: Malignant PE was defined as when
pleural fluid cytology or pleural biopsy confirmed malig-
nancy, or when a patient was previously diagnosed with
cancer and also had PE but PE could not be explained
by other causes [7]. Tuberculous pleurisy was defined as
when the Mycobacterium tuberculosis was isolated from
the respiratory specimens or pleural fluid using any
mycobacterial culture or molecular method, or when PE
was improved by antituberculosis treatment after a clin-
ical diagnosis of tuberculosis by a physician [8]. Para-
pneumonic effusion was defined as when a patient
diagnosed with pneumonia had simultaneous PE and did
not meet the definition of malignant PE or tuberculous
pleurisy [7]. PE due to heart failure, liver cirrhosis, or
renal failure was defined as when individual diseases
were identified, and PE improved following treatments
for the individual diseases. Miscellaneous PE referred to
PE due to other uncommon specific causes (e.g., chy-
lothorax, traumatic hydrothorax, hemothorax, acute
pancreatitis, drug-induced PE, atelectasis, other infec-
tious diseases). Lastly, idiopathic PE was defined as when
the above definitions were not met.
The present study was approved by the Institutional
Review Board of Ulsan University Hospital (IRB number:
UUH 2020-04-028).
Pleural fluid processing
Pleural fluid samples were collected in EDTA tubes and
immediately sent to the laboratory at ambient
temperature. Manual cell counts were performed using a
hemocytometer at high magnification (×400) under a
light microscope, and the cell suspension of pleural fluid
was adjusted to an optimal concentration (approximately
5.0 × 10
5
cells/mL). The suspension was then cytocentri-
fuged at 600 rpm for 5 min (Cellspin; Hanil Science In-
dustrial, Korea), and the preparations were stained with
Wright-Giemsa stain. The differential count of WBCs
was determined by counting 100 cells under a light
microscope (×400). Lymphocytes, neutrophils, histio-
cytes, eosinophils, mesothelial cells, malignant cells, and
atypical cells were differentiated (Figs. 1and 2).
Data analysis
Results were derived through descriptive analyses, and
data are expressed as numbers (percentages) and me-
dians (interquartile range [IQR]).
Fig. 1 Microscopic image of histiocytes in pleural fluid (Wright-Giemsa
stain, ×1000). Histiocytes can be observed as single or grouped cells,
and their sizes vary considerably, ranging from approximately 15 to
100 μm in diameter. The nucleus (a) is located on one side of the
cytoplasm in a distorted form or a kidney shape. The cytoplasm
contains vacuoles (b) and ingested red blood cells (c) and has an
unclear boundary
Chae et al. World Journal of Surgical Oncology (2021) 19:180 Page 2 of 7
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Results
Among the 201 exudative HisPE patients, the most com-
mon diagnosis was malignant PE (n= 102 [50.7%]),
followed by idiopathic PE (n= 36 [17.9%]); PE due to
heart failure, liver cirrhosis, or renal failure (n=24
[11.9%]); miscellaneous PE (n= 21 [10.4%]); parapneu-
monic effusion (n= 9 [4.5%]); and tuberculous pleurisy
(n= 9 [4.5%]).
The baseline characteristics of exudative HisPE pa-
tients, with the exception of miscellaneous and idio-
pathic conditions are presented in Table 1. Patients with
parapneumonic effusion were older than those with
other causes. The proportions of females and non-
smokers were higher among patients with malignant PE,
which is thought to be due to the high incidence of
breast cancer in our study. In comparison, the propor-
tion of males was higher among those with PE due to
heart failure, liver cirrhosis, or renal failure.
In the pleural fluid analysis, there was no apparent dif-
ference in the RBC count, but the WBC count was
higher among patients with parapneumonic effusion
than those with other causes. Additionally, in the differ-
ential count of pleural fluid WBCs, the parapneumonic
effusion group had a slightly higher proportion of neu-
trophils than lymphocytes (histiocytes 66.0%, neutrophils
10.0%, lymphocytes 7.0%). Meanwhile, patients with ma-
lignant PE and tuberculous pleurisy had a higher pro-
portion of lymphocytes than neutrophils (malignant PE:
histiocytes 62.5%, neutrophils 5.0%, lymphocytes 16.5%;
tuberculous pleurisy: histiocytes 69.0%, neutrophils 5.0%,
lymphocytes 19.0%). The proportion of mesothelial cells
was very low in all groups. In addition, the pleural fluid
ADA level was markedly higher among those with tuber-
culous pleurisy than those with other causes (IU/L, me-
dian [IQR]: tuberculous pleurisy, 71.4 [47.1–107.1];
malignant PE, 24.7 [15.9–34.3]; parapneumonic effusion,
27.0 [17.7–38.0]; heart failure, liver cirrhosis, or renal
failure, 14.5 [9.4–19.3]). Further, the pleural fluid protein
level was markedly lower in those with PE due to heart
failure, liver cirrhosis, or renal failure relative to those
with other causes (g/dl, median [IQR]: heart failure, liver
cirrhosis, or renal failure, 2.8 [1.7–3.3]; malignant PE,
4.2 [3.4–4.6]; parapneumonic effusion, 4.3 [3.9–5.0]; tu-
berculous pleurisy, 3.5 [2.9–3.7]). The pleural fluid LDH
level was higher in those with malignant PE than in
those with other causes (IU/L, median [IQR]: malignant
PE, 305.0 [202.0–706.5]; parapneumonic effusion, 254.0
[184.0–361.0]; tuberculous pleurisy, 207.0 [179.0–266.0];
heart failure, liver cirrhosis, or renal failure, 173.0
[138.0–219.0]). There was no apparent difference in the
serum protein level, but the serum LDH level was higher
among those with PE due to heart failure, liver cirrhosis,
or renal failure than those with other causes (IU/L, me-
dian [IQR]: heart failure, liver cirrhosis, or renal failure,
492.0 [277.0–685.0]; malignant PE, 317.0 [210.0–435.0];
parapneumonic effusion, 149.0 [128.0–212.0]; tubercu-
lous pleurisy, 331.0 [191.0–488.0]).
Regarding cancer types among the 102 patients with
malignant PE, lung cancer (n= 42 [41.2%]), breast cancer
(n= 16 [15.7%]), and stomach cancer (n= 11 [10.8%])
were the most common causes (Fig. 3). Among lung
cancers, which was the most common cause of malig-
nant PE, adenocarcinoma (n= 34 [81.0%]) was the most
common histology, followed by small cell lung cancer
Fig. 2 Microscopic image of white blood cells in pleural fluid (Wright-Giemsa stain, ×400). Histiocytes (a) appear as described in Fig. 1. Neutrophils (b)
are 12–14 μm in diameter and appear larger than the surrounding RBCs. They have a single nucleus, which contains 2–5 lobes, and their cytoplasm
has many granules. Lymphocytes (c) are small (approximately 6–9μm) and have a spherical nucleus. The cytoplasm is small and basophilic
Chae et al. World Journal of Surgical Oncology (2021) 19:180 Page 3 of 7
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(n= 4 [9.5%]), squamous cell carcinoma (n= 3 [7.1%]),
and non-small cell lung cancer—not otherwise specified
(n= 1 [2.4%]).
Thoracentesis for exudative HisPE patients was typic-
ally performed in the general ward (66.7%) and emer-
gency room (30.6%). There was no apparent difference
in the location according to the causal disease (Table 2).
In addition, when confirming the component to which
Light’s criteria were applied, both the protein and LDH
criteria were mostly satisfied among those with malig-
nant PE (60.8%), parapneumonic effusion (66.7%), and
tuberculous pleurisy (66.7%). In comparison, those with
PE due to heart failure, liver cirrhosis, or renal failure
generally satisfied only the LDH criteria (66.7%)
(Table 3).
Discussion
This study aimed to determine the clinical characteris-
tics and etiologies of HisPE. We found that HisPE was
not uncommon (9.0%) among patients with PE, and
>50% of exudative HisPE cases were caused by malig-
nancy (50.7%). The major malignancies were lung can-
cer, breast cancer, and stomach cancer. Thus, physicians
must consider the possibility of underlying cancer if they
encounter HisPE.
In a previous study on the cellular content of pleural
fluid from patients with normal pleura who were under-
going thoracoscopy for hyperhidrosis, approximately
75% of the cells in the pleural fluid were macrophages,
belonging to histiocytes [9]. That is, histiocytes com-
prised a considerable proportion of normal pleural fluid.
However, the characteristics and etiologies of patients
with HisPE due to pathologic conditions have not been
studied. In the present study, we defined HisPE as when
histiocytes comprised 50% or more of the pleural fluid
WBCs. In our clinical experience, we have found that
HisPE is not uncommon, and felt that it is associated
with malignant PE. We presumed that pleural metastasis
of cancer would trigger immune responses and induce
reactive histiocytic proliferation [10]. Thus, we started
this study because of this insightful experience.
Previous studies investigating HisPE consist of only
case reports. One such report observed proliferating his-
tiocytes in the pleural fluid with no palpable lymphaden-
opathy or organomegaly; this was an atypical case of
Rosai-Dorfman disease (also known as sinus histiocytosis
with massive lymphadenopathy), which involves the
overproduction of non-Langerhans sinus histiocytes
[11]. Another case report described histiocytic prolifera-
tion mimicking metastatic signet ring cell
Table 1 Baseline characteristics of patients with exudative HisPE
Malignant PE Parapneumonic effusion Tuberculous pleurisy Heart failure, liver cirrhosis, or renal failure
Number 102 (50.7) 9 (4.5) 9 (4.5) 24 (11.9)
Age (years) 62.0 (52.0–74.0) 71.0 (64.0–73.0) 63.0 (54.0–79.0) 64.5 (54.0–79.0)
Sex
Male 49 (48.0) 5 (55.6) 5 (55.6) 17 (70.8)
Female 53 (52.0) 4 (44.4) 4 (44.4) 7 (29.2)
Smoking status
Non-smoker 64 (62.7) 4 (44.4) 3 (33.3) 9 (37.5)
Current/ex-smoker 8 (7.8)/30 (29.4) 2 (22.2)/3 (33.3) 2 (22.2)/4 (44.4) 7 (29.2)/8 (33.3)
Pleural fluid
RBC (/uL) 3750 (740–27000) 6240 (70–11,200) 560 (250–3800) 495 (180–7110)
WBC (/uL) 460 (200–1000) 2500 (430–3680) 570 (310–720) 320 (105–560)
Histiocyte (%) 62.5 (55.0–70.0) 66.0 (53.0–78.0) 69.0 (62.0–74.0) 63.0 (55.0–77.5)
Neutrophil (%) 5.0 (2.0–12.0) 10.0 (3.0–12.0) 5.0 (2.0–6.0) 2.0 (1.0–6.5)
Lymphocyte (%) 16.5 (10.0–26.0) 7.0 (1.0–11.0) 19.0 (11.0–28.0) 16.0 (10.0–29.5)
Mesothelial cell (%) 0.0 (0.0–2.0) 0.0 (0.0–15.0) 0.0 (0.0–1.0) 0.5 (0.0–11.0)
ADA (IU/L) 24.7 (15.9–34.3) 27.0 (17.7–38.0) 71.4 (47.1–107.1) 14.5 (9.4–19.3)
Protein (g/dL) 4.2 (3.4–4.6) 4.3 (3.9–5.0) 3.5 (2.9–3.7) 2.8 (1.7–3.3)
LDH (IU/L) 305.0 (202.0–706.5) 254.0 (184.0–361.0) 207.0 (179.0–266.0) 173.0 (138.0–219.0)
Serum
Protein (g/dL) 6.2 (5.6–6.6) 6.4 (5.6–7.3) 6.1 (6.0–6.6) 6.3 (5.5–6.7)
LDH (IU/L) 317.0 (210.0–435.0) 149.0 (128.0–212.0) 331.0 (191.0–488.0) 492.0 (277.0–685.0)
Data are presented as n (%) or median (interquartile range)
HisPE histiocytic pleural effusion, PE pleural effusion, RBC red blood cell, WBC white blood cell, ADA adenosine deaminase, LDH lactate dehydrogen ase
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adenocarcinoma and highlighted the importance of dif-
ferentiation between histiocytic proliferation and signet
ring cell carcinoma [12]. There was also a report of his-
tiocytic sarcoma presenting with HisPE. In this case re-
port, a patient presented with anterior mediastinal
tumor accompanied by HisPE, and the cause of the mass
was histiocytic sarcoma [13].
The term “histiocytes”was originally used to describe
the large cells commonly found in the lymph nodes and
spleen that were morphologically nonspecific. Currently,
histiocytes are considered to be tissue macrophages that
are differentiated from the monocyte lineage, including
alveolar macrophages in the lung, Kupffer cells in the
liver, Langerhans cells in the skin, and dendritic cells in
the germinal centers of lymph nodes [14]. These cells
(histiocytes) play an important role in antigen presenta-
tion, phagocytosis, and removal of pathogens and cellu-
lar debris, and can be found anywhere on the human
body including the PE [15,16].
There are two situations in which histiocytes could
increase: reactive and neoplastic histiocytic prolifera-
tion [10]. Neoplastic proliferation refers to the clonal
proliferation of histiocytes, such as acute/chronic
myelomonocytic leukemia, acute monocytic leukemia,
and histiocytic sarcoma [10]. Reactive proliferation is
caused by inflammatory responses secondary to infec-
tion, autoimmune diseases, or malignancies. Granu-
loma is a representative reactive proliferation, wherein
Table 2 Location of thoracentesis in patients with exudative HisPE
Malignant PE
(n= 102)
Parapneumonic effusion
(n=9)
Tuberculous pleurisy
(n=9)
Heart failure, liver cirrhosis, or renal
failure (n= 24)
Total (n=
144)
General ward 74 (72.5) 6 (66.7) 4 (44.4) 12 (50.0) 96 (66.7)
Intensive care
unit
0 (0) 1 (11.1) 0 (0) 3 (12.5) 4 (2.8)
Emergency
room
28 (27.5) 2 (22.2) 5 (55.6) 9 (37.5) 44 (30.6)
Data are presented as n (%)
HisPE histiocytic pleural effusion, PE pleural effusion
Fig. 3 Distribution of the causes of malignancy in histiocytic pleural effusion (n= 102). Among the 102 patients with malignancy and histiocytic pleural
effusion, the causes of cancer were as follows: lung cancer (n= 42 [41.2%]), breast cancer (n= 16 [15.7%]), stomach cancer (n= 11 [10.8%]), biliary and pancreas
cancer (n= 7 [6.9%]), colorectal cancer (n= 5 [4.9%]), ovary and cervix cancer (n= 4 [3.9%]), and other malignancies (n= 17 [16.7%])
Chae et al. World Journal of Surgical Oncology (2021) 19:180 Page 5 of 7
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histiocytes fuse to form giant cells [10]. Severe in-
flammation may cause hemophagocytic lymphohistio-
cytosis via hypercytokinemia [16].
The causative mechanism of reactive histiocytosis is
poorly understood. It is presumed that histiocytes, which
are antigen-presenting cells, are likely increased by anti-
genic or microbial stimuli [14]. In the current study, his-
tiocytes were primarily increased in those with PE
caused by malignant tumors (50.7% of all exudative
HisPE). The mechanism of histiocytosis in malignant PE
seems to be associated with the immune response to
cancer (cancer cells as antigens) [10].
Further, in our study, lung cancer was the most com-
mon cause of malignant PE (41.2%), followed by breast
cancer (15.7%) and stomach cancer (10.8%). It is re-
ported that lung cancer, breast cancer, and lymphoma
account for most cases of malignant PE [2,17]. How-
ever, it is rather interesting that stomach cancer was the
third most common cause in our study. This is thought
to be due to the higher incidence of stomach cancer in
South Korea than in other countries [18]. In addition, it
is known that malignant PE can occur in all types of
lung cancer, but adenocarcinoma is the most common
cause [19,20]. The present study confirmed that adeno-
carcinoma is the most common cause (81.0%) of lung
cancer-induced malignant PE.
Aside from malignancy, in the present study, HisPE
occurred in patients with parapneumonic effusion (4.5%)
and tuberculous pleurisy (4.5%). These diseases must be
differentiated by using a variety of clinical situations.
However, our findings provide some insights. In para-
pneumonic effusion, neutrophils were the second most
common WBCs after histiocytes, whereas in tuberculous
pleurisy, the most common cell type was lymphocytes.
In tuberculous pleurisy, a prominent rise in ADA was
also observed. These findings could aid discrimination of
the causative disease of HisPE. Moreover, there were
multiple cases of PE due to heart failure, liver cirrhosis,
or renal diseases (11.9%). However, since we only ap-
plied Light’s criteria, approximately 25% of transudative
PE could have been misclassified as exudative PE [2].
Further consideration of the serum-pleural fluid protein
gradient as well as Light’s criteria would have
significantly reduced the proportion of PE due to heart
failure, liver cirrhosis, or renal diseases.
This study has some limitations. First, this was a retro-
spective study. Second, it was conducted at a single cen-
ter and the sample was small. It is necessary to confirm
whether the HisPE characteristics identified herein can
be replicated through prospective studies involving a
large number of PE patients. In addition, further studies
are needed to determine the mechanism by which histio-
cytes reactively increase in PE.
Conclusions
In conclusion, the leading cause of exudative HisPE was
malignancy, particularly lung cancer. Physicians should
consider the possibility of malignant diseases if histio-
cytes are predominantly present in pleural fluid analysis.
Acknowledgements
Not applicable
Authors’contributions
GC, JJ, and TL conceived the study concept and planned the design as the
principal investigator. GC, SHP, and TL analyzed the data. GC and JJ wrote
the manuscript draft. HSJ, CYP, JHK, BJK, HHK, SWR, KWS, YJ, and JJA
provided their critical comments to improve the manuscript. The authors
read and approved the final manuscript for submission.
Funding
None
Availability of data and materials
The datasets used and/or analyzed during the current study are available
from the corresponding author on reasonable request.
Declarations
Ethics approval and consent to participate
This study was approved by the Institutional Review Board of Ulsan
University Hospital (UUH 2020-04-028).
Consent for publication
Not applicable
Competing interests
The authors declare that they have no competing interests.
Author details
1
Department of Pulmonary and Critical Care Medicine, Asan Medical Center,
University of Ulsan College of Medicine, Seoul, Republic of Korea.
2
Division of
Infectious Diseases, Department of Internal Medicine, Ulsan University
Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea.
3
Division of Pulmonary and Critical Care Medicine, Department of Internal
Table 3 Component to which Light’s criteria are applied in exudative HisPE
Malignant PE
(n= 102)
Parapneumonic
effusion (n=9)
Tuberculous
pleurisy (n=9)
Heart failure, liver cirrhosis, or renal
failure (n= 24)
Total (n=
144)
Only protein criteria
a
19 (18.6) 1 (11.1) 1 (11.1) 5 (20.8) 26 (18.1)
Only LDH criteria
b
21 (20.6) 2 (22.2) 2 (22.2) 16 (66.7) 41 (28.5)
Both protein and LDH
criteria
62 (60.8) 6 (66.7) 6 (66.7) 3 (12.5) 77 (53.5)
Data are presented as n (%)
HisPE histiocytic pleural effusion, PE pleural effusion, LDH lactate dehydrogenase
a
The ratio of pleural fluid to serum protein is over 0.5
b
The ratio of pleural fluid to serum LDH is over 0.6 or the absolute pleural fluid LDH level is over 2/3 of the upper normal limit
Chae et al. World Journal of Surgical Oncology (2021) 19:180 Page 6 of 7
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Medicine, Samsung Medical Center, Sungkyunkwan University School of
Medicine, Seoul, Republic of Korea.
4
Division of Pulmonary and Critical Care
Medicine, Department of Internal Medicine, Ulsan University Hospital,
University of Ulsan College of Medicine, 877 Bangeojinsunhwando-ro,
Dong-gu, Ulsan 44033, Korea.
5
Department of Laboratory Medicine, Ulsan
University Hospital, University of Ulsan College of Medicine, Ulsan, Republic
of Korea.
Received: 17 April 2021 Accepted: 9 June 2021
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