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Mean Platelet Volume, Platelet Distribution Width,
and Platelet Count, in Connection with Immune
Thrombocytopenic Purpura and Essential
Thrombocytopenia
Eunyup Lee, MD, Miyoung Kim, MD*, Kibum Jeon, MD, Jiwon Lee, MD, Jee-Soo Lee, MD,
Han-Sung Kim, MD, Hee Jung Kang, MD, Young Kyung Lee, MD
Laboratory Medicine 2019;XX:1–7

DOI: 10.1093/labmed/lmy082

ABSTRACT
Objective: To examine the kinetic characteristics of platelet (PLT)
destruction and thrombopoiesis by using mean platelet volume (MPV)
and platelet distribution width (PDW).
Methods: Using the ADVIA2120i instrument, we measured PLT counts,
MPV, and PDW in 153 healthy individuals, 35 patients with immune
thrombocytopenic purpura (ITP), and 48 patients with essential
thrombocytopenia (ET).
Results: In the ITP group, the MPV and PDW were higher than those
values in healthy individuals. In the ET group, the MPV was lower
than in the ITP group and in healthy individuals, and the PDW was
lower than in the ITP group. When the ITP group was subdivided (PLT
counts <45 × 103/µL vs ≥ 45 × 103/µL), the MPV and PDW tended
to be higher in patients with PLT counts less than 45 × 103 per µL.
When patients with ET were subdivided (PLT counts <770 × 103/µL
vs ≥770 × 103/µL), the MPV and PDW were lower in patients with PLT
count of 770 or greater × 103 per µL.
Conclusions: In ITP, the overall PLT composition varies, and PLT
sequestration is nondiscriminatory. In ET, PLTs quickly shrink and remain
small, resulting in a high proportion of small-sized PLTs.
Keywords: thrombopoiesis, mean platelet volume, platelet
distribution width, immune thrombocytopenic purpura, essential
thrombocythemia, complete blood count

Chronic immune thrombocytopenic purpura (ITP) is charac-
terized by an immune-mediated isolated thrombocytopenia
that is caused by the destruction of platelets (PLTs) by Fc
receptor–bearing macrophages in the reticuloendothelial
system.1 Thrombopoiesis is usually observed in ITP and is a
Abbreviations
ITP, immune thrombocytopenic purpura; PLTs, platelets; ET, essential
thrombocythemia; rRNA, ribosomal RNA; MPV, mean platelet volume;
PDW, platelet distribution width; CBC, complete blood count; WHO, World
Health Organization; Hb, hemoglobin; MCV, mean corpuscular volume;
MCHC, mean corpuscular hemoglobin concentration; RDW, red-blood-
cell distribution width; WBC, white blood cell; MCH, mean corpuscular
hemoglobin; IQR, interquartile range
Department of Laboratory Medicine, Hallym University Sacred Heart
Hospital, Hallym University College of Medicine, Anyang, South Korea
*To whom correspondence should be addressed.
rabbit790622@gmail.com
result of megakaryocytes in the bone marrow compensating
for the peripheral destruction of PLTs.2
Conversely, essential thrombocythemia (ET) is character-
ized by a hyperproductive type of thrombocytosis. As a
myeloproliferative neoplasm, it is a clonal disorder chiefly
caused by JAK2, CALR, or MPL gene mutations. The
production of PLT precursors is markedly increased in the
bone marrow with a concomitant increase in the number
of dysplastic megakaryocytes; consequently, isolated
thrombocytosis is observed in the peripheral blood.3 It is
unknown whether the life span of the PLTs is affected by
this clonal process.
Although the PLT count by itself does not reveal the under-
lying pathomechanism, the volume and the distribution of
PLTs reflect the pathophysiology of PLT-associated dis-
orders. Immature, young PLTs that are newly released into
the circulating blood from bone marrow megakaryocytes

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are large, reticulated, and contain elevated levels of ribo-
somal RNA (rRNA).4 Thus, young PLTs can be differenti-
ated from older ones, which are smaller in size and have
reduced rRNA levels. Consequently, information on the
rates of thrombopoiesis and of PLT turnover can be de-
rived by determining the proportion of young PLTs in the
blood.5,6 Further, the activation of PLTs causes morphologic
changes, including in their spherical shape and pseudo-
podia formation, possibly affecting the PLT volume and size
distribution.7
Automated blood cell counters provide additional informa-
tion on circulating PLTs.8 Among several PLT parameters,
mean platelet volume (MPV) and platelet distribution width
(PDW) are the 2 most widely used indices. The results
from previous studies9,10 have shown that MPV and/or
PDW are helpful in distinguishing ITP from hypoproductive
thrombocytopenia, although Nakadate et al 11 reported that
neither the MPV nor PDW value differed in pediatric patients
with ITP vs those without ITP. Studies on PLT indices in
patients with ET are less common, and whether alterations
in MPV and/or PDW exist in ET is still controversial.3,12
Nevertheless, to our knowledge, no comprehensive studies
of the MPV and PDW values in ITP and ET, 2 diseases with
distinct PLT production pathophysiologic manifestations
(compensatory and intrinsic/clonal, respectively), exist.
In this study, we hypothesized that the MPV and PDW can
reflect the pathophysiological profiles of these 2 separate
diseases: hyperdestructive thrombocytopenia with compen-
satory thrombopoiesis in ITP, and hyperproductive thrombo-
cytosis with clonal thrombopoiesis in ET. In this first study
of its kind, we analyzed the MPV and PDW values in both
diseases and compared them, respectively, to those values
in healthy individuals.
Materials and Methods
Specimens
A total of 153 individuals whose complete blood count
(CBC) results were within the reference ranges and who
did not have any underlying diseases were enrolled in
the control group. The hyperdestructive-thrombocyto-
penia group comprised 35 patients with ITP, and the
2  
Lab Medicine 2019;XX;2–7
DOI: 10.1093/labmed/lmy082
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hyperproductive-thrombocytosis group comprised 48
patients with ET; none of the patients in either group had
previously received treatment. ET was diagnosed based
on bone-marrow examination and molecular study of JAK2
and/or CALR mutation status, as well as clinical obser-
vations and other laboratory data according to the World
Health Organization (WHO) classification.13
The specimens were collected randomly at Hallym Sacred
Heart Hospital, Anyang, South Korea, between January
2009 and April 2016. This study was approved by the
Institutional Review Board/Ethics Committee of Hallym
University Sacred Heart Hospital (IRB no. 2016-I030).
CBCs and Measurement of MPV and PDW
In the control group, CBCs (including simultaneous
measurements of MPV and PDW) were obtained using the
ADVIA2120i (Siemens AG) within 1 hour of specimen col-
lection according to manufacturer instructions. Hemoglobin
(Hb), mean corpuscular volume (MCV), mean corpuscular
hemoglobin concentration (MCHC), red blood cell distribu-
tion width (RDW), white blood cell (WBC) count, PLT count,
PDW, and MPV results were included in the analyses.
Statistics
The Shapiro-Wilk test was used to test for normality. Values
are expressed as mean (SD) for normally distributed data and
as medians (interquartile ranges) for non–normally distributed
data. We used Kruskal-Wallis and Mann-Whitney analyses
to compare CBC parameters (Hb, MCV, mean corpuscular
hemoglobin [MCH], MCHC, PDW, WBC, PLT count, and
MPV) among the 3 groups and their subgroups. Spearman
rank correlation analysis was used to determine associations
between parameters. We performed all statistical analyses
using SPSS software, version 22.0 (IBM Corporation). P val-
ues less than .05 were considered statistically significant.
Results
Patient Profile
The distributions of age, sex, and measured CBC parame-
ters, including Hb, MCVs, MCHCs, RDWs, WBCs, and PLTs,
from the study subject individuals are summarized in Table 1.
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Table 1. Demographics and Complete Blood Count Results of Healthy Individuals, Patients with ITP, and
Patients with ET
Variable Healthy Individuals ITP ET

(n = 153) (n = 35) (n = 48)

Age (y), mean (SD) 43.3 (20.4) 52.1 (35.9) 65.3 (32.5)
Sex, no. (M/F) 119/34 4/31 23/25
Hb (g/dL), median (IQR) 14.7 (13.8–15.2) 12.6 (10.8–14.3) 12.7 (11.5–14.2)
MCV (fL), median (IQR) 89.9 (87.8–92.2) 88.3 (86.0–90.4) 93.0 (88.2–100.3)
MCHC (g/dL), median (IQR) 34.7 (33.9–35.3) 34.5 (33.7–35.3) 33.0 (32.2–33.8)
RDW (%), median (IQR) 12.6 (12.3–12.9) 12.9 (12.5–13.9) 14.0 (13.3–14.9)
WBC/μL, median (IQR) 5960 (5010–6890) 7400 (4500–9600) 9000 (7400–12,425)
PLTs ×103/µL, median (IQR) 246 (213–274) 43 (16–73) 762 (589–954)
Abbreviations: ITP, immune thrombocytopenic purpura; ET, essential thrombocythemia; Hb, hemoglobin; IQR, interquartile range; MCV, mean corpuscular volume; MCHC, mean corpuscular
hemoglobin concentration; RDW, red blood cell distribution width; WBC, white blood cell; PLTs, platelets.

A B
P < .001 P = .048
P < .001 P < .001 P < .001 P < .001
13.5 85

75
11.5
MPV (fL)
MPV (fL)

65
9.5
55
7.5
45

5.5 35
Control ITP ET Control ITP ET
(n = 153) (n = 35) (n = 48) (n = 153) (n = 35) (n = 48)

Figure 1
Difference in platelet parameters among healthy individuals, patients with immune thrombocytopenic purpura (ITP), and patients with
essential thrombocythemia (ET). A, Mean platelet volume (MPV) in patients with immune thrombocytopenic purpura (ITP) vs in healthy
individuals. B, Platelet distribution width (PDW) in patients with essential thrombocythemia (ET) vs in healthy individuals.

Comparisons of PLT Indices (MPV and PDW) [7.7–8.9] fL; P <.001) (Figure 1A). Further, patients with ET
in Healthy Individuals and Patients with ITP showed higher PDW values than healthy individuals (Figure
and ET 1B). However, patients with ET showed significantly lower
PDW values than patients with ITP (54.1% [45.8%–60.0%]
MPV and PDW in ITP vs 66.3% [57.4%–70.1%]; P <.001).

The MPV in patients with ITP was 10.2 (8.6–11.0) fL, which
was significantly higher than the 8.8 (8.4–9.3) fL observed in
healthy individuals (P <.001) (Figure 1A). The PDW values in
patients with ITP (66.3% [57.4%–70.1%]) were significantly
higher than those in healthy individuals (50.5% [47.1%–
55.3%]) (Figure 1B).
MPV and PDW in ET
The MPV of patients with ET was significantly lower than
that in patients with ITP and that in healthy individuals (8.3
Correlations among MPV, PDW, and PLT Counts
in ITP and ET
Patients with ITP
When patients with ITP were subdivided into 2 groups
based on their PLT counts (<45 × 103/µL vs ≥ 45 × 103/µL),
there was no statistically significant difference in MPV or
PDW between the 2 groups (Table 2). On Spearman corre-
lation analysis, neither MPV nor PDW showed any signifi-
cant correlation with PLT counts (ρ = −0.129, P = .46 and

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DOI: 10.1093/labmed/lmy082
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Table 2. MPV, PDW, and PLT Counts in Patients with ITP and ET
Variable ITP
3 3
PLT <45 × 10 /µL PLT≥ 45 × 10 /µL
(n = 18) (n = 17)
MPV (fL), median (IQR) 10.5 (8.8–12.3) 9.4 (8.5–10.6)
PDW (%), median (IQR) 67.8 (58.4–72.0) 63.7 (57.1–69.0)
Abbreviations: MPV, mean platelet volume; PDW, platelet distribution width; PLT, platelet; ITP, immune thrombocytopenic purpura; ET, essential thrombocythemia; IQR, interquartile range.
ρ = −0.162, P = .35, respectively). The PDW and MPV were
moderately correlated with each other (ρ= 0.458, P = .006).
Patients with ET
When patients with ET were subdivided into 2 groups
according to their PLT counts (<770 × 103/µL or ≥
770 × 103/µL), MPV and PDW were significantly lower
in patients with ET who had PLT counts of 770 or
greater × 103 per µL than in those with counts less than
770 × 103 per µL (Table 2). The mean MPVs were 8.5
(7.8–9.2) fL in patients with ET who had PLT counts less
than 770 × 103 per µL and 8.1 (7.6–8.4) fL in those with
counts of 770 or greater × 103 per µL (P = .04). In contrast,
the PDWs were 57.1% (52.2%–64.3%) in patients with ET
who had PLT counts greater than 770 × 103 per µL and
50.2% (41.7%–57.3%) in patients with counts of 770 or
greater × 103 per µL (P = .008).
On Spearman correlation analysis, the MPV showed a weak
negative correlation with PLT counts (ρ = −0.394; P = .006),
as did the PDW (ρ = −0.492; P <.001). Also, the PDW and
MPV values showed moderate positive correlation with
each other (ρ = 0.609; P <.001).
Discussion
Previous studies of MPV or PDW focused on the discrim-
inatory power of the 2 indices, mostly in patients with
thrombocytopenia and sometimes in those with thrombo-
cytosis. Most of these studies did not compare the values
from patients with these disorders with the corresponding
values in healthy individuals. In our study, we hypothesized
that the MPV and PDW values of circulating PLTs reflect the
pathophysiology of these 2 diseases, which have different
mechanisms of altering PLT production.
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ET
3
P Value PLT <770 × 10 /µL PLT≥ 770 × 103/µL P Value
(n = 25) (n = 23)
.21 8.5 (7.8–9.2) 8.1 (7.6–8.4) .04
.14 57.1 (52.2–64.3) 50.2 (41.7–57.3) .008
The finding that we believe is most notable is that thrombo-
poiesis and PLT sequestration in ITP and ET involve com-
plex mechanisms. Patients with ITP showed higher MPV
and PDW values than healthy individuals, irrespective of
the instrument used. Previous studies have shown that the
PDW and/or MPV were higher in patients with ITP than in
those with thrombocytopenia of different pathologies, such
as hypoproductive thrombocytopenia. Keito et al14 reported
that MPV and PDW were significantly higher in ITP than
in aplastic anemia. Ntaios et al9 reported increased MPV
and PDW in patients with ITP, compared with patients with
hypoproductive thrombocytopenia. However, the aforemen-
tioned studies did not include comparisons to values from
healthy individuals. A possible explanation for the higher
MPV values in patients with ITP than in healthy individuals is
that the proportion of young, large PLTs is higher in ITP than
in normal conditions because of compensatory thrombo-
poiesis in the bone marrow in response to antibody-medi-
ated peripheral destruction.
We expected that PDW values in ITP would be low because
we theorized that the continuous destruction of peripheral
PLTs would eliminate already existing, relatively old PLTs
of smaller sizes; however, our data showed the opposite
result. This finding indicates that although the proportion of
young, large PLTs is increased in ITP, the high PDW shows
that the overall composition of the circulating PLTs varies,
with increased proportions of PLTs at both ends of their size
distribution. This, in turn, may be occurring because PLTs are
not necessarily targeted for destruction because of their older
age; rather, the process is nondiscriminatory. Hence, the dis-
tribution of the surviving PLTs in patients with ITP is not much
different from that in healthy individuals; however, the PDW is
higher because of excess younger PLTs. Future investigations
of individual PLT sizes and their life spans in patients with ITP
ought to yield clarity regarding these notions.
Further, we believed it was notable that the ranges of the
distributions of MPV and PDW values were wider in patients
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with ITP than in those with ET, demonstrating a larger
coefficient of variation in the former. Ours is the only study
to compare MPV and PDW in ITP and ET; therefore, this
finding is novel and could be attributed to the difference
in the rates of PLT production in the 2 diseases that have
distinct mechanisms for thrombopoiesis (compensatory vs
clonal). Compensatory thrombopoiesis in ITP is reactive and
therefore, it can be highly sporadic, whereas clonal throm-
bopoiesis in ET is a relatively stable process.
Another possible explanation for this phenomenon could
be that patients with ITP have lower PLT counts than those
with ET, and therefore, there are smaller denominators when
calculating the coefficient of variation, resulting in a larger
value. Further biological studies are required to validate
these hypotheses.
We subdivided patients with ITP into 2 groups according
to their PLT counts by using a PLT count cut-off value of
45 × 103 per µL, which is generally used to distinguish
severe from moderate thrombocytopenia in South Korea.
In most cases, MPV and PDW tended to be higher in
patients with lower PLT counts (<45 × 103/µL) than in
patients with higher counts (≥45 × 103/µL), despite that
the difference was not statistically significant. This finding
suggests that PLT destruction is increased in ITP, as
demonstrated by the higher PDW, and that compensatory
thrombopoiesis is more active, as demonstrated by the
higher MPV. Again, this hypothesis ought to be tested in a
future study.
In contrast, patients with ET showed lower PDW and MPV
than healthy individuals. This finding contrasted with our
expectation that MPV and PDW would be elevated in ET,
owing to the increased production of PLTs, and suggested
that clonal PLT production is a complex process. Regarding
MPV and PDW in ET, there are few previous studies with
which to compare our results. In an investigation comparing
MPV and PDW in ET, reactive thrombocytosis, and healthy
individuals, Sehayek et al15 reported that ET was character-
ized by a 5-fold increase in small PLTs less than 7.5 fL and a
3-fold increase in larger-sized PLTs, resulting in lower MPVs
in patients with ET than in those with reactive thrombocyto-
sis, who in turn had lower MPVs than healthy controls.
The findings of Sehayek et al may explain our observations.
However, a PDW of 10.5 or greater was reported in 50%,
21%, and 14% of patients with ET, patients with reactive
thrombocytosis, and healthy controls, respectively, in their
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study. In contrast, Arellano-Rodrigo et al12 reported that
patients with ET had significantly higher MPV values than
controls (n = 55 in each group). They also reported that the
PDW was elevated in patients with ET, which they attributed
to possible PLT activation and excessive heterogeneity in
PLT volume in those patients.
Our observations may suggest that newly generated young
PLTs in ET are not necessarily large as previously thought
but vary in size. Alternately, our observations may hint at the
speed at which PLTs decrease in size as they age. Although
the production of young, large PLTs is increased, these PLTs
quickly shrink and remain small for most of their life spans,
resulting in a high proportion of small-sized circulating PLTs
in ET. Because ET is a malignant, clonal process, PLTs gen-
erated in patients with this condition might not be the same
as those produced in normal or compensatory conditions,
in terms of size and lifespan.
Despite their statistical significance, the actual differences
in MPV and PDW values between healthy individuals and
patients with ET were fairly small (only 5.7% in MPV and
7.1% in PDW), in relation to the median values of healthy
individuals (ie, when the difference was expressed as a per-
centage using the median values of healthy individuals as
denominators). Therefore, our data may not be sufficiently
conclusive; hence, a further analysis with a larger number
of study subjects will be helpful to clarify and potentially
validate our findings.
The analysis of MPV and PDW in patients with ET divided
according to their PLT counts support our explanations,
as presented earlier herein, as do the findings of Sehayek
et al,15 who report that MPVs were found to be significantly
lower in patients with PLT counts of 770 or greater × 103
per µL than in those with PLT counts of less than 770 × 103
per µL. This finding suggests that the more advanced the
disease, the higher the proportion of relatively small-sized cir-
culating PLTs (as is the case in ET). This finding also suggests
that the increased production of PLTs does not necessarily
lead to a higher proportion of large PLTs but of small ones.
The PDW was also lower in patients with PLT counts of 770
or greater × 103 per µL than in those with counts less than
770 × 103 per µL, which suggests that the more advanced
the ET, the more uniform the sizes of the PLTs, with a
probable shift towards small-sized ones. Further studies
on the role of age on PLT sizes in healthy individuals and in
patients with ET would help address these theories.
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One limitation of our study was that the distributions of age
and sex in the healthy individual, ITP, and ET groups were
different. However, in a study of 306 individuals (101 male
and 205 female), Giovanetti et al16 showed that MPV and
PDW do not differ significantly with respect to sex and age
except when comparing those values in the 1- to 10-year-
old age group to those in most other age groups (the
10–20-year-old age group was the exception). Our analysis
also showed that neither the MPV nor the PDW correlates
with age and sex in healthy individuals.2
Another limitation of our study was that data on immature
platelet fractions (IPFs) were not included. The IPF among
circulating PLTs, which can be measured using automated
hematologic analyzers, directly reflects the status of throm-
bopoiesis from the bone marrow. The results from previous
studies6,8,17,18 showed that the IPF could be a useful marker
for distinguishing ITP from other types of thrombocytopenia,
including acute lymphoblastic leukemia, thrombocytopenia
due to chemotherapy, bone-marrow failure, or hereditary
macrothrombocytopenia. Further, IPF predicts PLT recovery
and can thus serve as a gauge for requiring PLT transfusion
in patients who undergo hematopoietic stem-cell trans-
plantation or chemotherapy.19,20 Studies of IPF in patients
with ET are relatively rare; Kissova et al21 showed that IPF
positively correlated with JAK2 V617F mutation status and
thrombotic complications.
Because our study was performed retrospectively in
patients lacking IPF data, we were not able to assess their
IPF status, despite that doing so would have provided
useful information. Nevertheless, our study has the advan-
tage of having analyzed MPV and PDW in the context of
understanding PLT biology in ITP and ET—these param-
eters reflect the overall features of immature and mature
circulating PLTs. Further, both these parameters indirectly
reflect IPF to some extent. A future study that includes IPF
data will be helpful in potentially elucidating PLT biology in
terms of the pathophysiologies of ITP and ET.
In conclusion, we discovered alterations in the composition
of the circulating PLTs of patients with ITP and those with
ET using MPV and PDW values; to our knowledge, this
study (in which we also compared healthy individuals) is
the first of its kind. MPV and PDW were increased in ITP,
suggesting an upregulation in the production of young, large
PLTs in conjunction with the indiscriminate destruction of
circulating PLTs regardless of their age. Separately, MPV
and PDW were decreased in patients with ET, suggesting
6  
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that the proportion of small PLTs was higher than normal
although PLT production is increased. The more severe the
disease, the stronger the tendency for the MPV and/or PDW
to be altered—this principle is consistent with our interpre-
tations herein. LM
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DOI: 10.1093/labmed/lmy082