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


Lab Med. 2019;50(3):279-285. 

In This Article

Abstract and Introduction


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.


Chronic immune thrombocytopenic purpura (ITP) is characterized 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 result of megakaryocytes in the bone marrow compensating for the peripheral destruction of PLTs.[2]

Conversely, essential thrombocythemia (ET) is characterized 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 underlying pathomechanism, the volume and the distribution of PLTs reflect the pathophysiology of PLT-associated disorders. Immature, young PLTs that are newly released into the circulating blood from bone marrow megakaryocytes are large, reticulated, and contain elevated levels of ribosomal RNA (rRNA).[4] Thus, young PLTs can be differentiated 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 derived 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 pseudopodia formation, possibly affecting the PLT volume and size distribution.[7]

Automated blood cell counters provide additional information 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 studies[9,10] 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 compensatory thrombopoiesis in ITP, and hyperproductive thrombocytosis 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.