Alcoholic fatty liver disease and alcoholic liver cirrhosis may be differentiated with mean platelet volume and platelet distribution width

To the Editor

We read with interest the article by Ozhan and colleagues on mean platelet volume in patients with non-alcoholic fatty liver disease [1]. In this article, they stated that mean platelet volume (MPV) was significantly increased in patients with non-alcoholic fatty liver disease (NAFLD) compared to control subjects.

MPV and platelet distribution width (PDW) are the platelet indices measured by automatic cell analyser and this may be helpful to distinguish hypoproductive thrombocytopenia (aplastic anemia) and hyperproductive thrombocytopenia (idiopathic thrombocytopenic purpura) and for the differential diagnosis of thrombocytosis [2–4], as well as to predict the prognosis of coronary artery disease. Recently, Yazici et al. reported that MPV reflects the disease activity of rheumatoid arthritis [5].

We aimed to observe whether platelet indices are helpful in distinguishing fatty liver disease from liver cirrhosis. To do so, we selected 241 healthy control subjects, 200 patients with NAFLD, 55 patients with alcoholic fatty liver disease (AFLD) and 48 patients with alcoholic liver cirrhosis (ALC) and measured platelet count (PLT), MPV and PDW. Non-alcoholic liver cirrhosis was excluded due to the small case number.

A high concentration of citrate (1:4 volume/volume with blood) for MPV measurement is recommended as an anticoagulant since ethylene diamine tetraacetic acid (EDTA), which is commonly used anticoagulant for complete blood cell count (CBC), is known to expand the volume of platelets [6]. However, citrate for CBC is not ideal because a high concentration of citrate may lower the cell counts due to a dilution effect and it brings the difficulty of providing the accurate ratio of blood sample and anticoagulant. We chose EDTA as an anticoagulant and ran the test within an hour of blood collection, as Dastjerdi et al. [7] reported that MPV measured within an hour of sampling using both citrate and EDTA are not significantly different when compared to each other.

Healthy controls and the patients with NAFLD and AFLD showed no significant difference in PLT, MPV and PDW. However, the patients with ALC showed significantly different PLT, MPV and PDW when compared to the patients with NAFLD and AFLD (Table I). In contrast to the results of Ozhan et al. [1], where patients with NAFLD showed decreased PLT and increased MPV, our results showed no significant difference. The patients with AFLD presented with no significantly different MPV but the patients with ALC showed increased MPV, PDW and decreased PLT when compared to those with NAFLD and AFLD and the healthy controls.

Table I.  Platelet numbers and platelet indices of studied groups.

	Controls	NAFLD*	AFLD*	ALC*	P-value^**
	(n = 241)	(n = 200)	(n = 55)	(n = 48)
PLT (×10^9/L)^§	239.8	232.2	220.7	131.7	<0.001
MPV (fL)^§	10.52	10.40	10.52	11.03	0.007
PDW (fL)^§	11.99	11.76	11.97	12.79	0.04

*The diagnosis was based on history of alcohol consumption, blood testing and ultrasound imaging [8]; **Student's t-test for comparing AFLD with ALC; ^§Measured with Sysmex XE-2100 automatic cell counter (Sysmex, Kobe, Japan).

NAFLD, non-alcoholic fatty liver disease; AFLD, alcoholic fatty liver disease; ALC, alcoholic cirrhosis; PLT, platelet count; MPV, mean platelet volume; PDW, platelet distribution width.

In conclusion, we observed that MPV and PDW may be an important clue in the distinction between patients with AFLD and ALC. We suggest that further studies on the clinical applications of MPV and PDW in various diseases should be performed in the future.