Controversies over the interpretation of changes of mean platelet volume in rheumatoid arthritis

To the Editor

We read with interest the article published in your journal, “The platelet indices in patients with rheumatoid arthritis: Mean platelet volume reflects disease activity” by Yazici et al. [1]. They presented that mean platelet volume (MPV) was increased in a rheumatoid arthritis (RA) group compared to a control group. However, on the contrary of this, Kisacik et al. [2] reported that MPV was decreased in a rheumatoid arthritis (RA) group compared to a control group. About this contradictive result, Yazici et al. argued that Kisacik's study had a limitation because of its small number of subjects. However, according to our usual observation, there was decreased tendency of MPV in cases of severe inflammation, just the opposite of the authors’ results. Gasparyan et al. [3], [4], in the meanwhile, reported that MPV was affected by various factors, as was increased in the patient on anti-TNFa therapy and in patients hypertensive more than 140/90 mmHg. Therefore, we performed this study in an intention to confirm such confusing issue.

We performed this study on 1072 patients who visited The Hospital for Rheumatic Diseases and were diagnosed as either RA or osteoarthritis (OA). Eight hundred and nine RA patients were grouped into active or inactive group according the C-reactive protein (CRP) test results. Two hundred and sixty three OA patients all tested negative for CRP test. Patients were predominantly female (F : M = 888 : 184; age = 54.0 ± 13.1 years). The three groups showed no significant differences by sex and age. Also 93 active RA patients were prospectively followed up to measure mean platelet volume (MPV) at, before, and after the treatment when erythrocyte sedimentation rate (ESR) became normalized. Complete blood cell count (CBC) analyses were performed with the use of Sysmex® XE-2100 automated blood cell counter. Samples were anticoagulated by EDTA and processed within 1 hour of venipuncture to avoid bias due to excessive platelet swelling [5], [6]. Platelet count (PLT) and platelet hematocrit (PCT) were measured using the hydrodynamic focusing method. MPV was calculated from the equation (PCT × 1000/PLT). ESR was measured using Westergren method, and CRP test was performed by nephelometry system.

MPV in the active RA group was 9.80 ± 0.74 fL, which was lower than 10.13 ± 0.79 fL (P-value < 0.001) in the OA group; the result in the inactive RA group was 10.08 ± 0.71 fL, which sat between the previously mentioned two groups. For 93 active RA patients, MPV results before treatment was 9.86 ± 0.66 fL while the result after the treatment increased to 10.25 ± 0.74 fL (P-value < 0.001). However, other test results that this article presented (white blood cell count, hemoglobin level, platelet count, ESR) were similar to our results. Besides the parameters that they presented, red cell distribution width (RDW) and absolute neutrophil count (ANC) were increased in the active RA group while platelet distribution width (PDW) was decreased (Table I).

Table I.  Complete blood cell count data in RA and OA (mean ± SD).

	Active RA (n = 368)	Inactive RA (n = 441)	OA (n = 263)	P-value*
WBC (/uL)	7812 ± 2299	6664 ± 2096	6117 ± 1492	<0.001
Hb (g/dL)	12.1 ± 1.5	12.7 ± 1.5	13.3 ± 1.2	<0.001
RDW	14.3 ± 1.5	13.7 ± 1.3	12.8 ± 0.8	<0.001
PLT (×10^3/uL)	293 ± 78	259 ± 119	249 ± 54	<0.001
MPV (fL)	9.80 ± 0.74	10.08 ± 0.71	10.13 ± 0.79	<0.001
PDW	10.38 ± 1.38	10.92 ± 1.36	11.10 ± 1.51	<0.001
ANC (/uL)	5325 ± 2113	4152 ± 1894	3275 ± 1198	<0.001
ESR (mm/h)	51.2 ± 31.9	18.4 ± 13.8	15.5 ± 11.8	<0.001

RA, rheumatoid arthritis; OA, osteoarthritis; WBC, white blood cell count; RDW, red cell distribution width; PLT, platelet; MPV, mean platelet volume; PDW, platelet distribution width; ANC, absolute neutrophil count; ESR, erythrocyte sedimentation rate.

*Student's t-test for comparing active RA with OA.

We considerably increased the patient group to the previous two studies and observed that MPV is decreased in the active RA group when compared to OA group. Also, when we compared the MPV results on 93 patients at, before, and after the treatment, MPV was increased after the treatment and this was different than the results by Yazici et al., showing again that MPV was decreased by the inflammation.

In this study, we did not evaluate all the possible factors that might affect MPV, such as serum lipid, blood pressure, conventional drug therapy and rheumatoid factors, but we think that the effects on MPV due to the factors mentioned above were minimal since we studied a large number of patients. Apparently, MPV may be measured higher in thrombotic events that may be provoked in diabetic and hypertensive patients, and in altered megakaryopoiesis in RA. Seemingly, MPV also requires standardization of its measurement system since commercial instruments are run by differing platelet (PLT) measurement methods. In addition, we observed that PDW could also be effectively used as inflammatory markers for active RA. Therefore, studies of clinical utility of not only MPV but also PDW on various types of diseases should be performed in the future.