Mean Platelet Volume in Chronic Urticaria and Beyond

We thank Dr Varol for his interest in our study. Mean platelet volume (MPV) and platelet distribution width (PDW) are commonly used platelet indices for clinical research, since they can easily be measured at a relatively low cost. As Dr Varol has pointed out, MPV is affected by various factors besides cardiovascular diseases. Several demographic and clinical variables can change MPV. Furthermore, drugs, compounds, and dietary components can affect platelet function. Therefore, it is difficult to avoid all of these variables in a study. This is a limitation. In our study, patient selection excluded cases with hereditary/acquired angioedema and anaphylaxis, both of which are characterized by excess histamine release, similar to chronic urticaria (CU). Also, hepatic and cardiac diseases, urticariarelated or systemic vasculitis were among our exclusion criteria. None of our patients received any oral anticoagulant drugs, had any infections, thromboembolism, or underwent any surgical treatment in the last 6 months. Diabetic patients have been shown to have larger MPV. In a recent cohort study in 1272 diabetic patients, increased MPV was associated with aging, treatment with angiotensin-receptor blockers, cholesterol, and hemoglobin levels, whereas it was not independently associated with diabetes mellitus (DM) and glycemic control. Although MPV has been proposed as an indicator of platelet reactivity, there is as yet no ideal test for the detection of platelet activation. Hyperaggregation of platelets in response to various agonists has been observed in patients with DM. In our study, we investigated the response of platelets to several agonists together with the possibility whether any changes in MPV and PDW may occur. Platelet counts were measured using an automated blood analyzer by the impedance method within 2 hours of blood collection. Platelet aggregation after adenosine diphosphate and arachidonic acid (AA) stimulation was not different from the healthy controls, but aggregation after ristocetin and thrombin receptor agonist peptide (TRAP) agonists was significantly decreased in CU patients, in contrast to the increased response seen in diabetics. Accordingly, decreased MPV in patients with CU was observed as compared with the controls, whereas PDW remained unchanged. Data from studies related to MPV and CU are controversial. Similar MPV was reported in patients with mild and more severe CU as well as in healthy participants. In contrast, the previous reports showed that MPV is increased or decreased in patients with CU. Conflicting results regarding MPV in CU may be due to the difficulty in excluding factors that can influence MPV. As concluded by Beyan et al, MPV alone is not sufficient to evaluate platelet function. Their observation was derived from the lack of correlation of MPV and PDW with optical platelet aggregation responses in healthy volunteers. In addition, large and variable in size platelets have been observed in several clinical conditions, without simultaneous activation of hemostasis. Also, the shape and volume of platelets are variable, even in healthy participants. It has been suggested that serial measurements of MPV and PDW would be insufficient for the recognition of progressive platelet activation. Studies with respect to whole blood platelet aggregation in response to AA or ristocetin are scarce in patients with CU. Therefore, the main objective of our study was to examine this process. Yet, our study has limitations. First, we did not assess CU severity scores; hence, we were unable to evaluate correlation between the measured parameters and CU severity. Second, our patients consisted of a Turkish population and were recruited from 1 center. A multicenter cohort study with a larger patient population should be carried out to minimize the confounding factors with respect to platelet function in CU.