Letter to the Editor
Mean Platelet Volume in Chronic Urticaria and Beyond
Angiology 1-2 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003319714561082 ang.sagepub.com
Figen Gurdol, MD1, Nilgun Isıksacan, PhD2, and Murat Koser, MD3
We thank Dr Varol for his interest in our study.1 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.2 Therefore, it is difficult to avoid all of these variables in a study. This is a limitation. In our study,3 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.4 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.5 Although MPV has been proposed as an indicator of platelet reactivity, there is as yet no ideal test for the detection of platelet activation.6 Hyperaggregation of platelets in response to various agonists has been observed in patients with DM.7 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.8 In contrast, the previous reports showed that MPV is increased9 or decreased10 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.11 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.11 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. References 1. Varol E. Confounding factors may affect mean platelet volume in chronic urticaria [published online on November 7, 2014]. Angiology. 2014. doi: 10.1177/0003319714557941.
1
Department of Biochemistry, Istanbul Faculty of Medicine, Istanbul University, Capa, Istanbul 2 Central Laboratory, Dr. Sadi Konuk Training and Research Hospital, Bakirkoy, Istanbul 3 Central Laboratory, Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Halkali, Istanbul Corresponding Author: Murat Koser, Central Laboratory, Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Halkali 34303, Istanbul, Turkey. Email: [email protected]
Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on March 31, 2015
2
Angiology
2. Kottke-Marchant K, Corcoran G. The laboratory diagnosis of platelet disorders. Arch Pathol Lab Med. 2002;126(2):133-146. 3. Isiksacan N, Koser M, Cemsitoglu F, Kucuksezer UC, Gurdol F. Platelet and other hemostatic characteristics in patients with chronic urticaria [published online September 30, 2014]. Angiology. 2014. 4. Ozder A, Eker HH. Investigation of mean platelet volume in patients with type 2 diabetes mellitus and in subjects with impaired fasting glucose: a cost-effective tool in primary health care? Int J Clin Exp Med. 2014;7(8):2292-2297. 5. Verdoia M, Schaffer A, Barbieri L, et al; Novara Atherosclerosis Study (NAS) group. Diabetes, glucose control and mean platelet volume: a single-centre cohort study. Diabetes Res Clin Pract. 2014;104(2):288-294. 6. Tsiara S, Elisaf M, Jagroop IA, Mikhailidis DP. Platelets as predictors of vascular risk: is there a practical index of platelet activity? Clin Appl Thromb Hemost. 2003;9(3):177-190. 7. Rosove MH, Frank HJL, Harwig SSL. Plasma b-thromboglobulin, platelet factor 4, fibrinopeptide A, and other hemostatic
8.
9.
10.
11.
functions during improved, short-term glycemic control in diabetes mellitus. Diabetes Care. 1984;7(2):174-179. Kasperska-Zajac A, Grzanka A, Jarzab J, et al. The association between platelet count and acute phase response in chronic spontaneous urticaria. Biomed Res Int. 2014; doi:10.1155/ 2014/650913. Magen E, Mishal J, Zeldin Y, et al. Increased mean platelet volume and C-reactive protein levels in patients with chronic urticaria with a positive autologous serum skin test. Am J Med Sci. 2010;339(6):504-508. Akelma AZ, Mete E, Cizmeci MN, Kanburoglu MK, Malli DD, Bozkaya D. The role of mean platelet volume as an inflammatory marker in children with chronic spontaneous urticaria [published online August 19, 2013]. Allergol Immunopathol (Madr). 2013. doi:10.1016/j.aller.2013.06.002. Beyan C, Kaptan K, Ifran A. Platelet count, mean platelet volume, platelet distribution width, and platelet crit do not correlate with optical platelet aggregation responses in healthy volunteers. J Thromb Thrombolysis. 2006;22(3):161-164.
Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on March 31, 2015
Mean Platelet Volume in Chronic Urticaria and Beyond
Angiology 1-2 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003319714561082 ang.sagepub.com
Figen Gurdol, MD1, Nilgun Isıksacan, PhD2, and Murat Koser, MD3
We thank Dr Varol for his interest in our study.1 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.2 Therefore, it is difficult to avoid all of these variables in a study. This is a limitation. In our study,3 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.4 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.5 Although MPV has been proposed as an indicator of platelet reactivity, there is as yet no ideal test for the detection of platelet activation.6 Hyperaggregation of platelets in response to various agonists has been observed in patients with DM.7 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.8 In contrast, the previous reports showed that MPV is increased9 or decreased10 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.11 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.11 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. References 1. Varol E. Confounding factors may affect mean platelet volume in chronic urticaria [published online on November 7, 2014]. Angiology. 2014. doi: 10.1177/0003319714557941.
1
Department of Biochemistry, Istanbul Faculty of Medicine, Istanbul University, Capa, Istanbul 2 Central Laboratory, Dr. Sadi Konuk Training and Research Hospital, Bakirkoy, Istanbul 3 Central Laboratory, Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Halkali, Istanbul Corresponding Author: Murat Koser, Central Laboratory, Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Halkali 34303, Istanbul, Turkey. Email: [email protected]
Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on March 31, 2015
2
Angiology
2. Kottke-Marchant K, Corcoran G. The laboratory diagnosis of platelet disorders. Arch Pathol Lab Med. 2002;126(2):133-146. 3. Isiksacan N, Koser M, Cemsitoglu F, Kucuksezer UC, Gurdol F. Platelet and other hemostatic characteristics in patients with chronic urticaria [published online September 30, 2014]. Angiology. 2014. 4. Ozder A, Eker HH. Investigation of mean platelet volume in patients with type 2 diabetes mellitus and in subjects with impaired fasting glucose: a cost-effective tool in primary health care? Int J Clin Exp Med. 2014;7(8):2292-2297. 5. Verdoia M, Schaffer A, Barbieri L, et al; Novara Atherosclerosis Study (NAS) group. Diabetes, glucose control and mean platelet volume: a single-centre cohort study. Diabetes Res Clin Pract. 2014;104(2):288-294. 6. Tsiara S, Elisaf M, Jagroop IA, Mikhailidis DP. Platelets as predictors of vascular risk: is there a practical index of platelet activity? Clin Appl Thromb Hemost. 2003;9(3):177-190. 7. Rosove MH, Frank HJL, Harwig SSL. Plasma b-thromboglobulin, platelet factor 4, fibrinopeptide A, and other hemostatic
8.
9.
10.
11.
functions during improved, short-term glycemic control in diabetes mellitus. Diabetes Care. 1984;7(2):174-179. Kasperska-Zajac A, Grzanka A, Jarzab J, et al. The association between platelet count and acute phase response in chronic spontaneous urticaria. Biomed Res Int. 2014; doi:10.1155/ 2014/650913. Magen E, Mishal J, Zeldin Y, et al. Increased mean platelet volume and C-reactive protein levels in patients with chronic urticaria with a positive autologous serum skin test. Am J Med Sci. 2010;339(6):504-508. Akelma AZ, Mete E, Cizmeci MN, Kanburoglu MK, Malli DD, Bozkaya D. The role of mean platelet volume as an inflammatory marker in children with chronic spontaneous urticaria [published online August 19, 2013]. Allergol Immunopathol (Madr). 2013. doi:10.1016/j.aller.2013.06.002. Beyan C, Kaptan K, Ifran A. Platelet count, mean platelet volume, platelet distribution width, and platelet crit do not correlate with optical platelet aggregation responses in healthy volunteers. J Thromb Thrombolysis. 2006;22(3):161-164.
Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on March 31, 2015
