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ORIGINAL ARTICLE
Year : 2019  |  Volume : 22  |  Issue : 5  |  Page : 727-730

Plateletcrit: A possible biomarker of inflammation in hepatitis A infection


1 Department of Paediatrics, University of Gaziantep, Gaziantep, Turkey
2 Department of Paediatric Haemotology, University of Gaziantep, Gaziantep, Turkey
3 Department of Paediatric Gastroenterology, Hepatology and Nutrition, Ankara Yıldırım Beyazıt University, Ankara, Turkey

Date of Acceptance06-Feb-2019
Date of Web Publication15-May-2019

Correspondence Address:
Assist. Prof. M E Coskun
Department of Paediatrics, University of Gaziantep, Gaziantep
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/njcp.njcp_331_18

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   Abstract 


Objectives: Hepatitis A (HepA) virus is a common infection worldwide that causes inflammation of the liver. Platelet index, particularly plateletcrit (PCT) which shows percentage of blood occupied by platelets, is thought to be potential marker of inflammation. Therefore, we aimed to investigate the changes in PCT percentages during HepA infection. Subjects and Methods: Seventy-three children with a diagnosis of acute HepA infection and 68 age- and sex-matched healthy controls were enrolled in this study. Their values of platelet indices [PCT and mean platelet volume (MPV)] obtained from complete blood counts, which were analyzed by XN-1000 analyzer, were statistically compared with each other. Results: PCT and MPV of the patients were found to be higher than those of controls (8.89 ± 1.30 vs 8.03 ± 0.89 for MPV and 0.29 ± 0.11 vs 0.24 ± 0.05 for PCT; P = 0.000, P = 0.002, respectively). In addition, PCT and platelet counts showed a significant negative correlation with alanine aminotransferase (ALT) levels, which indirectly represents inflammation in the liver (PCT: r = −0.368, P = 0.002; platelet count: r = −0.304, P = 0.009). In contrast, MPV levels were not found to demonstrate any correlation with ALT (r = −0.205, P = 0.082). Conclusion: Both MPV and PCT are capable of reflecting the inflammation during acute HepA inflammation. Also, PCT shows a significant negative correlation with the degree of inflammation.

Keywords: Children, hepatitis A, inflammation, plateletcrit


How to cite this article:
Coskun M E, Alidris A, Temel M T, Akbayram S, Hizli S. Plateletcrit: A possible biomarker of inflammation in hepatitis A infection. Niger J Clin Pract 2019;22:727-30

How to cite this URL:
Coskun M E, Alidris A, Temel M T, Akbayram S, Hizli S. Plateletcrit: A possible biomarker of inflammation in hepatitis A infection. Niger J Clin Pract [serial online] 2019 [cited 2019 Aug 24];22:727-30. Available from: http://www.njcponline.com/text.asp?2019/22/5/727/258270




   Introduction Top


Hepatitis A (HepA) is one of the most common infections worldwide resulting from the inflammation of the liver caused by hepatitis A virus (HAV). Its clinical presentation may differ from mild disease to fulminant hepatic failure.[1] During the infection, hepatic inflammation, which results from the secretion of various cytokines, may not only affect the prognosis of the disease but also change some of the indices of platelets[2],[3] which may be used to monitor the inflammation. Among these indices, mean platelet volume (MPV), which shows the platelet size and correlates with its functions,[4] has been researched on a wide range of clinical conditions.[3] On the other hand, literature regarding plateletcrit (PCT), which is another platelet index, is scarce, although it provides more comprehensive data about platelet mass and it is either available directly from complete blood count or calculated from the formula: platelet count (PLT) × MPV/10.

To the best of our knowledge, a research on PCT in HepA-infected children is not available, and therefore we aimed to investigate the potential role of PCT as a biomarker of inflammation in HepA infection.


   Subjects and Methods Top


The electronic records of patients who were diagnosed with acute HepA in the Department of Paediatrics at the University of Gaziantep, Turkey, between January 2010 and December 2012 were reviewed. Nine of 82 patients who had either corrupted or missing data or whose IgG levels were higher than IgM were excluded from the study. In addition, a gender- and age-matched control group composed of 68 individuals from the healthy children admitted to the social pediatrics outpatient clinic were also included. The hematological parameters, such as white blood cells (WBCs), hemoglobin (Hb), mean corpuscular volume (MCV), red cell distribution width (RDW), PLT, MPV, and (PCT), which were analyzed using XN-1000 analyzer by method of hydrodynamic focusing, flow cytometry, and SLS Hb, were used in this study. Hb, PLT, and PCT are directly analyzed, and the other parameters are calculated by the analyzer. These parameters were compared between patients with acute HepA and controls. In addition, correlation analysis of alanine aminotransferase (ALT) with some blood parameters and some platelet indices was made within the patient group.

The ethical approval for the study was obtained from ethical commission of the University of Gaziantep, and all patients were informed about the use of data related to them; in addition, the families of children assigned to the control group also signed informed consents.

For the parametric values, Student's t-test was used and Pearson's correlation test was used to analyze correlations P values < 0.05 were accepted as statistically significant. All analysis was computed using SPSS 20 software in the University of Gaziantep, Turkey.


   Results Top


A total of 73 patients comprising 38 males and 35 females diagnosed with HepA infection between January 2010 and December 2012 and whose records were available were enrolled in this study. Some of their some hematologic parameters including platelet indices were compared with those of age- and sex-matched 68 healthy controls. The mean age of both patient and control groups was 88.58 ± 37.63 and 92.29 ± 61.0 months, respectively. The patients' laboratory parameters supporting the diagnosis of acute HepA infection are shown in [Table 1]. The gender distribution was similar for both the groups (P = 0.867). MPV and PCT values of the patients were found to be significantly higher than those of healthy controls (8.89 ± 1.30 vs 8.03 ± 0.89 for MPV and 0.29 ± 0.11 vs 0.24 ± 0.05 for PCT; P = 0.000, P = 0.002, respectively) [Table 2]. The rest of the compared full blood count parameters were similar for the groups (P > 0.05, detailed P values are provided in [Table 2]). Furthermore, negative correlations of ALT with PCT and platelet counts were found in HepA-diagnosed patients (PCT: r = −0.368, P = 0.002; PLT: r = −0.304, P = 0.009). WBC, MPV, and Hb did not show any correlation with ALT in the patient group [Table 3].
Table 1: Laboratory parameters of patients with hepatitis A

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Table 2: The comparison of demographic and hematologic parameters between study groups

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Table 3: Correlation analysis of ALT within acute hepatitis A group

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   Discussion Top


Platelet indices have been widely studied either to establish a diagnostic marker or to show an association with a particular condition or to monitor the activity of a disease. Among these, MPV, which is a measure of platelet size and shows the rate of platelet production and activation, is one of the most researched platelet parameters in various conditions.[4] Its value was found to change during inflammation or infection because of the secreted cytokines and hormones affecting the proliferation and activation of the platelets.[5]

MPV is thought to be a potential inflammatory marker; however, the results of different studies revealed that it may act either as a positive or as a negative acute phase reactant. For instance, MPV was found to be increased in acute coronary syndromes or rheumatoid arthritis (RA).[6],[7] In contrast, a decrease in MPV during active disease was reported in familial  Mediterranean fever More Details (FMF).[8] Regarding infections, although the data are scarce, contradictory results were reported. For example, in a research, the relationship of increased MPV levels with tuberculosis was reported, whereas decreased MPV values were found during HIV and Respiratory syncytial virus (RSV) infections in separate studies.[9],[10],[11] Looking at HepA infection, to our knowledge, there has been only two studies and they found contradictory results of MPV values during the illness. Almış et al.[12] reported decreased levels of MPV in patients with HepA, while MPV was found to be higher in children diagnosed with HepA compared with that of controls in the study by Akın et al.[13] In our study, MPV levels were found to be higher than that of controls. The discrepancies between the aforementioned studies and our research could be attributed to the phase of infection, which was not provided in those studies. From this point of view, the population of this study could be regarded homogeneous in terms of the phase of the infection as patients who had higher anti-HAV IgM than IgG levels were enrolled in the study. It was not clear why there were contradictory results in the studies nonetheless; another possible explanation was brought to this inconsistence by Gasparyan et al.[14] who proposed that high inflammatory conditions such as active inflammatory bowel diseases (IBDs), attacks of FMF, or RA are associated with low MPV values possibly due to consumption of newly produced large-sized platelets at the site of the inflammation, whereas conditions causing low-grade inflammation are associated with high MPV due to conservation of large platelets.[14] However, this explanation was insufficient because it did not include infectious conditions; the tendency of hematopoietic system to maintain homeostasis by means of conserving constant platelet mass might be responsible.[15] In this regard, another platelet index, PCT, which shows percentage of blood volume occupied by platelets, could be more reliable than MPV in terms of evaluating the effect of different medical conditions on platelets as a mass.

Literature review showed more consistent data providing positive correlation between PCT and inflammation compared with MPV. For instance, high PCT was reported to be correlated with the development of nonalcoholic fatty liver disease in females.[16] Furthermore, high PCT percentages were found to be associated with autoimmune gastritis[17] and acute coronary syndromes;[18] in addition, PCT was reported to be correlated with either the severity or activation of IBDs,[19],[20] hyperemesis gravidarum,[21] and juvenile RA.[22] When we look at the infectious conditions, there have been a limited number of studies on PCT, an example of these is tuberculosis in which increased PCT percentages were reported.[9],[23] Similarly, in our study, PCT percentages along with MPV levels of HepA-infected patients were found to be significantly higher than those of controls. On the other hand, there were two studies that observed lowered PCT percentages in different conditions. In one of these studies, patients who died in the intensive care unit probably due to sepsis showed decreased PCT,[24] and in the other one, lowered PCT was found in neonates who had invasive fungal infection and bacterial sepsis.[25] Both of these studies reported that PLTs were found to be reduced along with PCT percentages; however, in the study regarding died patients in the intensive care unit, no significant change in MPV was reported. In the other research about neonates, MPV was found to be increased in neonates with fungal infection or bacterial sepsis.

Moreover, in our study, negative correlations of ALT with PCT and PLTs were found in acute HepA-infected patients' groups. This finding seems like contradictory, but it reflects a kind of biphasic response. In simple words, overall PCT percentages were found significantly increased in patients with HepA compared with that of healthy children in this study. However, when we looked in details, PCT showed a decreasing trend as the ALT levels increased in HepA-infected cases, but its mean value still remained higher than that of controls. Literature review revealed some correlation findings between PCT and inflammatory markers or disease activities. For instance, in patients with active Crohn's disease (CD), while PCT was found to be increased compared to patients in remission and in healthy controls, high-sensitive C-reactive protein (CRP), which was thought to be the most sensitive parameter in terms of discriminating active CD from inactive CD, showed no change.[20]

In addition, in our research, no correlation between MPV and ALT was seen in the patient group. However, a previous study about FMF reported positive correlation between MPV and disease activity.[8] On the other hand, another study reported a negative correlation between MPV and CRP in the active phase of ulcerative colitis.[19] Also, in a study evaluating the change pattern of MPV and its correlation with acute phase reactants in rota virus gastroenteritis, MPV was found to be lowered in rota-positive gastroenteritis cases compared with that of healthy controls and MPV was reported to display a negative correlation with CRP in the study group.[26]

Based on our results, we can only speculate that the negative correlation of PCT with ALT might be helpful in terms of estimating the course of HepA infection. However, as a limitation of this study, analysis did not include longitudinal follow-up figures of MPV, PCT, and ALT of HepA-infected patients, and that is why it has not been possible to demonstrate a complete change pattern of MPV and PCT in our research. Therefore, our speculation requires to be confirmed by further comprehensive investigations.

In conclusion, we found that both MPV and PCT increased as an acute phase reactant in acute HepA-infected patients. Also, in patients diagnosed with acute HepA, PCT was found to display a negative correlation with ALT, which is a marker of hepatic cell damage due to inflammation. However, the exact mechanism of this negative correlation can hardly be explained with the scope of this study. Therefore, further studies are required to investigate the change patterns of PCT and MPV in viral hepatitis cases.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

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Lippi G, Filippozzi L, Salvagno GL, Montagnana M, Franchini M, Guidi GC, et al. Increased mean platelet volume in patients with acute coronary syndromes. Arch Pathol Lab Med 2009;133:1441-3.  Back to cited text no. 6
    
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Yazici S, Yazici M, Erer B, Erer B, Calik Y, Ozhan H, et al. The platelet indices in patients with rheumatoid arthritis: Mean platelet volume reflects disease activity. Platelets 2010;21:122-5.  Back to cited text no. 7
    
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Makay B, Turkyilmaz Z, Unsal E. Mean platelet volume in children with familial Mediterranean fever. Clin Rheumatol 2009;28:975-8.  Back to cited text no. 8
    
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Tozkoparan E, Deniz O, Ucar E, Bilgic H, Ekiz K. Changes in platelet count and indices in pulmonary tuberculosis. Clin Chem Lab Med 2007;45:1009-13.  Back to cited text no. 9
    
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Qadri S, Holman S, Dehovitz J, Crystal H, Minkoff H, Lazar JM. Mean platelet volume is decreased in HIV-infected women. HIV Med 2013;14:549-55.  Back to cited text no. 10
    
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Renshaw AA, Drago B, Toraya N, Gould EW. Respiratory syncytial virus infection is strongly correlated with decreased mean platelet volume. Int J Infect Dis 2013;17:e678-80.  Back to cited text no. 11
    
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Almış H, Bucak IH, Celik V, Tekin M, Karakoc F, Konca C, et al. Mean platelet volume in hepatitis A. Eur Rev Med Pharmacol Sci 2016;20:2310-4.  Back to cited text no. 12
    
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Akin F, Sert A, Arslan S. Mean platelet volume in children with hepatitis A. J Health Popul Nutr 2016; 35:32.  Back to cited text no. 13
    
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Gasparyan AY, Ayvazyan L, Mikhailidis DP, Kitas GD. Mean platelet volume: A link between thrombosis and inflammation? Curr Pharm Des 2011;17:47-58.  Back to cited text no. 14
    
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Thompson CB. From precursor to product: How do megakaryocytes produce platelets? Prog Clin Biol Res 1986;215:361-71.  Back to cited text no. 15
    
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Wang LR, Zhou YF, Zhou YJ, Zhang SH, Liu WY, Wu SJ, et al. Elevation of plateletcrit increasing the risk of non-alcoholic fatty liver disease development in female adults: A large population-based study. Clin Chim Acta 2017;474:28-33.  Back to cited text no. 16
    
17.
Yuksel O, Helvaci K, Basar O, Koklu S, Caner S, Helvaci N, et al. An overlooked indicator of disease activity in ulcerative colitis: Mean platelet volume. Platelets 2009;20:277-81.  Back to cited text no. 17
    
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Ergelen M, Uyarel H. Plateletcrit: A novel prognostic marker for acute coronary syndrome. Int J Cardiol 2014;177:161.  Back to cited text no. 18
    
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Ozturk ZA, Dag MS, Kuyumcu ME, Cam H, Yesil Y, Yilmaz N, et al. Could platelet indices be new biomarkers for inflammatory bowel diseases? Eur Rev Med Pharmacol Sci 2013;17:334-41.  Back to cited text no. 19
    
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Tang J, Gao X, Zhi M, Zhou HM, Zhang M, Chen HW, et al. Plateletcrit: A sensitive biomarker for evaluating disease activity in Crohn's disease with low hs-CRP. J Dig Dis 2015;16:118-24.  Back to cited text no. 20
    
21.
Tayfur C, Burcu DC, Gulten O, Betul D, Tugberk G, Onur O, et al. Association between platelet to lymphocyte ratio, plateletcrit and the presence and severity of hyperemesis gravidarum. J Obstet Gynaecol Re 2017;43:498-504.  Back to cited text no. 21
    
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Vakili M, Ziaee V, Moradinejad MH, Raeeskarami SR, Kompani F, Rahamooz T. Changes of platelet indices in juvenile idiopathic arthritis in acute phase and after two months treatment. Iran J Pediatr 2016;26:e5006.  Back to cited text no. 22
    
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Sahin F, Yazar E, Yildiz P. Prominent features of platelet count, plateletcrit, mean platelet volume and platelet distribution width in pulmonary tuberculosis. Multidiscip Respir Med 2012;7:38.  Back to cited text no. 23
    
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Golwala ZM, Shah H, Gupta N, Sreenivas V, Puliyel JM. Mean platelet volume (MPV), platelet distribution width (PDW), platelet count and plateletcrit (PCT) as predictors of in-hospital paediatric mortality: A case-control Study. Afr Health Sci 2016;16:356-62.  Back to cited text no. 24
    
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Zhao D, Qiu G, Luo Z, Zhang Y. Platelet parameters and (1, 3)-beta-D-glucan as a diagnostic and prognostic marker of invasive fungal disease in preterm infants. PLoS One 2015;10:e0123907.  Back to cited text no. 25
    
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Mete E, Akelma AZ, Cizmeci MN, Bozkaya D, Kanburoglu MK. Decreased mean platelet volume in children with acute rotavirus gastroenteritis. Platelets 2014;25:51-54.  Back to cited text no. 26
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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