|Year : 2019 | Volume
| Issue : 2 | Page : 740-744
Mean platelet volume as a diagnostic marker in children with acute hepatitis A
Soheir S Abou El-Ella1, Maha A Tawfik1, Amany F Ismael2
1 Department of Pediatrics, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Pediatrics, Ministry of Health, Quesna Central Hospital, Menoufia, Egypt
|Date of Submission||22-Oct-2018|
|Date of Acceptance||04-Dec-2018|
|Date of Web Publication||25-Jun-2019|
Amany F Ismael
22 Negm Street, Quesna, Menoufia
Source of Support: None, Conflict of Interest: None
The aim of this study was to assess the level of mean platelet volume (MPV) in children with acute hepatitis A as compared with the control group.
MPV is a marker that indicates platelet size, function, and the rate of platelet production and activation.
Patients and methods
Our study was conducted on 100 Egyptian children, aged from 2 to 14 years (58 male and 42 female) previously diagnosed as having hepatitis A as a patient group and 100 apparently healthy age-matched and sex-matched children as a control group. All of them were subjected to full history, physical examination, C-reactive protein, erythrocyte sedimentation rate, complete blood count, MPV levels, liver function tests (alanine aminotransferase and aspartate aminotransferase), serum bilirubin level (total and direct), prothrombin time, and platelet count. The diagnosis of hepatitis A virus infection was based on antihepatitis A virus immunoglobulin M positivity.
MPV in the study group was significantly lower than the control group (P < 0.001). The MPV levels revealed no correlation with the alanine aminotransferase and aspartate aminotransferase (P > 0.05), but the MPV level was directly proportionate to the platelet counts (P < 0.05). Our study showed that there was 9% of cases with complications, mainly dehydration.
This study demonstrated that MPV is a negative acute-phase reactant for children with acute hepatitis A.
Keywords: child, hepatitis A, inflammation, mean platelet volume, viral
|How to cite this article:|
Abou El-Ella SS, Tawfik MA, Ismael AF. Mean platelet volume as a diagnostic marker in children with acute hepatitis A. Menoufia Med J 2019;32:740-4
|How to cite this URL:|
Abou El-Ella SS, Tawfik MA, Ismael AF. Mean platelet volume as a diagnostic marker in children with acute hepatitis A. Menoufia Med J [serial online] 2019 [cited 2019 Sep 17];32:740-4. Available from: http://www.mmj.eg.net/text.asp?2019/32/2/740/260891
| Introduction|| |
Hepatitis A is an inflammation of the liver that results from infection with the hepatitis A virus (HAV). HAV is a nonenveloped RNA virus, with an icosahedral structure, that is in the genus of Hepatovirus in the family of Picornaviridae. HAV is usually caused by self-limited acute hepatitis and is transmitted via the fecal-oral route. Although the course of HAV infection is usually asymptomatic, it rarely develops into fulminant hepatitis. HAV infection is the most prevalent of the five types of viral hepatitis (A, B, C, D, and E). This virus is also responsible for most forms of acute and benign hepatitis; although fulminant hepatic failure can occur, it is rare and occurs more often in adults than in children Endemicity is closely linked to sanitation, hygiene, socioeconomic status, and vaccination. Outbreaks of HAV infection can occur, although it is less common in developed countries. It can range in severity from a mild illness lasting a few weeks to a severe illness lasting several months. Hepatitis A is associated with various hematologic abnormalities, such as autoimmune hemolytic anemia, leukopenia, leukocytosis, thrombocytopenia, and thrombocytosis. Platelets play a critical role in the inflammatory process. Many cytokines with different functions are secreted by platelets in inflammation,. Various cytokines play a role in viral clearance and tissue damage. Changes in cytokine activities might favor viral persistence and consequently disease progression. Platelet volume is an indicator of platelet function and activation. Mean platelet volume (MPV) is readily measured within the complete blood count results. During hepatic viral infection, MPV, which is commonly used as a measure of platelet size, indicates the rate of platelet production and platelet activation. It also reflects the existence of thrombotic and inflammatory processes. MPV and changes in the activity and function of platelets affect many diseases, such as acute pancreatitis, acute appendicitis, inflammatory bowel disease, chronic hepatitis C, and pulmonary tuberculosis. This study aimed to evaluate the relationship between MPV in patients hepatitis A as compared with a healthy control group.
| Patients and Methods|| |
After approval of the Local Institutional Ethical Committee of Menoufia University Hospital and after taking an oral consent from parents of studied children to share in the study, our study was a case–control study conducted on 100 Egyptian children, aged from 2 to 14 years. They were classified into two groups: patient group including 100 patients (58 male and 42 female) previously diagnosed as having hepatitis A (group A), comprising nine cases with complications mainly dehydration (five male and four female), and a control group (group B) including 100 apparently healthy age-matched and sex-matched children. They were randomly selected from those attending the pediatric clinic and inpatient department of pediatrics at the Liver Institute in Menoufia, Shebin El Koum Teaching Hospital and Quesina Central Hospital in Menoufia in a period from from September 2017 to August 2018. Inclusion criteria were children aged 2–14 years, and patients diagnosed as having hepatitis A (the diagnosis of HAV infection was based on anti-HAV immunoglobulin M positivity). The exclusion criteria were patients with any other infectious disease or chronic disease including hematologic and hepatic diseases not enrolled into this study; the use of any drugs that might change platelet activity and function; presence of diabetes mellitus, asthma, peripheral and cerebrovascular disease, malignancies and chronic diseases; patients with total bilirubin more than 10 (cholestasis); and children with any sign of infection or systemic illness. All patients and controls were subjected to complete detailed history in the form of name, age, sex, residence, socioeconomic status, complaint detail, history of the present illness, past history, history of similar conditions, vaccination history, nutritional history, and family history. Thorough physical examination included anthropometric measurement for calculation of BMI and special emphasis on abdomen examination. Investigations done were by taking blood from patient and healthy groups obtained through venipuncture. The skin over the vein was sterilized by 70% alcohol, and 5 ml each sample of whole venous blood was collected into an EDTA tube, with 3 ml into serum tube, and 2 ml in citrate tube. When the blood was collected, the patients were instructed to apply pressure to the site where the needle entered the skin (by their fingers or bandage) for 5–10 min. Blood from the patient group and the healthy group was evaluated for anti-HAV I'm and anti-HAV Gig antibodies. The diagnosis of acute HAV infection was based on anti-HAV IgM positivity by using kits for hepatitis A as a rapid test. The EDTA samples were used for complete blood count [including platelet count (PC) and MPV]. Automated analyzer (PHONIX-NCC 3300, Bulevar sv. Cara Konstantina, Serbia, Europa) was used for whole blood sample for the blood counts. The reference range for MPV was between 7.0 and 11 fl. The serum samples were used for anti-HAV IgM and anti-HAV IgG antibodies, C-reactive protein (CRP), serum bilirubin level (total and direct), and liver function tests (alanine aminotransferase - aspartate aminotransferase). The citrate samples were used for erythrocyte sedimentation rate (ESR) and prothrombin time (PT). The data were collected and entered to the computer using SPSS 18 (statistical package for the social sciences) (SPSS Inc., Chicago, Illinois, USA) program for statistical analysis. Data were entered as numerical or categorical, as appropriate. Two types of statistics were done: (a) descriptive statistics in which quantitative data were expressed in mean, SD of the mean, and SE, and (b) qualitative data, which were expressed in number (frequency), and percentage. Analytical statistics was done by using χ2-test and Fisher's exact test to measure association between qualitative variables as appropriate. Moreover, Student's t-test, which is a test of significance, was used for comparison between two groups having quantitative variables. Mann–Whitney test (nonparametric test), which is a test of significance, was used for comparison between two groups not normally distributed having quantitative variables. The level of significance used was 95%, so P (probability) value of greater than 0.05 was considered statistically nonsignificant, P value of less than 0.05 was considered statistically significant, and P value of less than 0.001 was considered statistically highly significant. To define the optimal cutoff level of MPV measured in the acute hepatitis A, the receiver operating characteristic curve analysis was used. The results of comparing the correlation between two continuous variables were indicated by the correlation coefficient (r) using correlation analysis.
| Results|| |
A total of 100 patients (58 male and 42 female) with acute hepatitis A, of whom nine developed complications mainly dehydration, and 100 healthy controls (57 males; 43 females) were included in this study. The mean age for the study group was 5.5 ± 2.6 years, and the mean age for the control group was 5.1 ± 1.7 years. There was no statistically significant difference regarding age and sex between the groups (P > 0.05) [Table 1]. The anthropometric measurements were comparable in the HAV and control groups and were not statistically significant (P > 0.05) [Table 2]. The laboratory findings for the study group and the control group are shown in [Table 3]. The mean levels of MPV in the study group were statistically significantly lower than in the control group (P < 0.05). The MPV levels showed no correlation with the alanine aminotransferase and aspartate aminotransferase levels (P > 0.05), but we detected a correlation between the MPV levels and the PCs (P < 0.05) [Table 4]. We measured the CRP and ESR levels in the patients with acute hepatitis A and found no statistically significant correlation between these levels and the MPV levels (P > 0.05) [Table 4]. A 9.05 fl (area under the curve: 0.805) optimal cutoff level of MPV with a sensitivity of 85% and specificity of 86% was determined in the children with acute hepatitis A [Figure 1].
|Table 1: The sex and age distribution and demographic data of the studied groups|
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|Table 2: Comparison of the proposed risk factors between group A and group B|
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|Figure 1: Receiver operating characteristic curve showing the performance of the mean platelet volume in discrimination between patients with hepatitis A and control groups.|
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| Discussion|| |
MPV is one of the platelet function markers that reflect platelet production rate and stimulation. It also reflects the existence of thrombotic and inflammatory processes. Platelets have three types of granules: granules, dense bodies, and lysosomes. The granules and the dense bodies play a role in the activation of hemostasis and in the production of inflammation and cytokines; they are also modulators of inflammation. Platelets are not only required for primary hemostasis but also play an important proinflammatory role. Platelets are activated by different cytokines. Interleukin (IL)-6 and tumor necrosis factor (TNF)-α contribute to the inflammatory process by which the platelets are activated after degranulation, and the size of the platelets is reduced. Anti-TNF-α agents increase MPV and the size of the platelets. Platelet size varies depending on the platelet function and activity. MPV can be easily measured by whole blood sample, one of complete blood picture results. Nowadays, MPV is a marker widely used to detect platelet function and activity and acute-phase reactant. In our study, group A male hepatitis A patients were 58.0%, whereas female patients were 42.0%. Both groups A and B were sex and age matched, with no statistically significant deference (P > 0.05), and the mean age of the studied children having hepatitis A was 5.5 ± 2.6 years [Table 1]. This is in accordance with Clemens et al. who reported that hepatitis A is common in young age children (2 years up to 18 years) in boys and girls, with no statistically significant deference. In our study, the hepatitis A children from the urban and rural residence in group A were 12.0 and 88.0%, respectively, with a higher prevalence of hepatitis A in rural than urban residence. This is in accordance with Afifi et al. who reported that hepatitis A prevalence is more in rural than urban residence [Table 1], and in accordance with Choi et al., who reported that hepatitis A is more common in a rural than urban residence. In our study, sewage problem reported in group A was by 86.0%, which is lower than group B (99.0%), with a significant difference (P < 0.05) [Table 1]. This is in accordance with Abou Ismail et al. who reported hepatitis A infection among children of different socioeconomic status, in Cairo. Seroprevalence was significantly higher with young age, and sewage disposal was a significant risk factor for hepatitis A infection among children for HAV seropositivity in children of. In our study, the presence of a water source, especially tap water, was reported by higher number of children in group B (97.0%) than group A (83.0%), with a significant difference (P < 0.05) [Table 1]. This is in accordance with Abou Ismail et al. who reported that water supply was the most significant risk factors for hepatitis A infection among children. In our study, we found that hygiene of the food served to the children, Mother hand hygiene and child hand hygiene are the incriminated risk factors for the acute hepatitis A infection [Table 2]. This is in accordance with Choi et al. who reported that most hepatitis A infections occur during early childhood, where risk factors include poor sanitation and living in a household with an infected person. Anyone who has not been vaccinated or previously infected can get infected with hepatitis A virus. In our study, liver function tests, white blood cells (WBCs), CRP, ESR, and PT, were significantly higher in the patients with acute hepatitis A (group A) than the control group (group B) whereas hemoglobin and platelets were significantly lower in the patients with acute hepatitis A than the control group (P < 0.05) [Table 3]. This is in accordance with Almiş et al. who reported that liver function tests, WBCs, CRP, ESR, and PT, were significantly higher in the patients with acute hepatitis A than the control group. The most important finding of our study showed that MPV levels significantly decreased in patients with acute hepatitis A compared with the healthy control group. This study showed that MPV may be a negative acute-phase reactant in acute hepatitis A. The MPV was significantly lower in the patients with acute hepatitis A (8.2 ± 0.98) than the control group (9.6 ± 1.1) (P < 0.05), [Table 3], which in accordance with Anitha et al. who reported that liver function tests, WBCs, CRP, ESR, and PT were significantly higher in the patients with acute hepatitis A than the control group, whereas PC was significantly lower in the patients with acute hepatitis A than the control group. In our study, there was a significant positive correlation between MPV and platelets count in the patients with acute hepatitis A (P < 0.05), and there was no significant correlation between MPV and control group parameters (P > 0.05) [Table 4]. MPV levels were significantly lower in patients with liver disease On the contrary, Alexander et al. reported normal levels of TNF-α in patients with acute hepatitis A or B without fulminant liver failure. Cho et al. report that thrombopoietin, which is synthesized in the liver, could play a role in increasing MPV in patients with hepatitis A. Akin et al. showed that there is increase MPV in patients with hepatitis A. MPV has an optimal cutoff level of 9.05 fl, with a sensitivity of 85% and specificity of 86% in the children with acute hepatitis A (area under the curve: 0.805) [Figure 1]. According to our knowledge, this current study is the first to assess the relationship between MPV and children with acute hepatitis A in Egypt. Although similar studies were done in other countries, we need to do the study in Egypt owing to different population and slightly different methodology.
| Conclusion|| |
MPV is a negative acute-phase reactant for children with acute hepatitis A. Further studies are needed to explain the role MPV plays in inflammation and on other viral infections.
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Conflicts of interest
There are no conflicts of interest.
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