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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 2  |  Issue : 2  |  Page : 72-78

Diagnostic value of ultrasonographic portal venous index in the assessment of liver fibrosis in chronic viral hepatitis in Lagos, Nigeria


1 Department of Radiation Biology, Radiotherapy and Radiodiagnosis, Faculty of Clinical Sciences, University of Lagos, Lagos, Nigeria
2 Department of Radiodiagnosis, Lagos University Teaching Hospital, Lagos, Nigeria
3 Department of Internal Medicine, Gastroenterology Unit, Lagos University Teaching Hospital, Idi-Araba, Lagos, Nigeria

Date of Submission16-Jul-2021
Date of Decision20-Sep-2021
Date of Acceptance04-Oct-2021
Date of Web Publication30-Nov-2021

Correspondence Address:
Kofo O Soyebi
Department of Radiation Biology, Radiotherapy and Radiodiagnosis, Faculty of Clinical Sciences, University of Lagos, Idi-Araba, Lagos
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrmt.jrmt_14_21

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  Abstract 


Background: Delayed intervention in chronic viral hepatitis results in progression to fibrosis and hepatocellular carcinoma. Determining the degree of liver fibrosis is invaluable in the initiation of clinical interventions, prevention of progression, and prognostication of end-stage liver disease. Considering the risks of liver biopsy (the standard for assessing fibrosis), safer methods are necessitated. Aim: The aim of this study was to determine the reliability of ultrasonographic Portal Venous Index (PVI) in assessing liver fibrosis. Subjects and Methods: Doppler Ultrasonography-determined Aspartate-Platelet Ratio Index (APRI) Score. Results: The mean age for the subjects was 35.79 ± 10.75 years and controls was 36.51 ± 11.31 years. They were sex matched. HBV was more common, with a 99:3 HBV: HCV ratio. HBV immunization compliance in both the groups was poor. The median PVI of the subjects and controls was 0.36 and 0.42, respectively, which was statistically significant (P = 0.025). There was no significant difference in median PVI between subjects with and without significant fibrosis as determined by APRI score. There was an inverse but moderate correlation between PVI and APRI score (r = −0.57, P = 0.569). The area under the receiver operating characteristic curve was 0.524 (95% confidence interval: 0.36–0.69). The cutoff for PVI was 0.34 with a sensitivity of 57.1% and a specificity of 57.4%. Conclusion: PVI is useful in distinguishing healthy individuals from virus-induced chronic liver diseases but could not adequately determine the degree of liver fibrosis.

Keywords: Aspartate aminotransferase-to-platelet ratio index, chronic liver disease, noninvasive assessment, portal venous index, ultrasonography, viral hepatitis


How to cite this article:
Soyebi KO, Agboola AS, Oyeleke GK. Diagnostic value of ultrasonographic portal venous index in the assessment of liver fibrosis in chronic viral hepatitis in Lagos, Nigeria. J Radiat Med Trop 2021;2:72-8

How to cite this URL:
Soyebi KO, Agboola AS, Oyeleke GK. Diagnostic value of ultrasonographic portal venous index in the assessment of liver fibrosis in chronic viral hepatitis in Lagos, Nigeria. J Radiat Med Trop [serial online] 2021 [cited 2022 Jan 28];2:72-8. Available from: http://www.jrmt.org/text.asp?2021/2/2/72/331523




  Introduction Top


The World Health Organization (WHO) estimates that 2 billion people worldwide have been infected with hepatitis B virus (HBV).[1] Nigeria has an average prevalence rate of 11.7% for HBV and 2.2% for hepatitis C virus (HCV).[2] Incidence of new cases of HBV is however decreasing since the introduction of preventive vaccination globally.[3] Despite this, chronic HBV infection is still a global health concern. Over 360 million people are persistently infected with HBV, with 1 million deaths each year due to HBV-associated chronic liver disease (CLD) such as chronic hepatitis, liver cirrhosis, or hepatocellular carcinoma (HCC).[1] The progression and outcome of liver disease due to HBV infection varies among individuals from spontaneous resolution in most cases, with about 5%–10% of adults developing chronicity to 40%–90% of children born to HBV-infected mothers progressing to persistent liver disease.[1]

HCV infection is also a global health concern, with 3% of the world's population infected with HCV and 3 million new cases each year, out of which 80% progress to chronic carriers.[1] Of these chronic carriers, 10%–20% will develop cirrhosis,[4] 1%–5% culminating in HCC, without medical intervention. Nigeria is one of the countries with the highest disease burden, with a prevalence rate of 10%–15%.[5] Owolabi and Ojo[6] work in Nigeria documented a stronger relationship between HBV-related CLDs than HCV.[2]

The pathophysiology of viral hepatitis is centered in the liver, where viral proteins interact with the immune system leading to cycle of liver parenchyma damage and repair,[7],[8] the repair involving deposition of extracellular matrix within the liver parenchyma, resulting in progressive liver fibrosis and CLD.[9] Fibrosis results in end-stage liver disease if medical intervention is delayed.

Assessment of fibrosis for extent of liver damage is therefore the most important determinant of commencement of management, preventing progression, prognostication, and management of end-stage liver disease. Fibrosis is broadly assessed through histology,[10],[11] laboratory,[12],[13],[14] and imaging methods.[12],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26]

While liver biopsy for histopathology remains the method of choice, it is less attractive for its invasiveness, risks, and errors such as misclassification of fibrosis by at least 1 grade in 20%–30% of cases[11] and failure to diagnose cirrhosis in 10%–30% of cases.[11] Mortality rate of 3 in 10,000 procedures after liver biopsy has also been documented in the literature.[11] Biopsy's adverse effects resulted in inconsideration of noninvasive methods for assessment of liver fibrosis[12] such as clinical presentation, biochemical and hematologic blood tests (aspartate aminotransferase-to-platelet ratio index [APRI]),[13],[14] serum markers of fibrosis and inflammation, combinations of clinical and blood test results, quantitative assays of hepatic function, genomics, and radiologic imaging studies.[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26]

APRI score involves the determination of ratios of two laboratory tests (aspartate aminotransferase and platelet count) with proven clinical value in predicting and assessing liver fibrosis[13] and inflammation from various etiologies. APRI has been recommended by the WHO in the evaluation and monitoring of liver disease status.[14]

Imaging modalities such as ultrasonography,[15],[16] transient elastography (FibroScan),[17] acoustic radiation force impulse (ARFI) measurements,[18],[19] computed tomography, and magnetic resonance imaging have also been used to assess diseased liver's morphologic changes. Abdominal ultrasonography has become an integral part of the noninvasive methods of evaluation of the liver in patients with CLD.[16] Duplex Doppler provides further hemodynamic information regarding the presence or absence of flow and the direction and velocity of flow of the hepatic vasculature predicting the status of liver disease.[20],[21],[22],[23],[24],[25],[26]

Doppler ultrasound of the portal vein (for the purpose of determining the PVI) has been a noninvasive means of diagnosing fibrosis in chronic hepatitis[25] assessing portal vein pulsatility. It is derived by obtaining the maximum (Vmax) and minimum (Vmin) portal vein velocities using the formula: PVI = (Vmax − Vmin)/Vmax.[25]

Liver fibrosis is known to alter liver hemodynamics, and the confirmation of a relationship between the PVV and liver fibrosis suggests that PVI can be used as a noninvasive and cheaper alternative over liver biopsy for assessing liver fibrosis in patients with chronic viral hepatitis.[23] The portal vein from which the PVI is determined is easily identified on abdominal ultrasound and the portal venous index itself is independent of Doppler angle which is a rate-limiting step in most Doppler studies, making PVI an easy to determine parameters for assessing liver fibrosis in chronic viral hepatitis. Hence, the purpose of this study is to determine the diagnostic value of PVI in research participants with chronic viral hepatitis and correlate the findings with other diagnostic parameters such as APRI, comparing these findings in both the research and control groups.


  Subjects and Methods Top


This was a prospective case-controlled study of 102 research precipitants with APRI confirmed liver fibrosis from hepatitis B or hepatitis C, attending the Gastroenterology clinic of Lagos University Teaching Hospital over a 6-month period. The control group was negative for HBsAg/HCV screening test and was matched for age and gender with the research participants. All the participants, 18 years+ with no significant history of alcohol consumption and no comorbidities, gave written consent to participate in the study. Administering a standard questionnaire clinical and social history, demographic parameters including height and weight from which body mass index was calculated were obtained. Laboratory values of aspartate aminotransferase and platelet count were obtained for each research participant and control.

All the participants had grayscale abdominal ultrasonography using Adeyekun and Tsebi's protocol[16] on Toshiba Ultrasound Machine (MODEL TUS-X100s) and 1–6 MHz curvilinear transducer for liver size, liver margin/outline, and parenchymal echo pattern [Figure 1]a.
Figure 1: (a-c) Images from B-mode ultrasound, Duplex ultrasound (grayscale ultrasound on which is superimposed color Doppler), and triplex ultrasound (duplex ultrasound with displayed spectral waveform). B-mode ultrasound (subcostal view) showing the main portal vein in longitudinal plane from which the main portal vein diameter was determined. Note the inferior vena cava which is a posterior relation of the portal vein. Duplex Doppler scan showing the hepatopetal flow of the portal vein (right intercostal view). Triplex study: Spectral velocity waveform of the portal vein showing pulsatility of the portal vein and the maximum (thin white arrow) and minimum velocity (thick white arrow) from which the portal venous index was determined

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Subsequently, Doppler ultrasound interrogation of the portal vein was carried out using Mahajan et al.'s methodology.[20] The status of portal vein patency, its diameter, direction of flow within the vein, and blood flow velocity were all determined [Figure 1]b and [Figure 1]c. All velocity measurements were performed, with insonation angle between longitudinal axis and sound wave being <60°. The lowest value of wall filter setting obtainable was utilized and the pulse repetition frequency was adjusted manually to the lowest setting without aliasing.[20] Measurements were taken during few seconds of apnea or slow inspiration where apnea was impossible, in order to avoid motion artifacts. Values obtained at portal vein Doppler hemodynamics, as well as B-mode ultrasonography of the liver, were recorded. The PVI was then determined from the obtained portal vein maximum and minimum velocity values (cm/s) using the formula: PVI= (Vmax − Vmin)/V max.

The derived PVI of the study group was then compared with the control group to determine the variability between the two groups. The PVI for the study group was subsequently correlated with their APRI score to determine the accuracy of Doppler PVI as a noninvasive method for assessing liver disease by establishing the relationship between PVI, APRI score, and liver fibrosis. The findings obtained were further compared with established results in published studies.

The Statistical Package for the Social Sciences (SPSS) version 25 software for Windows (Chicago, IL, USA, 2007) analyzed the data and presented findings as mean ± standard deviation for parametric data while nonparametric data were presented as median (interquartile range). Independent t-test and Mann–Whitney U-test were used for parametric and nonparametric data, respectively. Categorical variables were presented as frequencies and percentages. Chi-square test was also used on categorical variables. Spearman correlation coefficient was used to test relationship between PVI and APRI score. Receiver operating characteristic (ROC) curve was plotted for PVI in relation to APRI score to assess the sensitivity and specificity levels of PVI as a determinant of chronic liver fibrosis. P <0.05 was considered statistically significant.


  Results Top


[Table 1] displays the sociodemographic parameters of the research participants – 57 males and 45 females (55.9% and 44.1%, respectively) and statistically correlated control group – 52.2% and 47.8% of males and females, respectively (P = 0.61).
Table 1: Demographic, educational, and clinical characteristics of the participants

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The ages of all participants ranged from 18 to 70 years (study group: mean age was 35.79 ± 10.57 years and control group = 36.51 ± 11.31 years). The mean age difference was not statistically significant (P = 0.65). Seventy-one percent of the research participants were <40 years; 38.02% of whom were in the <30-year-old bracket; the 61–70 age range was the least featured (5%) of the entire study population.

The more common infection was HBV (99, 97.1%) while HCV infection was detected in 3 (2.9%) of the research participants.

Poor HBV immunization history was elicited in both the study and control groups with no statistically significant difference (P = 0.27) between the study group (5, 4.9%) and the control group (8, 8.9%). Past history of blood transfusion was not a prominent clinical event in both the research group and the control group (4, 4.4%, and 3, 2.9%, respectively, with P = 0.58).

Sonographic parameters

The portal vein flow velocity waveform was more pulsatile in the control group than the study group. The median PVI value of 0.42 (0.33–0.48) for the control group and 0.36 (0.29–0.47) for the study group was obtained. This was statistically significant (P = 0.025), however, the median PVI value within the study group when grouped into those with significant and insignificant fibrosis as determined by APRI score was not statistically significant (P = 0.836).

Seventy-eight percent of the study group and 80.9% of the control group have a PVI range of between 0.2 and 0.5 while 4% and 3.4% of the subjects and controls had a PVI <0.2.

Values of PVI >0.5 were obtained in 18% of the research participants and 15.7% of the controls.

The mean values for Vmin (cm/s) for the study group and the control group were 16.29 ± 6.42 and 17.48 ± 7.16 (P = 0.225), respectively, and the mean values for Vmax (cm/s) for the study group were 26.08 ± 8.14 and 29.02 ± 9.63 for the control group (P = 0.230) [Table 2].
Table 2: Sonographic parameters of the study participants

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The mean value of the portal vein diameter (cm) of the case and control groups was statistically significant (P < 0.0002). All participants in the study and control groups had normal centripetal (hepatopetal) flow.

Degree of fibrosis as determined by aspartate aminotransferase-to-platelet ratio index score

APRI score was used to group subjects into those with insignificant fibrosis (APRI score <1.5) and those with significant fibrosis (APRI score >1.5). Based on APRI scoring, 6.9% of the research participants had significant fibrosis (APRI score >1.5) while 78.2% and 14.9% had APRI scores of <0.5 and 0.5–1.5, respectively, and were grouped as having insignificant fibrosis [Table 3] inferring that the correlation between PVI and APRI was moderate and inverse (r = −0.57) but not statistically significant (P = 0.569) [Figure 2].
Figure 2: Scatter plot showing the correlation between aspartate aminotransferase-to-platelet ratio index score and PVI. The spearman correlation coefficient did not show any statistically significant relationship between aspartate aminotransferase-to-platelet ratio index score and PVI (r = -0.57, P = 0.569)

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Table 3: Median PVI of subjects based on aspartate aminotransferase-to-platelet ratio index score classification severity of fibrosis

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To define the PVI cutoff for the diagnosis of liver fibrosis in patients with chronic hepatitis due to HBV or HCV infection, a ROC curve was obtained [Figure 3]. The area under the ROC curve was 0.524 with a 95% confidence interval (0.36–0.69). The ideal cutoff point for PVI was calculated to be 0.34 with a sensitivity equal to 57.1% and a specificity equal to 57.4% at a PVI cutoff of 0.34 [Figure 3].
Figure 3: ROC curve graph for sensitivity plotted against PVI. Specificity for the diagnosis of fibrosis

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  Discussion Top


CLD refers to a long-term pathological process of continuous destruction of liver parenchyma and its gradual substitution with fibrous tissue, which ultimately results in liver cirrhosis associated with fatal outcomes.[12]

The most common cause of CLD in the world is viral hepatitis. Nigeria has one of the highest prevalence rates of HBV infections but a low prevalence rate of HCV infection. This low HCV prevalence rate in our locality is corroborated by this study as only 2.9% of the study group had HCV, a finding (2.2%) similar to Adegoke et al.'s[2] study.

Owolabi et al.[6] also reported HCV as not strongly implicated in the pathogenesis of CLD in Nigeria. However, more studies with a larger sample size are needed before definite conclusion can be arrived at.

This study shows that CLD is more common in males where 55.9% of the subjects in this study were males. This is similar to the result obtained in Nigeria by Maaji et al.[27] Ndububa et al.[28] also reported 45 males out of a total of 70 participants in the study on chronic hepatitis in Nigerian patients in Ile-Ife, Nigeria.

The age range of 18–70 years of all the participants in this study is similar to the age range of 18–70 years, Ndububa et al.'s[28] study at Ile-Ife and 23–78 years reported in a Greek study by Tziafalia et al.[26] The mean age of 36.15 years in this study is higher than Ndububa et al.'s[28] study (29.82 years) but lower than 53.6 years reported by Tziafalia et al.[26] This could be due to cultural and social differences including culture of National Health-Care Policies-enabled early help seeking.

Also evident is the poor compliance with HBV immunization among the participants: 95.1% and 91.1% of the subjects and controls, respectively, had not been immunized against HBV as documented (LUTH-based study).[29]

There is a need for assessment and continuous monitoring of degree of liver fibrosis in patients with chronic viral hepatitis as degree of fibrosis determines the management and prevention of end-stage liver disease. At present, there are three broad methods of assessing fibrosis, namely histology, serology, and imaging. Liver biopsy is the gold standard for diagnosis and assessment of liver fibrosis. However, it is highly invasive and fraught with complications. In resource-poor countries, the WHO recommends the use of APRI scoring for the assessment and monitoring of CLD due to viral hepatitis.[14]

Chronic viral hepatitis leads to varying degrees of liver inflammation and fibrosis which overtime result in detectable morphological and hemodynamic changes in the liver and its vasculature. Most imaging modalities of the liver that assess chronic viral hepatitis look for the morphologic and hemodynamic effect of inflammation and fibrosis on the liver unlike serological tests which assess function and metabolic changes.[13]

Grayscale sonography,[15],[16] elastography, and ARFI[18],[19] which evaluate the changes in the diseased liver parenchyma and its rigidity, respectively, are inadequate to fully assess the damages from the viral insults. Hemodynamic changes in the liver give more reliable information on the disease process of CLD, and these can be evaluated by a large number of Doppler ultrasound parameters[20],[21],[22],[23],[24],[25],[26] for evaluating these hemodynamic changes.

There have been studies which evaluated portal vein velocities in isolation. Our study in addition evaluated the Vmax and Vmin of the portal vein and found no statistically significant difference between the subjects and controls similar to Bernatik et al.[21] findings, who compared Vmax in patients with varying grades of liver fibrosis and found no significant difference in Vmax.

PVI is defined as a parameter that evaluates portal vein pulsatility. Changes in PVI were first observed in patients with cardiac failure; later, it was discovered that patients with CLD also demonstrated changes in portal vein waveform pattern.[30]

There were three pulsatility wave patterns of the portal vein obtained in this study; majority had the more common slight fluctuation pattern with a PVI range of >0.2 and <0.5 (78% and 80.9% of the study and control groups, respectively) similar to Barakat's[30] study who studied portal vein pulsatility and spectral width changes in patients with portal hypertension where 77.6% of the cases had a PVI >0.2 and <0.5. Other patterns obtained in this study were >0.5 (15.7% of the controls and 18% of the subjects). Barakat[30] had 22% of the cases having this pattern. No subject in this study had a PVI >1 (systolic flow interruption) like Barakat's study.[30] However, 3.4% of the control group and 4% of the study group had < 0.2 (nonpulsatile/flat wave envelope) in this study, a finding reported by Galix et al.[31] but not observed in Barakat's[30] study.

Also observed in this study is the lower pulsatility of the portal vein velocity waveform in patients with CLD due to HBV and HCV infection when compared to healthy controls after quantification using PVI, a finding which was statistically significant and in agreement with similar finding to Rocha et al.'s study.[25] It has been postulated that this phenomenon might be due to increase in portal venous resistance and also the pathological fibrotic changes in the liver which results in decreased transmission of atrial pressure changes through the hepatic veins.[32] PVI was however not reliable in grading fibrosis when compared to APRI score which grouped the subjects into those with significant and insignificant fibrosis, a finding similar to Barakat's study[30] and Rocha et al.'s study.[25]

This could be due to the small number of patients with significant fibrosis (6.9%) in this study as it is known that liver morphologic and hemodynamic changes occur more in patients with significant fibrosis and cirrhosis.

A PVI cutoff of 0.34 was obtained after constructing an ROC; this falls within the normal range for PVI of between 0.20 and 0.50, suggesting that PVI is not a good surrogate marker for liver fibrosis of chronic viral hepatitis origin, a finding also noted in the study by Bernatik et al.[21]

Portal vein diameter (PVD) was also assessed in the present study, with the mean PVD of the control group being 9.45 ± 1.36 mm; this is similar to the result from a study on PVD in apparently healthy adults in northern Nigeria by Luntsi et al.[33] where a mean PVD of 9.60 ± 1.41 mm was derived. Hawaz et al.[34] obtained a value of 7.9 ± 2 mm in an Ethiopian study. In this study, there was a significant difference between the mean PVD of the subjects and controls, with the mean PVD of 10.51 ± 1.60 mm for the subjects being of higher value than the controls (9.45 ± 1.36 mm). A similar finding was also obtained by Usman et al.[35] who reported a mean value of 18.68 ± 2.59 mm and 10.87 ± 0.81 mm for CLD patients and control cases, respectively. This was attributed to ongoing inflammatory and fibrotic changes which lead to increase portal vein circumference resistance, gradual decrease of PVV, and gradual increase in PVD.


  Conclusion Top


Therefore, since the velocimetry of the portal vein is only able to detect the changes in liver hemodynamics in chronic viral hepatitis but unable to evaluate the chronic changes of fibrosis in liver parenchyma, a parameter which APRI superiorly evaluates and an information required for adequate planning of successful management of chronic viral hepatitis, PVI cannot be adopted as a surrogate marker in the management of chronic viral hepatitis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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  [Full text]  


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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  In this article
Abstract
Introduction
Subjects and Methods
Results
Discussion
Conclusion
References
Article Figures
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