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Portal venous and hepatic artery hemodynamic variation in non-alcoholic fatty liver disease



Non-alcoholic fatty liver disease remains asymptomatic until advanced disease, when risk factor modification and available treatment become no longer effective. Studies on hepatic vasculature can be informative about parenchymal injury and disease severity through the study of changes affecting vascular compliance. This study aimed to study portal vein and hepatic artery hemodynamic variation in non-alcoholic fatty liver and to correlate it with disease severity.


This case control study included 80 participants; those were further divided into four groups; healthy volunteers and non-alcoholic fatty liver disease patients’ grade 1, 2, and 3. We did anthropometric measures, laboratory tests, transient elastography, and Doppler ultrasound for all participants, and then we collected the data and analyzed it using SPSS version 25.

Doppler findings showed that peak maximum velocity, peak minimum velocity, mean flow velocity, portal vein pulsatility index of portal vein, and hepatic artery resistivity index were significantly lower in non-alcoholic fatty liver disease patients than in healthy people. All indices were indirectly proportionate to the grade of the disease except for peak minimum velocity which was significantly lower on comparing grade 3 patients with grades 1 and 2 patients.


Reduction of portal flow and increase in hepatic artery flow in fatty liver correlates with disease severity and can help as a non-invasive measure in diagnosis and grading of non-alcoholic fatty liver disease.


Non-alcoholic fatty liver disease (NAFLD) affects about 25% of the population; NAFLD and/or its complications is considered the commonest chronic progressive liver disease especially in developed countries [1].

NAFLD is macrovesicular steatosis in more than 5% of hepatocytes, in the absence of a secondary cause as alcohol or drugs. Histological lesions ranging from non-alcoholic fatty liver to steatohepatitis, fibrosis, and cirrhosis are included in pathogenesis [2]. Liver biopsy is the sure method to assessment liver fibrosis; yet it is associated with several drawbacks as invasiveness, cost, high sampling errors, and possible related morbidity and mortality [3]. Accordingly, non-invasive methods to assess liver fibrosis have been developed including blood biomarkers and imaging modalities [4]. Transient elastography (TE) is a non-invasive and easy modality that detects the level of fibrosis through measuring liver stiffness using the transmission of mechanical waves. Controlled attenuation parameter (CAP) enables the measurement of stiffness and steatosis simultaneously [5]. However, obesity, ascites, and elevated alanine aminotransferase (ALT) value may affect the accurate measurement of liver stiffness [6]. Duplex Doppler ultrasonography (US) is an important non-invasive method in evaluating hepatic vasculature and diagnosing some liver parenchymal diseases [7] as diffuse fatty infiltration in the liver alters hemodynamics in the portal vein as well as hepatic artery resistance [8].


A case-control study including 80 participants, after ethical committee approval and informed consent approval, were selected and classified into the following:

  • Control group: 20 healthy volunteers (with CAP score < 220)

  • Grade 1: 20 patients with grade 1 NAFLD (CAP score 220–259)

  • Grade 2: 20 patients with grade 2 NAFLD (CAP score 260–289)

  • Grade 3: 20 patients with grade3 NAFLD (CAP score ≥ 290) [9]

Subjects with alcohol consumption of more than 20 g/day, other causes of chronic liver disease, morbid obesity, and diabetics were excluded from the study population.

All participants were subjected to clinical examination including anthropometric measures, laboratory investigations including complete blood count (CBC), international normalization ration (INR), blood urea nitrogen (BUN), serum creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT), total protein, albumin (Alb.), total bilirubin (T.Bil.), direct bilirubin (D.Bil.), gamma-glutamyl transferase (GGT), fasting blood sugar (FBS), glucosylated hemoglobin (HBA1C), and lipid profile (triglycerides, total cholesterol, HDL cholesterol, LDL cholesterol).

Fatty liver index was calculated in all subjects [10].

Transient elastography (fibroscan): single experienced operator performed all Fibro Scan examinations as per the manufacturer’s recommendations. With the patient lying in the dorsal decubitus position, the tip of the transducer probe was placed on the skin between the ribs over the right lobe of the liver.

Doppler US

Doppler US was performed by a single radiologist using a Philips HD5 ultrasound machine with a convex arrayed (1 ~ 6 Mhz) transducer and Linear arrayed (3 ~ 12 Mhz) transducer. All subjects fasted overnight

Portal vein assessment

Portal vein assessment was done with patient in the left lateral decubitus with breath held in inspiration and the measurements were taken at the level of the main portal vein before the bifurcation. The transducer was oriented along the longitudinal axis of the main portal vein using a para-median or slightly oblique plan. The point of measurement was midway between the confluence of the splenic and superior mesenteric veins and the bifurcation of the portal vein during quiet inspiration. The Doppler angle was always < 60°. The maximum (Vmax), minimum (Vmin), and mean flow (MFV) velocities (cm/s) were recorded in each patient, and the vein pulsatility index (VPI) was calculated using the formula VPI = (Vmax − Vmin)/Vmax) to detect any increase or decrease in portal vein pulsatility in NAFLD

Hepatic artery assessment

The hepatic artery indices were measured at the level of porta-hepatis with patient lying in the supine position. The main hepatic artery was selected for examination as it supplies both hepatic arteries and is seen at the portal triad, measurements of hepatic artery resistive index (HARI) were obtained with the patient in suspended respiration [peak-systolic velocity (PSV) minus the end-diastolic velocity (EDV) divided by the PSV of the hepatic artery (HARI = [PSV − EDV]/PSV)].


The collected data was analyzed using Statistical Package for Social Science (SPSS 25). Mean and standard deviation (± SD) was used for parametric numerical data. Student’s t test, ANOVA test, and post hoc Bonferroni test to compare between means and correlation analysis (using Pearson’s method) to assess the strength of association between two quantitative variables.

P value: level of significance: (P > 0.05: non-significant (NS), P < 0.05: significant (S), P < 0.01: highly significant (HS).


This study included 20 healthy volunteers (control group) and 60 NAFLD patients (case group); case group was further classified into 3 subgroups according to their CAP score (grade 1, grade 2, and grade 3). All patients were sex- and age-matched with average age of 45 years. NAFLD patients had significantly higher BMI and waist circumference, total cholesterol, triglycerides, LDL, FBS, AST, ALT, GGT, BUN, fatty liver index, and lower HDL than control group (P < 0.001 for all), yet there were no statistically significant differences between case and control groups regarding creatinine, HBA1C, or bilirubin (direct and indirect).

All examined Doppler indices (Vmax, Vmin, MFV, VPI, HARI) were significantly lower in NAFLD patients than in healthy individuals (Table 1).

Table 1 Doppler indices comparison between case and control groups

Vmax, MFV, VPI, and HARI were significantly indirectly proportionate to NAFLD grade, yet Vmin was significantly lower on comparing grade 3 with grades 1 and 2 (Table 2).

Table 2 Doppler indices comparison between 3 grades of NAFLD

On comparing different grades of NAFLD using ANOVA and post hoc Bonferroni tests, total cholesterol was directly proportionate to the grade of NAFLD, HDL was significantly higher in grade 1 NAFLD than grades 2 and 3, and triglycerides were significantly higher on comparing grade 3 to grade 1 NAFLD patients only (Table 3).

Table 3 Comparison between the 3 grades of NAFLD

On correlating Doppler indices in NAFLD patients with variable parameters, there was highly significant correlation between all Doppler indices and age, BMI, waist circumference, lipid profile, fatty liver index, and CAP score, yet there was no significant correlation with fasting blood sugar (Table 4).

Table 4 Correlation between Doppler indices and significant variables in NAFLD


In the present study, the mean age of NAFLD patients was 45.95 ± 7.2 years which is consistent with NICE guidelines 2018 [4]

This study showed a significant difference in BMI between case and control groups which agrees with Rui et al. [11]. Ghobadi et al. 2014 [12] as well found a significant correlation between BMI and grades of NAFLD, as our study showed a statistically significant difference regarding BMI between grade 1 versus grades 2 and 3.

Concerning blood sugar, this study showed statistically significant difference between case and control groups. This agrees with Zhengjun [13], as impaired hepatic lipid and lipoprotein settling and increased oxidative stress in liver cells may increase liver fat accumulation and result in insulin resistance, this leads to increase in hepatic glucose production and elevated blood glucose [14].

Zhengjun [13] postulated that triglyceride, total cholesterol, and LDL cholesterol in NAFLD group were significantly higher than those in control group, which matches our study, as we found statistically significant differences between case and control groups regarding lipid profile. Furthermore, our study showed that HDL in case group was significantly lower than in control group, but this was not consistent with the study of Zhengjun [13] as there was no significant difference regarding HDL.

This study showed that increasing grade of NAFLD was significantly associated with worse lipid profile, where there were differences between three grades as regard total cholesterol and LDL, there was statistically significant difference between grade 1 and grade 3 in triglycerides and HDL, and between grade 1 and grade 2 in HDL. This agrees with Dhumal et al. [15] who found that increasing grades of NAFLD were significantly associated with increasing serum total cholesterol, LDL, and VLDL and decreasing HDL, yet they found no significant association between serum triglyceride.

Regarding portal vein Doppler indices, this study revealed statistically significant differences between case and control groups in all Doppler indices.

Vmax, Vmin, and VPI in case group were significantly lower than in control group. This was compatible with Besir et al. [16]. Balasubramanian et al. [17], although agreed with our finding regarding Vmax, found no significant difference regarding Vmin.

On comparing 3 grades of NAFLD, this study showed significant decrease in Vmax and VPI with increasing the grade of NAFLD. This agrees with Besir et al. [16] and Balasubramanian [17]. Yet, not with Ehsan et al. [18] who found no significant difference in VPI between fatty liver grades.

Vmin showed significant decrease only on comparing grade 3 versus grades 1 and 2; this agrees with Besir et al. [16] who postulated that Vmin decreased as the degree of hepatosteatosis increased.

MFV in case group was significantly lower than in control group which corresponds with Ehsan et al. [18]. Moreover, MFV was significantly decreasing with increasing NAFLD grade which is consistent with Balasubramanian [17].

These findings regarding velocity of the portal flow and portal vein pulsatility index can be explained by the hypothesis that liver infiltration with fat increases flow resistance in portal vein reducing hepatic portal blood flow [19].

Regarding hepatic artery Doppler, this study revealed that HARI in case group was significantly lower than in control group. This agreed with Claudio et al. [20] and Balasubramanian [17] who agreed also with our finding that HARI was significantly decreasing with increasing NAFLD grade. These findings suggest an increased hepatic artery blood flow which may occur as a compensatory mechanism for reduced portal flow with the progression of hepatic steatosis [21].


Liver biopsy was not carried out to confirm the diagnosis and severity of fatty liver and there was no follow-up for the cases.


Reduction of portal flow and increase in hepatic artery flow in fatty liver correlates with disease severity and can help as a non-invasive measure for NAFLD diagnosis and grading.

Availability of data and materials

Data are available with corresponding author to be presented upon request.





Alanine aminotransferase


Aspartate aminotransferase


Body mass index


Blood urea nitrogen


Controlled attenuation parameter


Complete blood count


Direct bilirubin


End-diastolic velocity


Fasting blood sugar


Gamma-glutamyl transferase


Hepatic artery resistive index




Glucosylated hemoglobin


High-density lipoproteins


Highly significant


International normalization ration


Low-density lipoproteins


Mean flow velocity




Non-alcoholic fatty liver disease






Peak-systolic velocity




Standard deviation


Statistical Package for Social Science


Total bilirubin


Transient elastography


Total leucocyte count




Very low-density lipoprotein


Peak maximum velocity


Peak minimum velocity


Vein pulsatility index


  1. Hirode G, Vittingho E, Wong RJ (2019) Increasing clinical and economic burden of nonalcoholic fatty liver disease among hospitalized adults in the United States. J Clin Gastroenterol 10:1097

    Google Scholar 

  2. Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M (2016) Global epidemiology of nonalcoholic fatty liver disease – Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 64(1):73–84.

    Article  PubMed  Google Scholar 

  3. Janiec DJ, Jacobson ER, Freeth A, Spaulding L, Blaszyk H (2005) Histologic variation of grade and stage of non-alcoholic fatty liver disease in liver biopsies. Obes Surg 15(4):497–501.

    Article  PubMed  Google Scholar 

  4. NICE guideline NCGC (2018) Non-alcoholic fatty liver disease. Assessment and management of non-alcoholic fatty liver disease (NAFLD) in adults, children and young people. Guideline National Institute for Health and Care Excellence

    Google Scholar 

  5. Karlas T, Petro D, Sasso M et al (2017) Individual patients data meta-analysis of controlled attenuation parameter (CAP) technology for assessing steatosis. J Hepatol 66(5):1022–1030.

    Article  PubMed  Google Scholar 

  6. Sasso M, Tengher-Barna I, Ziol M, Miette V, Fournier C, Sandrin L, Poupon R, Cardoso AC, Marcellin P, Douvin C, de Ledinghen V, Trinchet JC, Beaugrand M (2012) Novel controlled attenuation parameter for noninvasive assessment of steatosis using Fibroscan (R): Validation in chronic hepatitis C. J Viral Hepat 19(4):244–253.

    CAS  Article  PubMed  Google Scholar 

  7. von Herbay A, Frieling T, Haussinger D (2016) Association between duplex Doppler sonographic flow pattern in right hepatic vein and various liver diseases. J Clin Ultrasound 29:25

    Article  Google Scholar 

  8. Mihmanli I, Kantarci F, Yilmaz MH et al (2015) Effect of diffuse fatty infiltration of the liver on hepatic artery resistance index. J Clin Ultrasound 33:95. 20

    Google Scholar 

  9. Nirav K, Sarah H, Roshan R et al (2016) Comparison of controlled attenuation parameter and liver biopsy to assess hepatic steatosis in pediatric patients. J Pediatr 173:160–164

    Article  Google Scholar 

  10. Bedogni G, Bellentani S, Miglioli L, Masutti F, Passalacqua M, Castiglione A, Tiribelli C (2006) The fatty liver index: a simple and accurate predictor of hepatic steatosis in the general population. BMC Gastroenterol 6:33 11., 1

    Article  Google Scholar 

  11. Rui F, Jufang W, Jinman D (2018) Association between body mass index and fatty liver risk: A dose-response analysis. Sci Rep 8:15273

    Article  Google Scholar 

  12. Ghobad A, Atefeh Y, Rouhangiz A et al (2014) Correlation of body mass index and serum parameters with ultrasonographic grade of fatty change in non-alcoholic fatty liver disease. Iran Red Crescent Med J 16(1):e12669

    Google Scholar 

  13. Zhengjun Z, Jijun W (2018) and HongmeiW. Correlation of blood glucose, serum chemerin and insulin resistance with NAFLD in patients with type 2 diabetes mellitus. Exp Ther Med 15(3):2936–2940

    Google Scholar 

  14. Bian H, Yan H, Zeng M et al (2011) Increased liver fat content and unfavorable glucose profiles in subjects without diabetes. Diabetes Technol Ther 13(2):149–155

    CAS  Article  Google Scholar 

  15. Dhumal U, Madole M, Aher J (2013) Comparison of lipid profile in different grades of non-alcoholic fatty liver disease diagnosed on ultrasound. Asian Pac J Trop Biomed 3(11):907–912

    Article  Google Scholar 

  16. Besir E, Ali T, Ramazan B et al (2016) Portal vein hemodynamics in patients with non-alcoholic fatty liver disease. J Clin Diagn Res 10(8):TC07–TC10

    Google Scholar 

  17. Balasubramanian P, Boopathy V, Govindasamy E et al (2016) Assessment of portal venous and hepatic artery haemodynamic variation in non-alcoholic fatty liver disease (NAFLD) patients. J Clin Diagn Res 10(8):TC07–TC10

    PubMed  PubMed Central  Google Scholar 

  18. Ehsan S, Ghanaei FM et al (2011) Comparison of portal vein doppler indices and hepatic vein doppler waveform in patients with nonalcoholic fatty liver disease with healthy control. Hepat Mon 11(9):740–744.

    Article  Google Scholar 

  19. Dos Reis G, Monteiro ML, Ferreira DE et al (2016) Liver haemodynamic patterns in nonalcoholic steatosis: Doppler ultrasonography and histological evaluation. Gastroenterol Dietol 62(1):19–29

    Google Scholar 

  20. Claudio T, Marco T, Stefano R et al (2016) Hepatic artery resistive index (HARI) and non-alcoholic fatty liver disease (NAFLD) fibrosis score in NAFLD patients: cut-off suggestive of non-alcoholic steatohepatitis (NASH) evolution. J Ultrasound 19(3):183–189

    Article  Google Scholar 

  21. Balci A, Karazincir S, Sumbas H, Oter Y, Egilmez E, Inandi T (2008) Effects of diffuse fatty infiltration of the liver on portal vein flow haemodynamics. J Clin Ultrasound 36(3):134–140.

    Article  PubMed  Google Scholar 

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Thanks should be applied to radiology staff at the Ain Shams University for their help in facilitating data collection.


No funding was obtained for this study.

Author information




T Y designed the study. N A did data analysis and interpretation. C A drafted the manuscript. M S did critical revision of the manuscript for important intellectual content. M S did radiology work-up, and M M supervised the study. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Nourhan Assem.

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Ethics approval and consent to participate

This study had been performed in accordance with the ethical standards. Faculty of Medicine, Ain Shams University Ethical Committee approval was taken before starting the study, and the study protocol conforms to the ethical guidelines of the 1975 Declaration of Helsinki. A written consent was obtained from each participant. Committee’s reference number is FWA 000017585.

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Sabry, M., Youssef, T., Shaker, M. et al. Portal venous and hepatic artery hemodynamic variation in non-alcoholic fatty liver disease. Egypt Liver Journal 11, 58 (2021).

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  • Non-alcoholic fatty liver
  • Hepatic artery
  • Portal vein