Portal vein thrombosis (PVT) and Budd-Chiari syndrome (BCS) are rare vascular disorders with both well-recognized and less commonly identified etiologies.

This study aims to investigate the etiologies of portal vein thrombosis (PVT) and Budd-Chiari syndrome (BCS), thereby enhancing improving early detection and management strategies for these conditions. A retrospective review was undertaken to identify the etiologies of PVT and BCS.

A detailed clinical evaluation was performed and all underlying diseases, such as MPD, and related conditions (e.g. surgery) associated with thrombosis were recorded.

The study comprised a total of 73 patients, with 58 diagnosed with PVT and 15 with BCS. Of these patients, 56 (76.7%) had at least one underlying disease. The most prevalent underlying diseases in patients with PVT were cirrhosis (32/58, 55.2%), myeloproliferative disease (3/58, 5.2%), malignancy (4/58, 6.9%), and rheumatological conditions (4/58, 6.9%). For BCS, 11/15 patients (73.3%) had at least one predisposing condition, including cirrhosis in six cases. Congenital causes were identified in 16/58 cases of PVT (27.6%), in 7/15 cases of BCS (46.7%). Thirty-two patients had previously undergone gastrointestinal surgery (PVT 24/58, BCS 8/15); surgery was the sole etiology in 15/73 patients (20.5%). Homocysteinemia was common (PVT 20/58, BCS 5/15). A multitude of rare etiologies were identified, including paroxysmal nocturnal haemoglobinuria, Crohn's disease, nephrotic syndrome, drug therapies, pregnancy, JAK2 mutation, and elevated factor VIII or fibrinogen.

The presence of a wide range of diverse frequent-infrequent etiologies of congenital or acquired splanchnic vein thrombosis in this cohort underscores the necessity for the implementation of appropriate diagnostic strategies in a broad spectrum of at-risk patients.

Portal vein thrombosis (PVT) is a common thrombotic complication of cirrhosis. It can lead to variceal bleeding and bowel ischemia and also complicate liver transplantation. Identifying the possible risk factors associated with PVT can aid in identifying patients at high risk, enabling their screening and potentially preventing PVT through the rational use of anticoagulants. This study focuses on examining the clinical characteristics of PVT in cirrhotic patients and identifying the clinical and biochemical factors that are linked to the development of PVT. Consecutive hospitalized cirrhotic patients between 2015 and 2023 were identified through the hospital's computerized medical records based on the Tenth Revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) coding system and retrospectively analyzed. 928 individuals were included in this study; 783 (84.3%) without PVT and 145 (15.7%) with benign PVT. Hepatitis B virus (HBV) was significantly more common in the PVT group (P-value = .02), while alcohol and primary sclerosing cholangitis (PSC) were less common in this group (P-value = .01 and .02, respectively). Hepatocellular carcinoma (HCC) (P-value < .01), ascites (P-value = .01), and spontaneous bacterial peritonitis (SBP) (P-value = .02) were more common in the PVT group. Patients with PVT had a higher international normalized ratio (INR) level (P-value = .042) and lower plasma albumin (P-value = .01). No differences were identified in white blood cell, hemoglobin, platelet, and bilirubin levels. However, patients with PVT had higher model for end-stage liver disease (MELD) (P-value = .01) and Child-Pugh scores (P-value = .03). This study demonstrated a higher likelihood of PVT presence in cirrhotic patients with advanced age, HBV, and HCC, along with ascites, SBP, splenomegaly, hypoalbuminemia, elevated INR, and a higher MELD score. Nevertheless, additional research endeavors are necessary to accurately ascertain and validate supplementary risk factors within a broader demographic.

Several tumor and non-tumor factors affect the prognosis of hepatocellular carcinoma (HCC) patients. This study aimed to investigate the effects of hepatitis B virus (HBV) viral load on tumor and non-tumor factors in patients with HBV-associated HCC.

Patients with hepatitis B and HCC who presented to the HCC council at the Faculty of Medicine, Marmara University Liver Transplantation Institute, were included in our study. Patients were divided into two groups according to the presence or absence of HBV-DNA, and it was determined whether there were differences between these two groups with respect to tumor and non-tumor parameters.

Comparison of serum alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), hepatitis B surface antigen (HBsAg), and C-reactive protein (CRP) levels between HBV-DNA negative and positive patients showed significant differences (respectively p<0.01, p<0.01, p<0.05, and p<0.05). A major finding was a very significant difference between the two patient groups in terms of portal vein invasion (PVI) and venous invasion (p<0.001 and p<0.01, respectively). However, there was no significant difference in metastasis or lymph node involvement between HBV-DNA negative and positive patients.

Our findings suggest that HBV viral load plays an important role in PVI in HCC patients, and there is a significant relationship between HBV viral load and inflammation.

Arterial resection (AR) during pancreatectomy for curative R0 resection of pancreatic ductal adenocarcinoma (PDAC) remains a controversial procedure with high morbidity.

To investigate the feasibility and oncological outcomes of pancreatectomy combined with AR at a high-volume center for pancreatic surgery.

We retrospectively analyzed our experience in PDAC patients, who underwent pancreatic resection with AR and/or venous resection (VR) between 2007 and 2021.

In total 259 PDAC patients with borderline resectable (n = 138) or locally advanced (n = 121) PDAC underwent vascular resection during tumor resection. From these, 23 patients had AR (n = 4 due to intraoperative injury, n = 19 due to suspected arterial infiltration). However, 12 out of 23 patients (52.2%) underwent simultaneous VR including 1 case with intraoperative arterial injury. In comparison, 11 patients (47.8%) underwent AR only including 3 intraoperative arterial injury patients. Although the operation time and bleeding rate of patients with AR were respectively longer and higher than in VR, no significant difference was detected in postoperative complications between VR and AR (P = 0.11). The final histopathological findings of PDAC patients were similar, including M stage, regional lymph node metastases, and R0 margin resection. The mortality of the entire cohort was 6.2% (16/259), with a tendency to increase mortality in the AR cohort, yet without statistical significance (VR: 5% vs AR: 21.1%; P = 0.05). Although 19 (82.6%) patients had PDAC in the final histopathology, only 6 were confirmed to have infiltrated arteria. The microscopic distribution of PDAC in these infiltrated arterial walls on hematoxylin-eosin staining was classified into 3 patterns. Strikingly, the perivascular nerves frequently exhibited perineural invasion.

AR can be performed in high-volume centers for pancreatic surgery with an acceptable morbidity, which is comparable to that of VR. However, the likelihood of arterial infiltration seems to be rather overestimated, and as such, AR might be avoidable or replaced by less invasive techniques such as divestment during PDAC surgery.

Portal Vein Thrombosis (PVT), a common complication of advanced liver disease, is defined as an obstruction of the portal vein due to thrombus formation that can extend to the superior mesenteric and splenic veins. It was believed that PVT occurred predominantly due to prothrombotic potential. However, recent studies have shown that decreased blood flow related to portal hypertension appears to increase PVT risk as per Virchow's triad. It is well known that there is a higher incidence of PVTs in cirrhosis with a higher MELD and Child Pugh score. The controversy for management of PVTs in cirrhotics lies in the individualized assessment of risks versus benefits of anticoagulation, since these patients have a complex hemostatic profile with both bleeding and procoagulant propensities. In this review, we will systematically compile the etiology, pathophysiology, clinical features, and management of portal vein thrombosis in cirrhosis.

Portal vein thrombosis (PVT) after liver resection is rare but can lead to life-threatening liver failure. This prospective study evaluated patients using contrast-enhanced computed tomography (E-CT) on the first day after liver resection for early PVT detection and management.

To evaluate patients by E-CT on the first day after liver resection for early PVT detection and immediate management.

Patients who underwent liver resection for primary liver cancer from January 2015 were enrolled. E-CT was performed on the first day after surgery in patients undergoing anatomical resection, multiple resections, or with postoperative bile leakage in the high-risk group for PVT. When PVT was detected, anticoagulant therapy including heparin, warfarin, and edoxaban was administered. E-CT was performed monthly until PVT resolved.

The overall incidence of PVT was 1.57% (8/508). E-CT was performed on the first day after surgery in 235 consecutive high-risk patients (165 anatomical resections, 74 multiple resections, and 28 bile leakages), with a PVT incidence of 3.4% (8/235). Symptomatic PVT was not observed in the excluded cohort. Multivariate analyses revealed that sectionectomy was the only independent predictor of PVT [odds ratio (OR) = 12.20; 95% confidence interval (CI): 2.22-115.97; P = 0.003]. PVT was found in the umbilical portion of 75.0% (6/8) of patients, and sectionectomy on the left side showed the highest risk of PVT (OR = 14.10; 95%CI: 3.17-62.71; P < 0.0001).

Sectionectomy on the left side should be chosen with caution as it showed the highest risk of PVT. E-CT followed by anticoagulant therapy was effective in managing early-phase PVT for 2 mo without adverse events.

Cirrhotic patients with portal vein thrombosis (PVT) may have a high risk of hepatic decompensation and increased mortality. This study aimed to investigate if increased portal vein diameter is associated with PVT development.

A total of 174 cirrhotic patients were enrolled between February 1 and August 31, 2017. All participants were divided into PVT (n=62) and non-PVT (n=112) groups based on the thrombus that was detected by ultrasonography and confirmed by computed tomography angiography (CTA).

The study participants, aged 54.7±10.5 years (PVT) and 55.8±11.6 years (non-PVT), were included in this analysis. The Child-Pugh score of PVT or non-PVT was 6.6±1.3 and 5.8±0.9, respectively. Hepatitis B virus (HBV) is the primary etiological agent of cirrhosis. Logistic regression, receiver operating characteristic (ROC), and nomograph analysis designated portal diameter as the strongest independent risk factor for predicting PVT development [odds ratio (OR): 3.96, area under the ROC curve (AUC): 0.88; P<0.01], and the cutoff with predictive value for PVT development was >12.5 mm. No differences were observed in the overall survival (OS) in cirrhosis with or without PVT or stratifying on portal diameter based on the cutoff value.

Increased portal diameter is associated with an increased risk of PVT development. Patients with cirrhosis and increased portal diameter are a high-risk subgroup that may need thromboprophylaxis.

Portal vein tumor thrombus (PVTT) and extrahepatic metastasis are associated with the prognosis of hepatocellular carcinoma (HCC). We aimed to investigate the effect of hepatitis B virus (HBV) infection on HCC patients with PVTT or extrahepatic metastasis.

The clinical data of 639 patients with HCC from our hospital were retrospectively analyzed to analyze the correlation between HBV and HCC with PVTT or extrahepatic metastasis.

Univariate analysis revealed that positive hepatitis B virus surface antigen (HBsAg), a detectable serum hepatitis B virus DNA load (>500 IU/ml), cirrhosis and ascites were associated with the presence of PVTT. Positive hepatitis B virus e antigen (HBeAg), cirrhosis and ascites were associated with the presence of extrahepatic metastasis. In a multivariate regression analysis carried out a detectable serum hepatitis B virus DNA load, cirrhosis and ascites were independent risk factors of PVTT. Ascites was an independent risk factor of extrahepatic metastasis. The patients in the PVTT of type III/IV group and the PVTT of type I/II group had a significantly higher rate of positive serum HBsAg, a detectable serum hepatitis B virus DNA load (>500 IU/ml) and HBsAg + HBeAb + HBcAb test positive compared with those in the PVTT-negative group. HBsAg + HBeAb + HBcAb test positive was significantly associated with the presence of extrahepatic metastasis (P=0.028).

HBV infection and replication status are associated with the formation of PVTT or extrahepatic metastasis in patients with HCC.

Portal vein thrombosis (PVT) is a common condition in cirrhotic patients and mostly attributed to portal hypertension. The objective of our study was to examine the association of PVT with hepatocellular carcinoma (HCC) in cirrhotic patients.

A retrospective study was performed to identify cirrhotic patients with thrombosis of the portal system. Clinical and laboratory characteristics were collected and analyzed.

Thirty-nine patients were identified. Twenty-four out of 39 patients with PVT did not develop HCC (group A) after follow-up time of 38.5 months from the diagnosis of PVT. Eight patients (20.5%) were diagnosed with HCC within two weeks following diagnosis of PVT (group B). Seven patients (17.9%) were diagnosed with tumor thrombus (group C) at time of PVT diagnosis. The average age was 53.5, 66.5, and 69 years for groups A, B, and C respectively. Most patients (75 and 87.5% for groups B and C respectively) diagnosed with PVT and HCC were males. The most common cause of cirrhosis in groups B and C was chronic hepatitis B virus infection (HBV) in 62.5% and 50% respectively. The most common clinical presentation of PVT in group A was abdominal pain in 55.5% compared to new/worsening ascites in 43% and 37.5% for groups B and C respectively. The platelet count in groups B and C was higher as compared to that in group A (126 and 125 vs. 107 thousand, P = NS).

In 38.4% of cases, new diagnosis of PVT was associated with concomitant diagnosis of HCC. Identifiable risk factors were chronic HBV infection and higher platelet count.

This study was designed to identify and assess risk factors for portal vein thrombosis (PVT) in patients with cirrhosis. A total of 98 cirrhosis patients with PVT were identified and 101 cirrhosis patients without PVT were chosen as the control group in this retrospective study. Several variables were measured and the two groups PVT and non-PVT were compared statistically. PVT was identified in 98 patients (10%). Significant differences in hematocrit, international normalized ratio, albumin, bilirubin and glucose were determined between the groups (P<0.05). Out of the thrombophilic risk factors in the patients with PVT factor V Leiden was identified in 8.8%, prothrombin gene 6.6% and methylenetetrahydrofolate reductase 2.2%. There was no difference in survival time between groups (P>0.05).

Portal vein thrombosis is a fairly common and potentially life-threatening complication in patients with liver cirrhosis. The risk factors for portal vein thrombosis in these patients are still not fully understood.

This study aimed to investigate the associations between various risk factors in cirrhotic patients and the development of portal vein thrombosis.

In this case-control study performed at the Shiraz organ transplantation center, Iran, we studied 219 patients (> 18 years old) with liver cirrhosis, who were awaiting liver transplants in our unit, from November 2010 to May 2011. The patients were evaluated by history, physical examination, and laboratory tests, including factor V Leiden, prothrombin gene mutation, Janus Kinase 2 (JAK2) mutation, and serum levels of protein C, protein S, antithrombin III, homocysteine, factor VIII, and anticardiolipin antibodies.

There was no statistically significant difference in the assessed hypercoagulable states between patients with or without portal vein thrombosis. A history of previous variceal bleeding with subsequent endoscopic treatment in patients with portal vein thrombosis was significantly higher than in those without it (P = 0.013, OR: 2.526, 95% CI: 1.200 - 5.317).

In our population of cirrhotic patients, treatment of variceal bleeding predisposed the patients to portal vein thrombosis, but hypercoagulable disorders by themselves were not associated with portal vein thrombosis.

The prognostic impact of portal vein thrombosis (PVT) in liver cirrhosis remains controversial among studies, primarily because the risk stratification of PVT is often lacking. A definition of clinically significant PVT should be proposed and actively improved. Moreover, the risk factors for the development of PVT in liver cirrhosis should be fully recognized to screen and identify high-risk patients. Currently, well-recognized risk factors include a reduced portal vein flow velocity, a worse liver function, splenectomy, liver transplantation, and factor V Leiden and prothrombin G20210A mutations. Novel risk factors include an increased flow volume of portosystemic collateral vessel, thrombopoietin receptor agnonists, and non-selective beta-blockers. In contrast to the traditional perspectives, the abnormalities of procoagulant and anticoagulant factors may not contribute to the development of PVT in liver cirrhosis. Further studies should explore the role of other risk factors, such as antiphospholipid antibodies, methylenetetrahydrofolate reductase C677T gene mutation, hyperhomocysteinemia, and myeloproliferative neoplasms.

To demonstrate that caudate lobectomy is a valid treatment in cases of hepatocellular carcinoma (HCC) rupture in the caudate lobe based on our experience with the largest case series reported to date.

A retrospective study of eight patients presenting with spontaneous rupture and hemorrhage of HCC in the caudate lobe was conducted. Two patients underwent ineffective transarterial embolization preoperatively. Caudate lobectomy was performed in all eight patients. Bilateral approach was taken in seven cases for isolated complete caudate lobectomy. Left-sided approach was employed in one case for isolated partial caudate lobectomy. Transarterial chemoembolization was performed postoperatively in all patients.

Caudate lobectomy was successfully completed in all eight cases. The median time delay from the diagnosis to operation was 5 d (range: 0.25-9). Median operating time was 200 min (range: 120-310) with a median blood loss of 900 mL (range: 300-1500). Five patient remained in long-term follow-up, with one patient becoming lost to follow-up at 3 years and two patients currently alive at 7 and 19 mo. One patient required reoperation due to recurrence. Gamma knife intervention was performed for brain metastasis in another case. Two patients survived for 10 and 84 mo postoperatively, ultimately succumbing to multiple organ metastases.

Caudate lobectomy is the salvage choice for HCC rupture in the caudate lobe. Local anatomy and physiologic features of the disease render caudate lobectomy a technically difficult operation. Postponement of surgical intervention is thus recommended while the rupture remains hemodynamically stable until an experienced surgeon becomes available. Prognosis is confounded by numerous factors, but long-term survival can be expected in the majority of cases.

In this study, we aimed to describe the characteristics of portal vein tumor thrombosis (PVTT), complicating hepatocellular carcinoma (HCC) in contrast-enhanced FDG PET/CT scan.

In this retrospective study, 9 HCC patients with FDG-avid PVTT were diagnosed by contrast-enhanced fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT), which is a combination of dynamic liver CT scan, multiphase imaging, and whole-body PET scan. PET and CT DICOM images of patients were imported into the PET/CT imaging system for the re-analysis of contrast enhancement and FDG uptake in thrombus, the diameter of the involved portal vein, and characteristics of liver tumors and metastasis.

Two patients with previously untreated HCC and 7 cases with previously treated HCC had FDG-avid PVTT in contrast-enhanced FDG PET/CT scan. During the arterial phase of CT scan, portal vein thrombus showed contrast enhancement in 8 out of 9 patients (88.9%). PET scan showed an increased linear FDG uptake along the thrombosed portal vein in all patients. The mean greatest diameter of thrombosed portal veins was 1.8 ± 0.2 cm, which was significantly greater than that observed in normal portal veins (P<0.001). FDG uptake level in portal vein thrombus was significantly higher than that of blood pool in the reference normal portal vein (P=0.001). PVTT was caused by the direct extension of liver tumors. All patients had visible FDG-avid liver tumors in contrast-enhanced images. Five out of 9 patients (55.6%) had no extrahepatic metastasis, 3 cases (33.3%) had metastasis of regional lymph nodes, and 1 case (11.1%) presented with distant metastasis. The median estimated survival time of patients was 5 months.

The intraluminal filling defect consistent with thrombous within the portal vein, expansion of the involved portal vein, contrast enhancement, and linear increased FDG uptake of the thrombus extended from liver tumor are findings of FDG-avid PVTT from HCC in contrast-enhanced FDG PET/CT.

Viral hepatitis may promote the development of venous thromboembolism (VTE) and, more specifically, portal vein thrombosis (PVT). In this narrative review, we summarize the clinical data and discuss the possible pathogenetic roles of cytomegalovirus (CMV), Epstein-Barr virus (EBV), and hepatitis A, B, and C viruses (HAV, HBV, HCV) in the occurrence of VTE. CMV is the first qualified candidate to enter the list of VTE minor risk factors, and in the rare case of fulminant infection, both EBV and CMV, like any severe infection or inflammatory disease, increase risk for thrombosis. In chronic hepatitis B and C, it remains controversial whether antiphospholipid antibodies are important for thrombotic complications or merely an epiphenomenon. Retinal vein occlusion described in chronic hepatitis C is usually attributed to the treatment with interferon. Eltrombopag, used for HCV-related thrombocytopenia, has been associated with increased thrombotic risk. The imbalance between procoagulant and anticoagulant factors associated with chronic liver disease may have clinical implications. This may help to explain why these patients are not protected from clinical events such as VTE, PVT, and the progression of liver fibrosis.

Herein, we report a 26-year-old patient with lymphangiomatosis of the spleen associated with multiple lymphatic and venous malformations. This patient underwent excision of a large lymphatic malformation of the left abdominal wall during childhood. A venous malformation of her left lower limb was excised during adolescence. Additional lymphatic malformations were found in the soft tissue of her left thigh at the age of 20. During hospitalization for a huge vulvar hemangioma at the age of 26, she was incidentally found to have asymptomatic splenomegaly, for which she underwent splenectomy. Examination of the spleen revealed diffuse involvement by a lymphatic anomaly predominantly forming small cystic spaces. Lymphangiomatosis of the spleen is rare and is classically separated into an isolated or pure form and a generalized form when it is associated with involvement of other viscera and/or multiple soft-tissue planes. This patient was affected by a borderline form of splenic lymphangiomatosis with limited somatic involvement of the superficial soft tissues and blood vessels. Notably, all the additional vascular malformations in this patient were left sided, and at this time there was no additional involvement of internal organ. No hereditary or known syndrome was identified.

Discrepancies exist in the reported prevalence of portal vein thrombosis (PVT), and its clinical characteristics and sites of occurrence need to be elucidated. The risk factors for PVT are also poorly understood. This single centre study was undertaken to determine the clinical characteristics, sites of occurrence, and risk factors associated with PVT in patients with liver cirrhosis.

Hospitalized cirrhotic patients (N = 162) were segregated into the PVT and non-PVT groups. Indices possibly associated with PVT were measured and PVT was detected by both Doppler ultrasonography and computed tomography portal angiography. The portal vein diameter and flow velocity and splenic thickness were measured by ultrasonography.

PVT was found in 40 patients (24.7%); in 34 PVT patients (85%), the liver cirrhosis resulted from hepatitis B virus infections. Most (90%) patients were Child-Pugh classes B and C, with similar distribution between the groups. PVT was seen in 20 patients in the portal and superior mesenteric veins; ascites, abdominal pain, gastrointestinal bleeding, and jaundice were common findings in PVT patients. Haemoglobin levels and blood platelet counts (BPCs) were significantly lower and splenic thickness was greater in PVT than in non-PVT patients (P<0.01). There was a significant positive correlation between BPCs and platelet aggregation rates (R = 0.533, P<0.01).

The occurrence of PVT was 24.7 per cent, primarily in post-hepatitis B liver cirrhosis patients. PVT occurred mainly in the portal vein trunk and superior mesenteric vein. Different PVT sites may account for the differing clinical presentations. The lower levels of haemoglobin and BPCs as well as splenic thickening were associated with PVT. Splenic thickening may be a risk factor for PVT.

Short bowel syndrome occurs as a result of insufficiency in the total length of the small intestine to provide adequate supply of nutrients. Seventy-five percent of cases are due to massive intestinal resection. A 35-year-old male complaining of abdominal pain was admitted to the gastroenterology department. A CT scan was performed, showing total occlusion of the portal vein and superior mesenteric vein. During the operation, widespread edema and necrosis of the small intestine were found. The necrotic segments of the small intestine were resected. The spleen was larger than normal and, in some parts, infarcts were evident, thus asplenectomy was also performed during surgery. A second-look procedure was performed 24 hours later, and an additional 10 cm jejunal resection and anastomosis was performed. His further evaluations revealed myeloproliferative disease and chronic active hepatitis B leading to thrombosis. Essential thrombocytosis and portal vein thrombosis are common in hepatitis B infection. Patients with complaints of abdominal pain in the context of essential thrombocytosis and hepatitis B should be handled with caution as they are at risk of developing portal vein thrombosis.

Hepatitis B virus (HBV)-related cirrhosis is known to be associated with chronic hepatic inflammation. The present study aimed to examine the correlation between inflammatory mediators INF-γ, IL-17, and sICAM-1 in HBV cirrhotic patients.

The levels of sICAM-1, interleukin-17, and IFN-γ were measured with enzyme-linked immunosorbent assays in 120 cirrhotic patients with HBV and 270 sex- and age-matched healthy controls. Total bilirubin (TB) was measured and the association between TB and IFN-γ, sICAM-1, interleukin-17 were analyzed. The levels of these cytokines in serum and the association between IFN-γ and sICAM-1 as well as interleukin-17 were investigated. Relationships between these cytokines and Child-Pugh classes were analyzed in patients.

Age and sex were similar, but TB values were significantly different between the two groups (P<0.001). Serum levels of sICAM-1, interleukin-17, and IFN-γ were significantly higher in cirrhotic patients with HBV than in controls (P<0.001 for both). TB levels were positively correlated with IFN-γ, interleukin-17 and sICAM-1 levels. Significantly positive correlations were also found between IFN-γ and interleukin-17 as well as sICAM-1 (r=0.817 and r=0.561, respectively, P<0.01). There were significant differences between the studied cytokines (sICAM-1, interleukin-17, and IFN-γ) and Child-Pugh classes (P<0.01).

The increased IFN-γ level was correlated with both IL-17 and sICAM-1, and it may primarily play a role as cytokines trigger in liver injury. Both IL-17 and sICAM-1 may synergistically contribute to liver damage.