Prevalence Of Portal Vein Thrombosis Research Articles

Prevalence of Risk Factors and Complications of Portal Vein Thrombosis in Patients with Cirrhosis

Liver cirrhosis, the twelfth leading cause of death in the United States and according to the latest WHO data published in May 2014 Liver Disease Deaths in Egypt reached 41,355 or 8.92% of total deaths. The age adjusted Death Rate is 67.54 per 100,000 of population ranks Egypt #2 in the world. It is the end result of the hepatocellular injury that leads to both fibrosis and regenerative nodules throughout the liver. Causes include chronic viral hepatitis, alcohol, drug toxicity, autoimmune, metabolic liver diseases, and miscellaneous disorders. Portal vein thrombosis (PVT) means obstruction of the portal vein or its branches by a blood clot. The prevalence of PVT in patients with cirrhosis has been reported more frequently in recent years. The reported prevalence of PVT is in the range of 0.6%-15.8% in patients with liver cirrhosis or portal hypertension. Moreover, the prevalence of PVT increases with patient age and liver disease severity, reaching 15% in patients awaiting liver transplantation. Inherited and acquired thrombophilic disorders, bacterial infection and sluggish portal flow may all play a role in the high prevalence of PVT in patients with liver cirrhosis.

African Americans have a lower prevalence of portal vein thrombosis at the time of liver transplantation

BackgroundPerioperative vascular thrombotic events in patients undergoing liver transplantation (LT) are associated with significant morbidity and mortality. MethodsIn this retrospective UNOS database analysis, we evaluated the prevalence of portal vein thrombosis (PVT) and factors contributing to PVT development in different ethnic groups. ResultsOf the 47 953 LT performed between 2002 and 2015, we identified 3642 cases of PVT. African Americans (AA) had a significantly lower prevalence of PVT compared to other ethnic groups (p = 0.0001). Multivariable regression analysis confirmed that AA were less likely than other ethnicities to have PVT (OR = 0.6). AA cohort was more likely to have infectious or autoimmune causes of liver failure (OR = 1.6, 1.7 respectively) as well as higher creatinine and INR compared to other groups (OR = 1.6, 1.3 respectively). AA's were less likely to have encephalopathy, ascites, or variceal bleeding, which might indicate lower portal pressures. AA's were listed for LT later than other ethnicities and had both a lower functional status and higher MELD score at the time of registration. DiscussionAA's had a significantly lower prevalence of preoperative PVT despite having a greater number of factors predisposing to thrombosis. This predisposition should be considered before instituting perioperative antithrombotic therapy.

The Prevalence of Portal Vein Thrombosis in Children under 3 Years Old with History of Neonatal Umbilical Vein Catheterization in the Neonatal Intensive Care Unit

Background Portal vein thrombosis (PVT) is one of the most common causes of extrahepatic portal hypertension in children, which may follow neonatal umbilical vein catheterization. The incidence rates of catheter-related PVT, in infants and children vary in different studies. This study aimed to determine PVT incidence in the children under 3 years old with a history of neonatal umbilical vein catheterization in the NICU of Ghaem Hospital, Mashhad- Iran. Materials and Methods This cross-sectional study included 38 children with a history of hospitalization in the NICU of Ghaem Hospital, Mashhad-Iran, during 2012 to 2013 for whom umbilical vein catheterization had been performed. The Children’s histories were taken and they were examined. Color Doppler ultrasound was performed on them. Data analysis was carried out using SPSS-13 and descriptive statistics, t-test, Fisher's exact test. Results Fourteen (36.8%) and 24 (63.2%) of the infants were males and females, respectively. Mean age of the infants was 33.1±3.55 months. PVT evidence in a child raises a 2.6% PVT incidence. No statistically significant relationship was observed among gender, age, catheter type, and catheterization duration and PVT. A statistically significant relationship was observed between spleen size and portal vein size in ultrasound and PVT (P<0.05). The liver and spleen examination was only abnormal, in the patient with thrombosis. Conclusion The study findings suggest a 2.6% incidence for PVT. In addition, neonatal umbilical catheterization causes PVT during childhood.

Prevalence and outcome of portal thrombosis in a cohort of cirrhotic patients undergoing liver transplantation.

The prevalence of portal vein thrombosis (PVT) in patients that have undergone liver transplantation (LT) is 9.7% (SD 4.5). The aim of our study was to determine the prevalence, assess the factors that are associated with PVT and clarify their association with prognosis in patients with liver cirrhosis (LC) and LT. From 2005 to 2014, laboratory, radiological and surgical data were collected from patients with LC in our center who had undergone LT for the first time. One hundred and ninety-one patients were included. The mean age was 55 (SD 9), 75.4% of patients were male and 48.7% had HCV. The Child-Pugh scores were A/B/C 41.9%/35.9%/25.5% and the MELD score was 15 (SD 6). Previous decompensations were: ascites (61.4%), hepatic encephalopathy (34.4%), variceal bleeding (25.4%), hepatocellular carcinoma (48.9%) and spontaneous bacterial peritonitis (SPB) (14.3%). The mean post-transplant follow-up was 42 months (0-113). PVT was diagnosed at LT in 18 patients (9.4%). Six patients were previously diagnosed using imaging tests (33.3%): 2 patients (11.1%) by DU and 4 patients (22.2%) by CT scan. All patients with PVT had DU in a mean time of 6 months before LT (0-44) and 90 patients (47.1%) had a CT scan in a median time of 6 months before LT (0-45). PVT was significantly related to the presence of SBP (33.3% vs 12.6%; p = 0.02) and lower levels of albumin (3.1g/dl vs 3.4g/dl; p = 0.05). MELD was higher in patients with PVT (16.6 vs 14.9; p = 0.3). There were no significant differences with regard to the need for transfusion of blood components. Moreover, the surgery time was similar in both groups. PVT correlated with a higher mortality in the first 30 days (8.8% vs 16.7%; p = 0.2). Prior history of SBP and lower levels of albumin were identified as factors associated with PVT. The pre-transplant diagnosis rate is very low and the presence of PVT may have implications for short-term mortality.

Increased risk of portal vein thrombosis in patients with cirrhosis due to nonalcoholic steatohepatitis.

Portal vein thrombosis (PVT) is a common complication of cirrhosis sometimes implicated in hepatic decompensation. There are no consistent epidemiologic data to suggest an increased risk of thrombotic complications in nonalcoholic steatohepatitis (NASH); however, research suggests an increased risk of thrombosis. Our aim was to examine the independent association between NASH cirrhosis and PVT in patients who underwent liver transplantation (LT) in a cross-sectional study. Data on all LTs occurring in the United States between January 1, 2003 and December 31, 2012 were obtained from the United Network for Organ Sharing. Multivariable models were constructed to assess the statistical associations and risk factors for the development of PVT. A total of 33,368 patients underwent transplantation. Of these, 2096 (6.3%) had PVT. Of the patients with PVT, 12.0% had NASH. When we compared these patients to a composite of all other causes of cirrhosis, an increased prevalence of PVT was again found, with 10.1% having PVT at the time of transplantation versus 6.0% without NASH (P < 0.001). The strongest risk factor independently associated with a diagnosis of PVT in a multivariable analysis was NASH cirrhosis (odds ratio, 1.55; 95% confidence interval, 1.33-1.81; P < 0.001). NASH cirrhosis appears to predispose a patient to PVT independently of other risk factors. These epidemiological findings provide support for the idea that NASH is a prothrombotic state, and they should lead to more research in treatment and prevention in this population.

Study on Portal Vein Thrombosis in Cirrhotic Patients

Background andObjectives: Portal vein thrombosis (PVT) is commonly found in liver cirrhosis. It is often detected incidentally by imaging studies. PVT is associated with life threatening complications. Prevalence of PVT varies from 1% to 28% in cirrhosis. Prevalence increases with severity of cirrhosis. Its clinical characteristics and sites of occurrence need to be made clear. The risk factors for PVT are also poorly understood. This study was done to identify the clinical characteristics, sites of involvement and risk factors associated with PVT in cirrhotic patients. Methods: Retrospective analysis of cirrhotic patients admitted in our center. Cirrhotic patients (N = 182) were grouped into the PVT and non-PVT groups. Parameters associated with PVT were measured. PVT was identified by both Doppler ultrasonography and computed tomography. The portal vein diameter, flow, velocity, presence of collaterals and cavernoma were measured by ultrasonography. Results:Most (90%) patients were Child-Pugh classes B and C, in both the groups. PVT was found in 33 patients (18.13%). In 24 PVT patients (72.7%), cirrhosis was due to hepatitis B virus infections. Ascites, abdominal pain, gastrointestinal bleeding and jaundice were common findings in PVT patients. Haemoglobin levels and platelet counts were significantly lower in PVT patients. 7 patients had thrombosis in portal and superior mesenteric vein. Conclusion: Prevalence of PVT was 18.1%. Site of involvement of PVT is mainly seen in portal vein trunk and superiormesenteric vein. PVT is commonly seen in patients with cirrhosis due to hepatitis B virus. Low haemoglobin and platelet count correlated well with PVT.

Portal vein thrombosis in patients with cirrhosis

Portal vein thrombosis (PVT) can be seen in patients with cirrhosis in association with hepatocellular carcinoma or following splenectomy for the treatment of hypersplenism. PVT can also occur spontaneously in patients with cirrhosis; it is this group that is the subject of this discussion. Incidence, Etiology, and Clinical Consequences PVT may be complete, partial, or associated with cavernous transformation of the portal vein (Fig. 1). The thrombi can be in any part of the portal venous system but are seen most commonly in the main portal vein or its intrahepatic branches. The prevalence of PVT varies widely in patients with cirrhosis, ranging from 5% to 26% in different series of patients who were either evaluated for or underwent liver transplantation. Most of these patients had partial PVT, and many were diagnosed at the time of surgery. 1 In a series of 701 hospitalized patients with cirrhosis undergoing Doppler ultrasound, 11.2% were found to have PVT. In 43% of those with PVT, there were no symptoms, whereas 39% had portal hypertensive bleeding and 18% had abdominal pain, usually associated with intestinal ischemia. 2 There were no clear clinical differences between those patients with cirrhosis who did and those who did not have PVT. In one prospective trial of patients with Child class B/C cirrhosis, 6 of 36 patients (16.6%) developed PVT during a 48week period of observation, 3 suggesting many patients with advanced cirrhosis are at significant risk for developing this complication. PVT may progress or resolve spontaneously. In one series of 42 patients, partial PVT progressed in 48%, improved in 45%, and remained the same in 7%. 4 The pathogenesis of PVT in cirrhosis is not clear. Factors thought to play a role include reduced flow in the portal vein as a consequence of increased resistance in the liver, inherited defects in coagulation (such as factor V Leiden or prothrombin mutations), and an imbalance between proand anticoagulant factors that develop in the patient with cirrhosis due to impaired hepatic function. 1,2 Individuals with PVT and abdominal pain frequently have mesenteric ischemia. The impact of PVT of insidious onset on disease progression and complications of cirrhosis is unclear. Patients with PVT tend to have smaller livers and more severe portal hypertension than those without PVT, but it is unclear whether this difference is a consequence of the PVT. Perhaps the most compelling argument for the negative impact of PVT on disease progression is the recent controlled trial in which 70 outpatients with Child class B/ C cirrhosis and no PVT were randomized to enoxaparin (4000 IU/day subcutaneously) or no treatment for 48 weeks. During active treatment, none of the patients receiving enoxaparin developed PVT compared with 17% of controls. In the treated group, the probability of decompensation was significantly reduced, and survival was improved. 3 The most common cause of decompensation was the development of ascites, which was significantly less in treated patients. Seventy percent of those who developed PVT in the control group developed ascites. The incidence of encephalopathy, sepsis, or variceal bleeding did not differ between the two groups. Which factor accounted for the beneficial effects of enoxaparin is unclear. The use of the drug clearly decreased the incidence of PVT, but its use was also associated with significantly fewer bacterial infections. The data suggest that PVT and perhaps microvascular thrombosis play a role in disease progression in patients with cirrhosis and that their prothrombotic state may require some type of treatment. Further studies are required before one can generally recommend anticoagulants in patients with cirrhosis as a preventative therapy. Limited data suggest the presence of asymptomatic PVT in patients with cirrhosis does not affect overall survival, although in some patients it may add to the technical difficulty of liver

Low molecular weight heparin in portal vein thrombosis of cirrhotic patients: only therapeutic purposes?

Cirrhosis has always been regarded as hemorrhagic coagulopathy caused by the reduction in the hepatic synthesis of procoagulant proteins. However, with the progression of liver disease, the cirrhotic patient undergoes a high rate of thrombotic phenomena in the portal venous system. Although the progression of liver failure produces a reduction in the synthesis of anticoagulant molecules, a test able to detect the patients with hemostatic balance shifting towards hypercoagulability has not yet been elaborated. The need of treatment and/or prophylaxis of cirrhotic patients is demonstrated by the increased mortality, the risk of bleeding from esophageal varices, and the mortality of liver transplantation, when portal vein thrombosis (PVT) occurs even if current guidelines do not give indications about PVT treatment in cirrhosis. In view of the general feeling that the majority of cirrhotic patients at an advanced stage may be in a procoagulant condition (suggested by the sharp increase in the prevalence of PVT), it is presumable that a prophylaxis of this population could be of benefit. The safety and the efficacy of prophylaxis and treatment with enoxaparin in patients with cirrhosis demonstrated by a single paper suggest this option only in controlled trials and, currently, there are no sufficient evidences for a recommendation in the clinical practice.

Incidence and Natural Course of Portal Vein Thrombosis in Cirrhosis

To the Editor: We have read with interest the recent article by Maruyama et al. (1) on the incidence and natural course of portal vein thrombosis (PVT) in viral cirrhosis. Despite the interest of the study being the third to report incidence of PVT in cirrhotics, it presents several inconsistencies and drawbacks in design and data analysis. First, reported incidence of PVT included six patients with only splenic vein thrombosis, thus being 36/150, 24%. Moreover, the occurrence of PVT is strangely not equally distributed during the follow-up, with a 12.8% incidence in the first years and about 2% per year during the follow-up. This is in contrast with the current knowledge of a greater prevalence of PVT in patients with more advanced liver disease. Second, patients were recruited for the study during 11 years, and it is stated that Doppler ultrasonography (US) were performed at least every 6–12 months. However, surprisingly, the median number of US per patient was only 4.4, leading to a period of time covered of a maximum of 4 years. Third, correlation of flows at US Doppler at inclusion with occurrence of PVT after years from the initial evaluation is unlikely due to changing hemodynamics in cirrhotic patients overtime. Fourth, it is difficult to understand why patients were tested for prothrombotic disorders at the beginning of the enrollment in the study (in year 1998 the potential role of these alterations in cirrhosis was still not defined). Fifth, US is characterized by diagnostic limitations, especially in extra-hepatic segments of PV or other splanchnic veins. Sixth, worsening of PVT has been described in only 1/23 patients, data very different from previous studies that described progression of PVT in 48–75% of cases at 2 years (2,3). Finally, the way that data on PVT and survival was analyzed does not allow to conclude that PVT does not have an impact on survival. Kaplan–Meyer curve of survival is faulty because the number of patients plotted in the figure is 156 and not 150, and survival was considered from the enrollment in the study. Therefore, for example a patient developing PVT after 7 years of follow-up and dying 1 month after it is considered as being alive for 7 years and 1 month. In conclusion, we believe that the interpretation of the described data is difficult and no recommendations can be drawn according to the results of the present manuscript.

Portal Vein Thrombosis in Patients with End Stage Liver Disease Awaiting Liver Transplantation: Outcome of Anticoagulation

The prevalence of portal vein thrombosis (PVT) increases with the severity of liver disease. Development of PVT is often accompanied by increased rate of morbidity and mortality and may affect patient candidacy for liver transplant. There is limited data regarding the role of anticoagulation therapy in patients with PVT and liver cirrhosis. The aims of this study were to describe the prevalence of hypercoagulable disorders in patients with liver cirrhosis and PVT, and to describe the outcome of anticoagulation in patients with liver cirrhosis and PVT. A retrospective chart review was conducted of patients with liver cirrhosis awaiting liver transplant who were diagnosed with PVT between January 2005 and November 2011. During the study period, 537 patients were evaluated for liver transplant. Sixty-nine (13 %) patients were diagnosed with portal vein thrombosis. Chronic hepatitis C was the cause of liver disease in 24/69 (35 %) patients, and hepatocellular carcinoma was present in 39 % of patients. In 22 patients screened for hypercoagulable disorders, hypercoagulable disorder was diagnosed in one patient (5 %). Twenty-eight (28/69) patients were treated during the study period with warfarin: PVT resolved in 11/28 (39 %), no change in 5/28 (18 %), and 12/28 (43 %) patients showed partial resolution of thrombus. Eight patients received liver transplant while on anticoagulation, and operative notes confirmed patency of PV in all eight patients. PVT is frequently seen in patients with end stage liver disease with prevalence of 13 %. Hypercoagulable disorder was detected in 5 % of the patients screened. Careful use of anticoagulation is safe and effective in patients with PVT.

Prevalence of Portal Vein Thrombosis Following Umbilical Catheterization in Neonatal Period

Introduction Group B streptococcus is the main reason of neonatal infection in developed countries and causes a widespread clinical indications. In developing countries such as Iran, its rate of appearance is not determined. With regard to colonization and the relative high epithelia of group B streptococcus, it is likely that the incidence of group B streptococcus in neonatal sepsis is so high.In the present study, we attempted to use the molecular methods to identify this bacterium and develop the culture environments as well. Methods In the present study, a hundred below three months year old infants with sepsis hospitalized in ICU sector of Ghaem hospital for one year were studied since Khordad 1388 (June 2010). After getting consent from the infants’ parents, three blood samples of these patients in the sterile container with lid were transferred to the laboratory (two samples for culturing in normal environment and the other for PRC). All of the information was filled out by doctors in the incidence. SPSS 11.5 and descriptive-analytic tests were used for data analysis. Results The findings have shown that 100 below three months year old infants with sepsis clinical symptoms were studied. In none of the environments, the B group Streptococcus grows. For identifying the group B streptococcus, PCR were positive in 3% of infants, but other germs have grown in 5 % of normal culture, and 6 % of developed culture environment. Findings have also shown that 64 % of mothers took antibiotic before delivery. Conclusion With regard to the high rate of anti-biotic consumption by mothers before delivery, it is necessary to use more sensitive methods like PCR to identify the Group B Streptococcus.

Increased PD-1 and decreased CD28 expression in chronic hepatitis B patients with advanced hepatocellular carcinoma

Hepatitis B infection is a well-known cause of hepatocellular carcinoma (HCC). This study aims to investigate the role that the co-stimulatory molecule CD28 and co-inhibitory molecule programmed death-1 (PD-1) play in compromising the function of tumour-infiltrating lymphocytes (TIL) in hepatitis B virus (HBV)-related HCC. A total of 45 patients with HBV-related HCC were enrolled during the period February 2008 to March 2010. The immune phenotype and the expression of PD-1, CD28 and CD127 in TIL in biopsy specimens and in peripheral blood lymphocytes (PBL) from the same patients were analysed by flow cytometry. Among the 45 patients, there was a male predominance (80%) and the mean age was 50 ± 13.68 years (range: 29-71). The majority of TIL were CD45RO(+) CD69(+). PD-1 expression was higher and CD28 and CD127 expression levels were lower in TIL than in PBL. The prevalence of portal vein thrombosis was 40%. Furthermore, tumour thrombosis invasion into the portal vein correlated with the expression level of the PD-1 co-inhibitory molecule. PD-1(+) tumour-infiltrating lymphocytes correlate with portal vein thrombosis and might serve as a potential prognostic marker of and a novel therapeutic target for HBV-related HCC.

Transcatheter Arterial Embolization in the Emergency Department for Hemodynamic Instability Due to Ruptured Hepatocellular Carcinoma: Analysis of 167 Cases

The purpose of this study was to analyze the prognostic factors associated with emergency transcatheter arterial embolization in the treatment of patients in hemodynamically unstable condition caused by rupture of hepatocellular carcinoma. An 8-year retrospective cohort study was conducted to evaluate emergency transcatheter arterial embolization in the treatment of 167 patients in unstable hemodynamic condition (systolic blood pressure < 90 mm Hg at presentation) due to rupture of hepatocellular carcinoma. The clinical, laboratory, and imaging findings of a group who died (survival period, < or = 30 days) were compared with those of a group who survived more than 30 days. On arrival in the emergency department, the group who died (n = 52) were in significantly worse condition than the group who survived (n = 115). The group who died had a poorer Child-Pugh class, lower hemoglobin and serum albumin levels, higher demand for blood transfusion, higher incidence of acute respiratory failure, worse neurologic status (Glasgow Coma Scale score, < or = 12), greater prevalence of portal vein thrombosis, and higher serum total bilirubin and creatinine levels (p < 0.05, two-sample Student's t test and Fisher's exact or chi-square test). Multivariate logistic regression analysis showed that patients who did not have portal venous thrombosis (odds ratio, 0.241; p = 0.012) or a lower creatinine level (odds ratio, 0.458; p = 0.003) had better probability of survival. Successful hemostasis with transcatheter arterial embolization was achieved in 99% of patients (30-day mortality rate, 31%). Patients with coexistent acute respiratory failure or impaired neurologic status and marked hyperbilirubinemia (> 2.7 mg/dL) had exceptionally high mortality rate (> 70%). Emergency transcatheter arterial embolization is effective for hemostasis of ruptured hepatocellular carcinoma in patients in hemodynamically unstable condition being treated in the emergency department. However, patients with portal venous thrombosis, a high serum creatinine level, acute respiratory failure, impaired neurologic status, and a high serum total bilirubin level continue to be at high risk of death.

Portal Vein Thrombosis Following Splenectomy for Hematologic Diseases: Prevalence and Risk Factors.

Portal vein thrombosis (PVT) is a potentially fatal complication of splenectomy; the prevalence of PVT remains up till now controversial, such as the related-risk factors. The hematologic patients who underwent splenectomy in Niguarda Hospital, Milan, Italy, between January 1995 and November 2004 were retrospectively reviewed to identify the prevalence of post-splenectomy PVT and risk factors associated with its development. Splenectomy was performed because of malignant (n = 41) or non-malignant (n = 44) hematologic diseases. Indications for splenectomy in the groups with and without PVT were compared with Fisher's exact test. We tested the reliability of platelet count as a marker of PVT, analysing the receiver operator characteristic (ROC) curve. Cut-off level was chosen for best prediction in term of sensitivity and specificity.Among 85 patients who underwent splenectomy, the associated non-malignant diseases were immune thrombocytopenic purpura (n = 40), hemolytic anemia (n = 2), Evan's syndrome (n = 1), cryoglobulinemia (n = 1); malignant diseases were lymphoproliferative (n = 39) and myeloproliferative disorders (n = 2). Four cases of PVT (4,71%) were diagnosed. One of 2 patients with a myeloproliferative disorder had PVT. PVT was also present in 3/39 (7.69%) patients with lymphoproliferative malignancies, all with splenic marginal zone B-cell variety non-Hodgkin's lymphoma (3/16) . The median splenic weight in patients who developed PVT was 1800 g (range 1500–1980 ) and the median post-surgery platelet count was 661 x 109/liter (range 211–1250). No patient with non-malignant diseases had portal vein thrombosis. The incidence of the event was of 0.0000523 new cases for day-patient, with a 0.005% new incidental case probability. Splenic weight, with a cut-off value of 500 grams for the risk analysis (p=0.029), was significantly correlated to thrombosis. PVT was also significantly correlated to the entity of the post-surgery thrombocytosis (p=0.024), setting the threshold value of thrombosis risk at 850.000/uL (Sensibility 0.50 - Specificity 0.95).Patients with myeloproliferative and lymphoproliferative disorders seem at higher risk for the development of PVT than those with non-malignant diseases. A splenic weight over 500 grams and a post-surgery thrombocytosis over 850.000/uL are significantly associated with the occurrence of PVT. The presence of these two risk factors should require the prophylactic use of adequate doses of low molecolar weight heparin.

Prognostic Significance of Simultaneous Measurement of Three Tumor Markers in Patients With Hepatocellular Carcinoma

We conducted a prospective study to evaluate the significance of simultaneous measurement of 3 currently used tumor markers in the evaluation of tumor progression and prognosis of patients with hepatocellular carcinoma (HCC). Three tumor markers for HCC, alpha-fetoprotein (AFP), Lens culinaris agglutinin A-reactive fraction of AFP (AFP-L3), and des-gamma-carboxy prothrombin (DCP), were measured in the same serum samples obtained from 685 patients at the time of initial diagnosis of HCC. Positivity for AFP >20 ng/dL, AFP-L3 >10% of total AFP, and/or DCP >40 mAU/mL was determined. In addition, tumor markers were measured after treatment of HCC. Of the 685 patients, 337 (55.8%) were positive for AFP, 206 (34.1%) were positive for AFP-L3, and 371 (54.2%) were positive for DCP. In a comparison of patients positive for only 1 tumor marker, patients positive for AFP-L3 alone had a greater number of tumors, whereas patients positive for DCP alone had larger tumors and a higher prevalence of portal vein invasion. When patients were compared according to the number of tumor markers present, the number of markers present clearly reflected the extent of HCC and patient outcomes. The number of markers present significantly decreased after treatment. Tumor markers AFP-L3 and DCP appear to represent different features of tumor progression in patients with HCC. The number of tumor markers present could be useful for the evaluation of tumor progression, prediction of patient outcome, and treatment efficacy.

Relationship Between Various Patterns of Transient Increased Hepatic Attenuation on CT and Portal Vein Thrombosis Related to Acute Cholecystitis

We sought to investigate the prevalence of portal vein thrombosis in patients with acute cholecystitis and the relationship between portal vein thrombosis and the various patterns of transient increased hepatic attenuation on CT. We studied 72 of 107 patients with acute cholecystitis who, during a 3-year period, underwent dual-phase contrast-enhanced CT before percutaneous cholecystostomy or cholecystectomy. CT scans were retrospectively reviewed for the presence of portal vein thrombosis and location of the thrombi and for patterns of transient increased hepatic attenuation, which were classified as either pericholecystic, segmental, or mixed. Portal vein thrombi (two in hepatic segment IV, three in the left portal vein, and one in the right posterior portal vein) were found in six (8.3%) of 72 patients, and in those patients, transient increased attenuation with a segmental (five patients) or mixed (one patient) pattern was seen on CT. The pattern of transient increased attenuation in the 54 patients without portal vein thrombosis was pericholecystic in 41 (75.9%) and mixed in 13 (24.1%). Nineteen patients had segmental distribution (segmental or mixed pattern) that in 31.6% (6/19) of the patients was associated with portal vein thrombosis. Segmental distribution was more frequently found in those patients who had acute cholecystitis with portal vein thrombosis than in those who had only acute cholecystitis (p = 0.001). In patients with acute cholecystitis, portal vein thrombosis is not uncommon. Patterns of transient increased hepatic attenuation were found to vary, depending on the presence or absence of portal vein thrombosis.