European Journal of Cardiovascular Medicine

The frequency of portal vein thrombosis (PVT) can fluctuate based on factors such as age, underlying liver conditions, portal venous blood flow rate, and the patient's pro-coagulant or anticoagulant status. In individuals with Child-Pugh score A and B cirrhosis, the occurrence of newly diagnosed PVT after 1 and 5 years has been documented at 4.6% and 10.7%, respectively. The risk of PVT development is substantially amplified, more than sevenfold, in the presence of cirrhosis compared to the estimated risk of less than 1% in the general population [2] While patients with compensated cirrhosis are seldom affected, PVT is more frequently observed in advanced stages, reaching rates of up to 25% in candidates for liver transplantation and 35% in cirrhotic patients with hepatocellular carcinoma (HCC). Notably, in extensive studies involving liver transplantation candidates, 6.3% were diagnosed with PVT, especially in cases where cirrhosis was associated with non-alcoholic steatohepatitis (NASH). Additionally, prevalence rates between 5% and 16% have been noted in patients with advanced cirrhosis and those undergoing liver transplantation [1-3].

The clinical manifestations of PVT exhibit a wide range, from incidental detection during unrelated diagnostic procedures to severe complications like intestinal infarction or portal hypertension-related issues such as variceal bleeding, which can manifest as esophageal and/or gastric fundic varices in the presence of splenic vein thrombosis. Consequently, the prognosis and management of PVT are contingent upon factors like its location, extent, rate of progression, thrombotic risk factors, and the stage of chronic liver disease [4-6]. This study aimed to describe clinical profiling of and correlations between portal vein thrombo

The study included 145 patients diagnosed with chronic liver disease, encompassing both alcoholic and non-alcoholic causes and representing both genders at an Indian tertiary care medical college and hospital. Consent was obtained from all participants prior to their inclusion in the study. Information such as name, age, gender, etc., was documented. Each patient underwent a comprehensive medical history assessment, clinical examination, and laboratory evaluations, including fasting glucose levels, liver function tests, and coagulation profiles (Prothrombin time, INR). The collected data were then analyzed statistically using SPSS 19.0, with a significance level set at p < 0.05.

Among the 145 participants, the majority fell within the 36-55 age group. The average age of participants was 44.78±12.51 years (Figure 1).

Figure 1: Age Distribution of study cases

Most participants exhibited hemoglobin levels below 11 gm%. Serum bilirubin levels exceeded normal ranges in 68 participants. Elevated SGPT/SGOT values were noted in 54 participants. Additionally, 48 participants had below-normal serum albumin levels, while 44 had reduced platelet counts (Table 1).

Participants diagnosed with portal vein thrombosis demonstrated a notably higher mean portal vein diameter compared to those without this condition (Table 2).

Biochemical markers revealed a significant correlation between the Child-Pugh score and platelet count, INR, and total bilirubin levels (Tables 3 and 4).

Table 1: Biochemical parameters in study population

Table 2: Association between PVT and diameters of portal and splenic veins

Table 3: Association between PVT and biochemical parameters

Table 4: Association between Child Pugh Score and biochemical parameters

Portal vein thrombosis (PVT) refers to either partial or complete blockage of blood flow within the portal vein due to the presence of a thrombus in the vessel's lumen. The first documented case of PVT dates back to 1868, reported by Balfour and Stewart, detailing a patient exhibiting splenomegaly, ascites, and variceal dilation. PVT is relatively uncommon, with an overall incidence ranging from 0.05% to 0.5% in autopsy studies. This incidence varies based on the studied patient cohorts and the diagnostic methodology employed to detect portal vein obstruction [7,8].

While PVT is rare in the general population, its prevalence among cirrhotic patients ranges from 4.4% to 15%, accounting for about 5-10% of all cases of portal hypertension. In developing countries, 40% of portal hypertension cases are attributed to portal vein obstruction, likely due to increased instances of pylephlebitis associated with abdominal infections. In Japan, the frequency of portal vein obstruction is lower compared to Western countries. Regarding demographic factors, no significant differences based on sex have been consistently reported, except for a slight male predominance in cases where obstruction is secondary to cirrhosis. The age at which PVT manifests depends on the underlying condition. Primary PVT from coagulopathies occurs equally in adults and children [9-11].

In our study involving 100 participants, the majority fell within the age group of 36 to 55 years. The mean participant age was 44.78±12.51 years. Bolondi et al. [12] noted that ultrasound (US) could only detect 42% of portal hypertension cases based solely on portal vein size, where a portal vein diameter of 15 mm is indicative of portal hypertension.

In terms of biochemical markers, most participants had hemoglobin levels below 11 gm%, elevated serum bilirubin, SGPT/SGOT levels, abnormal blood coagulation markers (INR and PT), and below-normal serum albumin and platelet counts. Iwao T et al. [13] emphasized the liver vascular index as a highly sensitive and specific Doppler ultrasound parameter for diagnosing cirrhosis and portal hypertension, with specific cut-off values indicating sensitivity and specificity rates. Participants with PVT showed a significantly larger portal vein diameter compared to those without PVT.

Furthermore, abnormalities in hemoglobin levels, platelet counts, PT/INR values, serum albumin, serum creatinine, total bilirubin, SGOT, and SGPT were more prevalent in the PVT group than the non-PVT group. Child-Pugh score correlated significantly with platelet count, INR, and total bilirubin levels in our biochemical analyses. Moriyasu et al. [14] also observed an increased cross-sectional area of the portal vein in patients with portal hypertension, with factors like portal venous pressure, liver portal vascular resistance, portal blood flow, and the duration of abnormal hemodynamics influencing portal vein compliance index. However, the compliance curve of the portal vein is nonlinear, with increased pressure resulting in larger changes compared to volume alterations under normal hemodynamics [15].

The researchers discovered that PVT may exacerbate the rate of hepatic decompensation and impact the survival of individuals with cirrhosis. The prognostic significance of PVT in cirrhosis remains uncertain. However, early diagnosis, appropriate treatment, and regular monitoring of patients can potentially prevent the occurrence of PVT in liver cirrhosis, leading to enhanced liver function and improved survival outcomes.

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