Aims: Portal hypertension is a major complication of liver cirrhosis. Hepatic venous pressure gradient (HVPG) appears to be one of the best surrogates of clinical outcomes. However, the utility of elevated HVPG in predicting subsequent clinical decompensation is unclear.Methods: We analyzed 410 patients who underwent HVPG assessment between 2014 and 2018. Of these, we identified and analyzed 20 patients with HVPG >12 mmHg without evidence of clinical decompensation (defined as ascites, nonbleeding esophageal varices or bleeding esophageal varices, hepatic encephalopathy, hepatopulmonary syndrome, or hepatic hydrothorax). Additionally, we compared this group to 40 randomly selected cirrhotic patients with HVPG >12 mmHg with signs of clinical decompensation. Clinical events were subsequently assessed (mean = 33 months) after HVPG measurement.Results: Patients with high HVPG without evidence of clinical decompensation had a significantly lower model for end‐stage liver disease (MELD) scores (8 ± 4) compared to decompensated patients (13 ± 8, p = 0.05). HVPG measurements were similar in compensated (17 ± 6 mmHg) and decompensated (18 ± 4 mmHg) patients. Over follow‐up for 33 months, 8/20 compensated patients had a decompensating event and neither MELD (8 and 8, respectively) nor HVPG (17 and 18 mmHg, respectively) differentiated patients who remained compensated versus those that decompensated. Serum albumin at the time of HVPG measurement was significantly higher in patients who remained compensated than those with a decompensating event (3.5 vs. 2.6 g/dl, respectively, p = 0.05).Conclusions: A small, unique, population of cirrhotic patients with substantially elevated HVPG appear to remain free of complications over long‐term follow‐up.

CD44 has been demonstrated to play a pivotal role in regulating tumor cell progression, including hepatocellular carcinoma (HCC) development. Here, we aimed to establish a scoring system to evaluate the risk of developing HCC utilizing CD44-rs187115 SNP polymorphism. A prospective cohort of 120 individuals was enrolled in four groups: 19 non-metastatic HCC patients, 21 metastatic, 40 patients with hepatitis C-related cirrhosis, and 40 controls. Allelic discrimination of the CD44-rs187115 gene polymorphism was assessed using TaqMan genotyping assay. HCC patients with CT/CC genotypes were more likely to have aggressive malignancy compared to TT carriers. A significant correlation was noted between the existence of CT/CC genotypes and tumor size, multicentricity, infiltration, portal vein thrombosis, and metastasis. A CD44-incorporated Hepatocellular Carcinoma Risk Index Scoring Tool (CHRIST) was formulated utilizing clinical and genetic variables. A score > 3 for HCC development demonstrated 87.5% sensitivity, 72.5% specificity, and a 76% positive predictive value (PPV) and 85% negative predictive value (NPV). Furthermore, a score > 5 for HCC metastasis demonstrated 90.4% sensitivity, 68.4% specificity, a 76% PPV and 86% NPV. A similarly significant score was noted following a six-month re-evaluation. We conclude that CD44-rs187115 may serve as a reliable prognostic biomarker for HCC and that the CHRIST prognostic model is highly predictive of the development of HCC and metastatic HCC.