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Objectives Porto-sinusoidal vascular disorder (PSVD) is a recently defined vascular liver disease. Since diagnosis remains challenging, we aimed to evaluate radiological features that are distinct between PSVD and cirrhosis. Methods Clinical, laboratory, and radiological parameters (CT/MRI) of patients with histologically-confirmed PSVD vs. cirrhosis vs. non-cirrhotic parenchymal liver disease were retrospectively evaluated. Results Sixty-three PSVD, 155 cirrhosis, and 41 non-cirrhotic patients were included. As compared to cirrhosis, PSVD patients were younger and had lower HVPG, liver stiffness, and MELD. Routine clinical and imaging findings indicative of portal hypertension were similarly common. Intrahepatic portal tract abnormalities (49% vs. 15%; p < 0.001), FNH-like lesions (30% vs. 1%; p < 0.001), and abnormal liver morphology defined as peripheral parenchymal atrophy and compensatory hypertrophy of central segments (32% vs. 7%; p < 0.001) were significantly more common in PSVD patients. Hypertrophy of segment I (70% vs. 84%; p = 0.019), atrophy of segment IV (24% vs. 47%; p = 0.001), and nodular liver surface (22% vs. 89%; p < 0.001) were more common in patients with cirrhosis. In patients with gadoxetic acid–enhanced MRI, we identified the distinct imaging feature of “periportal hyperintensity” in the hepatobiliary phase (HBP) in 42% of patients with PSVD (14/33) vs. 1% in cirrhosis (1/95) vs. 0% in non-cirrhotic controls (0/41); p < 0.001). Conclusions Diagnosis of PSVD must be considered in younger patients presenting with clinical features of portal hypertension, portal tract abnormalities, and FNH-like lesions on CT/MRI. ‘Periportal hyperintensity’ in the HBP of gadoxetic acid–enhanced MRI was identified as a specific radiological feature of PSVD. Key Points • Cross-sectional imaging can provide essential information to identify patients with porto-sinusoidal vascular disorder (PSVD). • Intrahepatic portal tract abnormalities, FNH-like lesions, and abnormal liver morphology are common in PSVD patients. • Periportal hyperintensity on the hepatobiliary phase of gadoxetic acid–enhanced MRI seems to be specific for patients with PSVD.

Background Fistula-associated anal adenocarcinoma (FAAC) is a rare consequence in patients with long-standing perianal fistulas. A paucity of data are available for this patient collective, making clinical characterization and management of this disease difficult. Objective This study aimed to describe a single-center experience with FAAC patients, their clinical course, and histopathological and molecular pathological characterization. Methods All patients receiving surgery for an anal fistula in 1999–2019 at a tertiary university referral hospital were included in this retrospective analysis. Patients with FAAC were eligible for histopathological analysis, including immunohistochemistry and molecular profiling. Results This study included 1004 patients receiving surgical treatment for an anal fistula, of whom 242 had an underlying inflammatory bowel disease (IBD). Ten patients were diagnosed with a fistula-associated anal carcinoma (1.0%), and six of these patients had an FAAC (0.6%). The mean overall survival of FAAC patients was 24 ± 3 months. FAAC immunohistochemistry revealed positive staining for CK20, CDX2 and MUC2, while stainings for CK5/6 and CK7 were negative. All FAAC specimens revealed microsatellite stability. Molecular profiling detected mutations in 35 genes, with the most frequent mutations being TP53, NOTCH1, NOTCH3, ATM, PIK3R1 and SMAD4. Conclusion FAAC is rare but associated with poor clinical outcome. Tissue acquisition is crucial for early diagnosis and therapy and should be performed in long-standing, non-healing, IBD-associated fistulas in particular. The immunophenotype of FAAC seems more similar to the rectal-type mucosa than the anal glands.

Tumor‐infiltrating immune cells are relevant prognostic and immunotherapeutic targets in hepatocellular carcinoma (HCC). Mast cells play a key role in allergic response but may also be involved in anticancer immunity. Digital morphometric analysis of patient tissue sections has become increasingly available for clinical routine and provides unbiased quantitative data. Here, we apply morphometric analysis of mast cells to retrospectively evaluate their relevance for HCC recurrence in patients after orthotopic liver transplantation (OLT). A total of 173 patients underwent OLT for HCC at the Medical University of Vienna (21 women, 152 men; 55.2 ± 7.9 years; 74 beyond Milan criteria, 49 beyond up‐to‐7 criteria for liver transplantation). Tissue arrays from tumors and corresponding surrounding tissues were immunohistochemically stained for mast cell tryptase. Mast cells were quantified by digital tissue morphometric analysis and correlated with HCC recurrence. Mast cells were detected in 93% of HCC tumors and in all available surrounding liver tissues. Tumor tissues revealed lower mast cell density than corresponding surrounding tissues (P < 0.0001). Patients lacking intratumoral mast cells (iMCs) displayed larger tumors and higher tumor recurrence rates both in the whole cohort (hazard ratio [HR], 2.74; 95% confidence interval [CI], 1.09‐6.93; P = 0.029) and in patients beyond transplant criteria (Milan HR, 2.81; 95% CI, 1.04‐7.62; P = 0.01; up‐to‐7 HR, 3.58; 95% CI, 1.17‐10.92; P = 0.02). Notably, high iMC identified additional patients at low risk classified outside the Milan and up‐to‐7 criteria, whereas low iMC identified additional patients at high risk classified within the alpha‐fetoprotein French and Metroticket criteria. iMCs independently predicted tumor recurrence in a multivariate Cox regression analysis (Milan HR, 2.38; 95% CI, 1.16‐4.91; P = 0.019; up‐to‐7 HR, 2.21; 95% CI, 1.05‐4.62; P = 0.035). Conclusion: Hepatic mast cells might be implicated in antitumor immunity in HCC. Morphometric analysis of iMCs refines prognosis of HCC recurrence after liver transplantation. We applied digital morphometric analysis to evaluate microscopic tissue images of mast cells in tumors and surrounding tissues of hepatocellular carcinoma patients who underwent liver transplantation. We found that intratumoral mast cell density is an independent prognostic factor of HCC recurrence. Mast cells were decreased in tumors as compared to surrounding tissues; lack of mast cells indicated higher tumor recurrence risk. To our best knowledge, this is the first report on the link between hepatic mast cells and HCC recurrence after transplantation. These data also suggest that hepatic mast cells might be implicated in anti‐tumor immunity in HCC.

BackgroundLiver stiffness (LS) measured by vibration-controlled transient elastography (VCTE) is influenced by liver fibrosis and hepatic perfusion pressure. VCTE-based controlled attenuation parameter (CAP) is a noninvasive marker for hepatic steatosis (HS).AimsTo investigate the diagnostic performance of CAP in patients with advanced chronic liver disease (ACLD)/portal hypertension (PHT: hepatic venous pressure gradient (HVPG) ≥ 6 mmHg).MethodsEighty-eight patients with LS ≥ 10 kPa and/or HVPG ≥ 6 mmHg who underwent simultaneous liver biopsy, CAP, and HVPG measurement were included. HS was histologically graded according to the modified Brunt classification.ResultsPatient characteristics: Mean MELD:11 (standard derivation [SD] ± 4), median HVPG:16 (interquartile range [IQR]10–19) mmHg, median LS:27.4 (IQR 16.2–48.9) kPa, and mean CAP:221 (SD ± 75) dB/m. According to histology, 47 (53.4%) patients had no HS (S0), 28 (31.8%) had S1, 11 (12.5%) had S2, and 2 (2.3%) had S3. The area under the receiver operating characteristic curve (AUROC) of CAP for diagnosing any HS (S0 vs. ≥ S1) was 0.692 (95% confidence interval [95% CI] 0.582–0.802) in the overall cohort, 0.830 (95% CI 0.637–1.0) in patients with HVPG < 10 mmHg, and 0.629 (95% CI 0.497–0.761) in patients with clinically significant portal hypertension (CSPH; HVPG ≥ 10 mmHg; n = 69). Using the established cutoff for any HS (248 dB/m), the sensitivity/specificity of CAP was only 48.8%/76.6%, respectively. In contrast, the AUROC and sensitivity/specificity (cutoff 268 dB/m) for diagnosing HS ≥ S2 were 0.842 (95% CI 0.747–0.936) and 84.6%/81.3%, respectively. CAP correlated with the percentage of steatotic hepatocytes (Spearman’s ρ = 0.402; p ≤ 0.001) and showed a weak correlation with liver stiffness (ρ = 0.225; p = 0.035).ConclusionsThe diagnostic performance of CAP for any HS seems to be limited in patients with ACLD, if CSPH is present.