Introduction Sclerosing angiomatoid nodular transformation (SANT) of the spleen is a rare benign vascular lesion with unknown etiopathogenesis and with definite features of imaging, histopathology, and immunohistochemistry. It was first described by Martel et al. in 2004, and to date, only 151 cases have been reported. Case Description We report a case of SANT of the spleen detected in a 66-year-old Caucasian, without comorbidities, presented to our department with epigastric pain. We, also, presented a review of the literature. Conclusions SANT is a benign incidentally vascular condition in the majority of cases. The wide age and gender distribution in our review is in accordance with that in previous studies in English literature. In our opinion, splenectomy is the choice treatment because it is at the same time diagnostic and therapeutic in a definitive way.

Background Nonalcoholic fatty liver disease (NAFLD) is increasingly prevalent and represents a growing challenge in terms of prevention and treatment. A minority of affected patients develops inflammation, subsequently fibrosis, cirrhosis and hepatocellular carcinoma (HCC). HCC is a leading cause of cancer-related death. An increased number of senescent cells correlate with age-related tissue degeneration during NAFLD-induced HCC. Senolytics are promising agents that target selectively senescent cells. Previous studies showed that whereas a combination of the senolytic drugs dasatinib and quercetin (D + Q) reduced NAFLD in mice, D + Q lacked efficacy in removing doxorubicin-induced β-gal-positive senescent cells in human HCC xenografted mice. Whether D + Q has an effect on the age-associated spectrum of NAFLD-inflammation-HCC remains unknown. Methods Here, we utilized an established model of age- and obesity-associated HCC, the low dose diethylnitrosamine (DEN)/high fat diet (HFD), a regimen promoting liver inflammation and tumorigenesis over a long period of 9 months. Four groups of mice each were created: group 1 included control untreated mice; group 2 included mice treated with D + Q; group 3 included mice undergoing the DEN/HFD protocol; group 4 included mice undergoing the DEN/HFD protocol with the administration of D + Q. At the end of the chemical/dietary regimen, we analyzed liver damage and cell senescence by histopathology, qPCR and immunoblotting approaches. Results Unexpectedly, D + Q worsened liver disease progression in the DEN/HFD mouse model, slightly increasing histological damage and tumorigenesis, while having no effect on senescent cells removal. Conclusions In summary, using an animal model that fully recapitulates NAFLD, we demonstrate that these compounds are ineffective against age-associated NAFLD-induced HCC.

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Background & Aims NAFLD patients usually have an increase in AST/ALT levels, but cholestasis can also be observed. We aimed to assess in subjects with NAFLD the impact of the (cholestatic) C pattern on the likelihood of developing major liver‐related outcomes (MALO). Methods Five hundred and eighty‐two consecutive patients with biopsy‐proven NAFLD or a clinical diagnosis of NAFLD‐related compensated cirrhosis were classified as hepatocellular (H), C and mixed (M) patterns, by using the formula (ALT/ALT Upper Limit of Normal‐ULN)/(ALP/ALP ULN). MALO were recorded during follow‐up. An external cohort of 1281 biopsy‐proven NAFLD patients was enrolled as validation set. Results H, M and C patterns were found in 153 (26.3%), 272 (46.7%) and 157 (27%) patients respectively. During a median follow‐up of 78 months, only 1 (0.6%) patient with H pattern experienced MALO, whilst 15 (5.5%) and 38 (24.2%) patients in M and C groups had MALO. At multivariate Cox regression analysis, age >55 years (HR 2.55, 95% CI 1.17–5.54; p = .01), platelets <150 000/mmc (HR 0.14, 95% CI 0.06–0.32; p < .001), albumin <4 g/L(HR 0.62, 95% CI 0.35–1.08; p = .09), C versus M pattern (HR 7.86, 95% CI 1.03–60.1; p = .04), C versus H pattern(HR 12.1, 95% CI 1.61–90.9; p = .01) and fibrosis F3–F4(HR 35.8, 95% CI 4.65–275.2; p < .001) were independent risk factors for MALO occurrence. C versus M pattern(HR 14.3, 95% CI 1.90–105.6; p = .008) and C versus H pattern (HR 15.6, 95% CI 2.10–115.1; p = .0068) were confirmed independently associated with MALO occurrence in the validation set. The immunohistochemical analysis found a significantly higher prevalence of moderate‐high‐grade ductular metaplasia combined with low‐grade ductular proliferation in C pattern when compared with the biochemical H pattern. Gene expression analysis showed a lower expression of NR1H3, RXRα and VCAM1 in patients with the C pattern. Conclusions The presence of a cholestatic pattern in patients with NAFLD predicts a higher risk of MALO independently from other features of liver disease.