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Objectives: Current guidelines recommend use of a diagnostic algorithm to assess disease severity in cases of suspected nonalcoholic fatty liver disease (NAFLD). We applied this algorithm to HIV‐monoinfected patients. Methods: We analysed three prospective screening programmes for NAFLD carried out in the following cohorts: the Liver Disease in HIV (LIVEHIV) cohort in Montreal, the Modena HIV Metabolic Clinic (MHMC) cohort and the Liver Pathologies in HIV in Palermo (LHivPa) cohort. In the LIVEHIV and LHivPa cohorts, NAFLD was diagnosed if the controlled attenuation parameter (CAP) was ≥ 248 dB/m; in the MHMC cohort, it was diagnosed if the liver/spleen Hounsfield unit (HU) ratio on abdominal computerized tomography scan was < 1.1. Medium/high‐risk fibrosis category was defined as fibrosis‐4 (FIB‐4) ≥ 1.30. Patients requiring specialist referral to hepatology were defined as either having NAFLD and being in the medium/high‐risk fibrosis category or having elevated alanine aminotransferase (ALT). Results: A total of 1534 HIV‐infected adults without significant alcohol intake or viral hepatitis coinfection were included in the study. Of these, 313 (20.4%) patients had the metabolic comorbidities (obesity and/or diabetes) required for entry in the diagnostic algorithm. Among these patients, 123 (39.3%) required specialist referral to hepatology, according to guidelines. A total of 1062 patients with extended metabolic comorbidities (any among obesity, diabetes, hypertension and dyslipidaemia) represented most of the cases of NAFLD (79%), elevated ALT (75.9%) and medium/high‐risk fibrosis category (75.4%). When the algorithm was extended to these patients, it was found that 341 (32.1%) would require specialist referral to hepatology. Conclusions: According to current guidelines, one in five HIV‐monoinfected patients should undergo detailed assessment for NAFLD and disease severity. Moreover, one in ten should be referred to hepatology. Expansion of the algorithm to patients with any metabolic comorbidities may be considered. [ABSTRACT FROM AUTHOR]

Lymphography by radioisotope or dye is a well-known technique for visualizing the lymphatic drainage pattern in a neoplastic lesion and it is in use in gastric cancer. Indocyanine green (ICG) more recently has been validated in fluorescent lymphography studies and is under evaluation as a novel tracer agent in gastric cancer. The amount and dilution of ICG injected as well as the site and the time of the injection are not standardized. In our unit, endoscopic submucosal injections of ICG are made as 0.5 mg in 0.5 mL at four peritumoral sites the day before surgery (for a total of 2.0 mg in 2.0 mL). Detection instruments for ICG fluorescence are evolving. Near-infrared systems integrated into laparoscopic or robotic instruments (near-infrared fluorescence imaging) have shown the most promising results. ICG fluorescence recognizes the node that receives lymphatic flow directly from a primary tumor. This is defined as the sentinel lymph node, and it has a high predictive negative value at the cT1 stage, able to reduce the extent of gastrectomy and lymph node dissection. ICG also enhances the number of lymph nodes detected during extended lymphadenectomy for advanced gastric cancer. Nevertheless, the practical effects of ICG use in a single patient are not yet clear. Standardization of the technique and further studies are needed before fluorescent lymphography can be used extensively worldwide. Until then, current guidelines recommend an extensive lymphadenectomy as the standard approach for gastric cancer with suspected metastasis., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)

Background & Aims: Some patients with compensated advanced chronic liver disease (cACLD) require use of an extralarge probe for liver stiffness measurement (LSM), owing to overweight or obesity. However, the ability of noninvasive markers of portal hypertension and the controlled attenuation parameter (CAP) to determine which of these patients are at risk for decompensation has not been fully assessed., Methods: We collected data from 272 patients with cACLD (LSM ≥10 kPa by XL probe; 57% with nonalcoholic steatohepatitis; mean body mass index, 33.8 ± 6.5 kg/m 2 ; median Child-Pugh score, 5; median LSM, 16.8 kPa; mean CAP, 318 ± 66 dB/m) evaluated at 2 academic centers from 2015 through 2018. We collected clinical data on decompensation (ascites, portal hypertension bleeding, jaundice, hepatic encephalopathy) and severe bacterial infections; patients were followed up for a median of 17 months (interquartile range, 11-24 mo). We evaluated associations between these events and LSM, CAP, LSM∗spleen size/platelet count (LSPS), and portal hypertension risk scores., Results: Decompensation occurred in 12 patients and severe bacterial infections developed in 5 patients. LSM, LSPS, and the portal hypertension risk score identified patients with decompensation with area under the receiver operating characteristic curve values of 0.848 (95% CI, 0.720-0.976; P < .0001), 0.881 (95% CI, 0.798-0.954; P < .0001), and 0.890 (95% CI, 0.814-0.966; P < .0001), respectively. In multivariate Cox regression analysis, in patients with nonalcoholic steatohepatitis, LSM and CAP were associated independently with decompensation and severe bacterial infection; CAP ≥ 220 dB/m was associated with a reduced risk of decompensation (hazard ratio, 0.043, 95% CI, 0.004-0.476; P = .01)., Conclusions: LSM, LSPS, and the portal hypertension risk score identify obese or overweight patients with cACLD who are at increased risk of decompensation and severe bacterial infection., (Copyright © 2020 AGA Institute. Published by Elsevier Inc. All rights reserved.)

Background: Inflammatory bowel disease (IBD) patients may be at risk for nonalcoholic fatty liver disease (NAFLD) due to chronic inflammation, hepatotoxic drugs, and alteration of the gut microbiota. Prospective data using accurate diagnostic methods are lacking., Methods: We prospectively investigated prevalence and predictors of NAFLD and liver fibrosis by transient elastography (TE) with associated controlled attenuation parameter (CAP) in IBD patients as part of a routine screening program. NAFLD was defined as CAP ≥248 dB/m. Significant liver fibrosis (stage 2 or higher out of 4) was defined as TE measurement ≥7.0 kPa. Predictors of NAFLD and significant liver fibrosis were determined by logistic regression analysis., Results: A total of 384 patients (mean age 42.4 years, 45.0% male, 64.6% with Crohn's disease) with no significant alcohol intake were included. Prevalence of NAFLD and significant liver fibrosis was 32.8% and 12.2%, respectively. Independent predictors of NAFLD were older age (adjusted odds ratio [aOR], 1.45; 95% confidence interval [CI], 1.15-1.82), higher body mass index (BMI; aOR, 1.31; 95% CI, 1.20-1.42) and higher triglycerides (aOR, 1.45; 95% CI, 1.01-2.09). Significant liver fibrosis was independently predicted by older age (aOR, 1.38; 95% CI, 1.12-1.64) and higher BMI (aOR, 1.14; 95% CI, 1.07-1.23). Extrahepatic diseases were more common in IBD patients with NAFLD compared with those without, namely chronic kidney disease (10.3 vs 2.3%; P < 0.001) and cardiovascular diseases (11.3 vs 4.7%; P = 0.02)., Conclusions: NAFLD diagnosed by TE with CAP is a frequent comorbidity in IBD patients and is associated with extrahepatic diseases. Noninvasive screening strategies could help early diagnosis and initiation of interventions, including weight loss, correction of dyslipidemia, and linkage to care. 10.1093/ibd/izy200&#95;video1izy200.video15794817619001.

Purpose of Review: The study reviews recent publications that build on previous studies showing that acute enteric infection can produce persistent dysfunction in the lower gut (postinfectious irritable bowel syndrome) and proximal gut (postinfectious functional dyspepsia). The review addresses risk factors, the pathophysiological basis of persistent gut dysfunction, and the factors that initiate and maintain it., Recent Findings: Recent work has identified several loci of host genetic predisposition to these syndromes that focus attention on host immune responses that may lead to gut dysfunction, including changes in intestinal barrier function and cytokine responses to the initial infection. Human and animal studies identify changes in the serotonergic and cannabinoid pathways regulating visceral pain responses and gut motility. Recent work has also focused attention on the putative role of the intestinal microbiota or dysbiosis in maintaining gut dysfunction and this is reviewed in depth., Summary: The development of long-term consequences following an acute episode of gastroenteritis reflects a convergence of host factors that include genetic predisposition and psychological factors, as well as the development of intestinal dysbiosis. It is anticipated that future research will generate biomarkers of susceptibility as well as novel microbiota-directed preventive and therapeutic strategies.

Aim: To determine intra-hepatic blood flow and liver stiffness in patients with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) using contrast-enhanced ultrasound and fibroscan., Methods: This prospective study included 15 patients with NAFLD, 17 patients with NASH and 16 healthy controls. In each patient, real-time ultrasound was used to locate the portal vein (PV) and the right liver lobe, and 5 mL of SonoVue(®) was then injected intravenous in a peripheral vein of the left arm over a 4-s span. Digital recording was performed for 3 min thereafter. The recording was subsequently retrieved to identify an area of interest in the PV area and in the right liver parenchyma (LP) to assess the blood flow by processing the data using dedicated software (Qontrast(®), Bracco, Italy). The following parameters were evaluated: percentage of maximal contrast activity (Peak%), time to peak (TTP, s), regional blood volume (RBV, cm(3)), regional blood flow (RBF, cm(3)/s) and mean transit time (MTT, s). At 24-48 h post-injection, liver stiffness was evaluated using Fibroscan and measured in kPa. The statistical evaluation was performed using Student's t test., Results: In the PV, the Peak%, RBV and RBF were significantly reduced in the NAFLD and NASH patients compared with the controls (Peak%: NAFLD 26.3 ± 6.6, NASH 28.1 ± 7.3 vs controls 55.8 ± 9.9, P < 0.001; RBV: NAFLD 4202.3 ± 3519.7, NASH 3929.8 ± 1941.3 vs controls 7473 ± 3281, P < 0.01; RBF: NAFLD 32.5 ± 10.8, NASH 32.7 ± 12.1 vs controls 73.1 ± 13.9, P < 0.001). The TTP in the PV was longer in both patient groups but reached statistical significance only in the NASH patients compared with the controls (NASH 79.5 ± 37.8 vs controls 43.2 ± 30, P < 0.01). In the LP, the Peak%, RBV and RBF were significantly reduced in the NAFLD and NASH patients compared with the controls (Peak%: NAFLD 43.2 ± 7.3, NASH 41.7 ± 7.7 vs controls 56.6 ± 6.3, P < 0.001; RBV: NAFLD 4851.5 ± 2009, NASH 5069.4 ± 2292.5 vs controls 6922.9 ± 2461.5, P < 0.05; RBF: NAFLD 55.7 ± 10.1, NASH 54.5 ± 12.1 vs controls 75.9 ± 10.5, P < 0.001). The TTP was longer in both patient groups but did not reach statistical significance. The MTT in both the PV and LP in the NAFLD and NASH patients was not different from that in the controls. Liver stiffness was significantly increased relative to the controls only in the NASH patients (NASH: 6.4 ± 2.2 vs controls 4.6 ± 1.5, P < 0.05)., Conclusion: Blood flow derangement within the liver present not only in NASH but also in NAFLD suggests that a vascular flow alteration precedes liver fibrosis development.