Simplified liver imaging reporting and data system for the diagnosis of hepatocellular carcinoma on gadoxetic acid-enhanced magnetic resonance imaging.

BACKGROUND: The liver imaging reporting and data system (LI-RADS) diagnostic table has 15 cells and is too complex. The diagnostic performance of LI-RADS for hepatocellular carcinoma (HCC) is not satisfactory on gadoxetic acid-enhanced magnetic resonance imaging (EOB-MRI). AIM: To evaluate the ability of the simplified LI-RADS (sLI-RADS) to diagnose HCC on EOB-MRI. METHODS: A total of 331 patients with 356 hepatic observations were retrospectively analysed. The diagnostic performance of sLI-RADS A-D using a single threshold was evaluated and compared with LI-RADS v2018 to determine the optimal sLI-RADS. The algorithms of sLI-RADS A-D are as follows: The single threshold for sLI-RADS A and B was 10 mm, that is, classified observations ≥ 10mm using an algorithm of 10-19 mm observations (sLI-RADS A) and ≥ 20 mm observations (sLI-RADS B) in the diagnosis table of LI-RADS v2018, respectively, while the classification algorithm remained unchanged for observations < 10 mm; the single threshold for sLI-RADS C and D was 20 mm, that is, for < 20 mm observations, the algorithms for < 10 mm observations (sLI-RADS C)and 10-19 mm observations (sLI-RADS D) were used, respectively, while the algorithm remained unchanged for observations ≥ 20 mm. With hepatobiliary phase (HBP) hypointensity as a major feature (MF), the final sLI-RADS (F-sLI-RADS) was formed according to the optimal sLI-RADS, and its diagnostic performance was evaluated. The times needed to classify the observations according to F-sLI-RADS and LI-RADS v2018 were compared. RESULTS: The optimal sLI-RADS was sLI-RADS D (with a single threshold of 20 mm), because its sensitivity was greater than that of LI-RADS v2018 (89.8% vs 87.0%, P = 0.031), and its specificity was not lower (89.4% vs 90.1%, P > 0.999). With HBP hypointensity as an MF, the sensitivity of F-sLI-RADS was greater than that of LI-RADS v2018 (93.0% vs 87.0%, P < 0.001) and sLI-RADS D (93.0% vs 89.8%, P = 0.016), without a lower specificity (86.5% vs 90.1%, P = 0.062; 86.5% vs 89.4%, P = 0.125). Compared with that of LI-RADS v2018, the time to classify lesions according to F-sLI-RADS was shorter (51 ± 21 s vs 73 ± 24 s, P < 0.001). CONCLUSION: The use of sLI-RADS with HBP hypointensity as an MF may improve the sensitivity of HCC diagnosis and reduce lesion classification time.

Gut dysbiosis-influence on amygdala-based functional activity in patients with end stage renal disease: a preliminary study.

Patients with end-stage renal disease (ESRD) are notably accompanied by cognitive disorder and anxiety or depressive symptom. We aimed to explore the linkages of the amygdala-based MR parameters, cognitive and mood performance, systematic inflammation and gut microbiota in ESRD. This prospective study enrolled 28 ESRD patients (13 males and 15 females, mean age of 43.9 ± 13.8 years) and 19 age- and sex-matched healthy control (HC) (12 males and 7 females, mean age of 44.1 ± 10.0 years). All subjects underwent cognitive assessment, inflammatory factor and stool microbiota analysis, and brain MRI analysis [amygdala-based functional connectivity and voxel-based morphometry (VBM)]. ERSD was separated by different microbiota strains. All factors were compared between ESRD and HC, as well as between ESRD subgroups. Pearson correlation analysis and causal mediation analysis were conducted to further investigate the relationship among the factors derived from the gut microbiota, brain and systemic inflammation. ESRD displayed gut dysbiosis and increased systemic inflammation when compared to HC (all P < 0.05). Meanwhile, ESRD showed smaller VBM in amygdala, decreased functional connectivity in left amygdala - right inferior parietal lobe [P < 0.05, Gaussian Random Field (GRF) corrected] and worse cognitive or mood performance. Moreover, ESRD-B (Prevutella mainly), when compared to ESRD-A (Bacteroides mainly), displayed increased interleukin-6, self-rating anxiety scale and functional connectivity in left amygdala - bilateral anterior cingulate cortex / medial superior frontal cortex (P < 0.05, GRF corrected). Furthermore, the correlation network of ESRD showed that both gut dysbiosis and amygdala-based alteration were correlated with cognitive performance and systemic inflammation. Causal mediation analysis validated that the disrupted distribution of Roseburia indirectly regulated the amygdala-based functional connectivity through tumor necrosis factor-alpha. The gut dysbiosis induced by ESRD was closely related to pro-inflammatory cytokines, amygdala-based phenotype, and mood performance. The lower abundance in Roseburia indirectly modulated amygdala-based functional connectivity pattern by tumor necrosis factor-alpha, which might provide a new way in diagnosis and treatment in patients of ESRD with depressive/anxious mood.

The gut microbiota-inflammation-brain axis in end-stage renal disease: perspectives from default mode network.

The gut-brain axis in end-stage renal disease (ESRD) is attracting more and more attention. However, the mechanism of gut-brain axis based cognitive disorders in ESRD patients remains unclear. The purpose of this study was to investigate the linkages between the gut microbiota, inflammatory cytokines, brain default mode network (DMN) and cognitive function in ESRD patients. Methods: This prospective study enrolled 28 ESRD patients (13 males and 15 females, mean age of 44 ± 14 years) and 19 healthy controls (HCs) (12 males and 7 females, mean age of 44 ± 10 years). All subjects underwent stool microbiota analysis, blood inflammatory cytokines examination, brain MRI scans and cognitive assessments. Resting state functional MRI (rs-fMRI) data were used to construct DMN and graph theory was applied to characterize network topological properties. Two samples t-test was applied for the comparisons between ESRD and HCs. Correlation analysis and mediation analysis were conducted among factors with significant group differences. Results: ESRD patients displayed gut microbiota alterations, increased systemic inflammation and worse cognitive performance compared to HCs (all p < 0.05). Graph analysis revealed disrupted DMN topological organization, aberrant nodal centralities and functional connectivities (FCs) in ESRD patients relative to HCs (all p < 0.05, FDR corrected). Significant correlations were found between gut microbiota, inflammatory cytokines, DMN network measures and cognitive assessments. Mediation analysis found that gut microbiota alteration impaired DMN connectivity by increasing systemic inflammation. Conclusion: The present study first revealed gut microbiota alterations, systemic inflammation, DMN dissociation and cognitive dysfunction in ESRD patients simultaneously and further illuminated their inner relationship.