Aim To determine the tolerance and acceptance of hepatic venous pressure gradient (HVPG) measurements in patients with liver cirrhosis. Methods This prospective international multicenter study included 271 patients with cirrhosis who were scheduled to undergo HVPG measurement between October 2019 and June 2020. Data related to the tolerance and acceptance of HVPG measurements were collected using descriptive questionnaires. Results HVPG measurements were technically successful in all 271 patients, with 141 (52.0%) undergoing HVPG measurement alone. The complication rate was 0.4%. Postoperative pain was significantly lower than preoperative expected pain (p < 0.001) and intraoperative pain (p < 0.001), and intraoperative pain was also significantly lower than preoperative expected pain (p = 0.036). No, mild, moderate, severe, and intolerable discomfort scores were reported by 36.9%, 44.6%, 11.1%, 6.3%, and 0.4% of these patients, respectively, during HVPG measurement and by 54.6% 32.5%, 11.4%, 1.5%, and 0%, respectively, after HVPG measurement. Of these patients, 39.5% had little understanding and 10% had no understanding of the value of HVPG measurement, with 35.1% and 4.1% regarding HVPG measurements as being of little or no help, respectively. Most patients reported that they would definitely (15.5%), probably (46.9%), or possibly (29.9%) choose to undergo additional HVPG measurements again, and 62.7% regarded the cost of the procedure as acceptable. Conclusion HVPG measurement was safe and well‐tolerated in patients with cirrhosis, but patient education and communication are warranted to improve the acceptance of this procedure.
The global burden of hepatocellular carcinoma (HCC) as a preeminent etiology of cancer‐related mortalities sheds light on the imperative necessity for a more profound comprehension of its fundamental biological mechanisms. In this context, the precise function of the 26S proteasome non‐ATPase regulatory subunit 11 (PSMD11) in HCC remains equivocal. To address this vital knowledge gap, we interrogated the cancer genome atlas, genotype‐tissue expression, International cancer genome consortium, gene expression omnibus, the cancer cell line encyclopedia, and tumor immune single‐cell hub databases to evaluate the expression pattern of PSMD11, further confirmed by reverse‐transcription quantitative polymerase chain reaction (RT‐qPCR) in LO2, MHCC‐97H, HepG2, and SMMC7721 cell lines. Additionally, we meticulously assessed the clinical significance and prognostic value of PSMD11, while also exploring its potential molecular mechanisms in HCC. Our findings demonstrated that PSMD11 was highly expressed in HCC tissues, correlating with pathologic stage and histologic grade, thereby conferring a poor prognosis. Mechanistically, PSMD11 appears to exert its tumorigenic effects through the modulation of tumor metabolism‐related pathways. Impressively, low PSMD11 expression was associated with increased immune effector cell infiltration, heightened responsiveness to molecular targeted drugs such as dasatinib, erlotinib, gefitinib, and imatinib, as well as reduced somatic mutation rate. Additionally, we demonstrated that PSMD11 might modulate HCC development through intricate interactions with cuproptosis‐related genes ATP7A, DLAT, and PDHA1. Our comprehensive analyses collectively suggest that PSMD11 represents a promising therapeutic target in HCC.
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