Xiaobing Wang

POEMS (Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal gammopathy, Skin changes) syndrome is a rare multisystem disease, often presenting diagnostic challenges. Here, we report a case of POEMS syndrome in an elderly patient with refractory peritoneal effusion and hypoalbuminemia as the main manifestations. Physical examination revealed cutaneous hyperpigmentation of upper and lower extremities. Tests revealed elevated vascular endothelial growth factor (VEGF) and hypogonadism, while imaging showed enlargement of armpits and groin lymph nodes. Lymph node biopsy excluded tuberculosis and malignancy. Electroneuromyography (EMG) disclosed polyneuropathy of the lower extremities. Finally, he was diagnosed with POEMS syndrome via bone marrow biopsy. Notably, he presented endoscopic snakeskin-like appearance of stomach, which was consistent with previous research. POEMS syndrome, a rare cause of ascites, is frequently missed or misdiagnosed. Thus, clinicians should maintain high vigilance. In patients with unexplained refractory ascites and symptoms like neuropathy, lymph nodes enlargement, and endocrine disorders, screening for VEGF levels and M protein should be performed to facilitate early identification of POEMS syndrome.

Purpose This study aimed to explore a modified direct intrahepatic portocaval shunt (DIPS) technique as an alternative approach for patients with portal vein occlusion (PVO) and cirrhosis who were not candidates for traditional transjugular intrahepatic portosystemic shunt (TIPS) due to anatomical challenges. Technique Three patients with esophageal or gastric fundus variceal hemorrhage complicated by severe PVO were treated using innovative DIPS approaches. Preoperative contrast-enhanced computed tomography was employed to assess anatomical feasibility. The modified DIPS techniques involved targeting dilated varicose veins or the confluence of the superior mesenteric and splenic veins to access the inferior vena cava. For broader clinical applications, we outlined the anatomical conditions necessary for adopting the method proposed in this study. Following the puncture, portal hypertension was effectively alleviated, and bleeding was controlled. There were no obvious complications during the follow-up period. Conclusion Modified DIPS targeting different vessels appears to be a feasible alternative for the treatment of severe PVO when conventional TIPS by ultrasound-guided percutaneous transhepatic or transsplenic pathway and DIPS are unsuccessful. Future validation in a larger patient population is needed. Level of Evidence Level 4, Case Series. Graphical Abstract

Objective: This study was performed to investigate whether a definite correlation exists between alteration of blood biochemical parameters and immunosuppressive therapies in patients with inflammatory bowel disease (IBD). Methods: A comprehensive search of PubMed, EMBASE, MEDLINE, and the Cochrane Library was conducted. Data on alterations in white blood cells, platelets, hemoglobin, serum creatinine, and liver enzymes in patients with IBD treated with immunomodulators were extracted. Results: Data from 1141 patients were included. The relative risk (RR) of leukopenia was significantly higher in the immunosuppressive therapies group than in the placebo group (RR, 12.91; 95% confidence interval [CI], 5.28–31.57). A statistically significant risk of leukocytosis during immunosuppressive therapies was observed (RR, 1.53; 95% CI, 1.05–2.23). Patients taking immunomodulators had increased risks of serum creatinine elevation (RR, 10.68; 95% CI, 2.07–55.12) and serum aminotransferase elevation (RR, 3.18; 95% CI, 1.24–8.17). Conclusion: Immunosuppressive therapies might have an impact on variations in blood biochemical parameters in patients with IBD. Although the conclusion regarding leukopenia was reliable in this study, some confounding factors might reduce the reliability of the conclusions about leukocytosis, creatinine elevation, and aminotransferase elevation. Close monitoring is recommended during immunosuppressive therapies for IBD.

This study aimed to investigate the role of JKAP in inflammatory bowel disease (IBD). JKAP expression was analyzed in the intestinal mucosa of 81 IBD patients and 25 healthy controls (HCs) by qPCR and immunoblotting. The correlations of JKAP with clinical activity and inflammatory cytokines were performed. JKAP expression before and after IFX treatment was also measured. CD4+ T cells were isolated from peripheral blood in active IBD patient and HCs, and transduced with lentivirus-encoding JKAP (LV-JKAP), anti-JKAP (LV-anti-JKAP), or empty vector (LV-scramble), and JKAP functions on IBD CD4+ T cells were subsequently investigated. JKAP expression was decreased in inflamed mucosa of active IBD patients, and was negatively correlated with disease activity (CDAI, Mayo index, CRP, and ESR), IL-17 and TNF-α levels. Anti-TNF-α treatment up-regulated JKAP expression in CD patients and baseline JKAP expression was elevated in response patients compared with failure patients. Transduction of LV-JKAP into CD4+ T cells inhibited the percentages of CD25+ and CD69+ cells, and proliferation. Moreover, inhibition of JKAP promotes Th1/Th17 cell differentiation. Our data indicated that decreased expression of JKAP in intestinal mucosa contributed to the pathogenesis of IBD, through facilitating CD4+ T cell activation, proliferation, and Th1/Th17 cell differentiation.

A major reason for the failure of advanced colorectal cancer (CRC) treatment is the occurrence of chemoresistance to oxaliplatin-based chemotherapy. Recently, studies have shown that long non-coding RNAs (lncRNAs) play an important role in drug resistance. Using HiSeq sequencing methods, we identified that lncRNAs show differential expression levels in oxaliplatin-resistant (OxR) and non-resistant CRC patients. RT-qPCR was then performed in tissues and serum samples, and lncRNA MEG3 was verified to be downregulated in non-responding patients and to have considerable discriminating potential to identify responding patients from non-responding patients. Moreover, decreased serum MEG3 expression was associated with poor chemoresponse and low survival rate in CRC patients receiving oxaliplatin treatment. Subsequently, OxR cell lines were established, and MEG3 was significantly downregulated in HT29 OxR and SW480 OxR cells. In addition, overexpression of MEG3 with pMEG3 reversed oxaliplatin resistance in both CRC cell lines. Flow cytometric apoptosis analysis indicated that MEG3 promoted CRC cell apoptosis. More importantly, MEG3 enhanced oxaliplatin‑induced cell cytotoxicity in CRC. In conclusion, our integrated approach demonstrated that decreased expression of lncRNA MEG3 in CRC confers potent poor therapeutic efficacy, and that MEG3 promotes chemosensitivity by enhancing oxaliplatin-induced cell apoptosis. Thus, overexpression of MEG3 may be a future direction by which to develop a novel therapeutic strategy to overcome oxaliplatin resistance of CRC patients.