Quantitative evaluation of colorectal tumour vasculature using contrast-enhanced ultrasound: Correlation with angiogenesis and prognostic significance.

BACKGROUND: Ultrasound is a vital tool for the diagnosis and management of colorectal cancer (CRC). Contrast-enhanced ultrasound (CEUS) is a non-invasive, safe, and cost-effective method for evaluating tumour blood vessels, that play a crucial role in tumour growth and progression. AIM: To explore CEUS's role in the quantitative evaluation of CRC blood vessels and their correlation with angiogenesis markers and prognosis. METHODS: This study prospectively enrolled 100 patients with CRC confirmed by histopathology. All patients received preoperative CEUS examinations. Quantitative parameters, such as peak intensity (PI), time to peak (TTP), and area under the curve (AUC), were derived from time-intensity curve (TIC) analysis. Tumour tissue samples were obtained during surgery and examined immunohistochemically to assess the expression of angiogenesis markers, including vascular endothelial growth factor (VEGF) and microvessel density (MVD). The correlation between CEUS parameters, angiogenesis markers, and clinicopathological features was evaluated using appropriate statistical tests. RESULTS: Quantitative CEUS parameters (PI, TTP, and AUC) showed significant correlations with VEGF expression (P < 0.001) and MVD (P < 0.001), indicating a strong link between tumour blood vessels and angiogenesis. Increased PI, reduced TTP, and expanded AUC values were significantly related to higher tumour stage (P < 0.001), lymph node metastasis (P < 0.001), and distant metastasis (P < 0.001). Furthermore, these parameters were recognized as independent predictors of overall survival and disease-free survival in multivariate analysis (P < 0.001). CONCLUSION: CEUS has a high potential in guiding treatment planning and predicting patient outcomes. However, more comprehensive, multicentre studies are required to validate the clinical utility of CEUS in CRC management.

Development of hypothyroidism over 13 years of follow-up of patients with hyperthyroidism after radioiodine therapy.

OBJECTIVE: To analyze the incidence and associated factors of hypothyroidism after radioiodine treatment for hyperthyroidism during a 13-year follow-up period. SUBJECTS AND METHODS: This was a retrospective study of consecutive patients with hyperthyroidism who were treated using a single dose of radioactive iodine (RAI) with a calculated dose regimen from 07/2005 to 12/2012. Univariate and multivariate Cox regression models were used to examine the factors that are associated with the occurrence of hypothyroidism after RAI therapy. Kaplan-Meier analysis was used for confirming associations between these models. RESULTS: A total of 182 patients were included during a 7.5-year median follow-up (range: 6-13 years). They were 36.4±11.1 years. The mean radioactive iodine dosage was 308.2±104.3 (range: 129.5-740.0) MBq. The rates of euthyroidism, early hypothyroidism, improvement, and ineffective treatment at 6 months were 48.4%, 37.9%, 8.8%, and 4.9%, respectively. The cumulative incidence of hypothyroidism in all patients with hyperthyroidism was 45.6% at 1 year, 48.9% at 5 years, and 52.3% at 10 years. Thyroid weight >46g (HR=0.643, 95%CI: 0.422-0.981, P=0.040) and a course of disease of 0.5-3 years (HR=0.592, 95%CI: 0.358-0.981, P=0.042) were identified as independent factors associated with an increased risk of hypothyroidism after radioactive iodine therapy. CONCLUSION: Radioactive iodine treatment with a calculated dose has a high cure rate for hyperthyroidism and has a low annual increase of hypothyroidism. Hypothyroidism after radioactive iodine treatment is more likely to occur in patients with small thyroid and a short disease course.

Biphasic GA 68-labeled prostate specific membrane antigen-11 positron emission tomography/computed tomography scans in the differential diagnosis and risk stratification of initial primary prostate cancer.

BACKGROUND: This study aimed to assess the value of biphasic GA 68-labeled prostate-specific membrane antigen-11 (68Ga-PSMA-11) positron emission tomography/computed tomography (PET/CT) scan in the differential diagnosis and risk stratification of initial primary prostate cancer (PCa). METHODS: A total of 51 patients with PCa (8 low- and intermediate-risk PCa patients and 43 high-risk PCa patients) and 36 patients with benign prostate lesions, who underwent standard whole-body imaging and delayed pelvic imaging of 68Ga-PSMA-11 PET/CT, were enrolled in this prospective study. The PET parameters, such as maximum and mean standard uptake value (SUVmax and SUVmean), and maximum and mean standard retention index of PET images were calculated and compared in different prostate lesions. The diagnostic performances of the PET parameters were evaluated by receiver operating characteristic (ROC) curves. RESULTS: All the PET parameters of PCa participants were significantly higher than those of participants with benign prostate lesions (P<0.001). The SUVmean of delayed imaging had the best performance in the diagnosis of PCa with an area under the curve (AUC) of 0.918 (95% CI: 0.858 to 0.977), the sensitivity of 90.0%, and specificity of 83.3%. The SUVmax and SUVmean of high-risk PCa participants were significantly higher than those of low- and intermediate-risk PCa participants (P<0.005). The SUVmax of standard imaging had the best performance in predicting high-risk PCa with an AUC of 0.890 (95% CI: 0.799 to 0.980), a sensitivity of 76.7%, and a specificity of 100.0%. CONCLUSIONS: The biphasic 68Ga-PSMA-11 PET/CT scan had good performance in discriminating prostate cancer from benign prostate diseases. The SUVmean of the prostate lesion at delayed imaging of 68Ga-PSMA-11 PET/CT had the best value in the differential diagnosis of PCa, and the SUVmax at standard imaging was most valuable in predicting the risk stratification of PCa.

Apoptosis gene reprograming of human peripheral blood mononuclear cells induced by radioiodine-131 (131I) irradiation.

Background & objectives: The nature of adaptable change of B-cell lymphoma-2 (BCL-2) and/or Bcl2-associated X protein (BAX) gene expression in the human peripheral blood mononuclear cells (PBMCs) irradiated by radioiodine in thyroid diseases therapy is not fully understood. In this study, the alternation of apoptotic gene expression was evaluated while the PBMCs collected from healthy volunteers were irradiated by the radioiodine-131 (131I). Methods: Fasting blood samples were obtained from healthy volunteers. PBMCs from group 0 to 6 were incubated and exposed to different doses of 131I in cell suspension for 6, 12, 24 and 48 h. The apoptosis rates and expression of BCL-2 and BAX genes of PBMCs were examined. Results: The apoptosis rate in the human PBMCs was gradually enhanced after six hour irradiation. The values of BCL-2 and BAX gene expression in groups 1-6 were higher than in group 0 within 6 h of irradiation, and then, these were decreased gradually from 6 to 12 h. BCL: -2 gene expression increased in groups 1-3 after 12 h irradiation, but there was no difference in groups 4-6. The ratio of BCL-2/BAX gene expression among groups 4-6 gradually decreased during the period from 6 to 12 h, and it was significantly lower than in the group 0 at 12, 24 and 48 h. Interpretation & conclusions: The expression of BCL-2 and BAX genes was initially upregulated following irradiation. Later, the balance of BCL-2/BAX genes expression was adjusted, and then, PBMCs underwent apoptosis at higher doses of radiation.

G9A promotes gastric cancer metastasis by upregulating ITGB3 in a SET domain-independent manner.

Tumor metastasis is the leading cause of death in patients with advanced gastric cancer (GC). Limited therapeutic regimens are available for this condition, which is associated with a poor prognosis, and the mechanisms underlying tumor metastasis remain unclear. In the present study, increased histone methyltransferase G9A expression in GC tissues correlated with advanced stage and shorter overall survival, and in vitro and in vivo experiments revealed that G9A promoted tumor invasion and metastasis. Moreover, we observed that Reg IV induced G9A via the p-ERK/p-SP1 pathway. SP1 directly binds the G9A promoter and enhances G9A expression, and upregulated G9A then forms a transcriptional activator complex with P300 and GR, thereby promoting ITGB3 expression induced by dexamethasone (DEX) and contributing to GC metastasis. However, the G9A-mediated increase in ITGB3 expression was not dependent on the SET domain and methyltransferase activity of G9A. This study demonstrates that G9A is an independent prognostic marker and promotes metastasis in GC, thus suggesting that it may be a tumor biomarker and potential therapeutic target in GC.

ALEX1, a novel tumor suppressor gene, inhibits gastric cancer metastasis via the PAR-1/Rho GTPase signaling pathway.

BACKGROUND: The ALEX is a novel member of the armadillo family and ALEX1 was reported to be reduced or even lost in multiple solid tumors. However, its expression profile and oncogenic role in gastric cancer (GC) remains largely unknown. METHODS: ALEX1 expression was detected in 161 GC samples by immunohistochemistry staining. NCI-N87 cells transfected by ALEX1 lentivirus vectors and MKN28 cells transfected by ALEX1 shRNA were used for biological function investigation. Western blot was applied to explore the molecular mechanism and pull-down assays were applied to measure the activity of Rho GTPases. In vivo tumorigenicity, peritoneal and lung metastasis experiments were performed by tumor cell engraftment into nude mice. Bisulfite genomic sequencing and methylation-specific PCR were applied to check the methylation status of the ALEX1 gene. RESULTS: The expression rate of ALEX1 was significantly reduced in gastric tumor samples compared to non-tumor samples (43.5 vs. 90.2%), and its expression was closely related to the tumor differentiation, TNM staging, and lymph nodes metastasis. ALEX1 overexpression in NCI-N87 cells significantly inhibited cell proliferation, migration, and invasion in vitro, and disrupted the structure of the cytoskeleton. ALEX1 overexpression attenuated xenografts growth, peritoneal, and lung metastasis in nude mice. Mechanistically, the overexpression of ALEX1 inhibits thrombin-induced metastasis and Rho GTPases activation. Bisulfite genomic sequencing and methylation-specific PCR revealed that the promoter of ALEX1 is highly methylated in GC cells and tissues. CONCLUSIONS: ALEX1 expression is reduced in GC and is involved in diverse cellular functions. ALEX1 inhibits metastasis through the PAR-1/Rho GTPase signaling pathway.

Long noncoding RNA UCA1 promotes tumour metastasis by inducing GRK2 degradation in gastric cancer.

Increasing evidence demonstrates that long noncoding RNAs (lncRNAs) regulate gene and protein expression by exerting an influence on transcriptional and post-transcriptional processes. Here, we report that the lncRNA UCA1 increases the metastatic ability of gastric cancer (GC) cells by regulating GRK2 protein stability by promoting Cbl-c-mediated GRK2 ubiquitination and degradation. This process then activates the ERK-MMP9 signalling pathway. Furthermore, we demonstrate that GRK2 is downregulated in GC cells and that silencing of GRK2 might cause similar phenotypic changes and signalling pathway activation as those induced by elevated UCA1 in GC cells. Our results suggest that UCA1 might function as a mediator of protein ubiquitination and may be a promising molecular target for GC therapy.

Long noncoding RNA UCA1 induced by SP1 promotes cell proliferation via recruiting EZH2 and activating AKT pathway in gastric cancer.

Long noncoding RNA UCA1 has emerged as a novel regulator in cancer initiation and progression of various cancers. However, function and underlying mechanism of UCA1 in the progression of gastric cancer (GC) remain unclear. In the present study, we report that UCA1 expressed highly in GC tissues and GC cells, which was partly induced by SP1. UCA1 promoted GC cell proliferation and G1/S transition in vitro and in vivo. Moreover, UCA1 exerted its function through interacting with EZH2, promoting direct interaction with cyclin D1 promoter to activate the translation of cyclin D1. Furthermore, AKT/GSK-3B/cyclin D1 axis was activated to upregulate cyclin D1 due to overexpression of UCA1. In addition, EZH2 and phosphorylated AKT induced by UCA1 could impact each other to form a positive feedback to promote cyclin D1 expression. This study demonstrated that UCA1 as a critical regulator involved in GC proliferation and cell cycle progression by promoting cyclin D1 expression, which indicates that it may be clinically a potential therapeutic target in GC.

Luteolin suppresses gastric cancer progression by reversing epithelial-mesenchymal transition via suppression of the Notch signaling pathway.

BACKGROUND: Gastric cancer (GC) is one of the most malignant tumors and the second leading cause of cancer-related deaths in the world. Luteolin, a flavonoid present in many fruits and green plants, suppresses cancer progression. The effects of luteolin on GC cells and their underlying mechanisms remain unclear. METHODS: Effects of luteolin on cell proliferation, migration, invasion, and apoptosis were examined in vitro and in vivo by cell counting kit-8 (CCK-8), transwell assays, and flow cytometry, respectively. Real-time reverse transcription polymerase chain reaction (RT-PCR) and Western blots were performed to evaluate Notch1 signaling and activation of epithelial-mesenchymal transition (EMT) in GC cells treated with or without luteolin. Immunohistochemistry was performed to examine proliferation and Notch1 expression in xenograft tumors. RESULTS: Luteolin significantly inhibited cell proliferation, invasion, and migration in a dose-dependent and time-dependent manner and promoted cell apoptosis. Luteolin reversed EMT by shrinking the cytoskeleton and by inducing the expression of epithelial biomarker E-cadherin and downregulating the mesenchymal biomarkers N-cadherin, vimentin and Snail. Furthermore, Notch1 signaling was inhibited by luteolin, and downregulation of Notch1 had similar effects as luteolin treatment on cell proliferation, migration, and apoptosis. In addition, luteolin suppressed tumor growth in vivo. A higher expression of Notch1 correlated with a poor overall survival and a poor time to first progression. Furthermore, co-immunoprecipitation analysis revealed that activated Notch1 and ß-catenin formed a complex and regulated cell proliferation, migration, and invasion. CONCLUSIONS: In this study, GC progression was inhibited by luteolin through suppressing Notch1 signaling and reversing EMT, suggesting that luteolin may serve as an effective anti-tumor drug in GC treatment.

Immunoglobulin G4-Related Lung Disease Presenting as Lung Cavitating Mass and Mimicking Lung Cancer.

Immunoglobulin G4-related lung disease (IgG4-RLD) is a disease in which abundant activated IgG4-positive plasma cells and lymphocytes infiltrate lung tissues with high 18F-fluorodeoxyglucose uptake. Although various forms of radiologic features of IgG4-RLD have been reported, cavitating mass is a rare imaging feature and should be differentiated from cancer. Therefore, in this article, we report two cases both with unprovoked cough, bloody sputum and presenting quite similar cavitating lesions with high 18F-fluorodeoxyglucose uptake on positron emission tomography/ computed tomography, one of which diagnosed as IgG4-RLD and the other as lung cancer based on biopsy eventually. The awareness of the imaging features of IgG4-RLD and lung cancer described in the present study may help physicians to distinguish one from the other. IgG4-RLD should be considered in the differential diagnosis of cavitary lung lesions.

Biglycan stimulates VEGF expression in endothelial cells by activating the TLR signaling pathway.

Biglycan (BGN) is an important component of the extracellular matrix (ECM) that is implicated in a variety of human cancers. In our previous study, we reported that BGN was overexpressed in gastric cancer (GC) tissues and promoted cancer metastasis. Moreover, the tubular formation capacity in HUVECs was promoted by stimulation with culture media from BGN-overexpressing GC cells, but the exact underlying mechanism is still unknown. The purpose of this study was to determine the role and molecular mechanism of BGN in VEGF expression in endothelial cells. We found that BGN stimulation of endothelial cells increased the interaction between NF-kB and the HIF-1α promoter, leading to enhanced promoter activity and increased HIF-1α mRNA levels, as well as augmented HIF-1 activity that resulted in VEGF expression. All of this was dependent on the interaction of BGN with its receptors, TLR2 and TLR4. Moreover, we found that BGN enhanced endothelial cell migration and proliferation, as well as tube formation, in a TLR signaling pathway-dependent manner. In addition, endothelial cell-derived VEGF in turn was found to act on GC cells and promotes their migration. The combined findings of our current and previous studies suggest that BGN secreted from GC cells into the tumor stroma promotes GC development, as well as its progression, potentially through the chronic activation of tumor angiogenesis.

Identification of a five-lncRNA signature for the diagnosis and prognosis of gastric cancer.

Gastric cancer (GC) is one of the most aggressive malignancies and has a poor prognosis. Identifying novel diagnostic and prognostic markers is of great importance for the management and treatment of GC. Long non-coding RNAs (lncRNAs), which are involved in multiple processes during the development and progression of cancer, may act as potential biomarkers of GC. Here, by performing data mining using four microarray data sets of GC downloaded from the Gene Expression Omnibus (GEO) database with different classifiers and risk score analyses, we identified a five-lncRNA signature (AK001094, AK024171, AK093735, BC003519 and NR_003573) displaying both diagnostic and prognostic values for GC. The results of the Kaplan-Meier survival analysis and log-rank test showed that the risk score based on this five-lncRNA signature was closely associated with overall survival time (p = 0.0001). Further analysis revealed that the risk score is an independent predictor of prognosis. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis of 30 pairs of GC tissue samples confirmed that the five lncRNAs were dysregulated in GC, and receiver operating characteristic (ROC) curves showed the high diagnostic ability of combining the five lncRNAs, with an area under the curve (AUC) of 0.95 ± 0.025. The five lncRNAs involved in several cancer-related pathways were identified using gene set enrichment analysis (GSEA). These findings indicate that the five-lncRNA signature may have a good clinical applicability for determining the diagnosis and predicting the prognosis of GC.

TET1 inhibits gastric cancer growth and metastasis by PTEN demethylation and re-expression.

Ten-Eleven Translocation 1 (TET1) is a member of ten eleven translocation enzymes, which convert 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC). TET1 can promote CpG islands demethylation in specific genes and often absent in various cancers. Herein, we found that TET1 expression and 5-hmC content were low in gastric tumors compared to its adjacent non-tumor tissues. Cell proliferation, migration and invasion were enhanced upon TET1 knockdown in gastric cancer cells in vitro. This phenomenon was confirmed by an animal xeongraft model. We also found that TET1 directly binds to the promoter region of PTEN and activates its transcription through demethylation of CpG islands. TET1 knockdown activated AKT and FAK pathways, which were suppressed by PTEN. The activation of AKT and FAK facilitated tumor migration, invasion and accelerated cell growth. In conclusion, we found a novel mechanism that TET1 suppresses tumor cell growth, migration and invasion through demethylation of CpG island in PTEN promoter by increasing 5-hmC content. The re-expressed PTEN subsequently down regulates AKT and FAK activity.

Helicobacter pylori CagA induces tumor suppressor gene hypermethylation by upregulating DNMT1 via AKT-NFκB pathway in gastric cancer development.

Methylation of CpG islands in tumor suppressor gene prompter is one of the most characteristic abnormalities in Helicobacter pylori (HP)-associated gastric carcinoma (GC). Here, we investigated the pathogenic and molecular mechanisms underlying hypermethylation of tumor suppressor genes in HP induced GC development. We found that tumor suppressor genes hypermethylation, represented by MGMT, positively correlated with CagA in clinical specimens, gastric tissues from HP infected C57 mice and GC cell lines transfected by CagA or treated by HP infection. CagA enhanced PDK1 and AKT interaction and increased AKT phosphorylation. The P-AKT subsequent activated NFκB, which then bound to DNMT1 promoter and increased its expression. Finally, the upregulated DNMT1 promoted tumor suppressor genes hypermethylation with MGMT as a representative. In conclusion, CagA increased tumor suppressor genes hypermethylation via stimulating DNMT1 expression through the AKT-NFκB pathway.

Contribution of Disulfide Bridges to the Thermostability of a Type A Feruloyl Esterase from Aspergillus usamii.

The contribution of disulfide bridges to the thermostability of a type A feruloyl esterase (AuFaeA) from Aspergillus usamii E001 was studied by introducing an extra disulfide bridge or eliminating a native one from the enzyme. MODIP and DbD, two computational tools that can predict the possible disulfide bridges in proteins for thermostability improvement, and molecular dynamics (MD) simulations were used to design the extra disulfide bridge. One residue pair A126-N152 was chosen, and the respective amino acid residues were mutated to cysteine. The wild-type AuFaeA and its variants were expressed in Pichia pastoris GS115. The temperature optimum of the recombinant (re-) AuFaeAA126C-N152C was increased by 6°C compared to that of re-AuFaeA. The thermal inactivation half-lives of re-AuFaeAA126C-N152C at 55 and 60°C were 188 and 40 min, which were 12.5- and 10-folds longer than those of re-AuFaeA. The catalytic efficiency (kcat/Km) of re-AuFaeAA126C-N152C was similar to that of re-AuFaeA. Additionally, after elimination of each native disulfide bridge in AuFaeA, a great decrease in expression level and at least 10°C decrease in thermal stability of recombinant AuEaeA variants were also observed.

Epigenetic silencing of microRNA-149 in cancer-associated fibroblasts mediates prostaglandin E2/interleukin-6 signaling in the tumor microenvironment.

Tumor initiation and growth depend on its microenvironment in which cancer-associated fibroblasts (CAFs) in tumor stroma play an important role. Prostaglandin E2 (PGE2) and interleukin (IL)-6 signal pathways are involved in the crosstalk between tumor and stromal cells. However, how PGE2-mediated signaling modulates this crosstalk remains unclear. Here, we show that microRNA (miR)-149 links PGE2 and IL-6 signaling in mediating the crosstalk between tumor cells and CAFs in gastric cancer (GC). miR-149 inhibited fibroblast activation by targeting IL-6 and miR-149 expression was substantially suppressed in the CAFs of GC. miR-149 negatively regulated CAFs and their effect on GC development both in vitro and in vivo. CAFs enhanced epithelial-to-mesenchymal transition (EMT) and the stem-like properties of GC cells in a miR-149-IL-6-dependent manner. In addition to IL-6, PGE2 receptor 2 (PTGER2/EP2) was revealed as another potential target of miR-149 in fibroblasts. Furthermore, H. pylori infection, a leading cause of human GC, was able to induce cyclooxygenase-2 (COX-2)/PGE2 signaling and to enhance PGE2 production, resulting in the hypermethylation of miR-149 in CAFs and increased IL-6 secretion. Our findings indicate that miR-149 mediates the crosstalk between tumor cells and CAFs in GC and highlight the potential of interfering miRNAs in stromal cells to improve cancer therapy.

Androgen receptor promotes gastric cancer cell migration and invasion via AKT-phosphorylation dependent upregulation of matrix metalloproteinase 9.

Androgen receptor (AR) plays an important role in many kinds of cancers. However, the molecular mechanisms of AR in gastric cancer (GC) are poorly characterized. Here, we investigated the role of AR in GC cell migration, invasion and metastatic potential. Our data showed that AR expression was positively correlated with lymph node metastasis and late TNM stages. These findings were accompanied by activation of AKT and upregulation of matrix metalloproteinase 9 (MMP9). AR overexpression induced increases in GC cell migration, invasion and proliferation in vitro and in vivo. These effects were attenuated by inhibition of AKT, AR and MMP9. AR overexpression upregulated MMP9 protein levels, whereas this effect was counteracted by AR siRNA. Inhibition of AKT by siRNA or an inhibitor (MK-2206 2HC) decreased AR protein expression in both stably transfected and parental SGC-7901 cells. Luciferase reporter and chromatin immunoprecipitation assays demonstrated that AR bound to the AR-binding sites of the MMP9 promoter. In summary, AR overexpression induced by AKT phosphorylation upregulated MMP9 by binding to its promoter region to promote gastric carcinogenesis. The AKT/AR/MMP9 pathway plays an important role in GC metastasis and may be a novel therapeutic target for GC treatment.

Biglycan enhances gastric cancer invasion by activating FAK signaling pathway.

Biglycan (BGN) is an important member of small leucine-rich proteoglycans family, and has been implicated in oncogenesis and development of various human cancer types. Here we report that BGN promotes tumor invasion and metastasis of gastric cancer both in vitro and in vivo. BGN expression is significantly higher in gastric cancer tissues and associated with lymph node metastasis, depth of tumor invasion and TNM stage. BGN enhances gastric cancer cell wound healing, migration and invasion ability as well as the tube formation ability of endothelial cells in vitro. Animal experiments results in vivo are consistent with outcomes in vitro. BGN induces increased phosphorylation of FAK (Tyr576/577, Tyr925 and Tyr397) and Paxillin. These results indicate that BGN is upregulated, and plays an oncogenic role, in gastric cancer metastasis by activating the FAK signaling pathway.

Comparison of laparoscopic Roux-en-Y gastric bypass with laparoscopic sleeve gastrectomy for morbid obesity or type 2 diabetes mellitus: a meta-analysis of randomized controlled trials.

BACKGROUND: Laparoscopic Roux-en-Y gastric bypass (LRYGB) is one of the most widely used bariatric procedures, and laparoscopic sleeve gastrectomy (LSG) as a single-stage procedure for treating morbid obesity is becoming more popular. We compared both techniques to evaluate their efficacy in treating morbid obesity or type 2 diabetes mellitus (T2DM). METHODS: We searched the Cochrane Controlled Trials Register databases, Medline, Embase, ISI databases and the Chinese Biomedical Literature Database to identify randomized controlled trials (RCTs) of LRYGB and LSG for morbid obesity or T2DM published in any language. Statistical analyses were carried out using RevMan software. RESULTS: Five worldwide RCTs with 196 patients in the LRYGB group and 200 in the LSG group were included in our analysis. Compared with patients who had LSG, those who had LRYGB had a higher remission rate of T2MD, lost more weight and had lower low-density lipoprotein, triglycerides, homeostasis model assessment index and insulin levels. There was no difference in the reoperation rate between the groups. However, patients treated with LRYGB had a higher incidence of complication than those treated with LSG. CONCLUSION: Our meta-analysis demonstrates that LRYGB is more effective than LSG for the surgical treatment of T2DM and control of metabolic syndrome. However, LSG is safer and has a reduced rate of complications. Further high-quality RCTs with long follow-up periods are needed to provide more reliable evidence.

CONTEXTE: La dérivation gastrique laparoscopique Roux-en-Y (DGRY) est l'une des interventions bariatriques les plus utilisées, et la gastrectomie longitudinale laparoscopique (GLL) gagne en popularité comme intervention en une seule étape pour le traitement de l'obésité morbide. Nous avons comparé les 2 techniques pour en évaluer l'efficacité dans le traitement de l'obésité morbide ou du diabète de type 2 (DT2). MÉTHODES: Nous avons interrogé les bases de données du Registre des essais cliniques contrôlés de la Collaboration Cochrane, de même que les bases de données Medline, Embase, ISI et la base de données de la littérature biomédicale chinoise pour recenser les essais randomisés et contrôlés (ERC) publiés dans toutes les langues sur la DGRY et la GLL dans les cas d'obésité morbide ou de DT2. Les analyses statistiques ont été effectuées au moyen du logiciel RevMan. RÉSULTATS: Cinq ERC ont été recensés dans le monde et ont été inclus dans notre analyse, totalisant 196 patients soumis à la DGRY et 200 soumis à la GLL. Comparativement aux patients soumis à la GLL, les patients soumis à la DGRY ont présenté des taux de rémission plus élevés de leur DT2, ils ont perdu plus de poids et ont présenté des taux plus faibles de lipoprotéines de faible densité et de triglycérides, une baisse de leur indice d'évaluation du modèle d'homéostasie) et de leur taux d'insuline. On n'a noté aucune différence entre les groupes pour ce qui est du taux de réintervention. Toutefois, l'incidence des complications a été plus élevée chez les patients traités par DGRY que chez ceux traités par GLL. CONCLUSION: Notre méta-analyse démontre que la DGRY est plus efficace que la GLL pour le traitement chirurgical du DT2 et le contrôle du syndrome métabolique. Toutefois, la GLL est plus sécuritaire et s'accompagne d'un taux moindre de complications. Il faudra procéder à d'autres ERC de grande qualité comportant des suivis prolongés pour amasser des preuves plus fiables.