circ-Amotl1 in extracellular vesicles derived from ADSCs improves wound healing by upregulating SPARC translation.

Aim: This study aims to explore the mechanism of circ- AMOT-like protein 1 (Amotl1) in extracellular vesicles (Evs) derived from adipose-derived stromal cells (ADSCs) regulating SPARC translation in wound healing process. Methods: The morphology, wound healing rate of the wounds and Ki67 positive rate in mouse wound healing models were assessed by H&E staining and immunohistochemistry (IHC). The binding of IGF2BP2 and SPARC was verified by RNA pull-down. Adipose-derived stromal cells (ADSCs) were isolated and verified. The Evs from ADSCs (ADSC-Evs) were analyzed. Results: Overexpression of SPARC can promote the wound healing process in mouse models. IGF2BP2 can elevate SPARC expression to promote the proliferation and migration of HSFs. circ-Amotl1 in ADSC-Evs can increase SPARC expression by binding IGF2BP2 to promote the proliferation and migration of HSFs. Conclusion: ADSC-Evs derived circ-Amotl1 can bind IGF2BP2 to increase SPARC expression and further promote wound healing process.

Circular RNA cVIM promotes hepatic stellate cell activation in liver fibrosis via miR-122-5p/miR-9-5p-mediated TGF-ß signaling cascade.

Hepatic stellate cell (HSC) activation is considered as a central driver of liver fibrosis and effective suppression of HSC activation contributes to the treatment of liver fibrosis. Circular RNAs (circRNAs) have been reported to be important in tumor progression. However, the contributions of circRNAs in liver fibrosis remain largely unclear. The liver fibrosis-specific circRNA was explored by a circRNA microarray and cVIM (a circRNA derived from exons 4 to 8 of the vimentin gene mmu_circ_32994) was selected as the research object. Further studies revealed that cVIM, mainly expressed in the cytoplasm, may act as a sponge for miR-122-5p and miR-9-5p to enhance expression of type I TGF-ß receptor (TGFBR1) and TGFBR2 and promotes activation of the TGF-ß/Smad pathway, thereby accelerating the progression of liver fibrosis. Our results demonstrate a vital role for cVIM in promoting liver fibrosis progression and provide a fresh perspective on circRNAs in liver fibrosis.

Serum ribonucleotide reductase M2 is a potential biomarker for diagnosing and monitoring liver fibrosis in chronic hepatitis B patients.

It is known that ribonucleotide reductase M2 (RRM2) could be induced by hepatitis B virus (HBV) via DNA damage response. However, whether RRM2 is a potential biomarker for diagnosing and monitoring liver fibrosis in chronic hepatitis B (CHB) patients is still unclear. In this study, CHB patients from GSE84044 (a transcriptome data from GEO data set) were downloaded and RRM2 was selected as a hub gene. Interestingly, a positive correlation was found between serum RRM2 and liver fibrosis stage. The similar results were found in CHB patients with normal alanine aminotransferase (ALT). Notably, RRM2 could effectively differentiate preliminary fibrosis from advanced fibrosis in CHB patients with/without normal ALT. In addition, RRM2 had a better performance in diagnosing liver fibrosis than two commonly used noninvasive methods (aspartate aminotransferase-to-platelet ratio index and fibrosis index based on the four factors), two classic fibrotic biomarkers (hyaluronic acid and type IV collagen) as well as Mac-2 binding protein glycosylation isomer, a known serum fibrosis marker. Moreover, CHB patients with high RRM2, who were associated with advanced fibrosis, had higher expressions of immune checkpoints. Overall, serum RRM2 may be a promising biomarker for diagnosing and monitoring liver fibrosis in CHB patients.

FUT2 promotes the tumorigenicity and metastasis of colorectal cancer cells via the Wnt/ß­catenin pathway.

The incidence of colorectal cancer (CRC), a leading cause of cancer­related mortality, has increased globally. Fucosyltransferase 2 (FUT2), catalyzing the α1, 2­linked fucose in mammals, has been reported to be overexpressed in several malignant cancers, including CRC. However, the effects of FUT2 on CRC remain largely unknown. Herein, it was determined that the FUT2 expression levels in CRC tissues were higher than those in adjacent non­tumor tissues, whereas no association with tumor stage was revealed. The results of biological functional analysis revealed that FUT2 knockdown inhibited the proliferation, migration and invasion of human CRC cells. Moreover, the knockdown of FUT2 arrested the CRC cells at the G0/G1 phase and promoted the apoptosis of human CRC cells. Western blot analysis demonstrated that the expression levels of ß­catenin, C­myc and cyclin D1 were decreased by FUT2 knockdown in CRC cells, whereas the expression of glycogen synthase kinase­3ß and the phosphorylation levels of ß­catenin were increased. Additionally, Wnt2 was fucosylated by FUT2 in CRC cells. Furthermore, the knockdown of FUT2 inhibited the growth of human CRC in vivo. Overall, the findings of the present study suggest that FUT2 may be used as a potential diagnostic biomarker and therapeutic target for CRC treatment.

Machine learning integrations for development of a T-cell-tolerance derived signature to improve the clinical outcomes and precision treatment of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is characterized by high rates of recurrence and metastasis and poor prognosis. A recently discovered concept of T cell tolerance (TCT) has become an entirely new target of cancer immunotherapy. Unfortunately, the effect of TCT on the outcomes of HCC has not been explored. In this study, 7 public datasets and one external clinical cohort, including 1716 HCC patients were explored. Through WGCNA analysis and differential analysis, we explored the key TCT-related modulates. A total of 95 machine learning integrations across all validation cohorts were compared and the optimal method with the highest average C-index value was selected to construct the TCT derived signature (TCTS). In all independent clinical cohorts, TCTS showed accurate prediction of the prognosis, and was significantly correlated with clinical indicators and molecular features. Compared with 77 published gene signatures, the TCTS exhibited superior predictive performance. In the external clinical cohort, a novel nomogram (comprising TNM stage, Hepatitis B, Vascular invasion, Perineural invasion, AFP and TCTS) was constructed to test the clinical performance of TCTS. The results showed that the high TCTS scoring group showed dismal prognosis, improved sensitivity to oxaliplatin and good response to anti-PD-1/PD-L1 immunotherapy. Moreover, the low TCTS score group had few genomic alterations, low immune activation and low PD-1/PD-L1 expression levels. In conclusion, TCTS is an ideal biomarker for predicting the clinical outcomes and improving precision treatment of HCC.

Identification and Validation of Genomic Subtypes and a Prognostic Model Based on Antigen-Presenting Cells and Tumor Microenvironment Infiltration Characteristics in Hepatocellular Carcinoma.

Currently, the prognosis of hepatocellular carcinoma (HCC) is poor, and there is a lack of effective targeted therapy. As key mediators of the immune response, the prognostic value of antigen-presenting cells (APCs) in HCC still remains unclear. In this study, we aimed to identify APC-related genomic subtypes and develop a novel prognostic model in HCC. Our results indicated that overall survival (OS) and the level of immune infiltration significantly differed between different APC clusters. By analyzing the gene expression profile between APC clusters, APC-related genomic subtypes were identified. There was a significant difference in OS and tumor microenvironment infiltration in HCC patients with different genomic subtypes. With the aid of genomic subtypes, significantly differentially expressed genes were screened to generate a novel prognostic model. The risk score of the model had a significant positive correlation with APCs and was associated with immune checkpoint expressions. Through the clinical cohort collected from the First Affiliated Hospital of Wenzhou Medical University, the prognostic value of the risk score was further validated. Moreover, after the risk score and clinical characteristics were combined, a nomogram was constructed to evaluate the prognosis for HCC patients. In conclusion, we mainly identified the APC-related genomic subtypes and generated a novel prognostic model to improve the prognostic prediction and targeted therapy for HCC patients.

Human umbilical cord-derived mesenchymal stem cells improve chronic pancreatitis in rats via the AKT-mTOR-S6K1 signaling pathway.

Chronic pancreatitis (CP) is a progressive inflammatory disease. In clinical treatment, many patients cannot get a timely diagnosis and effective treatment due to the lack of early diagnosis indicators. Mesenchymal stem cells have immunomodulatory and anti-inflammatory effects, and have broad application prospects in treating auto-immune diseases and inflammatory diseases. This study aimed to clarify the mechanisms of human umbilical cord mesenchymal stem cells (HUCMSCs) in the treatment of CP. The rats were randomly divided into four groups, with six rats in each group: control group, CP group, CP + HUCMSCs-treated group I, and CP + HUCMSCs-treated group II. We evaluated the levels of inflammatory factors, fibrosis and apoptosis markers, detected the protein expression levels of AKT-mTOR-S6K1 and assessed histological changes of the pancreas. The results showed that HUCMSCs not only inhibited the secretion of inflammatory cytokines and activation of pancreatic stellate cells but also suppressed the apoptosis of acinar cells. Further investigation revealed that HUCMSCs noticeably suppressed the AKT-mTOR-S6K1 pathway in the pancreatic tissue of DBTC-induced CP. In addition, the therapeutic effect of HUCMSCs injected into the inferior vena cava and left gastric artery in the CP model was also observed, thus providing the basis for the clinical application of intervention measures.

Adipose­derived mesenchymal stem cells ameliorate dibutyltin dichloride­induced chronic pancreatitis by inhibiting the PI3K/AKT/mTOR signaling pathway.

Adipose­derived mesenchymal stem cells (ASCs) play a positive role in tissue injury repair and regeneration. The aim of this study was to determine whether ASCs could ameliorate chronic pancreatitis (CP) induced by the injection of dibutyltin dichloride (DBTC) and to elucidate its potential mechanisms. Furthermore, this study also explored whether there was a significant difference if the ASCs were injected via the inferior vena cava or the left gastric artery. CP was induced in rats by a single intravenous administration of DBTC, and the accumulation of collagen and apoptotic rates of pancreatic acinar cells were analyzed. According to the results, ASCs markedly reduced DBTC­induced pancreatic damage and collagen deposition in the rat model of CP. Moreover, ASCs significantly decreased pancreatic cell apoptosis by regulating the expression levels of caspase­3, BAX and Bcl­2. These effects were observed regardless of whether the injection was in the inferior vena cava or the left gastric artery. It was also found that the expression levels of phosphorylated PI3K, AKT and mTOR in pancreatic tissues of the DBTC­induced CP model group were significantly increased, while the expression levels of phosphorylated PI3K, AKT and mTOR in the two treatment groups were markedly decreased. ASCs noticeably suppressed the PI3K/AKT/mTOR pathway in the pancreatic tissue of DBTC­induced CP. This study indicated that ASCs protect against pancreatic fibrosis by modulating the PI3K/AKT/mTOR pathway, and have the potential to be a new strategy for the treatment of CP in the future.

Comprehensive analysis of long noncoding RNA and mRNA in five colorectal cancer tissues and five normal tissues.

The present study investigated the role of abnormally expressed mRNA and long noncoding RNA (lncRNA) in the development of colorectal cancer (CRC). We used lncRNA sequencing to analyze the transcriptome (mRNA and lncRNA) of five pairs of CRC tissues and adjacent normal tissues. The total expression of mRNAs and lncRNAs in each sample was determined using the R package and the gene expression was calculated using normalized FPKM. The structural features and expression of all detected lncRNAs were compared with those of mRNAs. Differentially expressed mRNAs were selected to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. The functional analysis of differentially expressed lncRNAs was performed by analyzing the GO and KEGG enrichment of predicted cis-regulated target genes. A total of 18.2 × 108 reads were obtained by sequencing, in which the clean reads reached ≥ 94.67%, with a total of 245.2 G bases. The number of mRNAs and lncRNAs differentially expressed in CRC tissues and normal tissues were 113 and 6, respectively. Further predictive analysis of target genes of lncRNAs revealed that six lncRNA genes had potential cis-regulatory effects on 13 differentially expressed mRNA genes and co-expressed with 53 mRNAs. Up-regulated CTD-2256P15.4 and RP11-229P13.23 were the most important lncRNAs in these CRC tissues and involved in cell proliferation and pathway in cancer. In conclusion, our study provides evidence regarding the mRNA and lncRNA transcription in CRC tissues, as well as new insights into the lncRNAs and mRNAs involved in the development of CRC.

Induction of Macrophage M2b/c Polarization by Adipose Tissue-Derived Mesenchymal Stem Cells.

BACKGROUND: Adipose-derived mesenchymal stem cells (ADMSCs) can promote healing and inhibit inflammation/immune response in local tissues, while the detailed mechanism remains unknown. RESULTS: ADMSCs and peritoneal macrophages were collected from C57BL/6 mice. The culture medium (CM) from ADMSCs (24 hours cultured) was collected. The CM was added to the Mφ culture system with lipopolysaccharide (LPS) or IL-4/IL-13 or blank. And those Mφ cultures without adding CM were used as controls. A series of classification markers and signaling pathways for Mφ polarization were detected by using flow cytometry, RT-PCR, and western blotting. Furthermore, the cell viability of all the groups was detected by CCK8 assay. After CM induction in different groups, M1-Mφ markers and M2a-Mφ were decreased; however, M2b/c-Mφ markers increased. STAT3/SOCS3 and STAT6/IRF4 were suppressed in all 3 CM-treated groups. Moreover, the cell viability of all 3 groups which were induced by CM significantly increased as compared to that of the control groups without adding CM. CONCLUSION: ADMSCs can induce nonactivated macrophage and M1-Mφ into M2b/c-Mφ. Downregulation of the STAT3 and STAT6 pathway may involve in this process. This data shows that the anti-inflammatory role of ADMSC in local tissues may be partly due to their effect on Mφ to M2b/c-Mφ.

Luteolin inhibits angiogenesis of the M2­like TAMs via the downregulation of hypoxia inducible factor­1α and the STAT3 signalling pathway under hypoxia.

The imbalance between angiogenic inducers and inhibitors appears to be a critical factor in tumour pathogenesis. Angiogenesis serves a key role in the occurrence, invasion and metastasis of tumours. Macrophages are a major cellular component of human and rodent tumours, where they are usually termed tumour­associated macrophages (TAMs). In malignant tumours, TAMs tend to resemble alternatively activated macrophages (M2­like), promote TA angiogenesis, strengthen tumour migration and invasive abilities, and simultaneously inhibit antitumor immune responses. In our previous study, luteolin, commonly found in a wide variety of plants, had a strong antitumor effect under normoxia; however, it is unknown whether luteolin serves a similar role under hypoxia. In the present study, cobalt chloride (CoCl2) was used to simulate hypoxia. Hypoxia­inducible factor­1α (HIF­1α), which is difficult to detect under normoxic conditions, was significantly increased. Additionally, vascular endothelial growth factor (VEGF) was also significantly increased in response to CoCl2 treatment. Subsequently, luteolin was applied with CoCl2 to examine the effects of luteolin. Luteolin decreased the expression of VEGF and matrix metalloproteinase­9, which promote angiogenesis. In addition, luteolin also suppressed the activation of HIF­1 and phosphorylated­signal transducer and activator of transcription 3 (STAT3) signalling, particularly within the M2­like TAMs. The results of the present study provide novel evidence that luteolin, under hypoxic conditions, has a strong anticancer effect via the HIF­1α and STAT3 signalling pathways.

Long non-coding RNA 657 suppresses hepatocellular carcinoma cell growth by acting as a molecular sponge of miR-106a-5p to regulate PTEN expression.

Previous study has identified the aberrant expression of LINC00657, a long non-coding RNA (lncRNA), in human breast cancer. However, the expression pattern, biological function and underlying mechanism of LINC00657 in human hepatocellular carcinoma (HCC) remain obscure. The expression levels of LINC00657 in HCC tissues and cell lines were determined by quantitative real-time PCR. CCK-8 assay, cell colony formation assay, cell cycle analysis, Transwell assay were performed to determine whether LINC00657 could affect HCC progression. Luciferase reporter assay was used to assess the target of LINC00657. Expressions of the relevant proteins were analyzed by Western blot. Herein, we found that LINC00657 was downregulated in HCC tissue specimens as well as in malignant HCC cell lines. LINC00657 overexpression inhibited the proliferation, migration and invasion of HCC cells, while LINC00657 depletion promoted both cell viability and cell invasion in vitro. We also found that LINC00657 could inhibit tumor growth in vivo. Further experiments demonstrated that down-regulated LINC00657 increased the expression of miR-106a-5p. miR-106a-5p decreased the abundances of PTEN protein, while had no impact on PTEN mRNA. Moreover, we identified that both LINC00657 and PTEN mRNA were targets of miR-106a-5p by using dual-luciferase reporter assay. Our results provide the new evidence supporting the tumor-suppressive role of LINC00657 in HCC, suggesting that LINC00657 might play a role in HCC and can be a novel therapeutic target for treating HCC.

Laparoscopic surgery assisted by colonoscopy for a submucosal cecal fecalith presenting as acute appendicitis: A case report.

RATIONALE: A cecal submucosal fecalith is extremely rare and is likely to be misdiagnosed as appendicitis with an incarcerated fecalith. PATIENT CONCERNS: This review presents the case of a female patient complaining of recurrent abdominal pain in the right lower quadrant, similar to the clinical symptoms of appendicitis. Physical examination revealed an abdominal tenderness in the right lower quadrant without rebound tenderness or muscular tension. An ultrasound examination found a mass located in the right lower abdomen. Computed tomography showed a high-density shadow in the cecal cavity. DIAGNOSES: A fecalith was detected in the submucosal cecal wall. The postoperative pathologic examination showed that the fecalith was located in the submucosa. INTERVENTIONS: A partial cecal excision was performed under laparoscopic surgery assisted by colonoscopy. OUTCOMES: The patient was discharged 1 week after surgery without postoperative complications. LESSONS: Fecaliths should be considered in the differential diagnosis of submucosal occupying lesions of the cecum.

Synchronous renal cell carcinoma metastasis to the contralateral adrenal gland and pancreas: A case report with 7-year follow-up subsequent to surgical therapy.

Metastatic renal cell carcinoma (RCC) disseminates to a number of organ sites and few patients demonstrate long-term survival following surgery. However, synchronous metastasis of RCC to the contralateral adrenal gland and pancreas is rare. In the present report, a case of synchronous RCC metastasis to the contralateral adrenal gland and pancreas in a 55-year-old patient, with an 116×92×61 mm right renal tumor and a 96×79×57 mm left adrenal lesion, is described. In April 2007, right nephrectomy was performed to treat the RCC, left adrenalectomy was performed to treat the adrenal tumor and the pancreatic metastases were resected. The patient remained alive at the 7-year follow-up appointment.

Long-term oncologic outcomes of laparoscopic vs open surgery for stages II and III rectal cancer: A retrospective cohort study.

AIM: To evaluate the 5-year survival after laparoscopic surgery vs open surgery for stages II and III rectal cancer. METHODS: This study enrolled 406 consecutive patients who underwent curative resection for stages II and III rectal cancer between January 2000 and December 2009 [laparoscopic rectal resection (LRR), n = 152; open rectal resection (ORR), n = 254]. Clinical characteristics, operative outcomes, pathological outcomes, postoperative recovery, and 5-year survival outcomes were compared between the two groups. RESULTS: Most of the clinical characteristics were similar except age (59 years vs 55 years, P = 0.033) between the LRR group and ORR group. The proportion of anterior resection was higher in the LRR group than that in the ORR group (81.6% vs 66.1%, P = 0.001). The LRR group had less estimated blood loss (50 mL vs 200 mL, P < 0.001) and a lower rate of blood transfusion (4.6% vs 11.8%, P = 0.019) compared to the ORR group. The pathological outcomes of the two groups were comparable. The LRR group was associated with faster recovery of bowel function (2.8 d vs 3.7 d, P < 0.001) and shorter postoperative hospital stay (11.7 d vs 13.7 d, P < 0.001). The median follow-up time was 63 mo in the LRR group and 65 mo in the ORR group. As for the survival outcomes, the 5-year local recurrence rate (16.0% vs 16.4%, P = 0.753), 5-year disease-free survival (DFS) rate (63.0% vs 63.1%, P = 0.589), and 5-year overall survival (OS) rate (68.1% vs 63.5%, P = 0.682) were comparable between the LRR group and the ORR group. Stage by stage, there were also no statistical differences between the LRR group and the ORR group in terms of the 5-year local recurrence rate (stage II: 6.3% vs 8.7%, P = 0.623; stage III: 26.4% vs 23.2%, P = 0.747), 5-year DFS rate (stage II: 77.5% vs 77.6%, P = 0.462; stage III: 46.5% vs 50.9%, P = 0.738), and 5-year OS rate (stage II: 81.4% vs 74.3%, P = 0.242; stage III: 53.9% vs 54.1%, P = 0.459). CONCLUSION: LRR for stages II and III rectal cancer can yield comparable long-term survival while achieving short-term benefits compared to open surgery.

Serum microRNA-125a-5p, a useful biomarker in liver diseases, correlates with disease progression.

It has been demonstrated that liver microRNA-125a-5p (miR-125a-5p) is correlated with disease progression in different liver diseases, including liver fibrosis and hepatocellular carcinoma (HCC). The present study investigated whether serum miR-125a-5p correlated with the progression of different liver diseases. Serum samples were obtained from healthy individuals, patients with chronic hepatitis B who had undergone a liver biopsy, and patients with HCC and were analyzed for the levels of miR-125a-5p. Compared with the healthy controls, the serum levels of miR-125a-5p were significantly higher in the liver fibrosis serum, and were reduced in HCC. With the development of liver fibrosis, there was a significant increase in the expression of miR-125a-5p (P<0.05). In comparing histological activity index (HAI) scores, higher expression levels of miR125a-5p were observed in the high HAI score group (P<0.05). Furthermore, correlation between serum miR-125a-5p and viral replication (P<0.001) was observed. Notably, miR-125a-5p demonstrated significant correlation with other markers in the liver fibrosis group (P<0.001). In the patients with HCC, lower serum levels of miR-125a-5p were correlated with a poor prognosis, determined by Kaplan-Meier curve analysis (P=0.009). In the liver fibrosis and HCC groups, different expression levels of serum miR-125a-5p were observed, and were correlated with disease progression. The results of the present study suggested that serum miR-125a-5p may be used as a non-invasive biomarker for monitoring disease progression in liver diseases.

[Duodenojejunal bypass in treatment for 7 cases with non-severe obese type 2 diabetes mellitus].

OBJECTIVE: To investigate the efficacy and feasibility of duodenojejunal bypass(DJB)on non-severe obese patients with type 2 diabetes mellitus(T2DM). METHODS: The body mass index (BMI), fasting plasma glucose(FPG), 2h-postprandial plasma glucose(2hPG), fasting insulin(F-ins), fasting c-peptide(F-CP), glycated hemoglobin and hypoglycemic agents dose changes were tested in 7 patients with non-severe obese T2DM undergoing DJB, preoperatively and within 24 weeks after surgery during the follow-up. Data were collected and the clinical outcomes of T2DM were analyzed. RESULTS: In 7 cases of non-obese T2DM who underwent DJB, one patient was weaned off hypoglycemic agents with normal FPG, 2hPG and HbA1c postoperatively. Five required significantly lower dosage. No significant improvement in 1 case. Complete remission rate of hyperglycemia was 1/7, effective rate was 6/7, and effective rate of HbA1c was 5/7. No significant changes in BMI were observed between the preoperative and postoperative phases. CONCLUSION: Plasma glucose level can be markedly reduced by duodenojejunal bypass in non-obese T2DM, independent of weight loss, and the mechanism remains unclear.

[Laparoscopic total mesorectal excision combined with intersphincteric resection for ultra-low rectal cancer].

OBJECTIVE: To evaluate clinical outcomes after laparoscopic total mesorectal excision (TME) combined with intersphincteric resection (ISR) for ultra-low rectal tumors. METHODS: Clinical data of 36 patients with ultra-low rectal tumor undergoing laparoscopic TME combined with ISR were analyzed retrospectively. RESULTS: The median distance from the inferior margin of the tumor to the anal verge was 3.4 (2.0-5.0) cm. There were 33 cases of well/moderately differentiated adenocarcinoma and 3 rectal malignant villous adenoma. There were 16 patients with stage I disease, 15 with stage II A, 3 with stage III A, and 1 with III B. Postoperatively, one patient developed stenosis at the end ileostomy and 3 anastomotic leakage. After a median follow-up of 16(4-49) months, one patient developed local recurrence at the anastomosis and one case died of liver metastasis. In the 19 patients who had a minimum follow-up of one year, the bowel movements frequency ranged from 1-4 times per day, and these patients were able to withhold defecation for more than 5 minutes. CONCLUSIONS: Laparoscopic TME combined with ISR can achieve oncologic clearance, sphincter preservation, and minimal invasiveness for ultra-lower rectal cancer. However, patients selection should be cautious.

Laparoscopic vs open left hepatectomy for hepatolithiasis.

AIM: To explore the feasibility and therapeutic effect of total laparoscopic left hepatectomy (LLH) for hepatolithiasis. METHODS: From June 2006 to October 2009, 61 consecutive patients with hepatolithiasis who met the inclusion criteria for LLH were treated in our institute. Of the 61 patients with hepatolithiasis, 28 underwent LLH (LLH group) and 33 underwent open left hepatectomy (OLH group). Clinical data including operation time, intraoperative blood loss, postoperative complication rate, postoperative hospital stay time, stone clearance and recurrence rate were retrospectively analyzed and compared between the two groups. RESULTS: LLH was successfully performed in 28 patients. The operation time of LLH group was longer than that of OLH group (158 +/- 43 min vs 132 +/- 39 min, P < 0.05) and the hospital stay time of LLH group was shorter than that of OLH group (6.8 +/- 2.8 d vs 10.2 +/- 3.4 d, P < 0.01). No difference was found in intraoperative blood loss (180 +/- 56 mL vs 184 +/- 50 mL), postoperative complication rate (14.2% vs 15.2%), and stone residual rate (intermediate rate 17.9% vs 12.1% and final rate 0% vs 0%) between the two groups. No perioperative death occurred in either group. Fifty-seven patients (93.4%) were followed up for 2-40 mo (mean 17 mo), including 27 in LLH group and 30 in OLH group. Stone recurrence occurred in 1 patient of each group. CONCLUSION: LLH for hepatolithiasis is feasible and safe in selected patients with an equal therapeutic effect to that of traditional open hepatectomy.