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Objective:To study the detection rates of using different MRI sequences and enhanced CT in colorectal cancer liver metastasis (CRLM).Methods:The imaging data of CRLM patients who were treated at Peking University Third Hospital from March 2018 to September 2021 were retrospectively analyzed. Sixty-six CRLM lesions with a maximum diameter ≤10 mm were selected. Different MRI sequences such as T 1 weighted imaging (T 1WI), T 2 weighted imaging (T 2WI), diffusion weighted imaging (DWI), dynamic enhanced phase of MRI (MR-Dyn), gadolinium-etoxybenzyl-diethylenetriaminepentaacetic acid (Gd-EOB-DTPA), enhanced hepatobiliary phase of MRI (HBP) and CT enhancement phase (CT-Dyn) were reviewed independently to determine whether the target lesions were detected. The pathological results were used as the gold standard. Paired chi-square test was used to compare the detection rate of CRLM in each group. Results:Among the 66 liver metastases, 15, 31, 55, 21, 56 and 20 were detected by T 1WI, T 2WI, DWI, MR-Dyn, HBP and CT-Dyn, respectively. Their detection rates were 22.7%, 47.0%, 83.3%, 31.8%, 84.8% and 30.3%, respectively. The detection rates of HBP and DWI were higher than those of T 2WI, MR-Dyn, CT-Dyn and T 1WI, respectively (all P<0.05). The detection rate of T 2WI was higher than that of MR-Dyn, CT-Dyn and T 1WI (all P<0.05). The detection efficiencies of non-contrast MRI and Gd-EOB-DTPA enhanced MRI for CRLM were highly consistent ( Kappa=0.745). Conclusions:The detection rates of HBP, DWI and T 2WI for CRLM were high. Non-contrast MRI could replace Gd-EOB-DTPA enhanced MRI for detection of large CRLM.
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Objective:To explore the mechanism of proprotein convertase subtilisin/kexin type 9 (PCSK9) in the inflammatory response induced by Helicobacter pylori ( H. pylori) infection. Methods:From May 1, 2020 to January 31, 2021, 60 patients with gastritis (30 H. pylori positive and 30 H. pylori negative)and 30 healthy individuals, who initially visited the Department of Gastroenterology, Shiyan Taihe Hospital were collected, and their serum PCSK9 levels were detected. Normal gastric epithelial cell line GES-1 and macrophages induced from THP-1 cells, and GES-1 infected with H. pylori were selected to prepare different supernatant media. Phosphate buffer saline empty medium (negative control group), normal GES-1 cell supernatant medium ( H. pylori-uninfected GES-1 group), H. pylori infected GES-1 cell supernatant medium ( H. pylori infected GES-1 group), H. pylori infected GES-1 cell supernatant + PCSK9 neutralizing antibody medium (anti PCSK9 group), H. pylori infected GES-1 cell supernatant+ human immunoglobulin G medium (isotype control group) were established. The differences between H. pylori infected GES-1 group and H. pylori-uninfected GES-1 group, negative control group, anti PCSK9 group and isotype control group in number of migrated macrophages, relative expression level of CC chemokine receptor ( CCR2), the levels of released interleukin(IL)-6 and cell necrosis factor (TNF)- α, level of CD8 + T cell membrane phosphorylation, and the number of macrophage colonies were determined by Transwell assay, real time fluorescence quantitative polymerase chain reaction, plate colony assay, H. pylori and phagocytosis lysosome co-localization assay. The regulating mechanism of PCSK9 in H. pylori infection induced inflammation was analyzed. Independent sample t test was used for statistical analysis. Results:The serum level of PCSK9 of patients with H. pylori positive gastritis was higher than that of patients with H. pylori negative gastritis and healthy individuals ((384.00±57.57) g/L vs. (208.80±48.89) and (176.10±47.14) g/L), and the differences were statistically significant ( t=12.71 and 15.31; both P<0.001). Compared with negative control group, H. pylori standard strain and 4 isolated H. pylori strains could stimulate GES-1 to secrete PCSK9 ((1 267.00±287.50) g/L vs.(2 717.00±199.20), (4 858.00±302.40), (3 167.00±334.20), (6 075.00±597.30), (4 283.00±331.20) g/L), and the differences were statistically significant( t=10.15, 21.09, 10.56, 17.77, 16.85, all P<0.001). The number of migrated macrophages, CCR2 mRNA expression level in macrophage, expression levels of IL-6 and TNF-α, and the number of macrophage colonies of H. pylori-infected GES-1 group were all higher than those of H. pylori-uninfected GES-1 group and negative control group (132.20±5.67 vs.84.83±4.62, 39.83±4.12; 8.66±0.94 vs. 6.52±0.47 and 1.00±0.09, (281.00±8.56) ng/L vs. (115.00±7.72) and (64.00±5.44) ng/L, (619.80±18.47) ng/L vs.(373.30±12.85)and (225.70±6.44) ng/L, (357.00±16.31) colony forming unit (CFU) vs. (134.80±8.64) and (74.17±9.68) CFU), and the differences were statistically significant ( t=15.85, 32.27; 4.96, 19.79; 35.28, 52.43; 26.84, 49.37; 29.49, 36.53; all P<0.001). The percentage of co-localization of H. pylori and phagocytosis lysosome, and the expression of cell membrane CD3ζ Tyr142, granzyme B and perforin in CD8 + T cell of H. pylori-infected GES-1 group were lower than that of H. pylori-uninfected GES-1 group ((15.33±1.86)% vs. (34.50±3.72)% and (65.67±3.56)%, 464.20±120.80 vs. 1 924.00±262.10 and 2 390.00±484.10; (6.41±0.42)% vs.(17.37±0.73)% and (26.60±1.57)%; (6.84±1.37)% vs.(14.53±0.48)% and (26.22±1.21)%), and the differences were statistically significant( t=11.27 and 30.70, 12.39 and 9.45, 30.50 and 31.90, 25.96 and 13.00; all P<0.001). The number of migrated macrophages, the relative expression level of CCR2 mRNA, the expression levels of IL-6 and TNF-α, and the number of macrophage colonies of anti-PCSK9 group were all lower than those of isotype control group (72.50±4.97 vs. 128.30±6.74, 0.82±0.06 vs. 1.00±0.08, (85.50±4.37) ng/L vs. (277.70±8.98) ng/L, (291.80±13.69) ng/L vs. (615.30±12.65) ng/L, (111.50±10.21) CFU vs. (346.20±18.04) CFU), and the differences were statistically significant ( t=16.33, 4.40, 47.13, 42.50 and 27.73, all P<0.001). The percentage of co-localization of H. pylori and phagocytosis lysosome, the expression levels of CD3ζ Tyr142, granzyme B and perforin of anti-PCSK9 group were all higher than those of isotype control group ((51.05±3.03)% vs. (16.71±1.91)%, 2 948.00±384.00 vs. 1 156.00±178.60, (53.88±3.86)% vs. (5.88±0.93)%, (32.80±2.07)% vs. (6.83±0.54)%), and the differences were statistically significant ( t=23.49, 10.36, 29.60 and 29.76, all P<0.001). Conclusions:H. pylori can inhibit CD8 + T activation and cytotoxicity by inducing the release of PCSK9 from gastric epithelial cells, and can also recruit macrophages, activate nuclear factor-κB signal axis to up-regulate the level of released inflammatory factors from macrophages, inhibit the phagocytosis and killing effects of macrophages, so as to regulate the inflammatory response.
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Objective:To evaluate the regulatory role and potential mechanism of Urease B(UreB) on macrophages.Methods:Bone marrow-derived macrophages (M0) were stimulated by recombinant UreB protein and then flowcytometry and ELISA were used to detect the apoptosis, polarization and antigen presentation-related biomarkers expression. CD4 + T cell co-culture assay, CFSE stain and flowcytometry were used to evaluate the impacts of UreB on antigen presentation capacity of macrophages. Truncated UreB protein, NanoBiT assay and co-immunoprecipitation were used to identify the binding sites of UreB to TLR2. Results:UreB promoted apoptosis and skewed macrophages from M1 to M2 in the presence of M1-inducer LPS. Moreover, UreB inhibited the expression of antigen presentation biomarkers, MHCⅡ and CD86 on macrophages, and further inhibited the proliferation and IFN-γ expression of CD4 + T cells. Molecular analyses revealed that the binding between seven carboxy-terminal amino acid residues of UreB and TLR2 were required for the UreB-mediated inhibitory effects. Conclusions:The findings in this study demonstrate that UreB mainly depends on the binding between seven carboxy-terminal amino acid residues and TLR2 to perform immune-suppressive activities, and which may provide valuable information for the design and optimization of UreB-based vaccines against Helicobacter pylori infection.
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Objective:To explore the mechanism of potassium iodide-induced pyrolysis of thyroid follicular cells.Methods:Thyroid gland tissue was obtained from patients with thyroid cancer (TC) coexisting with Hashimoto′s thyroiditis, and the tumor-adjacent Hashimoto′s thyroiditis tissue was used as the control. ELISA was used to detect the concentration of the pyroptosis inflammatory cytokines interleukin (IL)-1β and IL-18 in the tissues, and Western blotting was used to detect the activation of gasdermin (GSDM) proteins, a biomarker for pyroptosis. Thyroid follicular cells treated with different concentrations of potassium iodide, and IL-1β, IL-18, lactate dehydrogenase (LDH), GSDMD were measured. Transcriptome chip analysis was used to explore the differentially expressed genes involved in pyroptosis of thyroid follicular cells induced by potassium iodide treatment.Results:The levels of IL-1β and IL-18 cytokines in the tissues of patients with Hashimoto′s thyroiditis and thyroid cancer were higher than control tissues ( P<0.01), and the activation of the pyroptosis executive protein GSDMD was significant increased, while GSDME was not activated. IL-1β, IL-18, and LDH secretion were significantly increased in response to potassium iodide stimulation in thyroid follicular cells ( P<0.01) and GSDMD was cleaved, which indicated that potassium iodide induced the pyroptosis of thyroid follicular cells. Moreover, potassium iodide could activate NLRP3 inflammasomes to promotethe pyroptosis of thyroid follicular cells. Transcriptome chip analysis further found that PARP1 protein was highly upregulated by the stimulation of potassium iodide, and then enhanced the activity of nuclear factor-κB (NF-κB) transcription factor to induce pyroptosis. Conclusions:The findings in this study reveal that potassium iodide promotesthe pyroptosis of thyroid follicular cells through activating NF-κB-NLRP3 inflammasome, which may be a novel mechanism that promots the development of Hashimoto′s thyroiditis under the condition of excessive iodine intake. PARP1 is a pivotal protein that mediates the pyroptosis induced by potassium iodide and may be a potential therapeutic target to control Hashimoto′s thyroiditis progression.
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Pancreatic neuroendocrine neoplasms (pNENs) are highly heterogeneous, and the management of pNENs patients can be intractable. To address this challenge, an expert committee was established on behalf of the Chinese Pancreatic Surgery Association, Chinese Society of Surgery, Chinese Medical Association, which consisted of surgical oncologists, gastroenterologists, medical oncologists, endocrinologists, radiologists, pathologists, and nuclear medicine specialists. By reviewing the important issues regarding the diagnosis and treatment of pNENs, the committee concluded evidence-based statements and recommendations in this article, in order to further improve the management of pNENs patients in China.
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Objective:To investigate the mechanism of PE_PGRS60 protein in the pathogenesis of Mycobacterium tuberculosis infection. Methods:The cloned and purified PE_PGRS60 protein from Mycobacterium tuberculosis was used to stimulate RAW264.7 cells. The expression of cyclooxygenase 2(COX2) mRNA and protein was detected by qRT-PCR and Western blot, respectively. The signal pathways that may regulate the expression of COX2 were screened, and the expression of inflammatory cytokines induced by PE_PGRS60 was detected by ELISA. The level of cell death was measured by lactate dehydrogenase(LDH) release test and flow cytometry PI staining. Western blot was used to detect the expression of COX2 in Peripheral blood mononuclear cell(PBMC) from active tuberculosis patients. Results:PE_PGRS60 protein was found to promote the expression of COX2 in RAW264.7 cells and activate the three major members of the mitogen-activated protein kinase(MAPK) family: extracellular regulated protein kinase(ERK), p38 and c-Jun N-terminal kinase(JNK). Interestingly, only JNK-IN-7, the inhibitor of JNK was observed to suppress the up-regulation expression of COX2 induced by PE_PGRS60. This up-regulated expression of COX2 was also found in PBMCs from active tuberculosis patients. The COX2 inhibitor celecoxib can effectively block the expression of the inflammatory factors IL-1β, TNF-α and IL-6 induced by PE_PGRS60 and promote macrophage death.Conclusions:PE_PGRS60 can promote macrophages to release inflammatory factors by activating JNK/COX2 signal axis. Some macrophages still die under the protection of COX2.
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Pancreatic cancer is an aggressive malignant tumor with poor prognosis.On the one hand,it has a narrow therapeutic window due to the lack of specific markers and obvious clinical symptoms.Once diagnosed,it has often developed to an advanced stage.On the other hand,located in a vital region of the body,pancreatic operation is difficult and the postoperative recurrence rate is high.Therefore,surgical treatment is only suitable for a small number of early patients.Pancreatic cancer has a tumor microenvironment with the characteristic of dense stroma,hypoxia,paucity of blood vessels and highly immunosuppression.It is often insensitive to traditional radiation and chemotherapy.Therefore,strategies targeting on tumor microenvironment have a potential prospect.This article reviews the research progress in tumor microenvironment of pancreatic cancer,in order to provide the references in the further research and treatment of oancreatic cancer.
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Pancreatic cancer is an aggressive malignant tumor with poor prognosis. On the one hand, it has a narrow therapeutic window due to the lack of specific markers and obvious clinical symptoms. Once diagnosed, it has often developed to an advanced stage. On the other hand, located in a vital region of the body, pancreatic operation is difficult and the postoperative recurrence rate is high. Therefore, surgical treatment is only sui-table for a small number of early patients. Pancreatic cancer has a tumor microenvironment with the characteristic of dense stroma, hypoxia, paucity of blood vessels and highly immunosuppression. It is often insensitive to traditional radiation and chemotherapy. Therefore, strategies targeting on tumor microenvironment have a potential prospect. This article reviews the research progress in tumor microenvironment of pancreatic cancer, in order to provide the references in the further research and treatment of pancreatic cancer.
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Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) can speed up the regeneration of future liver remnant (FLR) in short period of time, and offer a chance for surgical resection for patients without sufficient FLR. However, ALPPS still remains controversy due to its high perioperative morbidity and mortality, as well as the uncertain long-term oncological benefits. How to solve these problems is the key to ensure the safety of surgery.This article focus on the indication selection, liver function reserve evaluation and timing to perform the second stage surgery, surgical mode evolution and comparison with portal venous embolization/portal venous ligation+two-stage hepatectomy.
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Humans , Embolization, Therapeutic , Hepatectomy/methods , Ligation , Liver/surgery , Liver Neoplasms/surgery , Liver Regeneration , Portal Vein/surgery , Treatment OutcomeABSTRACT
The pathogenic mechanism of Mycobacterium tuberculosis (MTB) has always been the focus of tuberculosis research. The pathogenicity of MTB, especially latent infection, is closely related to its ability to escape immune killing. Macrophage is one of the important immune cells in the human body, but the escaping mechanism of MTB toward macrophage killing is still unclear. Frontier studies have found that MTB has effects on macrophage-related receptors, phagolysosomes, oxidative stress, apoptosis, autophagy and pyrolysis, thus escaping the killing effects of macrophages. This article reviewed these influences in order to provide more reference for follow-up researchers.
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Objective:To investigate the possible molecular mechanism of high-risk human papillomavirus (HPV) 16 E6 protein in promoting the proliferation, invasion and migration of cervical cancer cells.Methods:C33A cells were infected with HPV E6 protein overexpression lentivirus to construct a stable C33A-E6 cell line. The expression of heat shock protein 70 (HSP70) was detected by qRT-PCR and Western blot. Degradation rates of HSP70 at mRNA and protein levels were detected by qRT-PCR and Western blot at different time points after actinomycin D (ActD) and actinomycin ketone (CHX) treatment. Exosomes were extracted by hypervelocity centrifugation and the concentrations of HSP70 in exosomes were detected by enzyme-linked immunosorbent assay (ELISA). The concentrations of TNF-α, IL-1β, IL-6 and IL-10 in the supernatants of THP-1 cell culture that treated with exosomes isolated from C33A and C33A-E6 cells after interfering HSP70 expression were detected by ELISA. C33A cells were co-cultured with exosome-treated THP-1 cells to evaluate the changes in cell proliferation with CCK-8 method. The invasion and migration of C33A cells were assessed by Transwell assay.Results:Compared with the C33A cells, the expression of HSP70 at mRNA level in C33A-E6 cells was significantly increased ( P<0.05), but no significant change was observed at the protein level ( P>0.05). No significant difference in the degradation rate of HSP70 at mRNA or protein level was detected between C33A and C33A-E6 groups after treating with ActD and CHX for different times, but the concentration of HSP70 in exosomes was significantly increased in the C33A-E6 group ( P<0.001). The exosomes secreted by C33A-E6 cells could enhance the secretion of IL-6, TNF-α and IL-10 by THP-1 cells ( P<0.001), and the THP-1 cells treated with the exosomes could promote the proliferation, migration and invasion of C33A cells ( P<0.001). However, interfering the expression of HSP70 in C33A-E6 cells could significantly reduce the secretion of IL-6 and IL-10 by exosome-treated THP-1 cells, and inhibit the THP-1 cell-induced proliferation, migration and invasion of C33A cells ( P<0.001). Conclusions:High-risk HPV 16 E6 protein upregulated the level of HSP70 in the exosomes secreted by cervical cancer cells, thereby promoting the secretion of IL-6 and IL-10 by macrophages and enhancing the macrophage-induced proliferation, migration and invasion of cervical cancer cells.
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Objective:To investigate the influence and potential mechanism of mannose-capped lipoarabinomannan (ManLAM) to B cells responding to Mycobacterium tuberculosis (Mtb) infection. Methods:B cells were separated from patients with active pulmonary tuberculosis using magnetic beads and then stimulated with ManLAM in combination with CE protein. Flow cytometry was performed to evaluate the apoptosis, proliferation and activation of B cells. The secretion of cytokines and CE protein-specific IgG subclasses were detected by ELISA. ELISPOT assay was used to analyze the influence on the differentiation of B cells into CE protein-specific antibody-secreting cells (ASCs).Results:ManLAM inhibited the CE protein-induced proliferation and activation of B cells and the production of pro-inflammatory cytokines, resulting in significantly increased secretion of the immunosuppressive cytokine IL-10. It also inhibited the differentiation of B cells into CE protein-specific IgG secretory cells, but had no significant influence on the differentiation to IgM secretory cells. Moreover, ManLAM inhibited the secretion of CE protein-specific IgG1 and IgG3 and induced the secretion of immunosuppressive IgG4 via TLR2.Conclusions:This study suggested that ManLAM could inhibit the anti-tuberculosis immune response of B cells, which provided new theoretical reference for better understanding the immune escape mechanism in Mtb infection.
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Objective:This research was designed to investigate the safety and efficiency of laparoscopic simultaneous resection in the treatment of synchronous colorectal cancer liver metastases (sCRLM).Methods:From January 2009 to December 2019, 121 patients diagnosed as sCRLM received radical resection in Peking University Third Hospital were included in the research. According to the surgery approaches, the patients were divided into laparoscopic surgery group and open surgery group. Statistical analysis of general patient data, surgical data, postoperative complications and follow-up of the two groups of patients.Results:There were 79 cases in the laparoscopic surgery group including 30 females and 49 males, and the average age was 61.5 years. There were 42 cases in the open surgery group including 15 females and 27 males, and the average age was 63.2 years. There were no significant differences in the preoperative demographic characteristics, the location of primary tumor, gene status, the size of liver metastases, the proportion of multiple liver metastases, the level of tumor markers and the proportion of neoadjuvant chemotherapy between laparoscopic surgery group and the open surgery group ( P>0.05). The complication rate was 15.2% (12/79) in the laparoscopic surgery group and 23.8% (10/42) in the open surgery group. There were no significant differences between the two groups ( P>0.05). The 3-year and 5-year survival rates in laparoscopic surgery group were 52.9% and 44.4%, which were 42.5% and 23.0% respectively in open surgery group. There were no significant differences between the two groups ( P>0.05). The 1-year and 3-year disease-free survival rate in laparoscopic surgery group were 50.6% and 41.2%, which were 44.7% and 19.4% respectively in open surgery group. There were no significant differences between the two groups ( P>0.05). Conclusions:Laparoscopic simultaneous resection was safe and feasible for patients with sCRLM. Comparing with the open surgery, the laparoscopic surgeries had similar incidence of perioperative complications and long-term oncological efficiency.
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The tumor components of pancreatic ductal adenocarcinoma (PDAC) are composed of immune microenvironment of extracellular matrix, fibroblasts, endothelial cells and immune cells together with a minority of malignant cells. The failure of the therapeutic measures, such as chemotherapy, targeted therapy and immunotherapy, has been linked to the specific immune microenvironment of pancreatic cancer. By analyzing the components of immune microenvironment of pancreatic cancer, the mechanism of various components in pancreatic cancer such as highly immunosuppressive, hypoxic and connective tissue hyperplasia can be clarified. New efforts in single-cell profiling will enable a better understanding of the composition of the microenvironment in primary and metastatic PDAC, as well as an understanding of how the microenvironment may respond to novel therapeutic approaches.
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Pancreatic pseudocyst is the most common pancreatic cystic disease in clinical practice.In the surgical treatment of pancreatic pseudocysts, most surgeons preferred laparoscopic surgery in recent years.The options and the timing of laparoscopic surgery for pancreatic pseudocysts in different situations are explored in the paper.Pancreatic pseudocysts during the observation period, the imaging examination to detect whether the cyst has disappeared or increased, such as cysts found to be enlarged or still can not dissipate after 6 months, the largest diameter greater than 6 cm, and clinical symptoms, surgical drainage should be considered treatment.Surgery based on the location of the cyst and surgical experience of surgical options.Pancreatic cyst often choose laparoscopic cyst-gastric anastomosis, far from the stomach cyst should choose laparoscopic cyst-jejunal anastomosis.Laparoscopic surgery for the treatment of pancreatic pseudocyst has a unique advantage, short operation time, less bleeding, less trauma, less postoperative complications, rapid recovery, is a safe and effective treatment options.
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Objective To examine whether the boundary patterns of the superior mesenteric artery (SMA) in the preoperative contrasted enhanced computer tomography (CE-CT) could predict poor postoperative prognosis.Methods From January 2010 to December 2015,104 patients of pancreatic head ductal adenocarcinoma received radical pancreaticoduodenectomy by a single group of surgeons.All patients underwent CE-CT before operation.The clinicopathological characteristics and the prognosis were comparatively analyzed among the patients with different SMA boundary patterns.Results The patients with obscure SMA boundary in CE-CT had a lower overall survival rate (P =0.012) and a higher liver metastasis rate (P ＜ 0.01) compared to the patients with clear SMA boundary.38.2％ of patients with obscure SMA boundary died within 6 months,69.1％ of them died within 12 months while the mortality rate was 6％ within 6 months and 29.2％ within 12 months in patients with clear SMA boundary.Only 2.2％ of patients with clear SMA boundary presented liver metastasis within 6 months,but that was 53％ in patients with obscure SMA boundary.18.4％ of patients developed liver metastasis within 12 months in patients with clear SMA boundary,whereas the rate was 82％ in patients with obscure SMA boundary.Furthermore,the tissues around the SMA presented a higher CT value in any phase in patients with obscure SMA boundary than in patients with clear SMA boundary (P ＜ 0.01).Conclusions The patterns of the SMA boundary in CE-CT is a potential prognostic factor in pancreatic head ductal adenocarcinoma after radical operation,and the obscure SMA boundary may be associated with early liver metastasis and high mortality.
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Liver metastasis is the one of the main prognostic factors of pancreatic neuroendocrine neoplasm (PNEN). With the development of multidisciplinary collaboration among surgical oncology, medical oncology, and intervention treatment, the treatment of PNEN with liver metastasis gradually tends to become diversification. Surgery is still the only way for curing the patients with pancreatic neuroendocrine tumor with liver metastasis when the histological types are G1 and G2. Medical oncology and intervention treatment could be selected for those having PNEN with diffuse liver metastasis or those cannot tolerate surgery. Liver transplantation only suits for a small number of selected patients. The present article explored the relationship between histological classifications and the treatment options of PNEN with liver metastasis, and discussed the specific treatments from perspectives of surgical treatment, medical treatment and intervention treatment.
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Objective To evaluate laparoscopic partial splenectomy (LPS) for benign splenic tumors.Method Data of 55 patients undergoing laparoscopic partial splenectomy (20 cases) vs total splenectomy (LTS in 35 cases) at Peking University Third Hospital from August 2008 to July 2016 were collected and retrospectively analyzed.Results There was no difference in sex,BMI,preoperative H GB,preoperative PLT,operation time,operative blood loss and hospital stay between two groups.Age in LPS cases was younger than LTS group,while the tumor size was larger.On the 4th day postoperatively,PLT level was significnatly higher in LTP group.More patients in LTS group suffered from thrombocytosis.Conclusions Laprtoscopic partial splenectomy is a safe and effective procedure for the management of splenic benign tumors.
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Objective To evaluate the effect of distal splenorenal shunts (DSRS) in treatment of portal hypertension.Methods A retrospective analysis was made on 16 patients undergoing DSRS between 2009 and 2015 in a single institution.Perioperative free portal pressure (FPP),blood routine,liver function were collected and analyzed.Postoperative complications,long-term anastomotic status and the rate of re-bleeding were observed.Results Before and after DSRS,FPP were (43 ± 9) cmH2O and (31 ± 6) cmH2 O,a decrease of 29.1％ (t =7.326,P ＜ 0.01).Postoperative serum total bilirubin and peripheral blood leukocyte increased significantly (t =-3.462,t =-2.822,P ＜ 0.05).There was no significant difference in the changes of platelet and albumin before and after surgery.7 patients (7/16,43.8％) had one or more complications including 5 cases (31.3％) of portal vein thrombosis,massive ascites in 4 cases (25.0％),1 case (6.3％) of pulmonary infection and 1 case (6.3％) of wound infection.There was no inhospital mortality and all the 16 cases were followed up with no shunt anastomotic stenosis as showed by enhanced CT scan,meanwhile postoperative re-bleeding occurred in 1 case (6.3％) and 1 case (6.3％) died from liver failure.Conclusions Distal splenorenal shunts provides an effective method for the treatment of portal hypertension.
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Objective To examine whether the boundary patterns of the superior mesenteric artery (SMA) in the preoperative contrasted enhanced computer tomography (CE-CT) could predict poor postoperative prognosis.Methods From January 2010 to December 2015,104 patients of pancreatic head ductal adenocarcinoma received radical pancreaticoduodenectomy by a single group of surgeons.All patients underwent CE-CT before operation.The clinicopathological characteristics and the prognosis were comparatively analyzed among the patients with different SMA boundary patterns.Results The patients with obscure SMA boundary in CE-CT had a lower overall survival rate (P =0.012) and a higher liver metastasis rate (P ＜ 0.01) compared to the patients with clear SMA boundary.38.2％ of patients with obscure SMA boundary died within 6 months,69.1％ of them died within 12 months while the mortality rate was 6％ within 6 months and 29.2％ within 12 months in patients with clear SMA boundary.Only 2.2％ of patients with clear SMA boundary presented liver metastasis within 6 months,but that was 53％ in patients with obscure SMA boundary.18.4％ of patients developed liver metastasis within 12 months in patients with clear SMA boundary,whereas the rate was 82％ in patients with obscure SMA boundary.Furthermore,the tissues around the SMA presented a higher CT value in any phase in patients with obscure SMA boundary than in patients with clear SMA boundary (P ＜ 0.01).Conclusions The patterns of the SMA boundary in CE-CT is a potential prognostic factor in pancreatic head ductal adenocarcinoma after radical operation,and the obscure SMA boundary may be associated with early liver metastasis and high mortality.