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1.
Front Cell Dev Biol ; 9: 700553, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34671598

RESUMO

Hepatocellular carcinoma (HCC), a highly aggressive tumor, has high incidence and mortality rates. Recently, immunotherapies have been shown to be a promising treatment in HCC. The results of either the CheckMate-040 or IMbrave 150 trials demonstrate the importance of immunotherapy in the systemic treatment of liver cancer. Thus, in this study, we tried to establish a reliable prognostic model for liver cancer based on immune-related genes (IRGs) and to provide a new insight for immunotherapy of HCC. In this study, we used four datasets that incorporated 851 HCC samples, including 340 samples with complete clinical information from the cancer genome atlas (TCGA) database, to establish an effective model for predicting the prognosis of HCC patients based on the differential expression of IRGs and validated the prognostic model using the data from International Cancer Genome Consortium (ICGC). The top 6 characteristic IRGs identified by protein-protein interaction (PPI) network analysis, MMP9, FOS, CAT, ESR1, ANGPTL3, and KLKB1, were selected for further study. In addition, we assessed the correlations of the six characteristic IRGs with the tumor immune microenvironment, clinical stage, and sensitivity to anti-cancer drugs. We also explored whether the differential expression of the characteristic IRGs was specific to HCC or present in pan-cancer. The expression levels of the six characteristic IRGs were significantly different between most tumor tissues and adjacent normal tissues. In addition, these characteristic IRGs showed a strong association with immune cell infiltration in HCC patients. We found that MMP9 and ESR1 were independent prognostic factors for HCC, while CAT, ESR1, and KLKB1 were associated with the clinical stage. We collected HCC paraffin sections from 24 patients from Xijing hospital to identify the differential expression of the five genes (MMP9, ESR1, CAT, FOS, and KLKB1). Finally, the results of decision curve analysis (DCA) and nomogram revealed that our models provided a prognostic benefit for most HCC patients and the predicted overall survival (OS) was consistent with the actual OS. In conclusion, we systemically constructed a novel prognostic model that provides new insights into HCC.

3.
Free Radic Biol Med ; 172: 578-589, 2021 08 20.
Artigo em Inglês | MEDLINE | ID: mdl-34242792

RESUMO

Acetaminophen (APAP) is the leading cause of acute liver failure (ALF), which is characterized by GSH depletion, oxidative stress and mitochondrial dysfunction. However, the specific mechanism of APAP-induced ALF remains to be clarified. In this study, we demonstrated that indoleamine 2,3-dioxygenase 1 (IDO1) aggravated APAP-induced ALF associated with excess lipid peroxidation, which was reversed by lipid peroxidation inhibitor (ferrostatin-1). Meanwhile, IDO1 deficiency effectively decreased the accumulation of reactive nitrogen species. Additionally, IDO1 deficiency prevented against APAP-induced liver injury through suppressing the activation of macrophages, thereby reduced their iron uptake and export, eventually reduced iron accumulation in hepatocytes through transferrin and transferrin receptor axis. In summary, our study confirmed that APAP-induced IDO1 aggravated ALF by triggering excess oxidative and nitrative stress and iron accumulation in liver. These results offer new insights for the clinical treatment of ALF or iron-dysregulated liver diseases in the future.


Assuntos
Doença Hepática Induzida por Substâncias e Drogas , Dioxigenases , Falência Hepática Aguda , Acetaminofen/toxicidade , Animais , Doença Hepática Induzida por Substâncias e Drogas/genética , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Dioxigenases/metabolismo , Hepatócitos , Ferro/metabolismo , Fígado/metabolismo , Falência Hepática Aguda/induzido quimicamente , Falência Hepática Aguda/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Estresse Oxidativo
4.
Ann Transl Med ; 9(2): 101, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33569403

RESUMO

Background: Primary biliary cholangitis (PBC) is an immune-mediated chronic cholestasis, in which T cell homeostasis plays an important role. Lysosomal-associated membrane protein 2 isoform A (LAMP-2A) has been implicated in the regulation of CD4+T cell responses. Methods: We comprehensively evaluated the immunobiology of CD4+T cells in patients with PBC (PBC, n=42), chronic hepatitis B (CHB, n=20), and healthy control subjects (HC, n=20) by flow cytometry including activation status and LAMP-2A expression. Additionally, we investigated the activation responses of PBC-naïve CD4+T cells by stimulation in vitro and tested the changes caused by deleting the gene encoding LAMP-2A. Results: Firstly, we found an increased activation status of circulating CD4+T cells from PBC patients compared to the HC subjects, and PBC-naïve CD4+T cells showed enhanced responses after stimulation in vitro. Secondly, PBC-naïve CD4+T cells expressed a significantly higher level of LAMP-2A compared to the HC and CHB groups [PBC vs. HC, 1,954.74 (1,254.28-3,057.14) vs. 1,542.12 (961.18-2,277.98), P=0.03; vs. CHB, 1,153.59 (726.87-1,275.48), P=0.02], and the overreactions of PBC-naïve CD4+T cells could be reversed by interfering with LAMP-2A expression in vitro. Thirdly, the LAMP-2A expression level of PBC-naïve CD4+T cells was related to disease severity and drug response. Conclusions: An abnormally increased LAMP-2A expression of PBC-naïve CD4+T cells might be related to excessive activation responses. LAMP-2A could be a novel therapeutic target for the treatment of PBC by reversing excessive responses and consequently reducing biliary injury.

5.
J Clin Lab Anal ; 34(11): e23501, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32915500

RESUMO

BACKGROUND: Ursodeoxycholic acid (UDCA) has been widely recommended as the first-line drug for primary biliary cholangitis (PBC) in the current guidelines. However, its therapeutic effects are poor in nearly one-third of patients. The early identification and intervention of these patients is crucial for delaying disease progression. Therefore, we explored risk factors for inadequate biochemical response and constructed a nomogram to predict the potential risk. METHODS: We enrolled 356 patients and randomly divided them into training (70%) and validation groups (30%). We defined inadequate biochemical response as the study endpoint. Logistic analysis was used to identify the independent predictors of poor biochemical response. Based on these factors, a predictive nomogram was finally constructed. Then, discrimination and calibration were evaluated by internal validation. Additionally, the association between the model predictions and prognosis was further analyzed. RESULTS: Female sex, and albumin and bilirubin concentrations were identified as risk factors, and a nomogram was built based on these factors. The areas under the ROC curves of the training and validation groups were 0.809 and 0.791, respectively. Moreover, calibration curves showed that predictions of the nomogram had good concordance with the actual outcomes. The correlation analysis demonstrated that PBC patients with a high probability of a suboptimal biochemical response were more likely to have adverse outcomes. CONCLUSION: We constructed a nomogram, which can accurately predict the risk of inadequate biochemical response to UDCA, facilitating the early screening of high-risk patients with PBC who should be prioritized for additional therapy.


Assuntos
Cirrose Hepática Biliar , Nomogramas , Ácido Ursodesoxicólico/uso terapêutico , Adulto , Progressão da Doença , Feminino , Humanos , Cirrose Hepática Biliar/diagnóstico , Cirrose Hepática Biliar/tratamento farmacológico , Cirrose Hepática Biliar/epidemiologia , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Prognóstico , Fatores de Risco , Resultado do Tratamento , Ácido Ursodesoxicólico/efeitos adversos
6.
Biochem Pharmacol ; 180: 114153, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32679126

RESUMO

Caveolin-1 (Cav-1) is a multifunctional protein and critical for the production of nitric oxide (NO) in intestinal physiological and pathological conditions, but its role in the inflammatory bowel disease(IBD) are still controversial. In this study we tested the hypothesis that Cav-1 could be an important cellular defense against IBD through inhibiting nitrosative stress and mucosal barrier damage. Male wild-type mice and Cav-1 knockout (Cav-1-/-) mice were subjected to 3% dextran sodium sulfate(DSS) for 7d to establish the experimental colitis model. A representative iNOS inhibitor (1400 W) was adopted to suppress the activity of iNOS in parallel group. Body weight and disease activity index were monitored. The colon tissues were evaluated through histological analysis. We found Cav-1 was down-regulated in the colon tissue and accompanied with the increase of iNOS and NO levels after DSS administration. Cav-1-/- mice were greatly increased susceptibility to DSS-induced colitis with the more weight loss and higher disease score than WT mice. Ablation of Cav-1gene significantly resulted in RNS overproduction, tight junctions impaired and inflammation elevated, which aggravated the severity of the intestinal damages. Furthermore, pharmacologic inhibition of iNOS by 1400 W significantly attenuated DSS-induced colitis in both WT and Cav-1-/- groups. Our results revealed an important role of Cav-1 in preventing intestinal nitrosative stress and mucosal barrier damage in the development of DSS-induced colitis.


Assuntos
Caveolina 1/deficiência , Colite/induzido quimicamente , Colite/metabolismo , Sulfato de Dextrana/toxicidade , Mucosa Intestinal/metabolismo , Estresse Nitrosativo/fisiologia , Animais , Colite/prevenção & controle , Mucosa Intestinal/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Estresse Nitrosativo/efeitos dos fármacos
7.
BMC Public Health ; 20(1): 263, 2020 Feb 21.
Artigo em Inglês | MEDLINE | ID: mdl-32085727

RESUMO

BACKGROUND: In developing countries, ambient sulfur dioxide (SO2) is a serious air pollutant concern, but there is no enough and consistent epidemiological evidence about its health effects on stroke hospitalization. METHODS: We collected the daily air pollution data, meteorological data and number of daily hospital admissions for ischemic and hemorrhagic stroke, in Guangzhou from January 1st 2009 to December 31st 2014. Then we applied generalized additive model with a quasi-Poisson link to assess the relationship between short-term SO2 exposure and the total number of hospital admissions for ischemic and hemorrhagic stroke. In addition, we evaluated the effect of ambient SO2 by age (< 65 years and ≥ 65 years). RESULTS: During the study period, a 24-h mean concentration of ambient SO2 of 27.82 µg/m3, a total of 58,473 ischemic stroke and 9167 hemorrhagic stroke hospital admissions hospital were recorded. Ambient SO2 was found to increase the risk for both ischemic and hemorrhagic stroke hospital admission in single pollutant model. The maximum value of percentage changes for ischemic and hemorrhagic stroke occurred in lag 0 day and lag 1 day, per 10 µg/m3 increase in SO2 concentrations was corresponded to a 1.27% (95% confidence interval (CI), 0.42-2.12%) and 1.55% (95%CI, 0.02-3.11%) increased risk, respectively. The association between SO2 and ischemic stroke hospitalization was robust to two pollutant model, but for hemorrhagic stroke it's partially weakened after adjusting for co-pollutants. The effect of ambient SO2 on ischemic stroke appeared to be greater for people < 65 years old, but null effect on hemorrhagic stroke was identified for both age groups. CONCLUSIONS: We found short-term exposure to ambient SO2 may significantly increase the risks of hospitalization for ischemic stroke. The findings may contribute to a better understanding of the health effects of low-levels of SO2.


Assuntos
Poluição do Ar/efeitos adversos , Exposição Ambiental/estatística & dados numéricos , Hospitalização/estatística & dados numéricos , Acidente Vascular Cerebral/terapia , Dióxido de Enxofre/efeitos adversos , Idoso , Poluição do Ar/análise , China/epidemiologia , Humanos , Pessoa de Meia-Idade , Medição de Risco , Acidente Vascular Cerebral/epidemiologia , Dióxido de Enxofre/análise
8.
Free Radic Biol Med ; 152: 668-679, 2020 05 20.
Artigo em Inglês | MEDLINE | ID: mdl-31945497

RESUMO

Ferroptosis is a recently recognized form of regulated cell death that is characterized by lipid peroxidation. However, the molecular mechanisms of ferroptosis in acute immune hepatitis (AIH) are largely unknown. In this study, we investigated the classical ferroptotic events in the livers of mice with concanavalin A (ConA) to induce AIH. The dramatically upregulated gene indoleamine 2, 3-dioxygenase 1 (IDO1) was identified with AIH, and its role in generation of ferroptosis and reactive nitrogen species (RNS) was assessed both in vitro and in vivo by genetic deletion or pharmacologic inhibition of IDO1. We observed that ferroptosis contributed to the ConA-induced hepatic damage, which was confirmed by the therapeutical effects of ferroptosis inhibitor (ferrostatin-1). Noteworthy, upregulation of hepatic IDO1 and nitrative stress in ConA-induced hepatic damage were also remarkably inhibited by the ferroptosis abolishment. Additionally, IDO1 deficiency contributed to ferroptosis resistance by activating solute carrier family 7 member 11 (SLC7A11; also known as xCT) expression, accompanied with the reductions of murine liver lesions and RNS. Meanwhile, IDO inhibitor 1-methyl tryptophan alleviated murine liver damage with the reduction of inducible nitric oxide synthase and 3-nitrotyrosine expression. Consistent with the results in vivo, hepatocytes-specific knockdown of IDO1 led to ferroptosis resistance upon exposure to ferroptosis-inducing compound (Erastin) in vitro, whereas IDO1 overexpression aggravated the classical ferroptotic events, and the RNS stress. Overall, these results revealed a novel molecular mechanism of ferroptosis with the key feature of nitrative stress in ConA-induced liver injury, and also identified IDO1-dependent ferroptosis as a potential target for the treatment of AIH.


Assuntos
Ferroptose , Hepatite , Animais , Hepatócitos , Indolamina-Pirrol 2,3,-Dioxigenase/genética , Camundongos
9.
Free Radic Biol Med ; 148: 151-161, 2020 02 20.
Artigo em Inglês | MEDLINE | ID: mdl-31877357

RESUMO

Ferroptosis is a new regulated cells death manner defined as results of iron-dependent accumulation of lipid peroxidation. However, the specific mechanisms of regulating ferroptosis remain unclear. In our present study, we demonstrated that Caveolin-1 (Cav-1) played a central role in protecting hepatocytes against ferroptosis in autoimmunity-mediated hepatitis (AIH). The down-regulated Cav-1 in liver tissues, accompanied by ferroptotic events and RNS production, were contributed to the outcome of ConA-induced hepatic damage, which were rescued by ferrostatin-1 (an inhibitor of ferroptosis) in vivo and in vitro. Additionally, Cav-1 deficiency aggravated ConA-induced hepatocellular death and ferroptosis associated with excessive nitrogen stress response. Short hairpin RNA of Cav-1 in hepatocytes promoted ferroptosis and nitrative stress in response to erastin in vitro, which was ameliorated by Cav-1 over-expression. Meanwhile, administration of the iNOS inhibitor (1400W) or ONOO- scavenger (Fe-TMPyP), diminished reactive nitrogen species (RNS), remarkably reduced hepatocytes ferroptosis and attenuated ConA-induced liver damage. Furthermore, immune inhibition by gadolinium chloride (GdCl3), a well-known Kupffer cell depletor, elevated hepatic Cav-1 but inhibited ferroptosis and nitrative stress under ConA exposure. In conclusion, these data revealed a novel molecular mechanism of ferroptosis with the Cav-1 regulation was essential for pathogenesis of ConA-induced hepatitis. Downstream of Cav-1, RNS-mediated ferroptosis was a pivotal step that drives the execution of acute immune-mediated hepatic damage.


Assuntos
Ferroptose , Caveolina 1/genética , Hepatócitos , Peroxidação de Lipídeos , Nitrogênio
10.
Front Oncol ; 10: 597996, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33575212

RESUMO

Background: Evidence from prevailing studies show that hepatocellular carcinoma (HCC) is among the top cancers with high mortality globally. Gene regulation at post-transcriptional level orchestrated by RNA-binding proteins (RBPs) is an important mechanism that modifies various biological behaviors of HCC. Currently, it is not fully understood how RBPs affects the prognosis of HCC. In this study, we aimed to construct and validate an RBP-related model to predict the prognosis of HCC patients. Methods: Differently expressed RBPs were identified in HCC patients based on the GSE54236 dataset from the Gene Expression Omnibus (GEO) database. Integrative bioinformatics analyses were performed to select hub genes. Gene expression patterns were validated in The Cancer Genome Atlas (TCGA) database, after which univariate and multivariate Cox regression analyses, as well as Kaplan-Meier analysis were performed to develop a prognostic model. Then, the performance of the prognostic model was assessed using receiver operating characteristic (ROC) curves and clinicopathological correlation analysis. Moreover, data from the International Cancer Genome Consortium (ICGC) database were used for external validation. Finally, a nomogram combining clinicopathological parameters and prognostic model was established for the individual prediction of survival probability. Results: The prognostic risk model was finally constructed based on two RBPs (BOP1 and EZH2), facilitating risk-stratification of HCC patients. Survival was markedly higher in the low-risk group relative to the high-risk group. Moreover, higher risk score was associated with advanced pathological grade and late clinical stage. Besides, the risk score was found to be an independent prognosis factor based on multivariate analysis. Nomogram including the risk score and clinical stage proved to perform better in predicting patient prognosis. Conclusions: The RBP-related prognostic model established in this study may function as a prognostic indicator for HCC, which could provide evidence for clinical decision making.

11.
Sci Rep ; 8(1): 6932, 2018 05 02.
Artigo em Inglês | MEDLINE | ID: mdl-29720683

RESUMO

Danon disease (DD) is caused by the absence or malfunction of lysosomal-associated membrane protein 2 (LAMP2). Although Lamp2-deficient mice and DD patients have similar characteristics, these mice have clear limitations and are clinically inconsistent. The aim of our paper is to outline the characteristics of Lamp2-deficient rats and to contrast this model with currently available DD mouse models. The baseline levels of some serum enzymes were elevated in Lamp2y/- rats along with hypercholesterolemia and hyperglycaemia at 8 weeks. Echocardiography showed that IVSd (1.500 ± 0.071 vs. 2.200 ± 1.147, P < 0.01) and LVPWd (1.575 ± 0.063 vs. 1.850 ± 0.029, P < 0.01) were significantly increased, and GCS (-13.20 ± 0.4814 vs. -6.954 ± 0.665) and GRS (21.42 ± 1.807 vs. 7.788 ± 1.140) were sharply decreased. Meanwhile, substantial myocyte disruption, hypertrophic muscle fibres, interstitial fibrosis and microvascular hyperplasia could be observed in the heart tissue. Lamp2y/- rats also displayed abnormal behaviours in the open field and fear conditioning tests. Notably, Lamp2y/- rats manifested other system dysfunctions, such as retinopathy, chronic kidney injury and sterility. Based on these results, Lamp2-deficient rats exhibited greater similarity to DD patients in terms of onset and multisystem lesions than did mouse models, and these rats could be used as a valuable animal model for DD.


Assuntos
Deleção de Genes , Doença de Depósito de Glicogênio Tipo IIb/etiologia , Doença de Depósito de Glicogênio Tipo IIb/metabolismo , Proteína 2 de Membrana Associada ao Lisossomo/genética , Animais , Biomarcadores , Cardiomiopatia Hipertrófica/genética , Cardiomiopatia Hipertrófica/metabolismo , Cardiomiopatia Hipertrófica/patologia , Cardiomiopatia Hipertrófica/fisiopatologia , Modelos Animais de Doenças , Técnicas de Inativação de Genes , Doença de Depósito de Glicogênio Tipo IIb/patologia , Músculo Esquelético/metabolismo , Músculo Esquelético/patologia , Ratos , Ratos Transgênicos
12.
Clin Rev Allergy Immunol ; 53(1): 105-116, 2017 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-28124283

RESUMO

Danon disease is a genetic deficiency in lysosome-associated membrane protein 2 (LAMP-2), a highly glycosylated constituent of the lysosomal membrane and characterized by a cardiomyopathy, skeletal muscle myopathy, and cognitive impairment. Patients, however, often manifest hepatic abnormalities, but liver function has not been well evaluated and the syndrome is relatively uncommon. Hence, we have taken advantage of a rat that has been deleted of LAMP-2 to study the relative role of LAMP-2 on liver function. Interestingly, rats deficient in LAMP-2 develop a striking increase in serum alkaline phosphatase (ALP) and a decrease in bile flow compared with wild-type littermates. Importantly and by ultrastructural analysis, deficient rats manifest dilated canaliculi that lack microvilli with evidence of bile-containing bodies. Moreover, following bile duct ligation, LAMP-2-deficient rats develop rapid and severe evidence of advanced cholestasis, with an increase in serum bilirubin, as early as 6 h later. In wild-type control rats, multidrug resistance-associated protein 2 (Mrp2) normally concentrates at the bile canalicular membranes to secrete conjugated bilirubin into bile. However, in LAMP-2y/- rats, Mrp2 was detected in hepatocytes compared with other canalicular proteins including P-glycoproteins, dipeptidyl peptidase IV (CD26), and aminopeptidase (CD13). Our data further suggest that LAMP-2 interacts with the membrane cytoskeletal proteins radixin and F-actin in determining the localization of integral membrane proteins.


Assuntos
Doença de Depósito de Glicogênio Tipo IIb/genética , Doença de Depósito de Glicogênio Tipo IIb/imunologia , Fígado/imunologia , Fígado/metabolismo , Proteína 2 de Membrana Associada ao Lisossomo/genética , Animais , Biomarcadores , Colestase Intra-Hepática/genética , Colestase Intra-Hepática/imunologia , Colestase Intra-Hepática/patologia , Modelos Animais de Doenças , Técnicas de Inativação de Genes , Loci Gênicos , Doença de Depósito de Glicogênio Tipo IIb/patologia , Humanos , Fígado/patologia , Camundongos Transgênicos , Ratos
13.
Eur Radiol ; 25(12): 3431-7, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25903717

RESUMO

OBJECTIVES: To introduce a modified transjugular intrahepatic portosystemic shunt (TIPS) procedure, percutaneous transhepatic balloon-assisted TIPS (BA-TIPS), and to evaluate its feasibility and efficacy in patients with chronic totally occluded portal vein thrombosis (CTO-PVT) with symptomatic portal hypertension. METHODS: Eighteen patients (12 men, six women; mean age 49 years [range, 34-68 years]) with CTO-PVT with symptomatic portal hypertension undergoing BA-TIPS between July 2011 and June 2014 were enrolled in this retrospective study. Rates of technical success, efficacy, and complications were evaluated, and pre- and post-procedure portosystemic gradients compared. Clinical follow-up and periodic assessment of TIPS for patency were performed. RESULTS: BA-TIPS was successful in fourteen patients and converted to open portosystemic shunt placement in four. Mean portosystemic pressure gradient fell from 24.1 ± 2.3 mmHg to 12.1 ± 3.5 mmHg after BA-TIPS (P < 0.01). No procedure-related complications were observed. During a median follow up of 16 months (range, 3-41 months), there was one death from hepatocellular carcinoma, one death from severe heart disease, and shunt dysfunction 16 months after BA-TIPS in one patient. Shunt patency was maintained in the remaining patients without symptoms of recurrence. CONCLUSIONS: BA-TIPS is feasible, safe, and effective for CTO-PVT with symptomatic portal hypertension. KEY POINTS: • Transjugular intrahepatic portosystemic shunt is an important treatment for portal vein thrombosis (PVT). • TIPS is challenging for patients with chronic totally occluded portal vein thrombosis (CTO-PVT). • The use of a balloon increased the technical success of portal puncture. • Balloon-assisted TIPS (BA-TIPS) is feasible, safe, and effective for CTO-PVT.


Assuntos
Angioplastia com Balão/métodos , Hipertensão Portal/complicações , Veia Porta/cirurgia , Derivação Portossistêmica Transjugular Intra-Hepática/métodos , Trombose Venosa/complicações , Trombose Venosa/terapia , Adulto , Idoso , Doença Crônica , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Derivação Portossistêmica Transjugular Intra-Hepática/efeitos adversos , Estudos Retrospectivos , Resultado do Tratamento , Trombose Venosa/cirurgia
14.
Cardiovasc Intervent Radiol ; 38(5): 1303-7, 2015 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25148922

RESUMO

Bifurcation stenoses after end-to-side anastomosis of transplant renal artery (TRA) and external iliac artery (EIA), including stenoses at the anastomosis and the iliac artery proximal to the TRA, are rare. In the present article, we report two successfully managed cases of bifurcation stenoses after end-to-side anastomosis of the TRA and EIA using the technique of T-stenting and small protrusion (TAP stenting).


Assuntos
Artéria Ilíaca/cirurgia , Transplante de Rim , Complicações Pós-Operatórias/cirurgia , Obstrução da Artéria Renal/cirurgia , Artéria Renal/transplante , Stents , Adulto , Anastomose Cirúrgica , Constrição Patológica/cirurgia , Humanos , Masculino , Pessoa de Meia-Idade
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