RESUMO
AIMS: In cases of malignant distal biliary obstruction, ERCP is the preferred technique for bile duct drainage. In case of failure, the alternative techniques are percutaneous transhepatic biliary drainage (PTBD) and more recently endoscopic ultrasound-guided biliary drainage. A new type of stent called the electrocautery-enhanced lumen-apposing metal stent (EC-LAMS) has been developed to enable the performance of biliary-enteric anastomosis under EUS-guidance in a single step, without prior bile duct puncture or the need for a guidewire. The aim of our study was to compare the real-life efficacies of PTBD and EUS-BD with the EC-LAMS for cases of ERCP failure in patients with malignant biliary obstruction. METHODS: We performed a monocentric retrospective study comparing PTBD and EUS-BD with the use of electrocautery-enhanced lumen-apposing metal stent in the context of a malignant distal biliary obstruction after ERCP failure. RESULTS: 95 patients were included (50 in EUS-BD group and 45 in PTBD group). The main etiology of malignant obstruction was adenocarcinoma of the head of pancreas (85%). There was a significant difference in favor of endoscopic ultrasound-guided biliary drainage using electrocautery-enhanced lumen-apposing metal stent for the following criteria: clinical success: 89.3% vs. 45.5%; p < 0.0001; procedure-related adverse event rate: 2.12% vs. 22.7%; p = 0.003; duration of post-drainage hospitalization: 3.5 vs. 8.2 days; p < 0.0001, overall survival (median survival): 118.2 vs. 42 days; p = 0.012, overall cost of the strategy per patient: 5098 vs. 9363 euros; p < 0.001. CONCLUSION: Our results are in favor of EUS-BD using electrocautery-enhanced lumen-apposing metal stent in case of ERCP failure for a distal tumor biliary obstruction. Operators performing ERCP for distal tumor biliary obstruction must learn this backup procedure because of its superiority over percutaneous transhepatic biliary drainage in terms of clinical success, safety, cost, and overall survival.
Assuntos
Colestase , Neoplasias , Humanos , Colangiopancreatografia Retrógrada Endoscópica/métodos , Colestase/etiologia , Colestase/cirurgia , Drenagem/métodos , Eletrocoagulação/métodos , Endossonografia/métodos , Metais , Neoplasias/complicações , Estudos Retrospectivos , Stents/efeitos adversos , Ultrassonografia de Intervenção/métodosAssuntos
Artrografia , Lúpus Eritematoso Sistêmico/diagnóstico , Imageamento por Ressonância Magnética , Polimialgia Reumática/diagnóstico , Mielofibrose Primária/diagnóstico , Corticosteroides/uso terapêutico , Diagnóstico Diferencial , Feminino , Humanos , Úmero/patologia , Articulação do Joelho/patologia , Lúpus Eritematoso Sistêmico/tratamento farmacológico , Pessoa de Meia-IdadeRESUMO
PURPOSE: Tendinopathy is a frequent and ubiquitous disease developing early disorganized collagen fibers with neo-angiogenesis on histology. Peritendinous injection of corticosteroid is the commonly accepted strategy despite the absence of inflammation in tendinopathy. Platelet-rich plasma (PRP) might be a useful strategy to rapidly accelerate healing of the tendinopathy but there is a lack ok knowledge about the amount of PRP to be injected and the opportunity of a second injection in case of partial pain relief. The aim of our study was to assess the potential therapeutic effect of early second PRP intra-tendinous to treat persistent painful tendon tear and tendinosis in a long-term follow-up by ultrasonography (US) and clinical data in case of incomplete efficiency of first PRP treatment injection. MATERIALS AND METHODS: Twenty-four consecutive patients referred for US treatment of tendon tear or tendinosis (T+) were included retrospectively. All had previously received a single intra-tendinous injection of PRP under US guidance (PRPT+) and benefited of a second PRP injection (PRPT2+) under US guidance in order to treat persistent painful. US and clinical data were collected for each anatomic compartment for upper and lower limbs before treatment (D0), 6 weeks (W6) after first treatment, 6 weeks (W12) after second treatment and until 32-month follow-up. We used Mac Nemar test and regression model to compare US and clinical data. RESULTS: The residual US size of lesions was not significantly lower at W12 after PRPT2+ as compared to W6 (P=0.86 in upper and P=NS in lower member) independently of age (P=0.22), gender (P=0.97) and kind of tendinopathy (P=NS). Quick dash test values and WOMAC values were not significantly lower in PRPT+ at W12 (average: 21.5 months) as compared to W6 (P>0.66) and long-term follow-up (P>0.75) independently of age (P=0.39), gender (P=0.63) and kind of tendinopathy (P=NS). Nevertheless, comparison between D0 and long-term follow-up (LTF) functionnal score was statistically significant (p<0.001 in upper and lower member). CONCLUSION: Our study suggests that second early intra-tendinous PRP injection under US guidance does not permit rapid decrease of tendinopathy area in US, nor does it quickly improve clinical pain and functional data in case of incomplete efficiency of first PRP injection. However, in long-term follow-up, patients improved their ability to mobilize pathologic tendons.
Assuntos
Plasma Rico em Plaquetas , Tendinopatia/diagnóstico por imagem , Tendinopatia/terapia , Ultrassonografia de Intervenção/métodos , Adulto , Idoso , Feminino , Seguimentos , Humanos , Interpretação de Imagem Assistida por Computador , Injeções , Masculino , Pessoa de Meia-Idade , Medição da Dor , Retratamento , Estudos Retrospectivos , Falha de TratamentoRESUMO
Ectopic endometriosis is a common condition which is often underdiagnosed, where MRI can help make a diagnosis simply, non-invasively and without irradiation. However, imagery signs of it are enormously polymorphic with a wide range of possible locations. In this paper, we have tried to illustrate comprehensively all its MRI appearances depending on the different locations where it occurs.
Assuntos
Endometriose/patologia , Imageamento por Ressonância Magnética , Feminino , Humanos , PelveRESUMO
The authors report the first case of gas embolism arising during an upper gastrointestinal endoscopy to a patient carrier of a biliary drain placed by radiological way. The hypothesis of a biliary-vascular fistula with abnormal connection between the biliary tree and the hepatic vascular system and finally an arteriovenous intrapulmonary shunt was retained to explain the physiopathology. The immediate stop of the endoscopic procedure and the implementation of symptomatic treatment allowed a favorable neurological outcome without sequelas. The realization of an upper gastrointestinal endoscopy to a patient carrier of a biliary drain has to lead the anaesthesiologists and the gastroenterologists to take care given the incurred risk of gas embolism.
Assuntos
Procedimentos Cirúrgicos do Sistema Biliar/métodos , Sistema Biliar/diagnóstico por imagem , Sistema Biliar/patologia , Drenagem/efeitos adversos , Embolia Aérea/etiologia , Gastroscopia/efeitos adversos , Complicações Intraoperatórias/etiologia , Complicações Intraoperatórias/terapia , Idoso , Idoso de 80 Anos ou mais , Colecistectomia , Ecocardiografia Transesofagiana , Embolia Aérea/diagnóstico por imagem , Endoscopia do Sistema Digestório , Humanos , Doença Iatrogênica , Masculino , RadiografiaRESUMO
Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) exert various effects on immune cells. Here we studied, whether they influence the cytokine expression pattern in peripheral blood mononuclear cells (PBMCs) or antigen specific T-cells. In PBMCs BDNF and NGF had interindividually variable effects on T helper cell type (Th)1- and Th2-cytokines. However, there was a high correlation between the modulating properties of these neurotrophins (r=0.97) concerning the expression of interleukin (IL) 4, transforming growth factor-beta and tumour necrosis factor-alpha mRNA at a concentration of 100 ng/ml. In myelin basic protein-specific T-cell lines BDNF and NGF increased interferon -gamma mRNA to a moderate extent, but not IL4. No major effects were detected at the cytokine protein level. In conclusion, our results suggest a partial effect of neurotrophins on immune cells, which may be modified by other signals.
Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Citocinas/metabolismo , Leucócitos Mononucleares/metabolismo , Fator de Crescimento Neural/metabolismo , Linfócitos T/metabolismo , Fator Neurotrófico Derivado do Encéfalo/farmacologia , Técnicas de Cultura de Células , Citocinas/efeitos dos fármacos , Relação Dose-Resposta a Droga , Humanos , Interferon gama/metabolismo , Interleucina-4/metabolismo , Leucócitos Mononucleares/efeitos dos fármacos , Fator de Crescimento Neural/farmacologia , RNA Mensageiro/metabolismo , Linfócitos T/efeitos dos fármacos , Fator de Crescimento Transformador beta/metabolismo , Fator de Necrose Tumoral alfa/metabolismoRESUMO
Inflammatory stimuli within the central nervous system may not only induce tissue damage but may also convey neuroprotection. It has been shown that brain derived neurotrophic factor (BDNF) is a neuroprotective candidate. Here we show that BDNF is constitutively expressed in cultured human cerebral endothelial cells (HCEC) and can further be upregulated under proinflammatory conditions. TNF-alpha treatment resulted in an increase in BDNF mRNA expression and protein levels were significantly elevated after 72 h (69+/-33%, P<0.01). Using functional assays it was demonstrated that BDNF produced by HCEC is bioactive and supports motoneuron survival. In contrast, BDNF expression was reduced by TNF-alpha in human umbilical vein endothelial cells (HUVEC). We conclude that HCEC likely to contribute to neuronal survival under physiological and inflammatory conditions.
Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Endotélio/metabolismo , Telencéfalo/metabolismo , Fator Neurotrófico Derivado do Encéfalo/biossíntese , Fator Neurotrófico Derivado do Encéfalo/farmacologia , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Citocinas/metabolismo , Humanos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Telencéfalo/citologiaRESUMO
Oncostatin M (OSM) is a member of the interleukin (IL)-6 cytokine family and modulates inflammatory responses. Here we investigated the role of OSM as an immunoregulatory factor for human cerebral endothelial cells (HCEC). Using RT-PCR we detected transcripts of the receptor components involved in OSM signaling, gp130, OSM receptor (OSMR)-beta, and leukemia inhibitory factor receptor (LIFR), in HCEC. A parallel FACS analysis revealed surface expression of gp130 and OSMR-beta, but not of LIFR on these cells. Functionally, OSM upregulated intercellular adhesion molecule-1, but did not induce vascular cell adhesion molecule-1 in HCEC. Further, OSM upregulated IL-6 and monocyte chemoattractant protein (MCP)-1, whereas IL-8 was unaffected. Combined application of tumor necrosis factor (TNF)-alpha and OSM synergistically enhanced IL-6 and MCP-1 production, but downregulated TNF-alpha-induced IL-8. As OSM regulated molecules relevant in inflammatory brain diseases, we investigated its expression in normal and pathological human brains. OSM was detected by immunohistochemistry in brains from multiple sclerosis patients in microglia, reactive astrocytes, and infiltrating leukocytes, whereas in normal brains and noninflammatory neurological diseases. immunoreactivity was absent from the parenchyma. These data suggest that immunoregulatory functions in human cerebral endothelial cells may be a mechanism by which OSM participates in the pathophysiology of inflammatory brain disease.
Assuntos
Barreira Hematoencefálica/fisiologia , Endotélio Vascular/química , Esclerose Múltipla/imunologia , Esclerose Múltipla/fisiopatologia , Peptídeos/análise , Adulto , Idoso , Antígenos CD/análise , Antígenos CD/genética , Células Cultivadas , Quimiocina CCL2/análise , Quimiocina CCL2/genética , Receptor gp130 de Citocina , Endotélio Vascular/citologia , Feminino , Citometria de Fluxo , Expressão Gênica/imunologia , Humanos , Molécula 1 de Adesão Intercelular/metabolismo , Interleucina-6/análise , Interleucina-6/genética , Subunidade alfa de Receptor de Fator Inibidor de Leucemia , Masculino , Glicoproteínas de Membrana/análise , Glicoproteínas de Membrana/genética , Pessoa de Meia-Idade , Esclerose Múltipla/patologia , Oncostatina M , Peptídeos/genética , RNA Mensageiro/análise , Receptor do Fator Neutrófico Ciliar/genética , Receptores de Citocinas/análise , Receptores de Citocinas/genética , Receptores de Interleucina-6/genética , Receptores de OSM-LIF , Fator de Necrose Tumoral alfa/farmacologia , Regulação para Cima/imunologia , Molécula 1 de Adesão de Célula Vascular/metabolismoRESUMO
Matrix metalloproteinases (MMPs) are Zn2+-endopeptidases that seem to play an important role in chronic inflammatory diseases of the central nervous system by disrupting the blood-brain barrier (BBB) and mediating the destruction of myelin components. We therefore investigated the influence of the pro-inflammatory cytokine TNF-alpha. on the expression and activation of several MMPs in human cerebral endothelial cells (HCEC). HCEC constitutively express MMP-2 and MMP-3 mRNA, but only MMP-3 is upregulated on mRNA and protein level after TNF-alpha stimulation. MMP-9 and MMP-12 mRNA could only be detected under inflammatory conditions. Furthermore, MMPs are involved in shedding of cell surface molecules. We therefore investigated the influence of MMPs on the release of soluble adhesion molecules using marimastat, a specific broad-spectrum MMP inhibitor and other protease inhibitors like aprotinin or leupeptin. Only marimastat inhibited the TNF-alpha mediated release of sVCAM-1 in the supernatants of HCEC. Western blot results of culture supernatants supported the time dependent release of the complete extracellular portion of the VCAM-1 molecule. These data suggest that MMPs produced by HCEC are actively involved in the shedding of soluble adhesion molecules at the BBB.
Assuntos
Moléculas de Adesão Celular/metabolismo , Córtex Cerebral/irrigação sanguínea , Endotélio Vascular/metabolismo , Metaloproteinases da Matriz/metabolismo , Processamento Alternativo , Northern Blotting , Células Cultivadas , Córtex Cerebral/citologia , Meios de Cultivo Condicionados/metabolismo , Proteínas de Ligação a DNA , Relação Dose-Resposta a Droga , Endotélio Vascular/citologia , Endotélio Vascular/efeitos dos fármacos , Ensaio de Imunoadsorção Enzimática , Citometria de Fluxo , Deleção de Genes , Humanos , Metaloproteinases da Matriz/genética , Microcirculação/citologia , Inibidores de Proteases/farmacologia , RNA Mensageiro/biossíntese , Fatores de Transcrição , Fator de Necrose Tumoral alfa/farmacologia , Molécula 1 de Adesão de Célula Vascular/genética , Molécula 1 de Adesão de Célula Vascular/metabolismoRESUMO
Tumour necrosis factor-alpha ( TNF-alpha) has been proposed as one of the key mediators of inflammatory diseases of the CNS such as multiple sclerosis. It has been shown to induce the expression of adhesion molecules which is a prerequisite for the transmigration of immune cells through the blood-brain barrier. We therefore investigated the role of TNF-alpha in the expression and release of vascular cell adhesion molecule-1 (VCAM-1) in cultures of human cerebral endothelial cells (HCEC) in comparison with peripheral blood mononuclear cells (PBMC). A time- and dose-dependent expression of VCAM-1 and release of soluble VCAM-1 was detected in HCEC but not PBMC. TNF-alpha-induced release of soluble VCAM-1 was further increased by cotreatment with interferon-beta (IFN-beta), while IFN-beta alone did not affect VCAM-1 expression or the release of soluble VCAM-1. In addition, we observed that preincubation of PBMC with soluble VCAM-1 completely blocked their adhesion to HCEC. In conclusion, the proinflammatory effect of TNF-alpha on HCEC, which involves the induction of VCAM-1 expression and cellular adhesion, is followed by the consecutive effects of soluble VCAM-1 release in blocking adhesion and downregulating further cellular infiltration. Increasing soluble VCAM-1 release during active inflammation could be another mechanism by which IFN-beta treatment exerts protective effects in multiple sclerosis patients.