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1.
Clin Res Cardiol ; 112(5): 614-625, 2023 May.
Artigo em Inglês | MEDLINE | ID: mdl-36749418

RESUMO

BACKGROUND: Large-bore arteriotomies can be percutaneously closed with suture-based or plug-based vascular closure device (VCD) strategies. The efficacy of both techniques remains controversial. AIMS: We conducted a meta-analysis of comparative studies between both VCD strategies, focusing on the most commonly applied VCDs (MANTA and ProGlide). METHODS: We searched MEDLINE, the Cochrane Central Register of Controlled Trials and Google scholar for observational studies (OS) and randomized controlled trials (RCT) comparing vascular closure with the MANTA-based and the ProGlide-based technique. The principal endpoint of this analysis was access-site related vascular complications. Both study types were analyzed separately. RESULTS: Access-site related vascular complications were less frequent after vascular closure with the MANTA technique in the analysis of OS (RR 0.61 [95%CI 0.43-0.89], p = 0.01, I2 = 0%), but more frequent in the analysis of RCT data (RR 1.70 [95%CI 1.16-2.51], p = 0.01, I2 = 0%). Both data sets provided no significant difference between the VCD techniques in terms of overall bleeding events (OS: RR 0.57 [95%CI 0.32-1.02], p = 0.06, I2 = 70%; and RCT: RR 1.37 [95%CI 0.82-2.28], p = 0.23, I2 = 30%). RCT data showed that endovascular stenting or vascular surgery due to VCD failure occurred more often after MANTA application (RR 3.53 [95%CI 1.07-11.33], p = 0.04, I2 = 0%). CONCLUSIONS: While OS point to favorable outcomes for large-bore vascular closure with the MANTA-based technique, RCT data show that this strategy is associated with more access-site related vascular complications as well as endovascular stenting or vascular surgery due to device failure compared with the ProGlide-based technique.


Assuntos
Doenças Cardiovasculares , Dispositivos de Oclusão Vascular , Humanos , Doenças Cardiovasculares/complicações , Artéria Femoral/cirurgia , Hemorragia/epidemiologia , Hemorragia/etiologia , Hemorragia/prevenção & controle , Técnicas Hemostáticas/efeitos adversos , Resultado do Tratamento , Dispositivos de Oclusão Vascular/efeitos adversos , Procedimentos Cirúrgicos Vasculares , Estudos Observacionais como Assunto , Ensaios Clínicos Controlados Aleatórios como Assunto
3.
Respiration ; 90(5): 416-25, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26452008

RESUMO

BACKGROUND: Inhaled corticosteroids (ICS) are widely used in the treatment of obstructive lung diseases. Recent data suggest a higher pneumonia risk in chronic obstructive pulmonary disease (COPD) patients treated with ICS. OBJECTIVE: Since non-typeable Haemophilus influenzae (NTHi) is the most common pathogen associated with acute exacerbations of COPD, we investigated the effects of budesonide (BUD) on NTHi-induced inflammation and invasive infection. METHODS: The alveolar epithelial cell line A549 and specimens of human lung tissue (HLT) were used in our experiments. Intracellular infection was determined by a lysis/culture assay of infected cells. Activated p38 mitogen-associated protein kinase (MAPK) was assessed using Western blotting and immunohistochemistry, expression of toll-like receptor 2 (TLR2) was determined by PCR, and CXCL-8 levels were measured using ELISA. Immunohistochemistry was used for detection of CXCL-8, platelet-activating factor receptor (PAF-R) and NTHi. RESULTS: BUD significantly reduced CXCL-8 secretion in A549 cells and lung tissue infected with NTHi. Furthermore, BUD decreased the expression of PAF-R in HLT and A549 cells. In A549 cells and HLT, BUD inhibited intracellular infection and - synergistically with NTHi - increased the expression of TLR2 (in A549 cells). TLR2 stimulation did not influence the intracellular infection of A549 cells, but p38 MAPK inhibition resulted in a significant reduction of infection. CONCLUSION: The present study adds new insights into the effects of glucocorticoids on pulmonary host defence after NTHi infection. Although the inflammatory response to infection is suppressed by BUD, interestingly, the intracellular infection is also inhibited. This effect seems to depend on the inhibition of p38 MAPK - a key enzyme in many pro-inflammatory pathways - as well as of PAF-R expression.


Assuntos
Budesonida/farmacologia , Haemophilus influenzae/efeitos dos fármacos , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Administração por Inalação , Anti-Inflamatórios/farmacologia , Western Blotting , Budesonida/efeitos adversos , Células Cultivadas , Meios de Cultivo Condicionados , Indução Enzimática/efeitos dos fármacos , Ensaio de Imunoadsorção Enzimática , Células Epiteliais/efeitos dos fármacos , Infecções por Haemophilus/etiologia , Infecções por Haemophilus/fisiopatologia , Humanos , Imuno-Histoquímica , Reação em Cadeia da Polimerase , Doença Pulmonar Obstrutiva Crônica/microbiologia , Sensibilidade e Especificidade , Proteínas Quinases p38 Ativadas por Mitógeno/efeitos dos fármacos
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