ABSTRACT
OBJECTIVE: The objective of this prospective study was to test whether the treatment of Lisfranc injuries with open reduction and dorsal plate fixation would have the same or better functional outcomes as treatment with standard trans-articular screw fixation. METHODS: Sixty patients with primarily isolated Lisfranc joint injury were treated by open reduction and dorsal plate fixation or standard screw fixation. The patients were followed on average for 31 months. Evaluation was performed with patients' chief complaint, clinical examination, radiography, and AOFAS Midfoot Scale. RESULTS: Thirty two patients were treated with open reduction and dorsal plate fixation, and twenty eight patients were treated with open reduction and screw fixation. After two years follow-up, the mean AOFAS Midfoot score was 83.1 points in the dorsal plate fixation group and 78.5 points in the screw fixation group (p<0.01). Of the dorsal plate fixation group, radiographic analysis revealed anatomic reduction in twenty-nine patients (90.6%, 29/32) and nonanatomic reduction in three patients. Of the screw fixation group, radiographic analysis revealed anatomic reduction in twenty-three patients and nonanatomic reduction in five patients (82.1%, 23/28). CONCLUSIONS: Open reduction and dorsal plate fixation for a dislocated Lisfranc injury do have better short and median term outcome and a lower reoperation rate than standard screw ORIF. In our experience, we recommend using dorsal plate in ORIF on dislocated Lisfranc injuries. Level of Evidence II, Prospective Comparative Study.
ABSTRACT
O objetivo deste estudo prospectivo foi testar se o tratamentode lesões de Lisfranc com redução aberta e fixação da placadorsal teria os mesmos resultados funcionais, ou melhores, do quetratamento padrão com fixação com parafuso transarticular. Métodos:Sessenta pacientes com lesão articular de Lisfranc foram tratadospor redução aberta e fixação da placa dorsal ou pelo método padrãopor fixação de parafusos. Os pacientes foram acompanhados por,em média, 31 meses. A avaliação foi realizada com base na queixaprincipal dos pacientes, exame clínico, radiografia, e escala AOFAS.Resultados: Trinta e dois pacientes foram tratados com redução abertae fixação da placa dorsal, e vinte e oito pacientes foram tratadoscom redução aberta e fixação com parafuso. Depois de dois anos deacompanhamento, a média do escore AOFAS foi de 83,1 pontos nogrupo de fixação da placa dorsal e 78,5 pontos no grupo de fixaçãocom parafusos (p <0,01). Do grupo de fixação com placa dorsal, aanálise radiográfica revelou redução anatômica em vinte e nove pacientes(90,6%, 29/32) e redução não anatômica em três pacientes.Do grupo de fixação com parafuso, a análise radiográfica revelou reduçãoanatômica em vinte e três pacientes e redução não anatômicaem cinco pacientes (82,1%, 23/28). Conclusões: A redução abertae fixação com placa dorsal para lesão de Lisfranc deslocada têmmelhor resultado a curto e médio prazo e uma taxa de reoperaçãoinferior do que a técnica padrão de redução aberta e fixação interna(RAFI) com parafuso. Em nossa experiência, recomendamos o usode placa dorsal em RAFI nas lesões de Lisfranc deslocadas. Nívelde Evidência II, Estudo Prospectivo Comparativo...
The objective of this prospective study was to testwhether the treatment of Lisfranc injuries with open reductionand dorsal plate fixation would have the same or better functionaloutcomes as treatment with standard trans-articular screwfixation. Methods: Sixty patients with primarily isolated Lisfrancjoint injury were treated by open reduction and dorsal platefixation or standard screw fixation. The patients were followedon average for 31 months. Evaluation was performed with patientschief complaint, clinical examination, radiography, andAOFAS Midfoot Scale. Results: Thirty two patients were treatedwith open reduction and dorsal plate fixation, and twenty eightpatients were treated with open reduction and screw fixation.After two years follow-up, the mean AOFAS Midfoot score was83.1 points in the dorsal plate fixation group and 78.5 points inthe screw fixation group (p<0.01). Of the dorsal plate fixationgroup, radiographic analysis revealed anatomic reduction intwenty-nine patients (90.6%, 29/32) and nonanatomic reductionin three patients. Of the screw fixation group, radiographicanalysis revealed anatomic reduction in twenty-three patientsand nonanatomic reduction in five patients (82.1%, 23/28).Conclusions: Open reduction and dorsal plate fixation for adislocated Lisfranc injury do have better short and median termoutcome and a lower reoperation rate than standard screw ORIF.In our experience, we recommend using dorsal plate in ORIF ondislocated Lisfranc injuries. Level of Evidence II, ProspectiveComparative Study...
Subject(s)
Humans , Male , Female , Tarsal Joints , Joints/injuries , Arthrodesis , Prospective Studies , Internal Fixators , Bone ScrewsABSTRACT
A recent study showed that miR-26a is downregulated in hepatocellular carcinoma tissues and that this downregulation is an independent predictor of survival. Interestingly, the same study also reported that miR-26a downregulation causes a concomitant elevation of IL-6 expression. Because miR-26a expression was found to be transcriptionally downregulated by oncogene c-Myc in various cancers, and the expression of c-Myc was increased by IL-6 stimulation, we hypothesized that IL-6 contributes to reduction of miR-26a in hepatocellular carcinoma. Serum IL-6 was measured by ELISA and miR-26a was detected by qRT-PCR. The data of 30 patients with hepatocellular carcinoma who had undergone surgical tumor resection revealed that serum IL-6 could be considered to be a predictor of survival up to 5 years for hepatocellular carcinoma patients (log-rank test, P < 0.05). We observed that the serum IL-6 concentration was inversely correlated with miR-26a expression in cancerous tissues (Pearson correlation test, r = -0.651, P < 0.01). Furthermore, by in vitro experiments with HepG2 cells, we showed that IL-6 stimulation can lead to miR-26a suppression via c-Myc activation, whereas in normal hepatocyte LO2 cells incubation with IL-6 had no significant effect on miR-26a expression. Taken together, these results indicate that miR-26a reduction in hepatocellular carcinoma might be due to IL-6 upregulation.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Carcinoma, Hepatocellular/metabolism , /metabolism , Liver Neoplasms/metabolism , MicroRNAs/metabolism , Case-Control Studies , Carcinoma, Hepatocellular/genetics , Gene Expression Regulation, Neoplastic , Immunohistochemistry , /genetics , Liver Neoplasms/genetics , MicroRNAs/genetics , MicroRNAs/physiology , Recurrence , Transcriptional Activation/genetics , Up-RegulationABSTRACT
A recent study showed that miR-26a is downregulated in hepatocellular carcinoma tissues and that this downregulation is an independent predictor of survival. Interestingly, the same study also reported that miR-26a downregulation causes a concomitant elevation of IL-6 expression. Because miR-26a expression was found to be transcriptionally downregulated by oncogene c-Myc in various cancers, and the expression of c-Myc was increased by IL-6 stimulation, we hypothesized that IL-6 contributes to reduction of miR-26a in hepatocellular carcinoma. Serum IL-6 was measured by ELISA and miR-26a was detected by qRT-PCR. The data of 30 patients with hepatocellular carcinoma who had undergone surgical tumor resection revealed that serum IL-6 could be considered to be a predictor of survival up to 5 years for hepatocellular carcinoma patients (log-rank test, P < 0.05). We observed that the serum IL-6 concentration was inversely correlated with miR-26a expression in cancerous tissues (Pearson correlation test, r = -0.651, P < 0.01). Furthermore, by in vitro experiments with HepG2 cells, we showed that IL-6 stimulation can lead to miR-26a suppression via c-Myc activation, whereas in normal hepatocyte LO2 cells incubation with IL-6 had no significant effect on miR-26a expression. Taken together, these results indicate that miR-26a reduction in hepatocellular carcinoma might be due to IL-6 upregulation.