Pseudoaneurisma para-anastomótico gigante tras revascularización por baipás aorto-bifemoral: Informe de un caso / Giant para-anastomotic pseudoaneurysm after revascularization though aorto-bifemoral bypass grafting: Case report

RESUMEN El pseudoaneurisma es aquel hematoma pulsátil y encapsulado producido tras la rotura de todas las túnicas del vaso y contenido por tejidos vecinos circundantes. Es considerado una complicación tardía en la cirugía protésica aorto-ilíaca. Se presenta un paciente de 72 años al que se le realizó un baipás aorto-bifemoral 13 años atrás, y que posteriormente se le diagnosticó un pseudoaneurisma para-anastomótico que se dejó evolucionar por presentar varias comorbilidades asociadas. Transcurridos 2 años fue necesario realizarle una intervención quirúrgica por presentar crecimiento excesivo de la tumefacción y complicación isquémica con necrosis cutánea. La aparición de un pseudoaneurisma está relacionada con el sexo, el material protésico y con el tiempo que transcurre desde la cirugía. El seguimiento ultrasonográfico durante el postoperatorio es primordial para identificar tempranamente esta complicación.

ABSTRACT Pseudoaneurysm is that pulsatile and encapsulated hematoma produced after the rupture of all vessel layers and contained by surrounding neighboring tissues. It is considered a late complication in aorto-iliac prosthetic surgery. We present a 72-year-old patient who underwent an aorto-bifemoral bypass grafting 13 years ago, and who was subsequently diagnosed with a para-anastomotic pseudoaneurysm that was allowed to evolve due to presenting several associated comorbidities. After two years, it was necessary to perform a surgical intervention due to the excessive growth of the swelling, and ischemic complication with skin necrosis. The appearance of a pseudoaneurysm is related to sex, prosthetic material as well as the time that elapses since the surgery. Ultrasound follow-up during the postoperative period is essential for an early identification of this complication.

Indicadores de valor pronóstico de amputación en pacientes hospitalizados con pie diabético / Indicators of amputation´s prognostic value in hospitalized patients with diabetic foot

Introducción: La diabetes mellitus es la causa más importante de amputaciones no traumáticas en el mundo. El pronóstico de riesgo de amputación resulta vital para el tratamiento óptimo de los pacientes hospitalizados con pie diabético. Objetivo: Caracterizar las variables con valor pronóstico de amputación en pacientes hospitalizados con diagnóstico de pie diabético. Método: Se realizó un estudio analítico longitudinal prospectivo en el período desde diciembre de 2015 hasta diciembre de 2017, con una muestra constituida por 77 pacientes. Las variables recogidas fueron edad, sexo, resultados hemoquímicos al ingreso, co-morbilidad, control glucémico y amputaciones realizadas, estos dos últimos durante la estadía hospitalaria. Se hizo inclusión de las variables con asociación significativa en un análisis univariado (p < 0,05) en un modelo de regresión logística múltiple para evaluar su asociación independiente. Se determinaron los valores predictivos positivos, negativos, y el grado de sensibilidad y especificidad. Resultados: Los indicadores pronósticos resultantes del análisis de las variables fueron el índice leuco-hematocrito (p = 0,045), el nivel de albúmina en sangre (p = 0,004), la glicemia a mitad del ingreso (p = 0,045) y la glicemia al ingreso (p = 0,039). El índice leuco-hematocrito, menor de 6 al ingreso, se relacionó con una especificidad de 92 por ciento; la albúmina, menor de 29,9 g/L, presentó un valor predictivo positivo de 71 por ciento; la glicemia al ingreso, mayor de 21,5 mmol/L, mostró una sensibilidad de 75 por ciento; y la glicemia a mitad del ingreso, mayor de 12,9 mmol/L, manifestó una sensibilidad de 71 por ciento. Conclusiones: La evolución a la amputación de los pacientes ingresados por pie diabético se relaciona con el estado inflamatorio crónico, el estado nutricional y el control glucémico(AU)

Introduction: Diabetes mellitus is the most important cause of non-traumatic amputations in the world. The prognosis of amputation risk is vital for the optimal treatment of patients hospitalized with diabetic foot disease. Objective: Characterize variables with amputation´s prognostic value in hospitalized patients diagnosed with diabetic foot disease. Method: A prospective longitudinal analytical study was conducted in the period from December 2015 to December 2017, with a sample consisting of 77 patients. The variables collected were age, sex, hemochemical results upon admission, co-morbidity, glycaemic control and amputations performed, the latter two during the hospital stay. Variables with significant association were included in a one-variety analysis (p < 0.05) in a multiple logistic regression model to evaluate their independent association. Positive, negative predictive values, and the degree of sensitivity and specificity were determined. Results: The prognosis indicators resulting from the analysis of the variables were the leuko-hematocrit index (p = 0.045), the level of albumin in blood (p = 0.004), the glycaemia at the mid-time of the stay (p = 0.045) and the glycaemia at the admission time (p = 0.039). The leuko-hematocrit index, in less than 6 patients at admission time, was related to a specificity of 92 percent; albumin, in less than 29.9 g/L, had a positive predictive value of 71 percent; glycaemia at admission time, higher than 21.5 mmol/L, showed a sensitivity of 75 percent;and glycaemia at mid-time of the stay, higher than 12.9 mmol/L, showed a sensitivity of 71 percent. Conclusions: The evolution to amputation of patients admitted due to diabetic foot is related to chronic inflammatory state, nutritional state and glycaemic control(AU)

The functional relationship between transglutaminase 2 and transforming growth factor ß1 in the regulation of angiogenesis and endothelial-mesenchymal transition.

The importance of transglutaminase 2 (TG2) in angiogenesis has been highlighted in recent studies, but other roles of this multi-functional enzyme in endothelial cell (EC) function still remains to be fully elucidated. We previously showed that the extracellular TG2 is involved in maintaining tubule formation in ECs by a mechanism involving matrix-bound vascular endothelial growth factor (VEGF) signalling. Here, by using the ECs and fibroblast co-culture and ECs 3D culture models, we demonstrate a further role for TG2 in both endothelial tubule formation and in tubule loss, which involves its role in the regulation of transforming growth factor ß1 (TGFß1) and Smad signalling. We demonstrate that inhibition of tubule formation by TG2 inhibitors can be restored by add-back of exogenous TGFß1 at pg/ml levels and show that TG2 -/- mouse ECs are unable to form tubules in 3D culture and display negligible Smad signalling compared to wild-type cells. Loss of tubule formation in the TG2 -/- ECs can be reconstituted by transduction with TG2. We demonstrate that extracellular TG2 also has an important role in TGFß1-induced transition of ECs into myofibroblast-like cells (endothelial-mesenchymal transition), resulting in loss of EC tubules and tubule formation. Our data also indicate that TG2 may have a role in regulating TGFß signalling through entrapment of active TGFß1 into the extracellular matrix. In conclusion, our work demonstrates that TG2 has multi-functional roles in ECs where its ability to fine-tune of TGFß1 signalling means it can be involved in both endothelial tubule formation and tubule rarefaction.

Celiac Disease-Specific TG2-Targeted Autoantibodies Inhibit Angiogenesis Ex Vivo and In Vivo in Mice by Interfering with Endothelial Cell Dynamics.

A characteristic feature of celiac disease is the presence of circulating autoantibodies targeted against transglutaminase 2 (TG2), reputed to have a function in angiogenesis. In this study we investigated whether TG2-specific autoantibodies derived from celiac patients inhibit angiogenesis in both ex vivo and in vivo models and sought to clarify the mechanism behind this phenomenon. We used the ex vivo murine aorta-ring and the in vivo mouse matrigel-plug assays to address aforementioned issues. We found angiogenesis to be impaired as a result of celiac disease antibody supplementation in both systems. Our results also showed the dynamics of endothelial cells was affected in the presence of celiac antibodies. In the in vivo angiogenesis assays, the vessels formed were able to transport blood despite impairment of functionality after treatment with celiac autoantibodies, as revealed by positron emission tomography. We conclude that celiac autoantibodies inhibit angiogenesis ex vivo and in vivo and impair vascular functionality. Our data suggest that the anti-angiogenic mechanism of the celiac disease-specific autoantibodies involves extracellular TG2 and inhibited endothelial cell mobility.