Browsing by Author "Munoz, Claudia"

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    Embolization of spontaneous portosystemic shunts as treatment for refractory hepatic encephalopathy
    (2022) Benitez, Carlos; Munoz, Ana; Poniachik, Jaime; Ramirez, Felipe; Munoz, Claudia; Cermenati, Tomas; Martinez, Nicolas; Diaz, Pia; Meneses, Luis
    Background: Hepatic encephalopathy (HE) is a common complication of cirrhosis associated with a reduced survival. The presence of high-flux spontaneous porto-systemic shunts can induce HE even in patients with preserved liver function. Aim: To evaluate the effect of spontaneous porto-systemic shunt embolization (SPSE) over HE and its long-term evolution. Material and Methods: Retrospective analysis of 11 patients (91% males) with severe HE non-responsive to medical treatment in whom a SPSE was performed. The grade of HE (employing West Haven score), survival, MELD and Child-Pugh score, ammonia levels, degree of disability (employing the modified Rankin scale (mRs)) were evaluated before and at thirty days after procedure. Results: The most common etiology found was non-alcoholic steatohepatitis (63.6%). A reduction of at least two score points of HE was observed in all patients after thirty days. There was a significant reduction on median (IQR) West Haven score from 3 (2-3) at baseline to 1 (0-1) after the procedure (p < 0.01). Twelve months survival was 63.6%. There was a decrease in median ammonia level from 106.5 (79-165) (ug/dL) to 56 (43-61) after SPSE (p = 0.006). The median mRS score before and after the procedure was 3 (3-5) and 1 (1-2.5), respectively (p < 0.01). Conclusions: According to our experience, SPSE is a feasible and effective alternative to improve HE and functionality of patients with refractory EH.
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    Lipopolysaccharide Activates Toll-Like Receptor 4 and Prevents Cardiac Fibroblast-to-Myofibroblast Differentiation
    (HUMANA PRESS INC, 2017) Bolivar, Samir; Santana, Roxana; Ayala, Pedro; Landaeta, Rodolfo; Boza, Pia; Humeres, Claudio; Vivar, Raul; Munoz, Claudia; Pardo, Viviana; Fernandez, Samuel; Anfossi, Renatto; Diaz Araya, Guillermo
    Bacterial lipopolysaccharide (LPS) is a known ligand of Toll-like receptor 4 (TLR4) which is expressed in cardiac fibroblasts (CF). Differentiation of CF to cardiac myofibroblasts (CMF) is induced by transforming growth factor-beta 1 (TGF-beta 1), increasing alpha-smooth muscle actin (alpha-SMA) expression. In endothelial cells, an antagonist effect between LPS-induced signaling and canonical TGF-beta 1 signaling was described; however, it has not been studied whether in CF and CMF the expression of alpha-SMA induced by TGF-beta 1 is antagonized by LPS and the mechanism involved. In adult rat CF and CMF, alpha-SMA, ERK1/2, Akt, NF-kappa beta, Smad3, and Smad7 protein levels were determined by western blot, TGF-beta isoforms by ELISA, and alpha-SMA stress fibers by immunocytochemistry. CF and CMF secrete the three TGF-beta isoforms, and the secretion levels of TGF-beta 2 was affected by LPS treatment. In CF, LPS treatment decreased the protein levels of alpha-SMA, and this effect was prevented by TAK-242 (TLR4 inhibitor) and LY294002 (Akt inhibitor), but not by BAY 11-7082 (NF-kappa beta inhibitor) and PD98059 (ERK1/2 inhibitor). TGF-beta 1 increased alpha-SMA protein levels in CF, and LPS prevented partially this effect. In addition, in CMF alpha-SMA protein levels were decreased by LPS treatment, which was abolished by TAK-242. Finally, in CF LPS decreased the p-Smad3 phosphorylation and increased the Smad7 protein levels. LPS treatment prevents the CF-to-CMF differentiation and reverses the CMF phenotype induced by TGF-beta 1, through decreasing p-Smad3 and increasing Smad7 protein levels.