Browsing by Author "Boza Wilson, Camilo"

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    Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease
    (Elsevier España, 2011) Espino Espino, Alberto Antonio; Villagran Torres, Andrea Alejandra; Vollrath Reyes, Valeska Yolanda; Hanckes Mayo, Maria Paulina; Salas Ocaranza, Roberto Ignacio; Farah Samaan, Andrea Catherina; Solis, Nancy; Pizarro Rojas, Margarita Alicia; Escalona Perez, Alex Gamaliel; Boza Wilson, Camilo; Perez, Gustavo; Carrasco, Gonzalo; Padilla, Orlando; Francisco Miguel, Juan; Nervi Oddone, Flavio; Chavez Tapia, Norberto C.; Arab Verdugo, Juan Pablo; Alvarez Lobos, Manuel Marcelo; Arrese Jimenez, Marco Antonio; Riquelme Perez, Arnoldo Javier
    Background. The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis. Aim. To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients. Material and methods. Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism. Results. BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 +/- 4.82) compared to controls (14.26 +/- 11.4; p < 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 +/- 4.35) compared to patients without liver fibrosis (10.61 +/- 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6). Conclusions. Morbidly obese patients had significantly Lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients.