Browsing by Author "Arrese Jiménez, Marco Antonio"

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    A Precision Medicine Guided Approach to the Utilization of Biomarkers in MASLD
    (2024) Thakral, Nimish; Desalegn, Hailemichael; Diaz Piga, Luis Antonio; Cabrera, Daniel; Loomba, Rohit; Arrese Jiménez, Marco Antonio; Arab Verdugo, Juan Pablo
    The new nomenclature of metabolic dysfunction-associated steatotic liver disease (MASLD) emphasizes a positive diagnosis based on cardiometabolic risk factors. This definition is not only less stigmatizing but also allows for subclassification and stratification, thereby addressing the heterogeneity of what was historically referred to as nonalcoholic fatty liver disease. The heterogeneity within this spectrum is influenced by several factors which include but are not limited to demographic/dietary factors, the amount of alcohol use and drinking patterns, metabolic status, gut microbiome, genetic predisposition together with epigenetic factors. The net effect of this dynamic and intricate system-level interaction is reflected in the phenotypic presentation of MASLD. Therefore, the application of precision medicine in this scenario aims at complex phenotyping with consequent individual risk prediction, development of individualized preventive strategies, and improvements in the clinical trial designs. In this review, we aim to highlight the importance of precision medicine approaches in MASLD, including the use of novel biomarkers of disease, and its subsequent utilization in future study designs.
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    Direct antivirals for the treatment of chronic hepatitis C virus infection. Experience in 106 patients.
    (2017) Soza Ried, Alejandro; Benítez Gajardo, Carlos Esteban; Barrera Álvarez, Francisco Benjamín; Monrroy Bravo, Hugo Alfonso; Vargas Domínguez, José Ignacio; Arab Verdugo, Juan Pablo; Arrese Jiménez, Marco Antonio; Sarmiento, V.; Fuster, F.
    Background: The availability of direct-acting antivirals (DAA) for the treatment of chronic hepatitis C virus (HCV) infection is just starting to expand in Chile. Aim: To report the initial experience of patients treated with DAA and their evolution after treatment. Material and Methods: Prospective cohort study, from June 2013 to August 2016 of patients treated with DAA for HCV in three clinical centers. The presence of cirrhosis, clinical and laboratory features; adverse events (AE) and post-treatment changes in liver function were evaluated. Sustained viral response at 12 weeks post-treatment (SVR12) was determined. Results: One hundred six patients aged 58 +/- 13 years, 54% males, were included. HCV genotype 1b was present in 88% and 47% had cirrhosis. Treatment regimens were asunaprevir + daclatasvir (DCV) in 17% of patients, paritaprevir / ritonavir / ombitasvir + dasabuvir in 33%, sofosbuvir (SOF) + DCV in 19%, and SOF + ledipasvir in 30%. Twenty five percent of patients used generic drugs. SVR12 was 92.1%, with no differences between generic and brand-name drugs. Serious AE were recorded in 22% of patients, being more common in those with cirrhosis (34% vs 11.5%, p < 0.01). At 12 weeks post-treatment follow-up, there was a decrease in aminotransferase values (p < 0.01), improvement in Child-Pugh score (5.9 vs. 5.5, p = 0.03) and decreased presence of ascites (p = 0.02). Conclusions: In our setting, DAA for HCV was highly effective and safe in non-cirrhotic patients. Hepatic function and inflammation improved at 12 weeks of follow-up. AE were common in patients with cirrhosis, suggesting that these patients should be treated by experienced teams. Generic drugs had similar effectiveness compared to originals.
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    El síndrome metabólico: de factor agravante a principal factor de riesgo patogénico en diversas enfermedades crónicas
    (2010) Von Bernhardi Montgomery, Rommy Edth B.; Zanlungo Matsuhiro, Silvana; Arrese Jiménez, Marco Antonio; Arteaga Llona, Antonio Alberto; Rigotti Rivera, Attilio Gianpietro
    In recent years, a rapidly increasing number of studies have focused on the association between metabolic syndrome and several chronic diseases. However, it is difficult to determine a well defined pathogenic relationship, due to the etiological heterogeneity and comorbidities of these diseases. Research efforts are aiming to identify the convergent biological mechanisms that mediate the effects of hyperinsulinemia, hyperglycemia, dyslipidemia, and hypertension. All these conditions define the metabolic syndrome, that increases the risk for several diseases. The knowledge of these biological mechanisms associated with this syndrome will elucidate the pathogenic association between a variety of chronic diseases, including its pathogenic link with cardiovascular diseases and the most common forms of dementia. The development of new therapeutic and preventive strategies for these diseases will be a corollary of this research.
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    Emerging Drug Therapies for Metabolic Dysfunction-Associated Steatotic Liver Disease: A Glimpse into the Horizon
    (2024) Arnold Álvarez, Jorge Ignacio; Idalsoaga Ferrer, Francisco Javier; Diaz Piga, Luis Antonio; Cabrera García, Daniel Alejandro; Barrera Álvarez, Francisco Benjamín; Arab Verdugo, Juan Pablo; Arrese Jiménez, Marco Antonio
    Purpose of Review Metabolic dysfunction–associated steatotic liver disease (MASLD) and its aggressive form, metabolic dysfunction-associated steatohepatitis (MASH), are highly prevalent and can lead to fibrosis, cirrhosis, hepatocellular carcinoma, and liver failure. Currently, there is no approved pharmacological treatment for MASLD. In this review, we aim to summarize recent data on therapeutic agents under study in phase 2 and 3 trials.Recent FindingsBuilding on a better understanding of MASLD/MASH pathophysiology, a myriad of drugs has been developed. Recent results from clinical trials show promise, with some candidates demonstrating positive outcomes in phase 3 trials that are predictably expected to be approved in the near future. Notably, resmetirom, a thyroid receptor β agonist, is likely to be approved in 2024.SummaryIn the coming years, results from several landmark trials will be available and will likely provide options to prevent progression to cirrhosis and adverse liver outcomes in patients with MASLD/MASH.
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    Hypoadiponectinemia and its Association with Liver Fibrosis in Morbidly Obese Patients
    (2010) Nazal Ortiz, Leyla María; Riquelme Pérez, Arnoldo Javier; Solís López, Nancy De Las Mercedes; Pizarro Rojas, Margarita Alicia; Escalona Pérez, Alex Gamaliel; Burotto Pichun, Mauricio Emanuel; Méndez, Juan Ignacio; Saint-Jean, Catalina; Concha Bustos, María José; Giovanni, Stefano; Awruch Diego Ariel; Morales Soto, Arturo Javier; Baudrand Biggs, Rene Felipe; Carrasco Avino, Gonzalo; Domínguez De Landa, María Angelica; Padilla Pérez, Oslando; Espinoza, Manuel; Miquel, Juan Francisco; Nervi Oddone, Flavio; Arrese Jiménez, Marco Antonio
    Reduced serum levels of adiponectin have been associated with insulin resistance and non-alcoholic fatty liver disease (NAFLD). However, the relationship between serum adiponectin levels and hepatic histology in NAFLD is controversial. The aim of this study was to explore associations between plasma adiponectin concentrations and liver histology in morbidly obese patients.", "We conducted a case-control study including obese patients undergoing bariatric surgery and normal controls. Anthropometric, standard biochemical variables as well as plasma adiponectin and leptin levels were determined. Liver biopsy was performed in all patients at the time of surgery.", "Seventy morbidly obese patients (mean BMI, 40.6 +/- 5.6 kg/m(2)) met the inclusion criteria and were compared with 69 controls (mean BMI, 22.8 +/- 1.6 kg/m(2), p = 0.0001). Thirty patients (43%) had NAFLD and 20 (28%) of them fulfilled the histological criteria for steatohepatitis. Obesity was associated with increased leptin and decreased adiponectin levels. NAFLD patients exhibited decreased levels of serum adiponectin compared with matched controls [median (Q1-Q3), 3.9 (3.2-4.3) vs. 8.6 (6.5-9.2) mu g/mL, p < 0.0001]. In univariate analysis, age, gender, type 2 diabetes mellitus, BMI, HOMA-IR, aspartate aminotransferase (AST), alanine aminotransferase, serum glucose, and adiponectin levels were independently associated with hepatic fibrosis. In multivariate analysis, AST [OR = 1.082 (1.000-1.170)], age [OR = 1.119 (1.023-1.225)], and serum adiponectin levels [OR = 0.529 (0.299-0.936)] were significantly associated with the presence of liver fibrosis.", "NAFLD patients have lower plasma adiponectin concentrations than control subjects. Low adiponectin levels are associated with more severe liver histology. Serum adiponectin may be useful to estimate the severity of liver damage in obese patients with NAFLD.
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    Letter: Potential impact of Helicobacter pylori infection on oesophageal disorders in chronic liver disease—Authors' reply
    (2024) Idalsoaga Ferrer, Francisco Javier; Diaz Piga, Luis Antonio; Ayares Campos, Gustavo Ignacio; Cabrera, Daniel; Chahuan Abde, Javier Nicolas; Monrroy Bravo, Hugo Alfonso; Halawi, Houssam; Arrese Jiménez, Marco Antonio; Arab Verdugo, Juan Pablo
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    [Molecular biology and medicine: basic concepts]
    (1999) Zanlungo Matsuhiro, Silvana; Rigotti Rivera, Attilio Gianpietro; Arrese Jiménez, Marco Antonio
    Through the advancements of molecular genetics, physicians and researchers are in an extraordinary period of study concerning the molecular basis of medicine. Molecular biology is making a tremendous impact on both diagnosis and treatment of diseases through the clinical introduction of molecular methods. These techniques, restricted for many years to basic biological research, include the polymerase chain reaction, DNA and protein electrophoresis, cloning of genes into viral or bacterial vectors and methods to rapidly sequence DNA and identify mutations. In this article the authors attempt to provide basic concepts on these themes for the non-trained physicians in order to help them to understand recent developments and foresee their future implications.
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    Nutrition in Alcohol-Related Liver Disease
    (2022) Ayala-Valverde, María; Arnold Álvarez, Jorge Ignacio; Diaz Piga, Luis Antonio; Idalsoaga Ferrer, Francisco Javier; Arrese Jiménez, Marco Antonio; Arab Verdugo, Juan Pablo
    Purpose of Review Alcohol use represents one of the five major causes of morbimortality globally, and alcohol-related liver disease (ALD) is the most common cause of cirrhosis worldwide. Malnutrition is one of the most frequent complications in ALD and is associated with decreased survival. Additionally, protein-energy malnutrition causes sarcopenia, frailty, and immunosuppression. This review summarizes the diverse mechanisms involved in the pathophysiology of malnutrition in ALD and its management.Recent FindingsMechanisms regarding malnutrition in ALD have been recently described. There is also an important area of interest in patients with overnutrition and sarcopenic obesity. Early assessment of malnutrition is needed so the management and prognosis improve in ALD patients.SummaryMalnutrition worsens disease progression and increases infections and mortality risk, especially in decompensated patients. It is important to have early recognition and management of this ALD complication. It is also essential to stratify a patient’s risk for refeeding syndrome once the supplementation is given since this syndrome can increase morbimortality.
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    Recent insights on the role of cholesterol in non-alcoholic fatty liver disease
    (2015) Argüello Florencio, Graciela Rosalva; Balboa Castillo, Elisa; Arrese Jiménez, Marco Antonio; Zanlungo Matsuhiro, Silvana
    Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of hepatic histopathological changes ranging from non-inflammatory intracellular fat deposition to non-alcoholic steatohepatitis (NASH), which may progress into hepatic fibrosis, cirrhosis, or hepatocellular carcinoma. NAFLD hallmark is the excessive hepatic accumulation of neutral lipids that result from an imbalance between lipid availability and lipid removal. Recent data suggest that disturbed hepatic cholesterol homeostasis and liver free cholesterol (FC) accumulation are relevant to the pathogenesis of NAFLD/NASH. Hepatic FC accumulation in NAFLD results from alterations in intracellular cholesterol transport and from unbalanced cellular cholesterol homeostasis characterized by activation of cholesterol biosynthetic pathways, increased cholesterol de-esterification and attenuation of cholesterol export and bile acid synthesis pathways. FC accumulation leads to liver injury through the activation of intracellular signaling pathways in Kupffer cells (KCs), Stellate cells (HSCs) and hepatocytes. The activation of KCs and HSCs promotes inflammation and fibrogenesis. In addition, FC accumulation in liver mitochondria induces mitochondrial dysfunction, which results in increasing production of reactive oxygen species, and triggers the unfolded protein response in the endoplasmic reticulum (ER) causing ER stress and apoptosis. These events create a vicious circle that contributes to the maintenance of steatosis and promotes ongoing hepatocyte death and liver damage, which in turn may translate into disease progression. In the present review we summarize the current knowledge on dysregulated cholesterol homeostasis in NAFLD and examine the cellular mechanisms of hepatic FC toxicity and its contribution to ongoing liver injury in this disease. The therapeutic implications of this knowledge are also discussed.