Características clínicas y demográficas de pacientes con cirrosis hepática, Hospital Dr. Gustavo Nelson Collado Ríos, Chitré, Enero-Diciembre 2019.

Introducción La cirrosis es un padecimiento irreversible, de elevada mortalidad y de etiología variada, siendo las causas más asociadas: abuso de alcohol, hepatitis por virus B y C y hepatopatías autoinmunes. Objetivo Describir las características clínicas y demográficas de los pacientes con cirrosis hepática en el Hospital Gustavo Nelson Collado Ríos. Enero- Diciembre 2019. Metodología Se realizó un estudio observacional, descriptivo y retrospectivo, para lo cual se revisaron 42 expedientes clínicos de pacientes con cirrosis hepática que acudieron a sus citas con el servicio de Gastroenterología en el año 2019. Resultados El grupo de edad con mayor número de casos fue 60-69 años con predominio del género femenino. Los factores asociados más frecuentes fueron diabetes mellitus 2 (62%), sobrepeso (38%), obesidad (33%), hábito de alcohol (19%), hepatopatías autoinmunes (12%) y virus de la hepatitis B (7%). Se calculó una letalidad de 20% para esta cohorte, una mediana de sobrevida de 2 años para los pacientes vivos al momento del estudio y una mediana de sobrevida de 18 meses para los pacientes fallecidos por complicaciones de cirrosis en el año 2019. Conclusión en las provincias centrales de Panamá, vemos una tendencia a la disminución de casos de cirrosis por etiología alcohólica y viral, con aumento de enfermedades metabólicas predominantemente en el género femenino que provocan lesión hepática a largo plazo. La cirrosis continúa siendo una enfermedad de alta letalidad; sin embargo con una sobrevida que sobrepasa los 2 años si se mantiene al paciente compensado.

Remodeling of Mitochondrial Plasticity: The Key Switch from NAFLD/NASH to HCC

Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver and the third-leading cause of cancer-related mortality. Currently, the global burden of nonalcoholic fatty liver disease (NAFLD) has dramatically overcome both viral and alcohol hepatitis, thus becoming the main cause of HCC incidence. NAFLD pathogenesis is severely influenced by lifestyle and genetic predisposition. Mitochondria are highly dynamic organelles that may adapt in response to environment, genetics and epigenetics in the liver (“mitochondrial plasticity”). Mounting evidence highlights that mitochondrial dysfunction due to loss of mitochondrial flexibility may arise before overt NAFLD, and from the early stages of liver injury. Mitochondrial failure promotes not only hepatocellular damage, but also release signals (mito-DAMPs), which trigger inflammation and fibrosis, generating an adverse microenvironment in which several hepatocytes select anti-apoptotic programs and mutations that may allow survival and proliferation. Furthermore, one of the key events in malignant hepatocytes is represented by the remodeling of glucidic–lipidic metabolism combined with the reprogramming of mitochondrial functions, optimized to deal with energy demand. In sum, this review will discuss how mitochondrial defects may be translated into causative explanations of NAFLD-driven HCC, emphasizing future directions for research and for the development of potential preventive or curative strategies.

Remodeling of Mitochondrial Plasticity: The Key Switch from NAFLD/NASH to HCC

Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver and the third-leading cause of cancer-related mortality. Currently, the global burden of nonalcoholic fatty liver disease (NAFLD) has dramatically overcome both viral and alcohol hepatitis thus becoming the main cause of HCC incidence. NAFLD pathogenesis is severely influenced by lifestyle and genetic predisposition. Mitochondria are highly dynamic organelles which may adapt in response to environment, genetics and epigenetics in the liver (“mitochondrial plasticity”). Mounting evidence highlighted that mitochondrial dysfunction due to loss of mitochondrial flexibility, may arise before overt NAFLD and since the early stages of liver injury. Mitochondrial failure not only promotes hepatocellular damage, but also release signals (mito-DAMPs) which trigger inflammation and fibrosis, generating an adverse microenvironment in which several hepatocytes select anti-apoptotic programs and mutations that may allow survival and proliferation. Furthermore, one of the key events in malignant hepatocytes is represented by remodeling of glucidic-lipidic metabolism combined to reprogramming of mitochondrial functions, optimized to deal with energy demand. In sum, this review will discuss how mitochondrial defects may be translated into causative explanations of NAFLD-driven HCC, emphasizing future directions for research purposes and for development of potential preventive or curative strategies.

Hepatotoxicidad inducida por glucosamina-condroitina en un hospital público de Lima (Perú): reporte de un caso

En el cuerpo humano tenemos glucosamina y condroitina de forma natural. Estas sustancias constituyen un componente importante del sistema cartilaginoso. Como medicamentos, tienen múltiples indicaciones clínicas, principalmente la osteoartritis. La hepatotoxicidad inducida por estas biomoléculas es infrecuente, pues cuentan solo con reportes de casos aislados en la literatura mundial. En este trabajo, presentamos el caso de una paciente con una lesión hepática inducida por glucosamina-condroitina del tipo hepatocelular, que fue admitida en el hospital por causa de una sintomatología respiratoria y malestar general. En ella, se destacó una marcada hipertransaminasemia durante los exámenes de laboratorio. Asimismo, se descartaron etiologías como el alcohol, hepatitis virales y hepatopatías autoinmunes, principalmente. De igual forma, no se llegó a evidenciar una enfermedad hepática crónica mediante la ecografía abdominal. Al suspenderse el medicamento, se observó una disminución considerable de la hipertransaminasemia luego de 1 semana, y una mejoría total de esta a los 2 meses del alta hospitalaria. Este caso se añade a los pocos reportados a nivel mundial y cobra una importancia relevante para la publicación de posteriores estudios sistemáticos que aclaren el panorama de esta enfermedad.

Mangiferin improves hepatic damage-associated molecular patterns, lipid metabolic disorder and mitochondrial dysfunction in alcohol hepatitis rats

Mangiferin ameliorated the progression of AH by regulating the metabolic network associated with damage-associated molecular patterns, lipid metabolic disorder and mitochondrial dysfunction in AH rats.

Diagnosa Penyakit Hepatitis Menggunakan Metode Weighted Product

Hepatitis is an inflammatory process in the liver tissue. Hepatitis in lay language is often referred to as liver or jaundice. Viral hepatitis infection can develop into cirrhosis or hardening of the liver even liver cancer, inflammation / inflammation and injury to the liver due to hepatic reactions to various conditions, especially viruses, drugs and alcohol. Hepatitis Diagnosis Expert System has been developed with a weighted product method. The weight product method diverts the results of the assessment of each attribute. The results of these multiplications have not been meaningful if they have not been compared with standard values. The weight for the benefit attribute functions as a positive power in the multiplication process, while the cost weight functions as a negative power multiplying the attribute value of each symptom that has been weighted for.From the results of the trials that have been carried out the system has been able to diagnose hepatitis A, B, C, D, E based on the symptoms entered by the patient.