RESUMEN
Metabolic syndrome (MS) and chronic hepatitis C (CHC) are prevalent diseases with many serious and fatal outcomes. Many of these outcomes are attributed to increased level of TNF-α which causes insulin resistance (IR), liver damage, increased incidence and mortality of hepatorenal syndrome (HRS), liver fibrosis and nonalcoholic steatohepatitis (NASH). So, an approach that depends on reducing the TNF-α levels is considered a reasonable method to help treat these conditions. Putting together the available data in the previous literature about pentoxifylline (PTX) would highly suggest that this drug is perfect for managing these conditions. Through its inhibitory effect on the production of TNF-α, it would improve the IR state and improve MS. It would also improve the liver condition in NASH which is associated with IR. And by its effect on enhancing the blood flow and decreasing its viscosity, it could also have a protective role against the cardiovascular incidents that develop with IR and MS. In CHC, it would decrease the IR that is associated with HCV infection and this would subsequently increase the response to the antiviral therapy and reduce the liver damage. It was also proven to decrease the incidence and mortality of HRS that develops in cirrhosis. PTX also has anti-fibrotic effects which can stop the liver fibrosis. The PTX effect should be evaluated experimentally and by clinical trials on patients as it can be a breakthrough in the management of MS and CHC. Such an affordable drug would remarkably decrease the expense of the management of these conditions, and would reduce the morbidity and mortality in those patients, which would indirectly increase the productivity in the societies that have a high prevalence of these diseases.
Asunto(s)
Hepatitis C Crónica/complicaciones , Hepatitis C Crónica/tratamiento farmacológico , Síndrome Metabólico/complicaciones , Síndrome Metabólico/tratamiento farmacológico , Pentoxifilina/uso terapéutico , Antivirales/uso terapéutico , Enfermedades Cardiovasculares/fisiopatología , Humanos , Resistencia a la Insulina/fisiología , Cirrosis Hepática/tratamiento farmacológico , Cirrosis Hepática/patología , Enfermedad del Hígado Graso no Alcohólico/tratamiento farmacológico , Prevalencia , Resultado del Tratamiento , Factor de Necrosis Tumoral alfa/metabolismo , Vasodilatadores/uso terapéutico , ViscosidadRESUMEN
It is well known that chronic hepatitis C is associated with insulin resistance and metabolic syndrome which are risk factors for atherosclerosis and coronary heart disease. As a result, chronic hepatitis C might be thought, through its association with metabolic syndrome, to increase the risk of myocardial infarction. However, unexpectedly it was found that HCV infection is not associated with an increased risk of myocardial infarction. We are providing here an hypothesis of the mechanism through which HCV infection does not increase the risk for myocardial infarction and also may be protecting against some cardiovascular risks that typically develop in many patients with metabolic syndrome who do not have chronic hepatitis C. The suggested mechanism includes factors that are normal consequences of chronic hepatitis, such as: significant decrease in cholesterol and LDL levels; defected blood clotting system; impaired myocardial function; decreased venous return and central venous pressure; increased nitric oxide and TNF alpha levels; and diminished cardiac beta receptors signal transduction. All these factors contribute to a protective effect against cardiac ischemia and coronary heart disease. We suggest further studies to investigate this hypothesis.