Metadoxine accelerates fatty liver recovery in alcoholic patients: results of a randomized double-blind, placebo-control trial

Caballería, Joan; Parés, Albert; Brú, Concepció; Mercader, J.M.; Plaza, A García; Caballería, Llorenç; Clemente, G.; Rodrigo, Luı́s; Rodés, Joan

doi:10.1016/s0168-8278(98)80202-x

Cited by 69 publications

(44 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Metadoxine has proved efficacious in the treatment of alcoholic liver steatosis, as shown by biochemical data and echographical signs (110). This drug restores hepatic glutathione concentrations and acts as an antifibrogenic agent.…”

Section: Cytoprotective Agents and Antioxidantsmentioning

confidence: 97%

Approach to the Pathogenesis and Treatment of Nonalcoholic Steatohepatitis

et al. 2004

View full text Add to dashboard Cite

Nonalcoholic steatohepatitis (NASH) represents an advanced stage of fatty liver disease developed in the absence of alcohol abuse. Its increasing prevalence in western countries, the diagnostic difficulties by noninvasive tests, and the possibility of progression to advanced fibrosis and even cirrhosis make NASH a challenge for hepatologists. NASH is frequently associated with type 2 diabetes and the metabolic syndrome, and several genetic and acquired factors are involved in its pathogenesis. Insulin resistance plays a central role in the development of a steatotic liver, which becomes vulnerable to additional injuries. Several cyclic mechanisms leading to selfenhancement of insulin resistance and hepatic accumulation of fat have been recently identified. Excess intracellular fatty acids, oxidant stress, tumor necrosis factor-␣, and mitochondrial dysfunction are causes of hepatocellular injury, thereby leading to disease progression and to the establishment of NASH. Intestinal bacterial overgrowth also plays a role, by increasing production of endogenous ethanol and proinflammatory cytokines. Therapeutic strategies aimed at modulating insulin resistance, normalizing lipoprotein metabolism, and downregulating inflammatory mediators with probiotics have promising potential. Diabetes Care 27:2057-2066, 2004N onalcoholic steatohepatitis (NASH) is a liver disease characterized by steatosis and periportal and lobular inflammation. In its initial phases, during which fat accumulates in the liver, no clinical symptoms are evident. In advanced stages, fibrosis (eventually progressing to established cirrhosis in some patients) is detectable histologically, along with a mixed inflammatory cell infiltrate, glycogen nuclei, and Mallory's hyaline (1). Because its adequate diagnosis requires histological evaluation of the liver, the prevalence of NASH is probably underestimated. Nonalcoholic fatty liver disease has been suggested to be the most common cause of chronic liver disease in the U.S., with a suggested incidence of 10 -24% in the general population and probably similar figures in Europe and Japan (2,3).Two types of NASH exist: primary NASH (which is associated with metabolic syndrome-related conditions, such as obesity, type 2 diabetes, and hyperlipemia) and secondary NASH (which occurs after obesity-related intestinal surgery, rapid weight loss in the obese, total parenteral nutrition, treatment with drugs such as amiodarone or perhexiline maleate, lipodystrophy, or Wilson's disease). Although many aspects of the disease are common to both presentations, this short review focuses mainly on the pathogenesis of primary NASH.The actual prevalence of NASH in type 2 diabetes and obesity is unknown. It is estimated that 75% of type 2 diabetic patients present some form of nonalcoholic fatty liver of different degrees. An association of NASH with hyperinsulinemia, as well as with clinical features of insulin resistance, has frequently been reported (4 -9). As far as obesity is regarded, steatosis has been reported in 70% o...

show abstract

Section: Cytoprotective Agents and Antioxidantsmentioning

confidence: 97%

Approach to the Pathogenesis and Treatment of Nonalcoholic Steatohepatitis

et al. 2004

View full text Add to dashboard Cite

show abstract

“…These data support early preclinical studies on ethanol-exposed rats, where pyridoxidine reversed the reduction in the apoenzyme for tryptophan pyrrolase caused by chronic ethanol exposure (Ragusa et al, 1980). Notably, clinical studies support a role of metadoxine in reducing alcohol-related tissue damage, specifically in alcoholic liver disease (Higuera-de la Tijera et al, 2015; Caballeria et al, 1998). …”

Section: Medication Development For Aud By Using Ethanol-drug Interacmentioning

confidence: 99%

Altering ethanol pharmacokinetics to treat alcohol use disorder: Can you teach an old dog new tricks?

et al. 2017

View full text Add to dashboard Cite

Disulfiram was the first pharmacotherapy approved to treat alcohol use disorder (AUD) in the 1950s. Disulfiram alters ethanol pharmacokinetics (PK) and causes uncomfortable reactions (e.g.: headache, tachycardia, nausea, flushing and hypotension) when alcohol is consumed. Subsequently, a better understanding of the neurobiological pathways involved in AUD led to the development of other medications (e.g.: naltrexone and acamprosate) to treat AUD. These neurobiological-based medications act on AUD-related phenotypes including craving, stress, and/or withdrawal. The original approach to treat AUD, by altering ethanol PK has been much less investigated. Recent research on ethanol PK has shed light on the mechanisms of action underlying AUD and how some medications that alter ethanol PK may be helpful in treating AUD. This review summarizes and discusses the complex PK of ethanol, and proposes that altering ethanol PK via novel pharmacological approaches may be a viable approach to treat AUD.

show abstract

“…En cuanto al manejo de la lípidos hepática el uso de metadoxina ocasionó en el presente caso una disminución de la ictericia, debido a que su mecanismo de acción es el antagonismo de la peroxidación lipídica de las células hepáticas 10 , además la metadoxina actúa específicamente en los sistemas neurotransmisores, aumentando la liberación de GABA y acetilcolina, que en especial este último cumple una función importantísima en los procesos de vaciamiento de la vesícula biliar 6,10 , obteniendo un efecto colerético y colagogo muy positivo, además de evitar los daños mitocondriales en los hepatocitos, aunque le fármaco se ha descrito como uno de los tratamientos de elección en la lipidosis alcohólica 7 , no hay muchos reportes de su efectividad en la especie felina, la dosis recomendada es un inferencia de la humana entre 5-10 mg/kg cada 8-12 horas 1, 2, 17 , para el presente los autores usaron la dosis mayor de 10 mg/kg, que corresponde a la dosis descrita para humanos 10 . Además del tratamiento con metadoxina, se utilizó terapia conjunta con otro colerético y colagogo, que en este caso fue el ácido orótico y la oxipurina, el cual aunque no tiene un mecanismo descrito produce un incremento de la excreción de biliar, contrae la vesícula biliar y aumenta el efecto enzimático, lo cual fue descrito por Forbes y Neale en 1936, encontrando un efecto verdaderamente antinecrótico 6,10 .…”

Section: A R T í C U L O R E T R a C T A D Ounclassified

Manejo terapéutico de lipidosis hepática felina por Mycoplasma haemofelis

Molina

Pacheco²

2016

Ces. Med. Vet. Zootec.

View full text Add to dashboard Cite

con la excelencia Rcsol11ci6n del Minísterio de EduciJCión N.icionol No. I 37 I del 11 de nw:o de 1007 unpresos o electrónicos. La publicación del articulo duplicado es simultánea o subsiguiente al artículo original, se realiza por los mismos autores y sin el conocimiento de los redactores de las revistas implicadas".De otro lado, se evidenció en la tabla 2 una manipulación deliberada de los datos de las pruebas de la química sanguínea del paciente, dado que al día cero de su evaluación las cifras difieren ostensiblemente en ambos textos, lo que permitió a los autores concluir que dichas pruebas "demuestran alteraciones hepáticas dicientes, tanto de la estructura como de la.función" (Revista CES MVZ); y en el otro artículo: "no demuestran alteraciones hepáticas"

show abstract

Metadoxine accelerates fatty liver recovery in alcoholic patients: results of a randomized double-blind, placebo-control trial

Cited by 69 publications

References 28 publications

Approach to the Pathogenesis and Treatment of Nonalcoholic Steatohepatitis

Approach to the Pathogenesis and Treatment of Nonalcoholic Steatohepatitis

Altering ethanol pharmacokinetics to treat alcohol use disorder: Can you teach an old dog new tricks?

Manejo terapéutico de lipidosis hepática felina por Mycoplasma haemofelis

Contact Info

Product

Resources

About