Escolar Documentos
Profissional Documentos
Cultura Documentos
Como citar
Rev cubana med v.46 n.1 Ciudad de la Habana ene.-
este artculo
mar. 2007
Resumen
El problema terminolgico
Patogenia
En la diabetes tipo 2, aumentan los cidos grasos libres captados por el hepatocito
que se asocian al mecanismo de la insulinorresistencia. As mismo se incrementa
el CYP2 E1 y puede existir, al mismo tiempo, un sndrome de sobrecrecimiento
bacteriano que provoca un elevado nivel de TNF-a.
Histopatologa
La infiltracin grasa del hgado tiene diferentes grados que van desde la esteatosis
simple, pasan por la esteatohapatitis hasta la fibrosis y/o cirrosis. Cada uno de
ellos puede tener un estadio segn su severidad (porcentaje de hepatocitos afectos)
en leve, moderada y severa.26
El perfil clnico "tpico" es el de una mujer de edad mediana, obesa, con diabetes
tipo 2 o sin ella, dislipidemia e hipertensin.35 En ocasiones, se ha asociado
tambin con algunas drogas, como estrgenos sintticos a altas dosis, metotrexate,
amiodarona y tamoxifeno. La obesidad es, sin duda, la condicin clnica ms
frecuente y se describe en 86 % de los casos.36 Otros estudios han demostrado
que el perfil de pacientes puede ser mucho ms amplio que el inicialmente
planteado. Bacon y otros,37 en una serie de pacientes con EGNAH reportaron que
58 % de los pacientes eran varones, 61 % no eran obesos y 79 % tenan glucemia
y nivel de lpidos, normales. Craig y otros38 reportaron igual frecuencia en
hombres que en mujeres y que slo 40 % de los pacientes eran obesos, 15 %
diabticos y 20 % dislipidmicos.
Enfoque teraputico
Para evitar txicos conocidos que daen al hgado se debe recomendar a los
pacientes tratados que no consuman alcohol, ni drogas hepatotxicas y tratar los
factores condicionantes o asociados a la EGNAH (figura).52
Summary
Fatty liver. Diagnostic and therapeutic approach
The diagnostic and therapeutic approach on fatty liver, proposed in this review,
was made to meet the needs of the practitioner. A theoretical disquisition on the
terminological problem of this syndrome was stated, and the common pathogenic
mechanisms in the different clinical conditions predisposing to suffer from this
health problem, that may appear as a simple hepatic steatosis, but that may also be
the cause of liver cirrhosis leading the patient to a liver transplantation, were
approached. It was considered the importance of hefting the sum of the factors
predisposing the disease, the imaging studies, and the risk markers of the
development of fibrosis before indicating the liver biopsy. The treatment is
intended to reduce the flow of fatty acids to the liver, to protect the hepatocyte
from oxidative mechanisms, to avoid known toxic agents damaging the liver, and
to treat the conditioning or associated factors. An algorithm of care and follow-up
of these patients was suggested.
Referencias bibliogrficas
8. Kotish A, Diehl AM. Animal models of steatosis. Semi Liver Dis. 2001;21:89-
104.
9. Younossi ZM, Diehl AM, Ong JP. Nonalcoholic fatty liver disease: an agenda
for clinical research. Hepatology. 2002;35:746-52.
10. Youssef W, McCullogh AJ. Diabetes Mellitus, Obesity, and hepatic Steatosis.
Sem Gastrointest Dis. 2002;13(1):17- 30.
17. Clouston AD, Jonsson JR, Purdie DM, Macdonald GA, Pandeya N,
Shorthouse C, et al. Steatosis and chronic hepatitis C: analysis of fibrosis and
stellate cell activation. J Hepatol. 2001;34:314-20.
21. Wigg AJ, Roberts.Thomson IC, Dymock RB. The role of small intestinal
bacterial overgrowth, intestinal pereabiliity, endotoxaemia and tumour necrosis
factor alpha in the pathogenesis of nonalcoholic steatohepatitis. Gut. 2001;48:206-
11.
24. Kral JG, Shaffner F, Pierson RN Jr, Wang J. Body fat topography as an
independent predictor of fatty liver. Metabolism. 1993;42:548-51.
25. Diehl AM, Goodman Z, Isask KG. Alcohol-like liver disease in nonalcoholics.
a clinical and histologic comparison with alcohol induced liver injury.
Gastroenterology. 1988;95:1056-62.
27. Bacon BR, Farahvash MJ, Janney CG, Neuschwander-Tetri BA. Nonalcoholic
steatohepatitis: an expanded clinical entity. Gastroenterology. 1994;107:1103-9.
28. Brunt EM. Nonalcoholic Steatohepatitis: definition and Pathology. Sem Liver
Dis. 2001;21(1):3-16.
29. Teli MR, James OF, Burt AD, Bennett MK, Day CP. The natural history of
non-alcoholic fatty liver: a follow-up study. Hepatology. 1995;22:1714-9.
30. Friedman LS, Dienstag JL, Watkins E. Evaluation of blood donors with
elevated serum alanine aminotransferase. Ann Intern Med. 1987;107:137-44.
31. Clain DJ, Lefkowitch JH. Fatty liver disease in morbid obesity. Gastroenterol
Clin North Am. 1987;16(2):239-52.
33. Rantala. AO, Lilja M, Kauma H, Savolainen MJ, Reunanam.A, Kesaniemi YA.
Gamma-glutamyl transpeptidase and the metabolic syndrome. J Int Med
2000;248:230-38.
34. Evan S, Siegelman, Rosen MA. Imaging of Hepatic Seteatosis. Sem Liver Dis.
2001;21(1):71- 80.
39. Powell EE, Cooksley WG, Hanson R, Searle J, Halliday JW, Powell LW. The
natural history of nonalcoholic steatohepatitis: a follow-up study of forty two
patients for up to 21 years. Hepatology. 1990;11:74-80.
40. Rogers DW, Lee CH, Pound DC, Kumar S, Cummings OW, Lumeng L.
Hepatitis C virus does not cause non-alcoholic steatohepatitis. Dig Dis Scl.
1992;37:1644-7.
43. Angulo P, Keach JC, Butts KP. Independent predictors of liver fibrosis in
pacients with nonalcoholic steatohepatitis. Hepatology. 1999;30:421-9.
45. Poonawala A, Nair SP, Thuluvath PJ. Prevalence of obesity and diabetes in
patients with cryptogenic cirrhosis: A case- control study. Hepatology.
1999;32:6889-99.
49. Dixon JB, Bhathal PS, O Brian PE. Non alcoholic steatohepatitis and liver
fibrosis in the severely obese.Gastroenterology. 2001;121:91100.
50. Laurin J, Lindor KD, Crippin JS, Gossard A, Gores GJ, Ludwig J, et al.
Ursodeoxycholic acid or clofibrate in the treatment of non-alcohol-induced
steatohepatitis: a pilot study. Hepatology. 1996; 23:1464-7.
ecimed@infomed.sld.cu