Vol. 12. Núm. 11.
Páginas 597-605 (Mayo 2016)

Actualización
Cirrosis hepática

Hepatic cirrhosis

D. RincónaR. Bañaresab
Doi : https://10.1016/j.med.2016.05.010
Opciones
Resumen
Concepto

La cirrosis es un proceso caracterizado por la aparición progresiva de zonas de extinción del parénquima hepático, sustituidas por fibrosis, con desarrollo de nódulos de regeneración y alteración de la arquitectura normal del hígado.

Etiopatogenia

Sus causas más frecuentes en nuestro medio son el abuso de alcohol y la hepatitis crónica por virus C, con una importancia creciente de la esteatohepatitis no alcohólica.

Evolución y tratamiento

El desarrollo progresivo de hipertensión portal constituye el acontecimiento fisiopatológico clave en su evolución, y es el factor de riesgo más relevante para la descompensación de la cirrosis; por el contrario, la mejoría del grado de hipertensión portal como consecuencia del tratamiento etiológico o vasoactivo reduce el riesgo de complicaciones. Bajo determinadas condiciones, sobre todo el adecuado tratamiento de la enfermedad desencadenante, se puede esperar un cierto grado de reversibilidad en todos los niveles (histológico, hemodinámico y clínico), que es variable en función del grado de evolución de la cirrosis.

Palabras clave
Cirrosis
Hipertensión portal
Varices esofágicas
Fibroelastografía
Abstract
Concept

Cirrhosis is a process characterised by the progressive appearance of areas of hepatic parenchymal extinction, substituted by fibrosis, with the development of regenerative nodules and alterations in the normal liver architecture.

Aetiopathogenesis

The most common causes of cirrhosis in our community are alcohol abuse and chronic hepatitis caused by the C virus, with significant growth of nonalcoholic steatohepatitis.

Progression and treatment

The progressive development of portal hypertension constitutes the key pathophysiological event in its progression and is the most relevant risk factor for decompensated cirrhosis. Conversely, the improvement in portal hypertension as a result of aetiological or vasoactive treatment reduces the risk of complications. Under certain conditions, especially proper treatment of the triggering disease, a certain degree of reversibility can be expected at all levels (histological, haemodynamic and clinical), which varies according to the how much the cirrhosis has progressed.

Keywords
Cirrhosis
Portal hypertension
Oesophageal varices
Fibroelastography

Identifíquese

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Bibliografía
[1]
M.
201605270039175618
201605270039175619
Pinzani, M. Rosselli, M. Zuckermann.
Liver cirrhosis.
Best Pract Res Clin Gastroenterol, (2011), 25 pp. 281-290
[2]
P.P. Anthony, K.G. Ishak, N.C. Nayak, H.E. Poulsen, P.J. Scheuer, L.H. Sobin.
The morphology of cirrhosis. Recommendations on definition, nomenclature, and classification by a working group sponsored by the World Health Organization.
J Clin Pathol, (1978), 31 pp. 395-414
[3]
V.J. Desmet, T. Roskams.
Cirrhosis reversal: a duel between dogma and myth.
J Hepatol, (2004), 40 pp. 860-867
[4]
A.M. Rappaport, P.J. MacPhee, M.M. Fisher, M.J. Phillips.
The scarring of the liver acini (Cirrhosis). Tridimensional and microcirculatory considerations.
Virchows Arch A Pathol Anat Histopathol, (1983), 402 pp. 107-137
[5]
J.C. García-Pagan, J. Gracía-Sancho, J. Bosch.
Functional aspects on the pathophysiology of portal hypertension in cirrhosis.
J Hepatol, (2012), 57 pp. 458-461
[6]
C. Villanueva, A. Albillos, J. Genescà, J.G. Abraldes, J.L. Calleja, C. Aracil, R. Bañares, et al.
Development of circulation and response to ⊠-blockers in compensated cirrhosis with portal hypertension.
Hepatology, (2016), 63 pp. 197-206
[7]
E. Sola, P. Gines.
Renal and circulatory dysfunction in cirrhosis: current management and future perspectives.
J Hepatol, (2010), 53 pp. 1135-1145
[8]
R.W. Schrier, V. Arroyo, M. Bernardi, M. Epstein, J.H. Henriksen, J. Rodes.
Peripheral arterial vasodilation hypothesis: a proposal for the initiation of renal sodium and water retention in cirrhosis.
Hepatology, (1988), 8 pp. 1151-1157
[9]
R.W. Schrier, M. Niederberger, A. Weigert, P. Gines.
Peripheral arterial vasodilatation: determinant of functional spectrum of cirrhosis.
Semin Liver Dis., (1994), 14 pp. 14-22
[10]
D. Rincon, O. Lo Iacono, M. Tejedor, A. Hernando, C. Ripoll, M.V. Catalina, et al.
Prognostic value of hepatic venous pressure gradient in patients with compensated chronic hepatitis C-related cirrhosis.
Scand J Gastroenterol, (2013), 48 pp. 487-495
[11]
G. D’Amico, G. Garcia-Tsao, L. Pagliaro.
Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies.
J Hepatol, (2006), 44 pp. 217-231
[12]
R. de Franchis.
Evolving consensus in portal hypertension. Report of the Baveno IV consensus workshop on methodology of diagnosis and therapy in portal hypertension.
J Hepatol, (2005), 43 pp. 167-176
[13]
R.M. Morillas, G. D’Amico, C. Villanueva, A. Albillos, J. Marti¿nez, A.K. Burroughs, et al.
Estadios clínicos de la cirrosis: estudio multicéntrico de cohorte con 1.858 pacientes.
Gastroenterol Hepatol, (2011), 34 pp. 179
[14]
R.
2016052700391756110
2016052700391756111
Moreau, R. Jalan, P. Gines, M. Pavesi, P. Angeli, J. Cordoba, et al.
Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis.
Gastroenterology, (2013), 144 pp. 1426-1437
[15]
J.L. Vincent, R. Moreno, J. Takala, S. Willatts, A. De Mendonca, H. Bruining, et al.
The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine.
Intensive Care Med., (1996), 22 pp. 707-710
[16]
R.J.
2016052700391756112
2016052700391756113
Groszmann, G. García-Tsao, J. Bosch, N.D. Grace, A.K. Burroughs, R. Planas, et al.
Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis.
N Engl J Med., (2005), 353 pp. 2254-2261
[17]
C. Ripoll, R. Groszmann, G. García-Tsao, N. Grace, A. Burroughs, R. Planas, et al.
Hepatic venous pressure gradient predicts clinical decompensation in patients with compensated cirrhosis.
Gastroenterology, (2007), 133 pp. 481-488
[18]
A.
2016052700391756114
2016052700391756115
Berzigotti, S. Seijo, U. Arena, J.G. Abraldes, F. Vizzutti, J.C. Garcia-Pagan, et al.
Elastography, spleen size, and platelet count identify portal hypertension in patients with compensated cirrhosis.
Gastroenterology, (2013), 144 pp. 102-111
[19]
J. Vorobioff, R.J. Groszmann, E. Picabea, M. Gamen, R. Villavicencio, J. Bordato, et al.
Prognostic value of hepatic venous pressure gradient measurements in alcoholic cirrhosis: a 10-year prospective study.
Gastroenterology, (1996), 111 pp. 701-709
[20]
G.
2016052700391756116
D’Amico, J.C. García-Pagan, A. Luca, J. Bosch.
Hepatic vein pressure gradient reduction and prevention of variceal bleeding in cirrhosis: a systematic review.
Gastroenterology, (2006), 131 pp. 1611-1624
[21]
A.
2016052700391756117
2016052700391756118
Albillos, R. Banares, M. González, C. Ripoll, R. Gonzalez, M.V. Catalina, et al.
Value of the hepatic venous pressure gradient to monitor drug therapy for portal hypertension: a meta-analysis.
Am J Gastroenterol, (2007), 102 pp. 1116-1126
[22]
C.
2016052700391756119
2016052700391756120
Villanueva, J. Minana, J. Ortiz, A. Gallego, G. Soriano, X. Torras, et al.
Endoscopic ligation compared with combined treatment with nadolol and isosorbide mononitrate to prevent recurrent variceal bleeding.
N Engl J Med., (2001), 345 pp. 647-655
[23]
J.G. Abraldes, I. Tarantino, J. Turnes, J.C. García-Pagan, J. Rodes, J. Bosch.
Hemodynamic response to pharmacological treatment of portal hypertension and long-term prognosis of cirrhosis.
Hepatology, (2003), 37 pp. 902-908
[24]
S. Nagula, D. Jain, R.J. Groszmann, G. García-Tsao.
Histological-hemodynamic correlation in cirrhosis-a histological classification of the severity of cirrhosis.
J Hepatol, (2006), 44 pp. 111-117
[25]
S. Sethasine, D. Jain, R.J. Groszmann, G. García-Tsao.
Quantitative histological-hemodynamic correlations in cirrhosis.
Hepatology, (2012), 55 pp. 1146-1153
[26]
M.Y. Kim, M.Y. Cho, S.K. Baik, H.J. Park, H.K. Jeon, C.K. Im, et al.
Histological subclassification of cirrhosis using the Laennec fibrosis scoring system correlates with clinical stage and grade of portal hypertension.
J Hepatol, (2011), 55 pp. 1004-1009
[27]
A.E. Stueck, I.R. Wanless.
Hepatocyte buds derived from progenitor cells repopulate regions of parenchymal extinction in human cirrhosis.
Hepatology, (2015), 61 pp. 1696-1707
[28]
S. Manolakopoulos, C. Triantos, J. Theodoropoulos, J. Vlachogiannakos, A. Kougioumtzan, G. Papatheodoridis, et al.
Antiviral therapy reduces portal pressure in patients with cirrhosis due to HBeAg-negative chronic hepatitis B and significant portal hypertension.
J Hepatol, (2009), 51 pp. 468-474
[29]
D. Rincon, C. Ripoll, O. Lo Iacono, M. Salcedo, M.V. Catalina, E. Álvarez, et al.
Antiviral therapy decreases hepatic venous pressure gradient in patients with chronic hepatitis C and advanced fibrosis.
Am J Gastroenterol, (2006), 101 pp. 2269-2274
[30]
Y.F. Liaw, J.J. Sung, W.C. Chow, G. Farrell, C.Z. Lee, H. Yuen, et al.
Lamivudine for patients with chronic hepatitis B and advanced liver disease.
N Engl J Med., (2004), 351 pp. 1521-1531
[31]
S. Bruno, T. Stroffolini, M. Colombo, S. Bollani, L. Benvegnu, G. Mazzella, et al.
Sustained virological response to interferon-alpha is associated with improved outcome in HCV-related cirrhosis: a retrospective study.
Hepatology, (2007), 45 pp. 579-587
[32]
C.M. Fernández-Rodríguez, S. Alonso, S.M. Martínez, X. Forns, J.M. Sánchez-Tapias, D. Rincon, et al.
Peginterferon plus ribavirin and sustained virological response in HCV-related cirrhosis: outcomes and factors predicting response.
Am J Gastroenterol, (2010), 105 pp. 2164-2172
[33]
P. Jepsen, P. Ott, P.K. Andersen, H.T. Sorensen, H. Vilstrup.
Clinical course of alcoholic liver cirrhosis: a Danish population-based cohort study.
Hepatology, (2010), 51 pp. 1675-1682
[34]
A.A. Qamar, N.D. Grace, R.J. Groszmann, G. García-Tsao, J. Bosch, A.K. Burroughs, et al.
Platelet count is not a predictor of the presence or development of gastroesophageal varices in cirrhosis.
Hepatology, (2008), 47 pp. 153-159
[35]
J. Bosch.
Towards the non-invasive diagnosis of cirrhosis: the nuts-cirrhosis connection.
[36]
European Association for Study of L, Asociacion Latinoamericana para el Estudio del H. EASL-ALEH Clinical Practice Guidelines: Non-invasive tests for evaluation of liver disease severity and prognosis. J Hepatol. 2015;63(1):237-64.
[37]
D.C. Rockey, S.H. Caldwell, Z.D. Goodman, R.C. Nelson, A.D. Smith.
American Association for the Study of Liver D. Liver biopsy.
Hepatology, (2009), 49 pp. 1017-1044
[38]
C. Ripoll, P. Lastra, D. Rincon, V. Catalina, R. Banares.
Comparison of MELD, HVPG, and their changes to predict clinically relevant endpoints in cirrhosis.
Scand J Gastroenterol, (2012), 47 pp. 204-211