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Inicio Enfermedades Infecciosas y Microbiología Clínica Historia natural y manifestaciones clínicas de la hepatitis B crónica
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Vol. 26. Núm. S7.
La hepatitis B en 2008
Páginas 11-18 (mayo 2008)
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Vol. 26. Núm. S7.
La hepatitis B en 2008
Páginas 11-18 (mayo 2008)
Acceso a texto completo
Historia natural y manifestaciones clínicas de la hepatitis B crónica
Natural history and clinical manifestations of chronic hepatitis B virus
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23681
Miguel Carneiro de Moura
Autor para correspondencia
hsm.cm@mail.telepac.pt

Correspondencia: Clínica Universitária de Gastrenterologia e Instituto de Medicina Molecular. Faculdade de Medicina de Lisboa. Avda. Prof. Egas Moniz 1649-028 Lisboa. Portugal.
, Rui Marinho
Clínica Universitária de Gastrenterologia. Faculdade de Medicina de Lisboa e Hospital de Santa Maria. Lisboa. Portugal
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La infección por virus de la hepatitis B (VHB) representa un importante problema de salud pública en todo el mundo. En las últimas décadas se han producido importantes progresos que han contribuido a una mayor comprensión de la historia natural y las manifestaciones clínicas de esta infección. La fluctuación entre la replicación viral y la respuesta inmunológica del huésped tiene implicaciones en la patogenia y la evolución de la lesión hepática. En el adulto inmunocompetente, la mayor parte de infecciones por VHB se resuelven de forma espontánea, en comparación con una evolución hacia una infección crónica en la mayoría de los recién nacidos. Los pacientes con hepatitis crónica por VHB o hepatitis B crónica pueden presentarse en cuatro fases evolutivas: a) fase de tolerancia inmunológica o inmunotolerancia; b) hepatitis B crónica HBeAg positivo; c) estado de portador inactivo de HBsAg, y d) hepatitis crónica HBeAg negativo. La hepatitis crónica HBeAg positivo o negativo puede evolucionar hacia una cirrosis, una insuficiencia hepática y un carcinoma hepatocelular. Una progresión hacia estas complicaciones es más frecuente en las formas HBeAg negativo, asociadas con mutaciones que afectan a la región pre-core y que mantienen la replicación viral activa. Los factores de riesgo son unos valores altos de ADN-VHB, el aumento de la concentración sérica de transaminasas y algunos genotipos. Estos factores subrayan la necesidad de evaluar y supervisar a todos los portadores del VHB para identificar a los pacientes que pueden beneficiarse de un tratamiento antiviral precoz, evitando de este modo la progresión hasta formas más avanzadas de hepatopatía. Estas medidas pueden contribuir a una mejor prevención y a un tratamiento más eficaz de la hepatitis B.

Palabras clave:
Hepatitis B
Estado de portador crónico de virus de la hepatitis B
Manifestaciones extrahepáticas
Historia natural

Hepatitis B virus (HBV) infection is a serious public health problem worldwide. In the last few decades, major advances have been achieved that have contributed to greater understanding of the natural history and clinical manifestations of this infection. The fluctuation between viral replication and the host's immune response has implications in the pathogenesis and progression of the hepatic lesion. In immunocompetent adults, most HBV infections resolve spontaneously in contrast with progression to chronic infection in most infants. Patients with chronic hepatitis due to HBV or chronic hepatitis B can present at four phases: 1) the immune tolerance phase, 2) HBeAg-positive chronic hepatitis B, 3) inactive HBsAg carrier state, and 4) HBeAg-negative chronic hepatitis. HBeAg-positive or –negative chronic hepatitis can progress to cirrhosis, liver failure and hepatocellular carcinoma.

Progression to these complications is more frequent in HBeAg-negative forms, associated with mutations that affect the pre-core region and maintain active viral replication. Risk factors are HBV-DNA positive serum levels, an increase in serum transaminase levels and some genotypes. These factors highlight the need to evaluate and monitor all HBV carriers to identify those who could benefit from early antiviral treatment, thus avoiding progression to more advanced forms of liver disease. These measures could improve prevention and treatment of hepatitis B.

Key words:
Hepatitis B
Chronic HBV carrier state
Extrahepatic manifestations
Natural history
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Bibliografía
[1.]
D. Lavanchy.
Hepatitis B virus epidemiology, disease burden, treatment, and current and emerging prevention and control measures.
J Viral Hepat, 11 (2004), pp. 97-107
[2.]
R. Williams.
Global challenges in liver disease.
Hepatology, 44 (2006), pp. 521-526
[3.]
W.M. Lee.
Hepatitis B virus infection.
N Engl J Med, 337 (1997), pp. 1733-1745
[4.]
Y.-F. Liaw, N. Leung, R. Guan, et al.
Asian-Pacific consensus statement on the management of chronic hepatitis B : an update.
J Gastroenterol Hepatol, 18 (2003), pp. 239-245
[5.]
R. Marinho, J. Giria, M. De Moura.
Rising costs and hospital admissions for hepatocellular carcinoma in Portugal (1993-2005).
World J Gastroenterol, 13 (2007), pp. 1522-1527
[6.]
S.J. Hadziyannis, D. Vassilopous.
Hepatitis e antigen negative chronic hepatitis B.
Hepatology, 34 (2001), pp. 617-624
[7.]
E.K. Manesis.
HBeAg-negative chronic hepatitis B: from obscurity to prominence.
J Hepatol, 45 (2006), pp. 343-346
[8.]
J.H. Hoofnagle.
Hepatitis B-Preventable and now treatable.
N Engl J Med, 354 (2006), pp. 1074-1076
[9.]
A.S. Lock, B. McMahon.
Chronic hepatitis B.
Hepatology, 45 (2007), pp. 507-539
[10.]
S. Pungpapong, W.R. Kim, J.J. Poterucha.
Natural history of hepatitis B virus infection: an update for clinicians.
Mayo Clin Proc, 82 (2007), pp. 967-975
[11.]
H.J. Yim, A.S. Lok.
Natural history of chronic hepatitis B virus infection: what we knew in 1981 and what we know in 2005.
Hepatology, 43 (2006), pp. S173-S181
[12.]
W.R. Kim, J.J. Poterucha, W.K. Kremers, et al.
Outcome of liver transplantation for hepatitis B in the United States.
Liver Transpl, 10 (2004), pp. 968-974
[13.]
P.C. Chan, H.L. Chen, M.S. Kong, et al.
Factors affecting the mortality of pediatric fulminant hepatic failure in relation to hepatitis B virus infection.
Gastroenterol Hepatol, 20 (2005), pp. 1223-1227
[14.]
R. Montalti, B. Nardo, P. Beltempo, et al.
Liver transplantation in fulminant hepatic failure: experience with 40 adult patients over a 17-year period.
Transplant Proc, 37 (2005), pp. 1085-1087
[15.]
C.K. Hui, N. Leung, S.T. Yuen, et al.
Natural history and disease progression in Chinese chronic hepatitis B patients in immune-tolerant phase.
Hepatology, 46 (2007), pp. 395-401
[16.]
A.S.F. Lok, C.-L. Lai.
Longitudinal follow-up of asymptomatic hepatitis B surface antigen-positive chinese children.
Hepatology, 8 (1988), pp. 1130-1133
[17.]
M. Chen, M. SÃllberg, J. Hughes, et al.
Immune tolerance split between hepatitis B virus precore and core proteins.
J Virol, 79 (2005), pp. 3016-3027
[18.]
C. Boni, P. Fisicaro, C. Valdatta, et al.
Characterization of hepatitis B virus (HBV)-specific T-cell dysfunction in chronic HBV infection.
J Virol, 8 (2007), pp. 4215-4225
[19.]
C.M. Chu, Y.F. Liaw.
Intrahepatic distribution of hepatitis B surface and core antigens in chronic hepatitis B virus infection. Hepatocyte with cytoplasmic/membranous hepatitis B core antigen as a possible target for immune hepatocytolysis.
Gastroenterology, 92 (1987), pp. 220-225
[20.]
B.J. McMahon, P. Holck, L. Bulkow, M. Snowball.
Serologic and clinical outcomes of 1536 Alaska Natives chronically infected with hepatitis B virus.
Ann Intern Med, 135 (2001), pp. 759-768
[21.]
A.S. Lok, C.L. Lai, P.C. Wu, et al.
Spontaneous hepatitis B e antigen to antibody seroconversion and reversion in Chinese patients with chronic hepatitis B virus infection.
Gastroenterology, 92 (1987), pp. 1839-1843
[22.]
M.F. Yuen, H.J. Yuan, C.K. Hui, et al.
A large population study of spontaneous HBeAg seroconversion and acute exacerbation of chronic hepatitis B infection: implications for antiviral therapy.
Gut, 52 (2003), pp. 416-419
[23.]
H.I. Yang, S.N. Lu, Y.F. Liaw, Taiwan Community-Based Cancer Screening Project Group, et al.
Hepatitis B e antigen and the risk of hepatocellular carcinoma.
N Engl J Med, 347 (2002), pp. 168-174
[24.]
G. Fattovich, G. Giustina, S.W. Schalm, et al.
Occurrence of hepatocellular carcinoma and decompensation in western European patients with cirrhosis type B. The EUROHEP Study Group on Hepatitis B Virus and Cirrhosis.
Hepatology, 21 (1995), pp. 77-82
[25.]
Fattovich G, Olivari N, Pasino M, et al. Long-term outcome of chronic hepatitis B in caucasian patients: mortality after 25 years. Gut. 2007. En prensa.
[26.]
M. Manno, C. Camma, F. Schepis, et al.
Natural history of chronic HBV carriers in northern Italy: morbidity and mortality after 30 years.
Gastroenterology, 127 (2004), pp. 756-763
[27.]
Y.F. Liaw, I.S. Sheen, T.J. Chen, et al.
Incidence, determinants and significance of delayed clearance of serum HBsAg in chronic hepatitis B virus infection: a prospective study.
Hepatology, 13 (1991), pp. 627-631
[28.]
A.S. Lok, R.H. Liang, E.K. Chiu, et al.
Reactivation of hepatitis B virus replication in patients receiving cytotoxic therapy: report of a prospective study.
Gastroenterology, 100 (1991), pp. 182-188
[29.]
C.M. Chu, Y.F. Liaw.
HBsAg seroclearance in asymptomatic carriers of high endemic areas: appreciably high rates during a long-term follow-up.
Hepatology, 45 (2007), pp. 1187-1192
[30.]
A.S. Lok, C.L. Lai, P.C. Wu, et al.
Spontaneous hepatitis B eantigen to antibody seroconversion and reversion in Chinese patients with chronic hepatitis B virus infection.
Gastroenterology, 92 (1987), pp. 1839-1843
[31.]
M.F. Yuen, D.K. Wong, M. Sablon, et al.
HBsAg seroclearance in chronic hepatitis B in the Chinese: virological, histological, and clinical aspects.
Hepatology, 39 (2004), pp. 1694-1701
[32.]
T.I. Huo, J.C. Wu, P.C. Lee, et al.
Sero-clearance of hepatitis B surface antigen in chronic carriers does not necessarily imply a good prognosis.
Hepatology, 28 (1998), pp. 231-236
[33.]
M.R. Brunetto, F. Oliveri, B. Coco, et al.
Outcome of anti-HBe positive chronic hepatitis B in alpha-interferon treated and untreated patients: a long term cohort study.
J Hepatolo, 36 (2002), pp. 263-270
[34.]
J.P. Zarski, P. Marcellin, V. Leroy, et al.
Characteristics of patients with chronic hepatitis B in France: predominant frequency of HBe antigen negative cases.
J Hepatol, 45 (2006), pp. 355-360
[35.]
U.H. Iloeje, H.I. Yang, J. Su, et al.
Predicting cirrhosis risk based on the level of circulating hepatitis B viral load. Risk Evaluation of Viral Load Elevation and Associated Liver Disease/Cancer-In HBV (the REVEAL-HBV) Study Group.
Gastroenterology, 130 (2006), pp. 678-686
[36.]
H. Sumi, O. Yokosuka, N. Seki, et al.
Influence of hepatitis B virus genotypes on the progression of chronic type B liver disease.
Hepatology, 37 (2003), pp. 19-26
[37.]
C.L. Thio, E.C. Seaberg, R. Skolasky Jr., et al.
Multicenter AIDS Cohort Study. HIV-1, hepatitis B virus, and risk of liver-related mortality in the Multicenter Cohort Study (MACS).
Lancet, 360 (2002), pp. 1921-1926
[38.]
C.J. Hoffmann, C.L. Thio.
Clinical implications of HIV and hepatitis B co-infection in Asia and Africa.
Lancet Infect Dis, 7 (2007), pp. 402-409
[39.]
Y.F. Liaw, J.J. Sung, W.C. Chow, Cirrhosis Asian Lamivudine Multicentre Study Group, et al.
Lamivudine for patients with chronic hepatitis B and advanced liver disease.
N Engl J Med, 351 (2004), pp. 1521-1531
[40.]
C.L. Lai, M. Rosmawati, J. Lao, et al.
Entecavir is superior to lamivudine in reducing hepatitis B virus DNA in patients with chronic hepatitis B infection.
Gastroenterology, 123 (2002), pp. 1831-1838
[41.]
P. Marcellin, T.T. Chang, S. Lim, Adefovir Dipivoxil 437 Study Group, et al.
Adefovir dipivoxil for the treatment of hepatitis B e antigen-positive chronic hepatitis B.
N Engl J Med, 348 (2003), pp. 808-816
[42.]
C.M. Chu.
Natural history of chronic hepatitis B virus infection in adults with emphasis on the occurrence of cirrhosis and hepatocellular carcinoma.
J Gastroenterol Hepatol, 15 (2000), pp. E25-E30
[43.]
K. Ohnishi, S. Iida, S. Iwama, et al.
The effect of chronic habitual alcohol intake on the development of liver cirrhosis and hepatocellular carcinoma: relation to hepatitis B surface antigen carriage.
Cancer, 49 (1982), pp. 672-677
[44.]
C.J. Chen, H.I. Yang, J. Su, C.L. Jen, S.L. You, S.N. Lu, REVEAL-HBV Study Group, et al.
Risk of hepatocellular carcinoma across a biological gradient of serum hepatitis B virus DNA level.
JAMA, 295 (2006), pp. 65-73
[45.]
M. Van Zonneveld, P. Honkoop, B.E. Hansen, et al.
Long-term follow-up of alpha-interferon treatment of patients with chronic hepatitis B.
Hepatology, 39 (2004), pp. 804-810
[46.]
G.A. Ostapowicz, R.J. Fontana, F.V. Schiodt, et al.
Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States.
Ann Intern Med, 137 (2002), pp. 945-954
[47.]
D. Samuel, R. Mulledr, G. Alexander, et al.
Liver transplantation in European patients with the hepatitis B surface antigen.
N Engl J Med, 320 (1993), pp. 1842-1847
[48.]
Carneiro de Moura M, Gameiro R, Matos L, et al. Chronic hepatitis B in Portugal: a retrospective study of patients attenting National Health System Hospitals. 2007 [en prensa].
[49.]
D. Schupan, F. Stickel.
Markers of progression.
Diagnosis of liver diseases, pp. 15-25
[50.]
F. Serejo, A. Costa, M. Carneiro de Moura, et al.
Alfa interferon improves liver fibrosis in chronic hepatitis C. Clinical significance of the serum-N-terminal propeptide of Procollagen type III.
Dig Dis Sci, 46 (2001), pp. 1684-1689
[51.]
W.M. Rosenberg, M. Voelker, R. Thiel, et al.
Serum markers detect the presence of liver fibrosis: a cohort study.
Gastroenterology, 127 (2004), pp. 1704-1713
[52.]
G. Papatheodoridis, E. Hadziyannis, E. Tsochatzis, et al.
Serum apoptotic caspase activity as diagnostic marker in HBeAg-negative chronic hepatitis B virus infection.
Gastroenterology, 132 (2007), pp. A760
[53.]
L. Castera, J. Vergniol, J. Foucher, et al.
Prospective comparison of transient elastography, Fibrotest, APRI, and liver biopsy for the assessment of fibrosis in chronic hepatitis C.
Gastroenterology, 128 (2005), pp. 343-350
[54.]
J. Chang, H.H. Tan, B.S. Yew, et al.
Diagnostic accuracy and clinical utility of transient elastography (Fibroscan®) in the evaluation of hepatic fibrosis in an Asian population with chronic hepatitis B.
Gastroenterology, 132 (2007), pp. A761
[55.]
B. Coco, F. Oliveri, A.M. Mans, et al.
Transient elastography : a new surrogate marker of liver fibrosis influenced by major changes of transaminases.
J Viral Hepat, 14 (2007), pp. 360-370
[56.]
R.Y. Akhtar, D.T. Dieterich, D. Carriero.
Low viral load chronic hepatitis B and liver histology.
Gastroenterology, 132 (2007), pp. A761
[57.]
S.H. Han.
Extrahepatic manifestations of chronic hepatitis B.
Clin Liver Dis, 8 (2004), pp. 403-418
[58.]
A. Mason, J. Theal, V. Bain, et al.
Hepatitis B virus replication in damaged endothelial tissues of patients with extrahepatic disease.
Am J Gastroenterol, 100 (2005), pp. 972-976
[59.]
P. Cacoub, D. Saadoun, M. Bourliére, et al.
Hepatitis B genotypes and extrahepatic manifestations.
J Hepatol, 43 (2005), pp. 764-770
[60.]
J.D. Kim, A.H. Sherker.
Antiviral therapy: role in the management of extrahepatic diseases.
Gastroenterol Clin North Am, 33 (2004), pp. 303-708
[61.]
K.N. Lai, P.K. LI, S.F. Lui, et al.
Membranous nephropathy related to hepatitis B virus in adults.
N Engl J Med, 324 (1991), pp. 1457-1463
[62.]
H.S. Conjeevaram, J.H. Hoofnagle, H.A. Austin, et al.
Long term outcome of hepatitis B virus related glomerulonephritis after therapy with interferon alpha.
Gastroenterology, 109 (1995), pp. 540-546
[63.]
L. Guillevin, A. Mahr, P. Callard, et al.
Hepatitis B virus related polyarteritis nodosa: clinical characteristics, outcome, and impact of treatment in 115 patients.
Medicine (Baltimore), 84 (2005), pp. 313-322
[64.]
S. Onay, E. Baskin, F. Ozçay, et al.
Successful treatment of hepatitis B-associated leukocytoclastic vasculitis with lamivudine tretament in a child patient.
Rheumatol Int, 27 (2007), pp. 869-872
[65.]
F. Bonino, M.R. Brunetto.
Chronic hepatitis B e antigen (HbeAg) negative, anti-HBe positive hepatitis B: an overview.
J Hepatol, 39 (2003), pp. 160-163
[66.]
F. Gerner, E. Lausch, M. Friedt, et al.
Hepatitis B virus core promoter mutations in children with multiple anti-HBe/HBeAg reactivations result in enhanced promoter activity.
J Med Virol, 59 (1999), pp. 415-423
[67.]
J.L. Steinberg, W. Yeo, S. Zhong, et al.
Hepatitis B virus reactivation in patients undergoing chemotherapy for solid tumours: precore/core mutations play an important role.
J Med Virol, 60 (2000), pp. 244-255
[68.]
L. Xunrong, A.W. Yan, R. Liang, et al.
Hepatitis B virus (HBVC) reactivation after cytotoxic or immunosupressive therapy: pathogenesis and management.
Rev Med Virol, 11 (2001), pp. 287-299
[69.]
Visvanathan K, Lewin DR. Immunopathogenesis: role of innate and adaptative immune responses. En: Locarnini S, editor. The control of chronic hepatitis B: the role for chemoprevention. Sem Liver Dis. 2006;26:104-15.
[70.]
R.P. Perrillo.
Acute flares in chronic hepatitis B: the natural and unatural history of an immunologically mediated liver disease.
Gastroenterology, 120 (2001), pp. 1009
[71.]
G. Raimondo, C. Balsano, A. Craxi, et al.
Occult hepatitis B virus infection.
Dig Liver Dis, 32 (2000), pp. 822-826
[72.]
G.K. Lau, H.H. Yiu, D.Y. Fong, et al.
Early is superior to deferred preemptive lamivudine therapy for hepatitis B patients undergoing chemotherapy.
Gastroenterology, 125 (2003), pp. 1742-1749
[73.]
A. Marzano, F. Angeluci, P. Andreoni, et al.
Prophylaxis and treatment of hepatitis B in immunocompromised patients.
Dig Liver Dis, 39 (2007), pp. 397-408
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