Hepatitis B virus surface antigen in glomerular immune complex deposits of patients with systemic lupus erythematosus

Looi, Lai‐Meng; Prathap, K.

doi:10.1111/j.1365-2559.1982.tb02711.x

Cited by 22 publications

(13 citation statements)

References 21 publications

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“…The association between chronic HBV infection and focal segmental glomerulosclerosis, minimal change nephropathy [37, 52, 53]and lupus nephritis may be fortuitous [54, 55]. …”

Section: Pathology Of Hbv-associated Glomerulonephritismentioning

confidence: 99%

Hepatitis B Virus-Associated Nephropathy

Bhimma

Coovadia²

2004

Am J Nephrol

209

165

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A direct causal association between hepatitis B virus (HBV) infection and the development of nephropathy remains controversial. Epidemiological studies have shown that chronic carriage of HBV in some individuals (particularly children) leads to the development of nephrotic syndrome with a strong male predominance, the commonest histological type being membranous nephropathy (MN). Spontaneous clearance of HBV antigens (particularly the HBeAg) leads to abrogation of proteinuria. The isolation of immune complexes in the kidney suggests that the pathogenesis of the disease may have an immune-complex basis. Recent studies showing expression of HBV viral antigens in kidney tissue suggest direct viral-induced pathological alterations and chronic immunologic injury. Biosocial studies have detected no correlation between HBV carriage and proteinuria using both quantitative and qualitative urinary protein analysis. Genetic studies of HLA class I and II genes showed a predisposition to MN but no similar correlation in those with milder degrees of proteinuria. These findings suggest that milder proteinuria is unrelated to HBV carriage or genetic factors but the development of nephropathy, particularly MN, in patients with chronic HBV carriage (HBsAg and/or HBV DNA positive) is based on an interaction of virus and host factors. Although the natural history of the disease tends to remission with preservation of renal function, there is considerable morbidity and a small but significant mortality. Use of naturally occurring cytokines (such as interferon-α2b) and other candidate therapies accelerates clearance of the virus and proteinuria. The most effective tool in reducing the incidence of the disease is the use of HBV vaccines.

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“…The association between chronic HBV infection and focal segmental glomerulosclerosis, minimal change nephropathy [37, 52, 53]and lupus nephritis may be fortuitous [54, 55]. …”

Section: Pathology Of Hbv-associated Glomerulonephritismentioning

confidence: 99%

Hepatitis B Virus-Associated Nephropathy

Bhimma

Coovadia²

2004

Am J Nephrol

209

165

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“…As an additional line of evidence relating HBV antigens and lupus kidney disease, Looi and Prathap (1982) reported that HBV-associated antigen deposition was found in the renal tissue of 63.8% (30/47) of lupus patients. Consistent with their report, Wang et al (2012) demonstrated that HBV-associated antigen deposition was present in 50.6% (84/166) of renal biopsies from lupus patients.…”

Section: A Role Of Hbv Infection In the Pathogenesis Of Slementioning

confidence: 99%

Pretreatment Screening for Hepatitis B Virus Infection in Patients with Systemic Lupus Erythematosus

Watanabe

Ishii

Harigae

2015

Tohoku J. Exp. Med.

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Hepatitis B virus (HBV) infection is one of the most common diseases, and approximately two billion people are infected with HBV in the world. Until recently, hepatitis B surface antigen (HBsAg)-negative patients, carrying hepatitis B surface antibody (anti-HBs) and/or hepatitis B core antibody (anti-HBc), have been considered to have achieved the resolution of HBV infection; however, among those patients, the reactivation of HBV has been increasingly reported after chemotherapy, hematopoietic stem cell transplantation, or immunosuppressive therapy. The reactivation of HBV can cause lethal hepatitis called de novo hepatitis B. Therefore, serological examination for HBV infection before starting immunosuppressive therapy is now recommended for all patients with rheumatic diseases. Systemic lupus erythematosus (SLE) is one of the autoimmune diseases characterized by the production of autoantibodies and usually requires immunosuppressive therapy. However, to date, a few reports are available regarding the prevalence and time course of HBV infection in patients with SLE under immunosuppressive therapy. In this review, we update the prevalence and time course of HBV infection in lupus patients using our data and previous papers available, with a special emphasis on occult HBV infection and a decrease of HBV-related antibodies (anti-HBs and anti-HBc) under immunosuppressive therapy. This review also highlights the screening and management of HBV infection currently recommended and the potential role of HBV infection in the pathogenesis of SLE. Throughout the present review, we recommend the pretreatment screening for HBV infection in patients with SLE as well as patients with other rheumatic diseases.

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“…Many extrahepatic manifestations are recognized in patients with HBV, including glomerulonephoritis, arthritis, vasculitis, and cryoglobulinaemia, features which are also frequently seen in SLE patients. It is possible that the HBV induces the lupus syndrome in susceptible individuals [58].…”

Section: Hbv and Slementioning

confidence: 99%

“…Based on evidence of the presence of HBsAg in glomerular immune complexes in patients with renal disease of varying morphological patterns, including membranous, proliferative and mesangiocapillary glomerulonephritis and focal glomerulosclerosis, Looi et al [58] aimed to find the frequency of HBsAg immune deposits in lupus nephritis. Over a 3-year period, they examined renal tissue from 259 patients, including 47 with SLE.…”

Section: Hbv and Slementioning

confidence: 99%

Hepatitis B Virus (HBV) and Autoimmune Disease

Ram

Gershwin

Shoenfeld

2007

Clinic Rev Allerg Immunol

112

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The etiology and pathogenesis of autoimmune diseases have long been an enigmatic subject that have involved genetic and environmental factors. Recent intriguing data has contributed to the mechanisms involved, including the relationship of infectious agents and loss of tolerance. This loss of tolerance is illustrated by the data on the immune response to Hepatitis B virus such as the molecular mimicry between HBV antigens and self proteins, the generation of immune complexes between HBV antigens and antibodies, and apoptosis/tissue damage resulting in the exposure of intracellular antigens to the immune system. In this paper, we review the current database related to HBV infection and a variety of autoimmune conditions, including autoimmune hepatitis, systemic lupus erythematosus, aplastic anemia, antiphospholipid syndrome, polyarteritis nodosa, rheumatoid arthritis, type 1 diabetes, multiple sclerosis, thyroid disease and uveitis.

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Hepatitis B virus surface antigen in glomerular immune complex deposits of patients with systemic lupus erythematosus

Cited by 22 publications

References 21 publications

Hepatitis B Virus-Associated Nephropathy

Hepatitis B Virus-Associated Nephropathy

Pretreatment Screening for Hepatitis B Virus Infection in Patients with Systemic Lupus Erythematosus

Hepatitis B Virus (HBV) and Autoimmune Disease

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