Hépatite lupique : une série de 12 patients

Khalifa, M.; Benjazia, Elhem; Rezgui, A.; Ghannouchi, N.; Alaoua, A.; Braham, A.; Létaief, A.; Bahri, F.

doi:10.1016/j.revmed.2010.10.357

Cited by 16 publications

(12 citation statements)

References 10 publications

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“…Frequently, patients with SLE have comorbidities with many non-autoimmune hepatic diseases, such as drug-derived hepatic injury, viral or infectious hepatitis, and thrombotic liver diseases ( 11 – 14 ). The prevalence of lupus hepatitis lies between 6.1 and 24.5% ( 14 – 16 ); however, there are currently no diagnostic gold-standard criteria and specific treatment for lupus hepatitis and the diagnosis is mainly rule out on the bases of other liver diseases. Thus, it is important to understand the pathogenesis and features of lupus hepatitis.…”

Section: Introductionmentioning

confidence: 99%

Role of Hepatic Deposited Immunoglobulin G in the Pathogenesis of Liver Damage in Systemic Lupus Erythematosus

et al. 2018

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The onset of hepatic disorders in patients with systemic lupus erythematosus (SLE) is frequent; however, the etiology and liver pathogenesis of SLE remain unknown. In the present study, the role of hepatic deposited immunoglobulin G (IgG) in SLE-derived liver damage was investigated. From a retrospective analysis of the medical records of 404 patients with lupus and from experimental studies on mice models, we found that liver dysfunction is common in SLE and liver damage with IgG deposition spontaneously develops in lupus-prone mice. Liver injury was recreated in mice by injecting IgG from lupus serum intrahepatically. The inflammation intensity in the liver decreased with IgG depletion and the lupus IgG-induced liver inflammation in FcγRIII-deficient mice was comparatively low; while, inflammation was increased in FcγRIIb-deficient mice. Macrophages, Kupffer cells, natural killer cells, and their products, but not lymphocytes, are required for the initiation of SLE-associated liver inflammation. Blocking IgG signaling using a spleen tyrosine kinase (Syk) inhibitor suppressed the liver damage. Our findings provided evidence of spontaneously established liver damage in SLE. They also suggested that hepatic-deposited lupus IgG is an important pathological factor in the development of liver injury and that hepatic inflammation is regulated by the Syk signaling pathway. Thus, Syk inhibition might promote the development of a therapeutic strategy to control liver damage in patients with SLE.

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Section: Introductionmentioning

confidence: 99%

Role of Hepatic Deposited Immunoglobulin G in the Pathogenesis of Liver Damage in Systemic Lupus Erythematosus

et al. 2018

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“…Although the anti-ribosomal-P protein in our patient was normal, he responded well to high dose corticosteroid treatment, with complete resolution of symptoms and objective findings within weeks of treatment. There is some controversy about the utility of anti-ribosomal-P protein in assessing lupus hepatitis with some evidence of strong correlation [ 7 ], and other studies reporting limited utility in diagnosing lupus hepatitis [ 8 ]. The effective response to prednisone treatment is consistent with an immunologic etiology, as opposed to etiologies associated with infectious agents or adverse drug reaction.…”

Section: Discussionmentioning

confidence: 99%

Acute Hepatic Failure and Epididymitis in a Hispanic Patient With Active Systemic Lupus Erythematosus

et al. 2018

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Systemic lupus erythematosus (SLE) is an autoimmune disease known to affect a variety of organ systems. Patients with SLE are more prone to developing common infections that can mimic the complications of SLE. As such, it is essential to differentiate complications of SLE from infection to ensure appropriate management and to improve morbidity and mortality of this patient population. Here we present a 24-year-old, Hispanic male, with SLE complicated by dialysis-dependent end-stage renal disease and dilated cardiomyopathy. The patient presented to the emergency room with nausea, vomiting, and abdominal pain and admitted to the medicine service. Initial evaluation showed hypoalbuminemia coupled with elevated transaminases, INR, and total bilirubin consistent with acute liver failure. Further evaluation was negative for viral, toxic, metabolic, or vascular causes of acute failure. The patient was diagnosed with lupus hepatitis and associated acute hepatic failure, and started on high dose prednisone (60 mg daily). Complete resolution of liver function and symptoms was observed within 1 week at follow-up. The patient was readmitted 2 weeks after discharge with left scrotal pain and swelling after abruptly decreasing the prescribed prednisone dose 3 days after discharge. Physical exam and scrotal ultrasound in the emergency department were consistent with epididymitis. Urinalysis, urine culture, and gonorrhea and chlamydia PCR were all negative. Without evidence of infection, and upon reconfirmation of low serum complement levels, the patient was diagnosed with lupus epididymitis and restarted on high dose prednisone. Complete resolution of symptoms was attained within 1 week at follow-up. This case emphasizes the importance of differentiating the clinical manifestations of SLE from infection and the complexity of disease presentation in Hispanic patients.

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“…6 A wide range of hepatic disorders including congestion, fatty liver, arteritis, portal or hepatic vein thrombosis, hepatic infarction, fibrosis, chronic active or chronic persistent hepatitis, non-specific reactive hepatitis, cholecystitis, nodular regenerative hyperplasia, primary biliary cirrhosis and hemangioma have been reported in patients with SLE. 1,2,4,7 Hepatomegaly is reported in 39-40% and splenomegaly in 6% of patients with SLE, but huge splenomegaly is not expected. Abnormal liver function tests may be observed in more than half of the patients with SLE.…”

Section: Discussionmentioning

confidence: 99%

“…1 Liver involvement in SLE is frequently subclinical and is not expected as the initial presentation of the disease. 2 Moreover, SLE is infrequent in children and rare in infants. Granulomatous liver involvement is very rare in adults with SLE and has not been previously reported in children or infants suffering from this disease.…”

Section: Introductionmentioning

confidence: 99%

Granulomatous liver involvement in a child with systemic lupus erythematosus: a case report and review of the literature

Fallahzadeh

Mojtahedi

Dehghani

et al. 2013

Lupus

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Systemic lupus erythematosus (SLE) is uncommon in young children and unusual in infancy. Although a variety of liver pathologies have been reported in SLE, presentation of this disease with granulomatous liver involvement is very rare. In this article, for the first time, we report an infant girl presenting with unexplained hepatosplenomegaly and non-necrotizing granulomatous liver involvement at the age of six months who later developed pancytopenia and proteinuria and was finally diagnosed with SLE at the age of three years. Therefore, we suggest that SLE could be considered as one of the possible differential diagnoses when infants or children present with unexplained granulomatous liver involvement.

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Hépatite lupique : une série de 12 patients

Cited by 16 publications

References 10 publications

Role of Hepatic Deposited Immunoglobulin G in the Pathogenesis of Liver Damage in Systemic Lupus Erythematosus

Role of Hepatic Deposited Immunoglobulin G in the Pathogenesis of Liver Damage in Systemic Lupus Erythematosus

Acute Hepatic Failure and Epididymitis in a Hispanic Patient With Active Systemic Lupus Erythematosus

Granulomatous liver involvement in a child with systemic lupus erythematosus: a case report and review of the literature

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