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Systemic lupus erythematosus (SLE) is a multi-organic autoimmune disease with a wide variety of clinical manifestations. However, hepatic dysfunction is not included in the diagnostic criteria for the disease and has not been recognized properly. The spectrum of hepatic involvement described in these patients ranges from abnormalities in liver function tests (LFTs) to fulminant hepatic failure. Usually, abnormalities in LFTs are only mild and transient, have a hepatocellular pattern and are not related to SLE but rather are mostly drug related. The most frequent finding on liver biopsy is steatosis (non-alcoholic fatty liver disease). Patients do not frequently progress to advanced chronic liver disease, and their outcome is favourable. Those who develop cirrhosis have traditional risk factors, such as other non-SLE-related conditions. In this work, we aim to review hepatic manifestations in patients with SLE, as well as the diagnostic and therapeutic approaches used for different liver diseases in these patients.

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OBJECTIVES: Human T-cell lymphotropic virus type 1 (HTLV-1) infection is associated with neurological abnormalities, such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and peripheral neuropathy (PN). Hepatitis C virus (HCV) infection is the leading cause of chronic liver disease worldwide, and causes PN in approximately 9% of patients. Because the interplay between these potentially neuropathogenic viruses in the same individual is still poorly understood, the clinical and laboratory outcomes of co-infected patients were evaluated and compared with those of controls. METHODS: The prevalence rates of neurological and laboratory abnormalities were evaluated in HCV/HTLV-1 co-infected patients (n=50), and in subjects with single HCV (n=46) or HTLV-1 (n=150) infection. RESULTS: A higher frequency of isolated PN was present in HCV-infected patients; this was not associated with cryoglobulinemia. No difference was found in the frequency of PN or HAM/TSP when co-infected subjects were compared to singly infected subjects. Hepatic involvement was present in HCV-infected subjects, as shown by increased levels of serum alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, and bilirubin, in addition to thrombocytopenia. On the other hand, HCV/HTLV-1 co-infected individuals presented a better prognosis for hepatic involvement when compared with singly HCV-infected subjects. CONCLUSIONS: These data suggest that HCV/HTLV-1 co-infection does not mutualistically alter the outcome with regard to neurological manifestations. Nonetheless, changes in the immunological environment induced by HTLV-1 infection could lead to a reduction in hepatic damage, even without significant HCV clearance.

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O acometimento hepático nos pacientes com telangiectasia hereditária hemorrágica ou síndrome de Osler-Weber-Rendu é infreqüente e muitas vezes representa um desafio diagnóstico. Os autores apresentam o caso de uma paciente que procurou atendimento médico por aumento de aminotransferases, história prévia de epistaxe, exame físico e endoscopia digestiva alta evidenciando telangiectasia. A tomografia computadorizada de abdome sugeriu neoplasia primária ou metastática do fígado e a arteriografia demonstrou artéria hepática direita ectásica e neovascularização. Para confirmação do diagnóstico e exclusão de neoplasia foi realizada biópsia hepática, a qual evidenciou vasos anômalos e fibrose no espaço porta, espessamento e ectasia de ramos da artéria hepática e dilatação de sinusóides, achados já descritos nesta síndrome (AU)

Hepatic involvement in patients with hereditary hemorrhagic telangiectasia is infrequent and sometimes represents a diagnostic challenge. The authors present a case of a patient that presents with a elevation of aminotransferases, had history of epistaxis and telangiectases diagnosed by physical examination and upper gastrointestinal endoscopy. The computed tomographic scans suggested primary or metastatic liver neoplasia and angiographic studies showed enlarged right hepatic artery and neovascularization. Liver biopsy demonstrated findings of this syndrome like ectatic vascular structures, fibrosis, enlargement of hepatic artery and sinusoidal dilation. This confirmed diagnoses and exclude neoplasia (AU)

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