Hepatitis mortality in Brazil and regions, 2001-2020: temporal trend and spatial analysis / Mortalidade por hepatites no Brasil e regiões, 2001-2020: tendência temporal e análise espacial

ABSTRACT Objective: To analyze the spatial distribution and the temporal trend of the hepatitis mortality rate in Brazil from 2001 to 2020. Methods: Ecological, temporal, and spatial study on mortality from hepatitis in Brazil with data from the Mortality Information System (Sistema de Informações sobre Mortalidade - SIM/DATASUS). Information was stratified by year of diagnosis, region of the country, municipalities (of residence). Standardized mortality rates (SMR) were calculated. The temporal trend was estimated by Prais-Winsten regression and the spatial distribution by the Global Moran Index (GMI). Results: The highest SMR means in Brazil were for Chronic viral hepatitis with 0.88 deaths per 100,000 inhabitants (SD=0.16), followed by Other viral hepatitis with 0.22/100,000 (SD=0.11). In Brazil, the temporal trend of mortality from Hepatitis A was −8.11% per year (95%CI −9.38; −6.82), while for Hepatitis B it was −4.13% (95%CI −6.03; −2.20), of Other viral hepatitis of −7.84% (95%CI −14.11; −1.11) and of Unspecified Hepatitis −5.67% per year (95%CI −6.22; −5.10). Mortality due to chronic viral hepatitis increased by 5.74% (95%CI 3.47; 8.06) in the North and 4.95% in the Northeast (95%CI 0.27; 9.85). The Moran Index (I) for Hepatitis A was 0.470 (p<0.001), for Hepatitis B 0.846 (p<0.001), Chronic viral hepatitis=0.666 (p<0.001), other viral hepatitis=0.713 (p<0.001), and Unspecified Hepatitis=0.712 (p<0.001). Conclusion: The temporal trend of hepatitis A, B, other viral, and unspecified hepatitis was decreasing in Brazil, while mortality from chronic hepatitis was increasing in the North and Northeast.

RESUMO Objetivo: Analisar a distribuição espacial e a tendência temporal da taxa de mortalidade por hepatites no Brasil no período de 2001 a 2020. Métodos: Estudo ecológico, temporal e espacial sobre a mortalidade por hepatites no Brasil com dados do Sistema de Informações sobre Mortalidade (SIM/Datasus). As informações foram estratificadas por ano do diagnóstico, região do país, municípios (de residência). Foram calculadas as taxas padronizadas de mortalidade (TPM). A tendência temporal foi estimada pela regressão de Prais-Winsten e a distribuição espacial pelo Índice Global de Moran (IGM). Resultados: As maiores médias da TPM no Brasil foram para hepatite viral crônica, com 0,88 mortes para cada 100 mil habitantes (desvio padrão — DP=0,16), seguida de outras hepatites virais, com 0,22/100 mil (DP=0,11). No Brasil, a tendência temporal da mortalidade por hepatite A foi de −8,11% ao ano (intervalo de confiança de 95% — IC95% −9,38; −6,82), enquanto por hepatite B foi de −4,13% (IC95% −6,03; −2,20); de outras hepatites virais, foi de −7,84% (IC95% −14,11; −1,11) e de hepatite não especificada, de −5,67% ao ano (IC95% −6,22; −5,10). A mortalidade por hepatite viral crônica cresceu 5,74% (IC95%3,47; 8,06) no norte e 4,95% no nordeste (IC95% 0,27; 9,85). O Índice de Moran (I) para hepatite A foi de 0,470 (p<0,001), para hepatite B de 0,846 (p<0,001), hepatite viral crônica=0,666 (p<0,001), outras hepatites virais=0,713 (p<0,001) e hepatites não especificadas=0,712 (p<0,001). Conclusão: A tendência temporal das hepatites A, B, de outras hepatites virais e das não especificadas foi de diminuição no Brasil, enquanto a mortalidade por hepatites crônicas foi de crescimento nas Regiões Norte e Nordeste.

[Diagnosis and treatment of new-onset or uncontrolled hyperthyroidism-induced liver injury].

The thyroid gland is the largest endocrine gland in the human body, which mainly secretes thyroid hormones. Thyroid hormone acts on almost all tissues and cells at different level regulating growth and development, metabolism and other functional activities of the body. Therefore, abnormal thyroid function can affect the multiple organs throughout the body. Liver, as the largest biochemical plant in the whole body, is widely regulated by thyroid hormones, and is one of the important target organs of the thyroid gland. Hyperthyroidism (HT for short) is a common disease of the endocrine system, which can cause liver injury, such as hepatomegaly, abnormal liver function, jaundice, cirrhosis, and liver failure. This phenomenon is also known as hyperthyroidism-induced liver injury, and it is more common in new or untreated or improperly treated patients with hyperthyroidism. The basic liver function test at the beginning of antithyroid drugs (ATD) treatment can clarify the degree of liver injury caused by hyperthyroidism itself, and further predict the additional liver injury with ATD therapy initiation. The core of treating hyperthyroidism-induced liver injury is to rapidly control hyperthyroidism, and restore normal liver function. This review briefly summarizes the incidence rate, possible mechanisms, pathological changes, clinical manifestations, laboratory, imaging and pathologic findings, and the recent advances in diagnosis and treatment of the hyperthyroidism-induced liver injury.

Sofosbuvir/velpatasvir plus ribavirin for Child-Pugh B and Child-Pugh C hepatitis C virus-related cirrhosis.

BACKGROUND/AIMS: Real-world studies assessing the effectiveness and safety of sofosbuvir/velpatasvir (SOF/VEL) plus ribavirin (RBV) for Child-Pugh B/C hepatitis C virus (HCV)-related cirrhosis are limited. METHODS: We included 107 patients with Child-Pugh B/C HCV-related cirrhosis receiving SOF/VEL plus RBV for 12 weeks in Taiwan. The sustained virologic response rates at off-treatment week 12 (SVR12) for the evaluable population (EP), modified EP, and per-protocol population (PP) were assessed. Thesafety profiles were reported. RESULTS: The SVR12 rates in the EP, modified EP and PP were 89.7% (95% confidence interval [CI], 82.5-94.2%), 94.1% (95% CI, 87.8-97.3%), and 100% (95% CI, 96.2-100%). Number of patients who failed to achieve SVR12 were attributed to virologic failures. The SVR12 rates were comparable regardless of patient characteristics. One patient discontinued treatment because of adverse events (AEs). Twenty-four patients had serious AEs and six died, but none were related to SOF/VEL or RBV. Among the 96 patients achieving SVR12, 84.4% and 64.6% had improved Child-Pugh and model for endstage liver disease (MELD) scores. Multivariate analysis revealed that a baseline MELD score ≥15 was associated with an improved MELD score of ≥3 (odds ratio, 4.13; 95% CI, 1.16-14.71; P=0.02). Patients with chronic kidney disease (CKD) stage 1 had more significant estimated glomerular filtration rate declines than patients with CKD stage 2 (-0.42 mL/min/1.73 m2/month; P=0.01) or stage 3 (-0.56 mL/min/1.73 m2/month; P<0.001). CONCLUSION: SOF/VEL plus RBV for 12 weeks is efficacious and well-tolerated for Child-Pugh B/C HCV-related cirrhosis.

[Viral hepatitis A-E]. / Virushepatitis A­E.

Hepatitis viruses A-E cause acute and chronic liver inflammation and thus lead to significant morbidity and mortality worldwide. They differ significantly in their biology, course of disease and therapy options. While hepatitis A virus only causes acute infection, hepatitis B can become chronic, even reactivate or occur as coinfection with hepatitis D virus. Whereas these infections are preventable through vaccination, a vaccine does not exist against HCV. However, new direct antiviral agents reliably lead to cure of chronic hepatitis C. Hepatitis E virus frequently causes acute or-in case of immunosuppression-even chronic hepatitis. Continual screening of patients with elevated liver enzymes or risk groups using simple serological markers can enable virus-specific therapy of mostly asymptomatic chronic virus hepatitis, preventing the development of liver cirrhosis and hepatocellular carcinoma.

Autoimmune hepatitis in practice, from diagnosis to complications: What is the role of imaging? A clinicoradiological review.

Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease of unknown origin that can lead to liver cirrhosis, hepatocellular carcinoma (HCC), liver transplantation or death. The diagnosis is performed upon a multifactorial score. Treatment is based on the combination of immunosuppressants and aims at clinical, laboratory and histological remission, the latter being the most difficult to be achieved and proven. The absence of liver inflammation, defined by biopsy, is the main determinant in remission or therapeutic modification. Imaging exams have a limited role in this clinical management and the main findings are those related to chronic liver disease. Imaging's relevance, therefore, lies mainly in helping to exclude overlapping syndromes and in assessing complications related to cirrhosis, such as in screening for HCC. In recent years, however, the radiological literature has been witnessing increasing advances with regard to imaging biomarkers in liver disease, leading some authors to consider a future of virtual liver biopsy performed by magnetic resonance imaging. The present study aims to review the role of imaging in the management of AIH in the light of recent advances in the current literature and to provide an illustrated guide with the main findings described in the disease.

Hypovitaminosis D in Hepatitis C patients and its relation with demographic and laboratory data.

OBJECTIVE: To determine the frequency of vitamin-D deficiency in hepatitis C patients and its relation with demographic and baseline laboratory data. METHODS: The cross-sectional study was conducted at the University Institute of Medical Laboratory Technology, Faculty of Allied Health Sciences, The University of Lahore, Pakistan, from April 3 to July 24, 2017, and comprised diagnosed hepatitis C genotype 3 patients aged 18-60 years. Demographic data was collected on a predesigned proforma. Tests included complete blood counts, liver function test, hepatitis C viral load and 25-hydroxy Vitamin-D level. Data was analysed using SPSS 24. RESULTS: Of the 115 patients, 54(47%) were male and 61(53%) were females. Mean vitamin-D level was 22.3±11.3. Total 25(21.7%) patients showed normal level of vitamin-D while the level was low in 90(78.3%) patients; 41(35.6%) showed vitamin-D insufficiency and 49(42.6%) vitamin-D deficiency. Significant effect of sun exposure was recorded on patient's vitamin-D level (p=0.00). Significantly low hepatitis C viral load was seen in patients with normal vitamin-D (p= 0. 02 6 ). CONCLUSIONS: Patients with hepatitis C virus infection had high incidence of hypo-vitaminosis D.

[Effect of chronic hepatitis B virus DNA negative transformation and HBsAg clearance on the occurrence of hepatocellular carcinoma].

Achieving HBV DNA negative transformation and HBsAg clearance with effective antiviral therapy can reduce the incidence of HCC, but some patients are still at risk of developing HCC. Therefore, screening high-risk patients for close monitoring is essential to reduce the incidence of HCC. This paper reviews the occurrence of HCC, risk factors and risk prediction models of HBV DNA negative transformation and HBsAg clearance, and provides a basis for screening and follow-up management of high-risk group of HCC with chronic hepatitis B.

[Quantitative comparison of diffusion weighted image in liver at two field strengths for chronic hepatitis B].

Objective: To evaluate whether there were differences between apparent diffusion coefficient (ADC) values derived from 3.0 T and 1.5 T MR diffusion-weighted imaging (DWI) in liver of patients with chronic hepatitis B. Methods: From January 2016 to November 2016, a total of 40 chronic hepatitis B prospectively underwent both 1.5 T and 3.0 T DWI before liver biopsy, the interval between two scans was within 15 minutes, the protocol was respiratory-triggered DWI(RT-DWI). The ADC values were measured at both field strengths using ROI method. Bland-Altman tests and paired t-tests were used to compare ADC values obtained at 1.5 T and 3.0 T. Results: The ADC values of different b values for patients with mild inflammation at 1.5 T were(1.22-1.48(1.35±0.08)×10(-3) mm(2)/s), the ADC values of different b values for patients with mild inflammation at 3.0 T were(1.18-1.45(1.30±0.08)×10(-3) mm(2)/s); the ADC values of different b values for patients with moderate to severe inflammation at 1.5 T were(1.11-1.37(1.25±0.06)×10(-3) mm(2)/s), the ADC values of different b values for patients with moderate to severe inflammation at 3.0 T were(1.08-1.31(1.20±0.06)×10(-3) mm(2)/s). There were significantly differences between the ADC values of different b values for patients with chronic hepatitis B obtained at two field strengths (P<0.01). Conclusions: Different field strengths have influence on ADC values in liver, the ADC values derived from 3.0 T are lower than the ADC values derived from 1.5 T.

Rare hepatic metastases of colorectal cancer in livers with symptomatic HBV and HCV hepatitis.

AIM: The liver is the most common site of metastases in colorectal cancer but metastases seem to be less common in patients with a chronically liver damage. The aim of our study was to assess the development of metachronous liver metastases in patients affected by HBV or HCV related liver diseases. MATERIAL OF STUDY: We retrospectively evaluated above all the development of liver metastases and the 5-year disease free in 457 patients radically treated for colorectal cancer with healthy liver and in 31 patients radically treated for colorectal cancer affected by liver damage (HBV or HCV related). RESULTS: Overall incidence of liver metastases was 9% (44/488), in particular 3.2% in infected patients and 9.4% in non-infected patients (p= 0.34). Our results revealed that there is no statistically significant difference between the number of positive lymph nodes of primary colorectal cancer and the number of indifferentiated cancers in infected compared with non-infected patients (29% vs 34.1% and 9.7% vs 13.6% respectively), and the 5-year disease free is better for infected patients (93% and 80%, p = 0.17). DISCUSSION: In infected patients we registered a better crude 5-year disease free interval and a fewer incidence of metachronous liver metastases. This difference is in agreement with other results mentioned in literature. CONCLUSION: In the light of the reported data, the authors consider that the recent pathogenetic theory of the "metalloproteinase inhibitor" should be taken in account.

Clinical features and long term outcome of 102 treated autoimmune hepatitis patients.

BACKGROUND: There is limited data on the natural history of autoimmune hepatitis (AIH) and on the long-term follow-up of AIH patients who have been referred for regular medical attention. OBJECTIVES: We evaluated the clinical presentation and natural history of AIH in a large cohort of type I AIH patients from Iran. PATIENTS AND METHODS: Between 1997 and 2008, 102 patients were enrolled in the study. Patients were diagnosed using the International Autoimmune Hepatitis Group criteria and were followed up for an average of 60 months. Clinical and biochemical data were gathered from all the patients at both the beginning and the end of the follow-up period. Liver biopsy was performed in all patients before treatment, and the biopsies were performed in 28 patients after treatment. RESULTS: Biochemical remission was achieved by 80 (79.4%) patients. Of these, 53 (66.5%) showed near-normal liver histology or liver function test results and sonogram. The remaining 27 (33.5%) patients also achieved clinical and biochemical remission, but developed compensated cirrhosis. After a period of remission, 24 patients (32.5%) relapsed. Among the 22 (21.6%) patients who showed ultimate treatment failure, 6 underwent orthotopic liver transplantation and 3 died of liver failure while awaiting a transplant. Sixteen (72.7%) of the 22 patients who did not respond to therapy were non-compliant with medications and had irregular follow-up. The overall 10-year survival rate in the cohort was 96%. CONCLUSIONS: Long-term survival in AIH patients is very good. Prompt diagnosis and appropriate first-line and salvage therapy that includes close follow-up will make liver transplantation a rare necessity in the treatment of this disease.

Changes in serum Interleukin-33 concentration before and after treatment with pegylated interferon alfa-2a plus ribavirin in patients with chronic hepatitis C genotype 1b infection.

BACKGROUND: IL-33 is a novel member of the IL-1 family, which has been shown to play an important role in T helper 2 (Th2)-associated immune responses. Recent studies have suggested a possible role for IL-33 in the pathogenesis of liver damage during acute and chronic hepatitis; furthermore, IL-33 may be involved in the development and progression of liver fibrosis. OBJECTIVES: To evaluate serum IL-33 levels in a group of patients with chronic hepatitis C (CHC) genotype 1b at enrolment and after a course of pegylated (PEG)-IFN plus ribavirin. PATIENTS AND METHODS: 60 patients with chronic hepatitis C (CHC) and 65 healthy controls were examined and compared for serum IL-33 levels by ELISA. All CHC patients were submitted to liver biopsy either before starting antiviral treatment or during post-treatment follow up. We evaluated whether post-treatment IL-33 concentration was associated with histologic outcome as well as with virologic response to therapy. RESULTS: Serum IL-33 levels were significantly higher among CHC patients in comparison with healthy controls. IL-33 concentration was lower among patients with a METAVIR fibrosis score F1-F2, compared with those having a more advanced liver disease (METAVIR stage F3-F4). In addition, sustained virologic response (SVR) was associated with a significant drop in IL-33 levels, whereas no changes were found among relapsers and nonresponders. Analogously, patients experiencing liver histologic improvement after antiviral therapy had lower post-treatment IL-33 levels in comparison with baseline values. Contrarily, no variations were detected among subjects with worsened or stable histologic features. CONCLUSIONS: IL-33 may represent a new and easy-to-detect biomarker for the diagnosis of liver damage in CHC patients, as it appears to be modulated in parallel with biochemical and histologic parameters, such as ALT levels and liver fibrosis. Furthermore, considering that serum IL-33 concentration was significantly reduced following a successful course of antiviral treatment, this cytokine may also represent a sensitive indicator of SVR.

Increased expression of cyclooxygenase-2 is associated with the progression to cirrhosis.

BACKGROUND/AIMS: To investigate the degree of cyclooxygenase-2 (COX-2) protein expression in chronic hepatitis and cirrhosis. METHODS: COX-2 protein expression was evaluated in 43 cases of chronic hepatitis and 24 cases of cirrhosis using immunohistochemical techniques. The COX-2 immunohistochemical staining score was assessed using the scoring systems of Pazirandeh et al and Qiu et al. and each scoring system was based on a sum of the parameters of staining intensity and distribution. RESULTS: The mean COX-2 expression scores in chronic hepatitis and cirrhosis were 2.5 ± 1.3 vs. 3.3 ± 1.1 (p = 0.008), and 3.2 ± 2.0 vs. 4.5 ± 1.7 (p = 0.006), respectively, based on the Pazirandeh et al. and Qiu et al. scoring systems. The percentage samples of high COX-2 expression score (4 to 5) in chronic hepatitis and cirrhosis were 16.3% vs. 45.8% (p = 0.022), and 23.3% vs. 50% (p = 0.021), respectively, based on the two scoring systems. The mean COX-2 expression scores based on the severity of hepatic fibrosis scored using Ishak's modified staging system (fibrosis score 0 to 3 vs. 4 to 6) were 2.4 ± 1.3 vs. 3.2 ± 1.1 (p = 0.009), and 3.1 ± 2.0 vs. 4.3 ± 1.8 (p = 0.009), respectively, based on the two scoring systems. CONCLUSIONS: COX-2 expression was significantly higher in liver cirrhosis group than in chronic hepatitis. COX-2 expression scores according to Ishak's staging was significantly higher in the advanced fibrosis group. COX-2 may play a role in the progression of hepatic fibrosis.

Vascularização na cirrose hepática: estudo imunoistoquímico baseado em necropsias / Vascularization in hepatic cirrhosis: an immunohistochemical study on necropsies

RACIONAL: O processo patológico mais discutido na gênese da cirrose hepática é a fibrose progressiva, porém alterações na vasculatura do órgão têm sido apontadas como elementos fundamentais na fisiopatologia da doença e de suas complicações, como hipertensão portal, insuficiência hepática e carcinoma hepatocelular. OBJETIVO: Avaliar a densidade microvascular em 35 casos de necropsias de pacientes com cirrose hepática mediante pesquisa imunoistoquímica do marcador endotelial CD34 a fim de comparar os informes obtidos mediante semi-quantificação com aqueles registrados por método quantitativo morfométrico, além de relacionar as alterações vasculares encontradas com os principais agentes causais, padrões de lesão e complicações clínicas da doença. MÉTODOS: Foram estudados 35 casos de cirrose obtidos retrospectivamente de necropsias realizadas no SVOC/USP no período de março de 2002 a junho de 2003. Os casos foram reagrupados segundo padrão anatomopatológico em esteatohepatite e hepatite crônica. A microvasculatura foi avaliada através da reação imunoistoquímica com anticorpo anti-endotelio clone CD34, QBend. RESULTADOS: Observou-se associação significativa entre a abordagem semi-quantitativa e a quantificação morfométrica da densidade de vasos no parênquima, o mesmo não ocorrendo no septo. Não foram detectadas associações específicas entre a neovascularização e os tipos de complicação da hepatopatia aqui estudados. O principal achado foi que a neoformação vascular no parênquima é significantemente maior nas cirroses associadas a hepatites crônicas do que nas esteatohepatites. CONCLUSÃO: Todos esses achados requerem necessários estudos clínicos para avaliar a hipótese de que o estudo do rearranjo da microcirculação hepática, através de marcadores como o CD34, pode ser fator prognóstico em pacientes cirróticos.

BAKGROUND: Fibrosis has been the most cited variable in cirrhosis, but major alterations in hepatic vascularization have been pointed as basic elements in the physiopathology of the illness and its complications as portal hypertension, hepatic failure and hepatocellular carcinoma. METHODS: The present study aims at assessing microvascular density in 35 cases of necropsies of cirrhotic patients by immunohistochemical detection of endothelial marker CD34, comparing semi-quantification with morphometric quantitative method, also searching for a possible relation of vascular alterations with the main causal agents, injury patterns and major clinical complications. RESULTS: A significant association was detected between semi-quantitative and quantitative approach of microvessel density in parenchyma, but not in septa. No significant association was detected between neovascularization and any specific clinical complication of cirrhosis. Under our standpoint, the main achievement of the present study was the demonstration that the vascular neoformation in hepatic parenchyma is significantly higher in cirrhosis associated with chronic hepatitis than in cirrhosis resulting from steatohepatitis. CONCLUSION: These findings require further clinical studies to assess the hypothesis that the rearrangement of liver microcirculation through the detection of CD34 might be relevant in prognostic assessment of cirrhotic patients.

Perfil do HLA de classe II de pacientes com hepatite C e características de hepatite auto-imune / Class II HLA profile oh hepatitis C patients with autoimmune hepatitis features

Introdução: A infecção crônica pelo vírus da hepatite C (VHC) é uma epidemia que atinge mais de 170 milhões de pessoas em todo o mundo e frequentemente associa-se a fenômenos de auto-imunidade. O papel dos alelos de HLA de classe II vem sendo estudado em diversas condições autoimunes. Objetivos: investigar a presença de auto-imunidade em portadores de VHC; realizar análise de HLA de classe II em portadores de VHC com e sem marcadores de auto-imunidade. Casuística e Métodos: obtiveram-se retrospectivamente os dados clínicos, laboratoriais, histológicos hepáticos de 1312 indivíduos com VHC, e definiu-se a presença de HAI associada segundo critérios adotados pelo Grupo Internacional de Estudos da HAI (escore >= 10). Constituíram-se os subgrupos: VHC + HAI (n = 44); VHC + anticorpo antimicrossoma de fígado e rim tipo 1 (AAMFR-1) (n = 7); VHC+ anticorpo antimúsculo liso padrão tubular/antiactina (AAML-T/AAA) (n = 5) e controle de pacientes com VHC sem características de auto-imunidade (n = 29). A tipagem do HLA foi realizada em DNA leucócitário de sangue periférico, extraído pela técnica de DTAB/CTAB, seguido de SSCP com o kit Micro SSPTM HLA DNA Typing (One Lambda Inc., CA, USA). A análise estatística foi realizada com o teste de X2 de Pearson com correção de Yates ou teste exato de Fisher quando apropriado e nos casos de existência de associação foi calculado o coeficiente de Yule para quantificá-la. Resultados: observou-se no grupo VHC + HAI, em comparação com a casuística geral predominância de idade > 40 anos e níveis de ALT acima de três vezes o limite superior da normalidade, associação positiva com o HLADR4 (45,1% vs 3,4%, p = 0,0006, coeficiente de Yule = 0,92) e DQ3 (67,7% vs 37,9%, p = 0,04, coeficiente de Yule = 0,54) e associação negativa com o HLADR51 (9,6% vs 34,4%, p = 0,04, coeficiente de Yule = -0,66) e DR2 (9,6% vs 34,4%, p = 0,04, coeficiente de Yule = -0,66). Pacientes do grupo VHC + AAMFR-1...

Introduction: HCV chronic infection is an epidemic condition that affects more than 170 million of people around the world, and often is associated with autoimmunity phenomena. The role of HLA class II alleles has been studied in many autoimmune diseases. Aim: To investigate the presence of laboratory markers of autoimmunity and compatible anatomo pathologic histology for autoimmune hepatitis (AIH) in HCV patients; to perform HLA class II typing in HCV patients with and without autoimmunity markers. Material and Methods: Clinical, laboratory and liver histology data from 1312 HCV patients were obtained retrospectively. AIH was considered in association based on the International Group for the Study of AIH criteria score system (>= 10). The following groups were constituted: HCV + AIH (n = 44); HCV + anti-liver-kidney-microsome type 1 (LKM-1) (n = 7); HCV + antismooth muscle/anti-actin antibodies (SMA/AAA) (n = 5); control (HCV without autoimmunity) (n = 29). HLA typing was performed DNA extracted from leucocyte from periferic blood by DTAB/CTAB techniques, followed by SSCP with Micro SSPTM HLA DNA Typing kit (One Lambda Inc., CA, USA). Statistical analysis was performed with Pearson's X2 test, with Yates correction or Fisher exact test, when appropriated; when significant association was detected, Yule coefficient was calculated. Results: Age > 40 years old and ALT three times above upper normal limit predominated in the HCV + AIH group, when compared with the whole cohort (n = 1312). HLA typing in VHC+HAI group (n = 31) revealed positive association with HLA-DR4 (45.1% vs 3.4%, p = 0.0006, Yule = 0.92) and DQ3 (67.7% vs 37.9%, p = 0.04, Yule = 0.54) and negative association with HLA-DR51 (9.6% vs 34.4%, p = 0.04, Yule = -0.66) and DR2 (9.6% vs 34.4%, p = 0.04, Yule = -0.66), when compared with VHC control (n = 29). HCV + LKM-1 patients were younger than 40 years old at the time of initial disease manifestations (p = 0,001)...

Hepatitis crónica autoinmune / Chronic autoimmune hepatitis

La hepatitis autoinmune (HA) es una enfermedad inflamatoria crónica con destrucción progresiva del hígado produciendo necrosis, fibrosis y cirrosis. Diferentes estudios sugieren que es una enfermedad en la que existe una predisposición genética multifactorial que acoplada a algún factor desencadenante, gatilla una respuesta autoinmune dirigida contra los hepatocitos. La predisposición genética es un hecho reconocido en la HA llegándose a considerar la presencia de HLA-DR3 y DR4, como factores de riegos por si mismos para desarrollar la enfermedad. Se presenta el caso de una niña de 12 años cuyo cuadro clínico, hallazgos de laboratorio y de estudios de gabinete, fueron compatibles con hepatitis crónica autoinmune en fase de cirrosis e hipertensión portal.

The hepatitis autoinmune (HA) it is an illness inflammatory chronicle with progressive destruction of the liver producing necrosis, fibrosis and cirrhosis. Difíerent studies suggest that it is an illness in that it exists a bias genetic multifactori that coupled to some factor to unchail an answer managed autoinmune it is triggered against the hepatocell. The genetic bias is a fact recognized in there is her being ended up considering the presence of HLA-DR3 and DR4, as factors of waterings for if same to develop the illness.