Risk Factors For Steatosis Research Articles

Esteato-hepatite relacionada ao vírus da hepatite C: perfil clínico-histológico

INTRODUÇÃO: Esteatose ocorre com freqüência na hepatite crônica pelo vírus C (HCV) e parece estar relacionada a fatores clínicos e/ou virológicos. Contudo, a presença de esteato-hepatite, uma condição indutora de fibrose, tem sido pouco estudada. OBJETIVO: Estudar a associação de HCV com esteato-hepatite em material de biópsia hepática, correlacionando-a com dados clínicos. MÉTODOS: As biópsias hepáticas de pacientes com HCV foram avaliadas quanto a atividade, estádio e presença de alterações morfológicas de esteato-hepatite. Os dados morfológicos foram correlacionados a parâmetros clínicos que incluíam: consumo alcoólico, IMC, colesterol, triglicérides, glicemia, exposição a petroquímicos e genótipo viral. RESULTADOS: Esteato-hepatite foi encontrada em 42 de 252 (16,6%) pacientes com HCV. Entre os 42 casos, critérios para obesidade, diabetes e dislipidemia foram encontrados em 16,7%; 16,7% e 21,4%, respectivamente. O genótipo 3 esteve presente em 38,1% dos casos. Fatores de risco para esteato-hepatite não-alcoólica (NASH) foram encontrados em 73% dos casos em genótipos diferentes do 3, enquanto tais fatores foram presentes em 37,5% dos casos com genótipo 3 (p = 0,05). O padrão morfológico mais freqüente foi a esteatose macrovacuolar de moderada intensidade (61,9%) com distribuição difusa (64,3%). Tanto o padrão de fibrose de NASH quanto o de HCV foram notados: fibrose perissinusoidal (87,8%), portal (87,8%), septal (69,0%) e cirrose (30,9%). CONCLUSÕES: Esteato-hepatite é freqüente em pacientes com HCV, apresentando padrão peculiar de distribuição da esteatose e alta freqüência de cirrose. Em genótipos diferentes do 3, a esteato-hepatite parece estar relacionada à sobreposição de fatores de risco para NASH.

Hepatic steatosis in HIV–HCV coinfected patients: analysis of risk factors

To evaluate the prevalence and severity of steatosis and possible interactions between steatosis, host factors, viral factors, and treatment for HIV infection in HIV-hepatitis C virus (HCV) coinfected patients. Steatosis was assessed among 395 HIV-HCV coinfected patients who were enrolled in the ANRS trial HC02 Ribavic and for whom histological data were available. Steatosis was graded as follows: 0 (none); 1 (< 30% hepatocytes containing fat); 2 (30-70%); 3 (> 70%). Steatosis was present in 241 patients (61%), of whom 149 (38%) had grade 1, 64 (16%) grade 2 and 28 (7%) grade 3. In multivariate analysis, the following five independent risk factors were associated with steatosis: HCV genotype 3 [odds ratio (OR), 3.02; 95% confidence interval (CI), 1.91-4.79; P < 0.0001], the mean METAVIR fibrosis score (OR, 1.43; 95% CI, 1.11-1.84; P = 0.0053), the body mass index (BMI; OR, 1.13; 95% CI, 1.05-1.21; P = 0.0013), HCV viral load (OR. 1.65; 95% CI, 1.22-2.23; P = 0.0012) and ferritin (OR, 1.13; 95% CI, 1.06-1.21; P < 0.0003). As HCV genotype 3 was a risk factor for steatosis, further exploratory analyses were stratified according to the HCV genotype (1 and 3). Factors independently associated with steatosis were BMI and HCV viral load in patients with HCV genotype 3 infection and the mean METAVIR fibrosis score, the BMI and ferritin in patients with HCV genotype 1 infection. Steatosis is particularly frequent in HIV-HCV coinfected patients, who appear to have the same risk factors for steatosis as HCV monoinfected patients. None of the characteristics of HIV infection, including antiretroviral therapy, was independently associated with steatosis.

Steatosis in hepatitis C: What does it mean?

Hepatitis C and nonalcoholic fatty liver disease (NAFLD) are both common causes of liver disease. Thus, it is not surprising that they can coexist in the same individual. The prevalence of steatosis in patients with chronic hepatitis C differs between studies, probably reflecting population differences in known risk factors for steatosis, namely overweight, diabetes, and dyslipidemia. The pathogenic significance of steatosis likely differs according to its origin, metabolic (NAFLD or nonalcoholic steatohepatitis) or virus related (due to hepatitis C virus genotype 3). Whether or not steatosis determines fibrosis progression is not yet unproven.

Liver transplantation for jejunoileal bypass-associated cirrhosis: Allograft histology in the setting of an intact bypassed limb

Jejunoileal bypass (JIB) is a well known cause of steatohepatitis, which may, on occasion, progress to cirrhosis and require liver transplantation. We report 3 patients who underwent orthotopic liver transplantation (OLT) for steatohepatitic cirrhosis secondary to JIB in which the JIB was left intact. All 3 patients have demonstrated recurrent steatosis in the graft after liver transplantation. In two of the cases, the changes are moderately severe, whereas in one case the changes are mild. All 3 patients have essentially normal liver function tests and are clinically asymptomatic; 1 of the patients has undergone removal of the JIB 2.5 years after transplantation. Control hepatic allografts in patients with primary biliary cirrhosis and primary sclerosing cholangitis show negligible fatty change, and in patients who receive transplants for alcoholic steatohepatitis, they rarely (2 of 20 patients) contain greater than 10% fat. We conclude that transplantation alone is not associated with subsequent steatosis. Presence of JIB is, therefore, a continuing risk factor for steatosis in patients who have undergone OLT. Reversal of JIB after OLT may be considered if fatty changes are severe or associated with significant fibrosis.

Idiopathic steatohepatitis in childhood: A multicenter retrospective study

Objective: To describe the clinical, laboratory, and histopathologic features of idiopathic steatohepatitis in children. Study design: Retrospective review of all liver biopsies performed at Boston Children's Hospital, Massachusetts General Hospital, and the University of Massachusetts Medical Center from 1991 to 1994. Chart review was performed when biopsies demonstrated steatosis. Results: Eighty-two patients had biopsy-proven hepatic steatosis. Fourteen patients had fatty liver without evidence of inherited, infectious, autoimmune, endocrinologic, toxicologic, or iatrogenic causes. All 14 patients were obese, averaging 159% of ideal body weight (range, 121% to 222%). Nine patients initially had transient abdominal pain, two had hepatomegaly, and one was identified by incidental laboratory evaluation. These 12 patients had biopsies because of persistent elevations of aminotransferase levels. Two other patients without risk factors for steatosis were identified at staging laparotomy for Hodgkin lymphoma. The 10 boys and 4 girls had an average age of 13.5 years (range, 10 to 18 years). Aminotransferase elevations were modest, with aspartate aminotransferase and alanine aminotransferase values averaging 77 ± 38 IU and 129 ± 73 IU, respectively. All had imaging studies demonstrating diffuse fatty change. Histologic examination of biopsy specimens revealed varying degrees of steatosis with inflammation and fibrosis. Conclusion: Idiopathic steatohepatitis occurs predominantly or exclusively in obese peripubertal children. This entity represents a frequent reason for liver biopsy in this age group. The degree of steatosis, fibrosis, and inflammation does not correlate with symptoms or signs, and significant liver injury with bridging fibrosis may be present. (J P EDIATR 1995;127:700-4)