Navegando por Palavras-chave "Steatosis"
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- ItemAcesso aberto (Open Access)Diagnosis of hepatic steatosis by contrast-enhanced abdominal computed tomography(Colégio Brasileiro de Radiologia e Diagnóstico por Imagem, 2013-06-01) Monjardim, Rodrigo da Fonseca; Costa, Danilo Manuel Cerqueira; Romano, Ricardo Francisco Tavares; Salvadori, Priscila Silveira; Santos, Jaime de Vargas Conde dos; Atzingen, Augusto Castelli von [UNIFESP]; Shigueoka, David Carlos [UNIFESP]; D'Ippolito, Giuseppe [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Objective To evaluate the diagnostic capacity of abdominal computed tomography in the assessment of hepatic steatosis using the portal phase with a simplified calculation method as compared with the non-contrast-enhanced phase. Materials and Methods In the present study, 150 patients were retrospectively evaluated by means of non-contrast-enhanced and contrast-enhanced computed tomography. One hundred patients had hepatic steatosis and 50 were control subjects. For the diagnosis of hepatic steatosis in the portal phase, the authors considered a result of < 104 HU calculated by the formula [L - 0.3 × (0.75 × P + 0.25 × A)] / 0.7, where L, P and A represent the attenuation of the liver, of the main portal vein and abdominal aorta, respectively. Sensitivity, specificity, positive and negative predictive values were calculated, using non-contrast-enhanced computed tomography as the reference standard. Results The simplified calculation method with portal phase for the diagnosis of hepatic steatosis showed 100% sensitivity, 36% specificity, negative predictive value of 100% and positive predictive value of 75.8%. The rate of false positive results was 64%. False negative results were not observed. Conclusion The portal phase presents an excellent sensitivity in the diagnosis of hepatic steatosis, as compared with the non-contrast-enhanced phase of abdominal computed tomography. However, the method has low specificity.
- ItemSomente MetadadadosLate-onset systemic lupus erythematosus-associated liver disease(Springer, 2012-09-01) Schiavon, Leonardo L. [UNIFESP]; Carvalho-Filho, Roberto J. [UNIFESP]; Narciso-Schiavon, Janaina Luz [UNIFESP]; Lanzoni, Valeria P. [UNIFESP]; Ferraz, Maria Lucia G. [UNIFESP]; Silva, Antonio Eduardo B. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease, which predominantly affects women under 50 years old. Although liver disease is not included in the diagnostic criteria, abnormal liver tests are common among patients with SLE and, in a significant proportion of those patients, no other underlying condition can be identified. We described a case of liver involvement in late-onset SLE presenting with a predominantly cholestatic pattern. Other conditions associated with abnormal liver tests were excluded, and the patient showed a prompt response to steroid therapy. the spectrum of the liver involvement in SLE is discussed, with emphasis on the differential diagnosis with autoimmune hepatitis.
- ItemAcesso aberto (Open Access)Limolipin, um repressor transcricional que promove esteatose hepática(Universidade Federal de São Paulo (UNIFESP), 2017-10-26) Fernandes, Gustavo Werpel [UNIFESP]; Bianco, Antonio Carlos [UNIFESP]; Ribeiro, Miriam Oliveira; http://lattes.cnpq.br/7069953370349465; http://lattes.cnpq.br/3164827775137971; http://lattes.cnpq.br/9002769050037329; Universidade Federal de São Paulo (UNIFESP)Liver-specific disruption of the type 2 deiodinase gene (Alb-D2KO), that encodes the key enzyme that activates thyroid hormone, results in resistance to diet-induced obesity and to liver steatosis in mice. Here we report that this is caused by ~60% reduction in liver zinc finger protein-125 (Zfp125) expression. Zfp125 is a Foxo1-inducible transcriptional repressor that causes lipid accumulation in AML12 mouse hepatic cell line and liver steatosis in mice by reducing hepatocyte secretion of triglycerides and cholesterol. It acts by repressing 18 genes involved in lipoprotein structure, lipid binding and transport. There is a functional Zfp125-binding element located in the ApoE promoter, also present in 16 other lipid-related genes repressed by Zfp125. Liposome-mediated Zfp125 expression in liver causes steatosis and a ~3-fold increase in circulating VLDL+LDL-cholesterol. While liver-specific knockdown of Zfp125 in control mice causes a “Alb-D2KO-like” metabolic phenotype, liver-specific normalization of Zfp125 expression in Alb-D2KO mice rescues the metabolic phenotype, restoring normal susceptibility to diet-induced obesity, liver steatosis and hypercholesterolemia. These findings explain how a brief perinatal hepatic surge in local thyroid hormone activation affects the Foxo1-Zfp125 pathway and modulate susceptibility to obesity, liver steatosis and hypercholesterolemia later in life.
- ItemAcesso aberto (Open Access)Prebiotic and Synbiotic Modifications of Beta Oxidation and Lipogenic Gene Expression after Experimental Hypercholesterolemia in Rat Liver(Frontiers Media Sa, 2017) Alves, Claudia Cristina [UNIFESP]; Waitzberg, Dan Linetzky; Andrade, Laila Santos de [UNIFESP]; Aguiar, Lais dos Santos [UNIFESP]; Reis, Milene Barcelos [UNIFESP]; Guanabara, Camila Chaves [UNIFESP]; Aguiar, Odair [UNIFESP]; Ribeiro, Daniel Araki [UNIFESP]; Sala, PriscilaBackground and aims: Non-alcoholic fatty liver disease (NAFLD) is characterized by the presence of fat in hepatocytes because of decreased β-oxidation and increased lipogenesis. Prebiotics, probiotics, and synbiotic have modulatory effects on intestinal microbiota and may influence the gut-liver axis. Our aim was to evaluate the effects of prebiotic, probiotics, and synbiotic on liver histopathology and gene expression related to β-oxidation and lipogenesis after hypercholesterolemia. Methods: Wistar male adult rats (n = 40) were submitted to hypercholesterolemic conditions (HPC) (60 days). On Day 30 of HPC, rats were subdivided in 5 groups: negative control (NC): without HPC + Gv (distilled water); positive control (PC): with HPC + Gv (distilled water); prebiotic (PRE): HPC + Gv with prebiotic (Fiber FOS®); probiotic (PRO): HPC + Gv with probiotic strains Gv (Probiatop®); and synbiotic (SYN): HPC + Gv with synbiotic (Simbioflora®). All rats were sacrificed on Day 30 post-treatment. Blood was collected to verify total serum cholesterol, and liver tissue was sampled to verify histopathological changes and gene expression. Gene expression related to ß-oxidation (PPAR-α and CPT-1) and lipogenesis (SREBP-1c, FAS and ME) was evaluated in liver tissue using RT-qPCR. Results: PC had higher cholesterol levels when compared to NC. PRE and SYN rats had lower cholesterol levels than PC. PC rats showed more histopathological changes than NC rats; PRE and SYN rats showed fewer alterations than PC rats. PPAR-α was expressed at higher levels in SYN and PC rats compared with PRE and PRO rats. CPT-1 expression was similar in all groups. SREBP-1c was expressed at higher levels in PC rats compared with NC rats; levels were lower in SYN rats compared with PRO rats; levels were lower in PRE rats compared with PC and PRO rats. FAS was expressed at lower levels in PRE rats compared with SYN rats. ME expression was lower in PC rats compared with NC rats. Conclusion: Prebiotic and synbiotic supplementation improve hepatic alterations related to hypercholesterolemia. These changes appear to be mediated by altered expression of genes related to β-oxidation and lipogenesis.