[Hepatic steatosis in chronic hepatitis C: study of risk factors and relationship with the fibrosis stage]. / Esteatosis hepática en la hepatitis crónica por virus C: estudio de los factores de riesgo y relación con el estadio de fibrosis.

BACKGROUND AND OBJECTIVE: Liver steatosis (LS) is a frequent histological finding in chronic hepatitis C virus (HCV) infection with prognostic implications. The aim of the present prospective study was to analyse the risk factors of steatosis and its relationship with the fibrosis stage in patients with chronic HCV infection. MATERIAL AND METHOD: Eighty four consecutive HCV RNA positive patients, not treated previously, in whom a liver biopsy was performed, were enrolled. In each patient demographic, clinical, laboratory, viral, and histological variables were obtained at the time of biopsy. Bivariate and multivariate analysis, calculating the odds ratio (OR) and the 95% confidence interval (95%CI), were performed. RESULTS: LS was present in 69% of patients. Risk factors of steatosis were an increase of the body mass index (OR: 1.17; 95%CI: 1.01-1.35) and chronic alcohol consumption (OR: 3.58; 95%CI: 1.1-11.6) whereas those of fibrosis were chronic alcohol consumption (OR: 3.58; 95%CI: 1.1-11.6) and increase of the liver inflammatory activity (OR: 1.31; 95%CI: 1.13-1.53). LS was associated with genotype 3 virus infection, which was present in all patients with this infection who had severe steatosis in a significantly greater proportion than in patients with non-genotype 3 virus infection (41.7% vs 2.8%; P<.001). LS was more frequent in patients with advanced fibrosis stages than in patients with non-advanced fibrosis (78,9% vs 60,9%; P=.074). CONCLUSIONS: LS is a frequent finding in HCV chronic infection related to both host and viral factors. LS could be a worsening factor of hepatic injury.

Esteatosis hepática en la hepatitis crónica por virus C: estudio de los factores de riesgo y relación con el estadio de fibrosis / Hepatic steatosis in chronic hepatitis C: study of risk factors and relationship with the fibrosis stage

Fundamento y objetivo: La esteatosis hepática (EH) es un hallazgo histológico frecuente en la infección crónica por el virus de la hepatitis C (VHC) que puede influir en el pronóstico de la enfermedad. El objetivo del presente estudio prospectivo es valorar los factores asociados a su presencia y su relación con el estadio de fibrosis en pacientes con infección crónica por VHC. Material y método: Se incluyó a 84 pacientes consecutivos con ARN-VHC positivo, no tratados previamente y a los que se practicó una biopsia hepática. En todos los pacientes se recogieron en el momento de la biopsia variables demográficas, clínicas, analíticas, virales e histológicas. Se practicaron análisis bivariante y multivariante, calculando la odds ratio (OR) y el intervalo de confianza (IC) del 95%. Resultados: La EH estuvo presente en 69% de los pacientes. Los factores de riesgo de esteatosis fueron el aumento del índice de masa corporal (OR=1,17; IC del 95%, 1,01¿1,35) y el consumo crónico de alcohol (OR=5,73; IC del 95%, 1,12¿29,63) mientras los de fibrosis avanzada fueron el consumo crónico de alcohol (OR=3,58; IC del 95%, 1,1¿11,6) y el aumento de la actividad inflamatoria hepática (OR=1,31; IC del 95%, 1,13¿1,53). La EH se asoció al genotipo viral 3, ya que estuvo presente en todos los pacientes con este genotipo, los cuales presentaron esteatosis grave en una proporción significativamente superior a la presentada por el resto de los pacientes (el 41,7 frente al 2,8%; p<0,001). La frecuencia de esteatosis fue mayor en los pacientes con estadios avanzados de fibrosis que en el resto de pacientes (el 78,9 frente al 60,9%; p=0,074). Conclusiones: La EH es un hallazgo frecuente en la infección crónica por VHC que se relaciona tanto con factores del huésped como virales. La presencia de esteatosis puede ser un factor de agravamiento de la lesión hepática (AU)

Background and objective: Liver steatosis (LS) is a frequent histological finding in chronic hepatitis C virus (HCV) infection with prognostic implications. The aim of the present prospective study was to analyse the risk factors of steatosis and its relationship with the fibrosis stage in patients with chronic HCV infection. Material and method: Eighty four consecutive HCV RNA positive patients, not treated previously, in whom a liver biopsy was performed, were enrolled. In each patient demographic, clinical, laboratory, viral, and histological variables were obtained at the time of biopsy. Bivariate and multivariate analysis, calculating the odds ratio (OR) and the 95% confidence interval (95%CI), were performed. Results: LS was present in 69% of patients. Risk factors of steatosis were an increase of the body mass index (OR: 1.17; 95%CI: 1.01¿1.35) and chronic alcohol consumption (OR: 3.58; 95%CI: 1.1¿11.6) whereas those of fibrosis were chronic alcohol consumption (OR: 3.58; 95%CI: 1.1¿11.6) and increase of the liver inflammatory activity (OR: 1.31; 95%CI: 1.13¿1.53). LS was associated with genotype 3 virus infection, which was present in all patients with this infection who had severe steatosis in a significantly greater proportion than in patients with non-genotype 3 virus infection (41.7% vs 2.8%; P<.001). LS was more frequent in patients with advanced fibrosis stages than in patients with non-advanced fibrosis (78,9% vs 60,9%; P=.074). Conclusions: LS is a frequent finding in HCV chronic infection related to both host and viral factors. LS could be a worsening factor of hepatic injury (AU)

Epstein-Barr virus negative clonal plasma cell proliferations and lymphomas in peripheral T-cell lymphomas: a phenomenon with distinctive clinicopathologic features.

Clonal B-cell populations have been described in peripheral T-cell lymphomas (PTCL) as secondary Epstein-Barr virus (EBV) driven B-cell expansions that may evolve to an overt B-cell lymphoma. EBV-negative B-cell proliferations associated with T-cell lymphomas are uncommon and not well characterized. We studied 15 patients who developed an EBV-negative B-cell proliferation or malignant lymphoma associated with PTCL. The T-cell tumors were 8 PTCL, not otherwise specified, 4 angioimmunoblastic T-cell lymphomas, and 3 cutaneous PTCL. The B-cell component was intermingled with the PTCL in all patients and it was classified as clonal/monotypic plasma cell proliferation in 8 lesions, clonal/monotypic large B-cell proliferation in 4 patients, and B-cell lymphoma with plasmacytic/plasmablastic differentiation in 3 patients. Two patients had 2 clonally unrelated plasma cell proliferations associated with the same PTCL. All cases showed cytoplasmic Ig light chain restriction. Clonal IgH and T-cell receptor rearrangements were detected in 11/12 and 11/13 cases examined, respectively. EBV, cytomegalovirus, and HHV-8 were not observed in any of the examined cases. Sequential samples in 7 patients showed persistence of the PTCL and the B-cell component in 4, the PTCL without the B-cell lymphoma in 2, and progression of the B-cell neoplasm in 1. Patients followed an aggressive clinical course similar to conventional PTCL. In conclusion, EBV-negative clonal or mononotypic B-cell proliferations in patients with PTCL present with a spectrum of lesions ranging from plasma cell proliferations to overt lymphomas with plasmacytic/plasmablastic features. The distinctive features of these patients suggest that these lesions represent a specific phenomenon in PTCL.