Liver eosinophilic infiltrate is a significant finding in patients with chronic hepatitis C
Cattedra ed Unità Operativa di Gastroenterologia ed Epatologia, Dipartimento Biomedico di Medicina Interna e Specialistica, University of Palermo, Italy. Journal of Viral Hepatitis
(Impact Factor: 3.91).
07/2008; 15(7):523-30. DOI: 10.1111/j.1365-2893.2008.00976.x
Eosinophilic infiltrate of liver tissue is described in primary cholestatic diseases, hepatic allograft rejection and drug-induced liver injury, but its significance and its implications in chronic hepatitis C are unknown. The aim of this study was to investigate the clinical significance of eosinophilic liver infiltrate in patients with chronic hepatitis C. We retrospectively evaluated 147 patients with chronic hepatitis C. The presence of eosinophilic infiltrate was investigated in liver biopsies, and a numeric count of eosinophilic leucocytes in every portal tract was assessed. An eosinophilic infiltrate of liver tissue (> or =3 cells evaluated in the portal / periportal spaces) was observed in 46 patients (31%), and patients who consumed drugs had an odds ratio (OR) of 4.02 (95% CI: 1.62-9.96) to have an eosinophilic infiltrate in liver biopsy. By logistic regression analysis, the presence of steatosis was independently associated with eosinophilic infiltrate (OR 5.86; 95% CI: 2.46-13.96) and homeostasis model assessment-score (OR 1.18; 95% CI: 1.00-1.39). Logistic regression analysis also showed that fibrosis staging > or = 2 by Scheuer score was associated with grading >1 by Scheuer score (OR 6.82; 95% CI 2.46-18.80) and eosinophilic infiltrate (OR 4.00; 95% CI 1.23-12.91). In conclusion, we observed that the eosinophilic infiltrate of liver tissue was significantly more frequent in patients who assumed drugs, and found a significant association between eosinophilic infiltrate, liver steatosis and liver fibrosis. These preliminary data could lead to a constant assumption of drugs as a co-factor of eosinophils-mediated liver injury in chronic hepatitis C.
Available from: Zheping Huang
- "However, the same doses of As(III) elicited severe necrosis in Nrf2 −/− mice with more infiltrated inflammatory cells including eosinophils (Fig 2, liver panel, G and H). This indicates progression to liver disease, since eosinophilic infiltration was recently found to be associated with liver steatosis and liver fibrosis (Tarantino et al., 2008). As expected, there was no significant malignant hyperplasia observed in bladder epithelium in either Nrf2 +/+ or Nrf2 −/− mice following six-weeks of As(III) exposure. "
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ABSTRACT: Arsenic compounds are classified as toxicants and human carcinogens. Environmental exposure to arsenic imposes a big health issue worldwide. Arsenic elicits its toxic efforts through many mechanisms, including generation of reactive oxygen species (ROS). Nrf2 is the primary transcription factor that controls expression of a main cellular antioxidant response, which is required for neutralizing ROS and thus defending cells from exogenous insults. Previously, we demonstrated a protective role of Nrf2 against arsenic-induced toxicity using a cell culture model. In this report, we present evidence that Nrf2 protects against liver and bladder injury in response to six weeks of arsenic exposure in a mouse model. Nrf2(-/-) mice displayed more severe pathological changes in the liver and bladder, compared to Nrf2(+/+) mice. Furthermore, Nrf2(-/-) mice were more sensitive to arsenic-induced DNA hypomethylation, oxidative DNA damage, and apoptotic cell death. These results indicate a protective role of Nrf2 against arsenic toxicity in vivo. Hence, this work demonstrates the feasibility of using dietary compounds that target activation of the Nrf2 signaling pathway to alleviate arsenic-induced damage.
Toxicology and Applied Pharmacology 07/2009; 240(1):8-14. DOI:10.1016/j.taap.2009.06.010 · 3.71 Impact Factor
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ABSTRACT: Chronic hepatitis C virus infection is the leading etiology for liver transplantation in the United States. Recurrent hepatitis C occurs nearly universally in these patients and represents a serious posttransplantation complication. Despite the detailed characterization of the histologic features of both recurrent hepatitis C and acute cellular rejection (ACR) over the last decades, the pathologic distinction between these 2 conditions remains one of the greatest diagnostic challenges in liver pathology. An accurate diagnosis, nevertheless, plays an essential role in patient management, as different therapeutic strategies are used for these conditions. In this review, the clinicopathologic features of posttransplantation recurrent hepatitis C and ACR are discussed, with emphasis on distinguishing histopathologic features, morphologic variants, ancillary techniques, and diagnostic pitfalls.
Advances in anatomic pathology 09/2011; 18(5):393-405. DOI:10.1097/PAP.0b013e31822a5a10 · 3.23 Impact Factor
Available from: Evaggelia Liaskou
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ABSTRACT: Innate immune system is the first line of defence against invading pathogens that is critical for the overall survival of the host. Human liver is characterised by a dual blood supply, with 80% of blood entering through the portal vein carrying nutrients and bacterial endotoxin from the gastrointestinal tract. The liver is thus constantly exposed to antigenic loads. Therefore, pathogenic microorganism must be efficiently eliminated whilst harmless antigens derived from the gastrointestinal tract need to be tolerized in the liver. In order to achieve this, the liver innate immune system is equipped with multiple cellular components; monocytes, macrophages, granulocytes, natural killer cells, and dendritic cells which coordinate to exert tolerogenic environment at the same time detect, respond, and eliminate invading pathogens, infected or transformed self to mount immunity. This paper will discuss the innate immune cells that take part in human liver inflammation, and their roles in both resolution of inflammation and tissue repair.
Mediators of Inflammation 08/2012; 2012(2):949157. DOI:10.1155/2012/949157 · 3.24 Impact Factor
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