Iron-rich foci in chronic viral hepatitis

Lefkowitch, Jay H.; Yee, Herman; J, Sweeting; Green, Peter H. R.; Magun, Arthur M.

doi:10.1016/s0046-8177(98)90219-2

Cited by 18 publications

(4 citation statements)

References 12 publications

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“…Even mild to moderate alcohol consumption has recently been shown to increase the prevalence of iron overload [110] . Iron localization has been reported in Kupffer cells [108] as well as in hepatocytes [111][112][113] . In our experience, iron accumulation is more common in hepatocytes than Kupffer cells in patients with ALD.…”

Section: Ethanol and Hcv Lead To Hepatic Iron Accumulationmentioning

confidence: 99%

Evaluation of standard liver volume formulae for Chinese adults

Shi¹,

Yan²,

Li³

et al. 2009

WJG

105

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Alcoholic liver disease (ALD) and hepatitis C virus (HCV) infection represent, either alone or in combination, more than two thirds of all patients with liver disease in the Western world. This review discusses the epidemiology and combined impact of ALD and HCV on the progression of liver disease. ALD and HCV affect the progression of liver disease to liver cirrhosis and hepatocellular carcinoma (HCC) in a synergistic manner. Thus, the risk for HCC increases five times with a daily alcohol consumption of 80 g; in the presence of HCV it is increased 20-fold, and a combination of both risk factors leads to a more than 100-fold risk for HCC development. Alcohol consumption also decreases the response to interferon treatment which is probably due to a lack of compliance than a direct effect on HCV replication. Several molecular mechanisms are discussed that could explain the synergistic interaction of alcohol and HCV on disease progression. They include modulation of the immune response and apoptosis, increased oxidative stress via induction of CYP2E1 and the hepatic accumulation of iron. Thus, both HCV and alcohol independently cause hepatic iron accumulation in > 50% of patients probably due to suppression of the liver-secreted systemic iron hormone hepcidin. A better understanding of hepcidin regulation could help in developing novel therapeutic approaches to treat the chronic disease in the future. For now, it can be generally concluded that HCV-infected patients should abstain from alcohol and alcoholics should be encouraged to participate in detoxification programs.

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Section: Ethanol and Hcv Lead To Hepatic Iron Accumulationmentioning

confidence: 99%

Evaluation of standard liver volume formulae for Chinese adults

Shi¹,

Yan²,

Li³

et al. 2009

WJG

105

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“…In such patients, macroscopical nodules that contain much more iron than the surrounding parenchyma are frequently present and are sometimes referred to as iron‐rich nodules or, more frequently, as siderotic nodules (80). Microscopical iron‐rich foci seem to be less common (81). Some of the siderotic nodules show cytological and architectural atypia and they are therefore referred to as high‐grade siderotic DN, while siderotic nodules without atypia are called regenerative siderotic nodules (80), although some authors consider siderotic nodules per definition as low‐grade DNs (82).…”

Section: Iron‐free and ‐Rich (Or Siderotic) Foci And Nodulesmentioning

confidence: 99%

Preneoplastic lesions in human hepatocarcinogenesis

Libbrecht¹,

Desmet

Roskams

2005

Liver International

180

109

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The early stages of hepatocarcinogenesis in human chronic liver diseases are characterized by the emergence of preneoplastic lesions of which some will eventually develop into hepatocellular carcinoma (HCC). Basic studies on the genetic and epigenetic alterations of these preneoplastic lesions may eventually lead to new therapeutic strategies. Clinicopathological studies are also important in order to determine optimal management of patients with a preneoplastic lesion. This article aims to provide a comprehensive review of the current concepts of preneoplastic lesion in chronic liver diseases. The microscopical small-cell dysplastic focus is the smallest morphologically recognizable precursor lesion of HCC and therefore is a logical target of study to elucidate the earliest events in hepatocarcinogenesis. In contrast, large-cell dysplasia is not a precursor lesion, but appears to be of clinical value because of its good predictive value for development of HCC. Dysplastic nodules (DNs) are macroscopically recognizable precursor lesions of HCC and high-grade DNs (HGDNs) have a risk of malignant transformation. Detection of DNs and correct differentiation from small HCC (<2 cm) is sometimes difficult, especially when only imaging techniques are used. Additional clinicopathological studies on identification and optimal treatment of DNs are necessary. Molecular studies on HGDNs and small HCCs may yield much information on the genetic mechanisms involved in the transition from severe dysplasia to early malignancy. In contrast, currently available data indicate that (large) regenerative nodules do not represent a distinct step in hepatocarcinogenesis. Animal models will be helpful in the further unravelling of human HCC development, provided that studies are performed on models that are good representatives of human hepatocarcinogenesis. We propose three criteria by which good mimickers can be identified.

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“…The presence of stainable iron in SLC, portal tract macrophages, and mesenchymal/stromal cells has garnered interest in both chronic viral hepatitis B and C as potential markers of poor response to treatment by some, 60 but not all, groups, 61 as reviewed. 62 Lefkowitch and associates 63 reported additional cases of ''iron-rich foci'' (2þ to 4þ) in chronic hepatitis C (2) and B (1), characterized as patchy granular hepatocellular iron deposition in periseptal or periportal regions adjacent to otherwise iron-free parenchyma; of note, two were cirrhotic (Fig. 6).…”

Section: Acute and Chronic Viral Hepatitismentioning

confidence: 99%

Pathology of Hepatic Iron Overload

Brunt¹

2005

Semin Liver Dis

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The role of liver biopsy in all chronic liver diseases continues to evolve with the emergence of new laboratory and imaging tests. However, the value of histologic examination for fibrosis, parenchymal architectural remodeling, and possible concurrent disease remains relatively unchallenged, including in patients with suspected iron overload. In addition, only histologic evaluation allows detailed analysis of cellular and acinar localization of iron. Routine use of an iron stain for all liver biopsy analysis enables detection of iron when not otherwise suspected. The broad classifications of iron overload include parenchymal ("primary") or reticuloendothelial ("secondary"), and mixed. These classifications, however, serve only as guidelines to differential diagnoses, as will be noted in the following review of pathology of iron overload. Ultimately, the role of the pathologist is to document cellular and acinar localization of iron and to provide a semiquantitative assessment of amount to alert the clinician to the possibility of a significant condition. In this article, histopathologic findings in conditions of iron overload and in several forms of liver disease are discussed.

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Iron-rich foci in chronic viral hepatitis

Cited by 18 publications

References 12 publications

Evaluation of standard liver volume formulae for Chinese adults

Evaluation of standard liver volume formulae for Chinese adults

Preneoplastic lesions in human hepatocarcinogenesis

Pathology of Hepatic Iron Overload

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