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<p><b>OBJECTIVE</b>To identify the type of iron deposition and describe its amount, distribution and associated lesions, in order to support an etiologic diagnosis for hemochromatosis.</p><p><b>METHODS</b>Hematoxylineosin (HE) stain, reticular fiber stain, Masson's stain and Perl's iron stain were used to assess liver biopsies from 31 patients with hemochromatosis. The Ishak scoring system and Deugnier scoring system were used to assess the histological change in liver and to semi-quantify the excess of hepatic iron. Genetic testing results were received from a portion of the patients and used in analysis.</p><p><b>RESULTS</b>One patient had hereditary (-HFE) hemochromatosis complicated with Gilbert's syndrome, for which the pattern of iron deposition was similar to that of the four patients with Gilbert's syndrome. Iron accumulation appeared as fine granules predominating at the biliary pole of cells and was distributed throughout the lobule with a decreasing gradient spanning from the periportal to centrolobular areas. Mild chronic inflammation was found to be commonly associated with low stage fibrosis.One patient had HFE hemochromatosis complicated with hepatitis B virus infection, and the pattern of iron deposition resembled that in the eight patients with viral hepatitis, wherein the deposition was mainly in the sinusoidal cells and/or portal macrophages. Histological grading and fibrosis staging differed among patients. The five patients with blood disordered showed iron accumulation mainly in the periportal hepatocytes, but mesenchymal iron deposits were also present. The grade of inflammation, as well as of fibrosis,was mild. The five patients with alcoholic disease and the five patients with drug-induced hepatitis showed hepatic iron deposition in swollen or ballooned hepatocytes. The two patients with excessive iron supply showed iron deposition localized within the parenchymal and mesenchymal cells.</p><p><b>CONCLUSION</b>Etiologic diagnosis of hemochromatosis relies on both the type of iron deposition and the nature of associated lesions. Liver biopsy is necessary for both diagnosis and prognosis.</p>
Subject(s)
Humans , Biopsy , Hemochromatosis , Iron , LiverABSTRACT
Objective To investigate the changes of CD4+ CD25+ regulatory T lymphocyte (Treg) and expressions of folkhead helix transcription factor 3 (FoxP3) in intestinal mucosa in human immunodeficiency virus (HIV) infected patients. Methods Twenty-one HIV infected patients and 17 control subjects without HIV infection were included in this study. The expression of FoxP3, which was considered as a specific marker of CD4+ CD25 + Treg, was detected in intestinal mucosa specimens from HIV infected patients by immunohistochemistry. Meanwhile, the in situ expression of CD4+ T lymphocyte was also determined by immunohistochemistry. The data were analyzed by t test. Results The positive labeling index of CD4+ T lymphocyte in intestinal mucosa was significantly lower in HIV infected patients compared to the controls (11. 56%±4. 44% vs 43. 49% ±8. 90% ,t=-11. 86,P<0. 01). The positive labeling index of FoxP3 in intestinal mucosa was also significantly lower in HIV infected patients compared to the controls (0.46% ± 0.20% vs 1. 18% ± 0. 44% ,t= - 5. 98,P<0.01). Conclusion The depletion of CD4+ CD25+ Treg is accompanied with the depletion of CD4 + T lymphocyte and the reduction of FoxP3 expression in intestinal mucosa of HIV infected patients.
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Objective To describe the development of nodules of altered hepatocytes (NAH) in chronic hepatitis B and to reveal progression of the nodules to hepatocellular carcinoma (HCC). Methods HCC, NAH and ordinary regenerative nodules (ORN) were identified and compared histologically. Expression levels of hepatitis B virus (HBV) antigens, mitoactivity and p53 accumulation in these lesions were evaluated by immunohistochemistry. Results Multiple foci of altered hepatocytes (FAH) and NAH were identified in the liver parenchyma surrounding HCC in all of the samples examined. Sequential architectural and cellular changes were observed during the progression of FAH to NAH and HCC. Expression levels of HBV surface and core antigens were found to be significantly decreased in ORN, NAH and HCC, with their positive rates being 70 % (35/50), 50 % (25/50), 10 % (5/50) and 60 % (30/50), 40 % (20/50), 6 % (3/50), respectively (P ＜0.05). Ki-67-1abelling indices were determined to be (0.58±0.49) %, (2.46±1.05) % and (40.36±26.27) %in these lesions, respectively (P ＜0.05). Nuclear p53 accumulation was found only in HCC. Its occurrence was associated to a high histological grade, with its frequencies being 13 % (1/8), 41% (11/27) and 73 % (11/15)in grade 1, 2 and 3 lesions, respectively. Conclusion NAH lesions, identified by their morphologic features and mitoactivity elevation, are detectable in resected liver samples with chronic hepatitis B and cirrhosis. They represent a common HCC precursor and can be used as a surrogate marker for the surveillance of high-risk individuals.
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Objective Focal nodular hyperplasia(FNH) is composed of multiple hyperplastic liver cell nodules,but its pathogenesis has not been elucidated. Foci (FAH) or nodules of altered hepatocytes (NAH) are precursors of hepatocellular adenoma (HCA) and carcinoma.This study aimed at identifying FAH and NAH from FNH and evaluating their role in FNH development.Methods 6 FNH lesions from 5 patients and 10 HCA from 9 patients were examined histologically,and expression levels of CD_(34) cytokeratin 19(CKl9) and Ki-67 antigen were demonstrated immunohistochemicailly.Proliferative activity was evaluated by Ki-67 antigen-labeling indices(Ki-67 LI).Results Multiple FAH and NAH were identified in all of the 6 FNH lesions. Whiie micmvasculatures were demonstrated by CD_(34) immunoreactivity in both HCA and FNH,their density and distribution were different in these two lesions,being diffuse in HCA and focal or nodular,mainly within NAH.CKl9 expression Was found in FNH,localized in ductal and ductular cells,but not within NAH and HCA.Average Ki.67 LI of 73 NAH(2.8%) was shown to be higher than that of the whole FNH lesions (0.6%),and had no statistieal difference comparable to that of HCA(1.8%).Conclusion Muhiple NAH are present in all classical FNH lesions.Unlike the surrounding parenchyma,NAH lesions are more proliferative and equipped with CD_(34)-positive microvasculatures as in HCA.
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Osteoclast (OC) are bone resorbing cells whose development and activity are under the influence of osteoblast (OB). The potential association between those two cell lineages is an area of significant interest. It was not until 1998 that osteoclast differentiation factor (ODF) and osteoprotegerin (OPG) was cloned. The two novel TNF superfamily members have been recently demonstrate to be the key extracellular regulators of osteoclasteogenesis and bone resorption both in vivo and in vitro, and they play important roles in osteoporosis development, diagnosis and treatment.