Objective To investigate the features and the probable affecting factors of the proliferation and differentiation of the hepatic progenitor cells (HPC) and the liver regeneration in the patients with severe hepatitis(SH). Methods Liver tissues taken from 59 cases with severe hepatitis were tested for the proliferating cell nuclear antigen (PCNA) by immunohistochemistry (IHC). Meanwhile, PCNA were also detected in liver tissues of 58 cases with common hepatitis as controls. Results The percentage of cases with positive PCNA in hepatocytes in severe hepatitis (30.5%) was significantly lower than that in common hepatitis (50.0%) (P

Objective To observe pulmonary fibrosis in severe acute respiratory syndrome (SARS) and to discuss the mechanisms of pulmonary fibrosis in SARS. Methods Hematoxylin and Eosin staining (H&E), histology staining and immuno-histochemical staining (SP methods) were used to investigate the lungs from 4 autopsy cases. Antibodies against collagen type Ⅲ, ?-smooth muscle actin(?-SMA), Fas, FasL and transforming growth factor ?1(TGF-?1) were used for immunohistochemical studies. Results All these four lung tissues showed different degree of pulmonary fibrosis, including the organization of exudative fibrin, glomerulus-like fibrosis in alveolar spaces, the thickening of the alveolar septum, proliferation of fibroblasts, the hyperplasia of collagen fibers and the consolidation of lungs. Sirius red staining and collagen type Ⅲ staining showed the type Ⅲ and the type Ⅰ collagen fibers were the main components of the hyperplastic collagen fibers. ?-SMA were expressed in fibroblasts, immunoreactivity to Fas, FasL, TGF-?1 were all positive and located in plasma of pneumocytes, macrophages and lymphocytes. Conclusions The pulmonary fibrosis can be observed early in SARS patients and the pathogenesis may be involved in the co-effect of many effective cells, inflammatory mediators and cytokines.

Objective To investigate the changes in serology and liver histology of patients with chronic hepatitis B after interferon treatment. Methods Twenty four patients with chronic hepatitis B were enrolled in this research. Sera of patients were obtained before and after interferon treatment respectively. Liver biopsy was performed in each patient before and after treatment respectively. Serum ALT, HBsAg, HBcAg, HBeAg, HBV DNA and TIMP 1 were evaluated, as well as HAI(histological activity index), HBsAg, HBcAg, HBeAg, TIMP 1 and activated HSC in liver. Results The patients responded to interferon accounted for 7/24(37.5%). Compared with pretreatment, the serum HBV DNA and TIMP 1 decreased significantly( P

Objective We report the pathological features of lung in the dead patients with severe acute respiratory syndrome (SARS). Methods Post-mortem lung and pulomonary hilar lymph nodes tissues of 3 patients dead from SARS were studied by histology and immuhistochemistry with rabbit anti-Fas polyclonal antibody, mouse anti-PCNA, mouse anti- CD83,mouse anti-CD4 and mouse anti-CD8 monoclonal antibodies. Results The surface of lung from 3 cases were shown red or purplish red color. Histopathological examination showed that diffuse interstitial exudative or leakage inflammation and alveolar damages with a pronounced increase of of monocytes in the interval at various levels of progression and severity. There were hyaline-membrane formation, desquamation and apoptosis of type-2 pneumocytes in alveolar spaces. Fibrin thrombus and thrombo-embolism could be found in blood capillary and bronchial artery respectively. We observed some fibrin deposition in alveoli interval. No obviously giant-cell infiltrate within the alveolar lumen. The positive cell of proliferative cell nuclear antigen (PCNA) was rare. Fas antigen were expressed in a lot of type-2 pneumocytes, monocytes of the interval and pulomonary hilar lymph nodes. Comparison with the lymph nodes of chronic inflammation, there were obviously disorganization and attenuation of lymphocyte in lymph nodes of SARS. The proportion of CD4 positive lymphocytes were rare, but CD83 and CD8 positive lymphocyte seemed no decreased, relatively. The seminal changes such as decreased lymphocytes ,white pulp atrophy,hemorrhage and necrosis,and decreased expression of lymphocytes for CD4 antigen could also observe in spleen. Conclusions Severe damages of lung and immunological system damages might lead to death of patients with SARS.

OBJECTIVETo raise the accuracy of clinical diagnosis of chronic hepatitis B.

METHODSThe correlation between the clinical features, biochemical tests (the serum total bilirubin-TBil, albumin-ALB, prothrobin activity-PTA, alanine aminotransferase-ALT, albumin/globulin-A/G, and r-globulin-r-G) and histopathological data in 202 patients with chronic hepatitis B (CHB) were studied.

RESULTSSome of presenting symptoms and signs were obviously associated with histological grade and stage. The grade of necroinflammatory activity of CHB was associated with the rising TBil, ALT, GGT and the declining ALB, A/G and PTA. The coincidence of clinical diagnosis and pathology was highest in mild chronic hepatitis, 63.8%~79.0%; then was in marked chronic hepatitis, 40.0%~62.5%. The coincidence was lowest in moderate chronic hepatitis, 10.0%~28.2%.

CONCLUSIONSGreat attention should be paid to the significance of symptoms and signs, meanwhile the standard of clinical diagnosis for moderate chronic hepatitis might be relaxed somewhat.

Adolescent ; Adult ; Aged ; Alanine Transaminase ; blood ; Bilirubin ; blood ; Biomarkers ; analysis ; blood ; Clinical Medicine ; Female ; Hepatitis B, Chronic ; blood ; diagnosis ; pathology ; physiopathology ; Histological Techniques ; Humans ; Male ; Middle Aged ; Prothrombin ; analysis

Adolescent ; Adult ; Aged ; Child ; Child, Preschool ; Female ; Hematologic Tests ; Humans ; Liver Cirrhosis ; pathology ; Male ; Middle Aged ; Portal Vein ; diagnostic imaging ; pathology ; Severity of Illness Index ; Spleen ; blood supply ; pathology ; Splenic Vein ; diagnostic imaging ; pathology ; Ultrasonography, Doppler, Color

Objective To develop a simple model for the noninvasive diagnosis of liver fibrosis in patients with chronic hepatitis B and to testify its diagnostic value. Methods One hundred and ninety patients with chronic hepatitis B who had undergone liver biopsy were divided into 2 groups:one for developing the model(n=110) and one for validation(n=80). Histological staging of liver fibrosis,assessed blindly and independently by 2 pathologists,was determined according to Scheuer fibrosis score.Twenty markers involved in the study were analyzed initially in the estimation group to derive a predictive model to discriminate the stages of fibrosis.The model created was then assessed with receiver operating characteristic curve(ROC)analysis. It was also applied to the validation group to test its accuracy. Results Haptoglobin(HPT),γ-glutamyl transpeptidase(GGT)and platelet were identified by logistic regression analysis as independent factors of fibrosis. A model developed from the above three markers was established to predict the stage of fibrosis(S). In ROC analysis,the area under curve(AUC) for identifying S≥1,S≥2,S≥3 and S=4 was 0.832,0.835,0.820 and 0.843 respectively. The model had a similar AUC in the vatidation group without statistically significant difierence. Using a cut-off of ＜0.18, significant fibrosis (S≥2)could be excluded in 27 patients of the total patient population(negative predictive value 90%).Similarly,applying a cut-off ≥0.70,significant fibrosis could be identified correctly in 67 patients of the total patient population(positive predictive value 82.7%).The model had a high level of diagnostic value in patients with HBeAg-positive chronic hepatitis B as well as in patients with HBeAg-negative chronic hepatitis B(AUC for identifying S≥2,0.857 vs 0.802). Restricting biopsy to patients with intermediate scores(≥0.70 and ＜0.18) may prevent liver biopsies in 58.4% of the patients while maintaining 84.7% accuracy. Conclusions A model including HPT,GGT and platelet is a simple and reliable index for predicting significant fibrosis in patients with HBeAg-positive chronic hepatitis B as well as in patients with HBeAg-negative chronic hepatitis B.

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.

OBJECTIVETo study the pathological characteristics of severe acute respiratory syndrome (SARS) and its relationship to clinical manifestation.

METHODSTissue specimens from 3 autopsies of probable SARS cases were studied by microscope, and the clinical data was reviewed.

RESULTSThe typical pathological changes of lungs were diffuse hemorrhaging on the surface. A combination of serous, fibrinous and hemorrhagic inflammation was seen in most of the pulmonary alveoli with the engorgement of capillaries and detection of micro-thrombosis in some of these capillaries. Pulmonary alveoli thickened with interstitial mononuclear inflammatory infiltrates, suffered diffuse alveolar damage, experienced desquamation of pneumocytes and had hyaline-membrane formation, fibrinoid materials, and erythrocytes in alveolar spaces. There were thromboembolisms in some bronchial arteries. Furthermore, hemorrhagic necrosis was also evident in lymph nodes and spleen with the attenuation of lymphocytes. Other atypical pathological changes, such as hydropic degeneration, fatty degeneration, interstitial cell proliferation and lesions having existed before hospitalization were observed in the liver, heart, kidney and pancreas.

CONCLUSIONSevere damage to the pulmonary and immunological systems is responsible for the clinical features of SARS and may lead to the death of patients.

Aged ; Humans ; Lung ; pathology ; Lymph Nodes ; pathology ; Male ; Middle Aged ; Severe Acute Respiratory Syndrome ; pathology ; Spleen ; pathology

OBJECTIVETo identify the type of iron deposition and describe its amount, distribution and associated lesions, in order to support an etiologic diagnosis for hemochromatosis.

METHODSHematoxylineosin (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.

RESULTSOne 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.

CONCLUSIONEtiologic 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.

Biopsy ; Hemochromatosis ; Humans ; Iron ; Liver