Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study correlated histopathology and diagnostic tests in hemodialysis patients with serologic markers for hepatitis C virus (HCV). Hepatitis C virus infection was found in 65 of 163 patients, as assessed by anti-c100-3 (ELISA 1), anti-c22-3, c33C (ELISA 2), and RIBA 2. Several histopathologic patterns were found in 33 liver samples from HCV-positive individuals: cirrhosis (n = 3), chronic active hepatitis (n = 14), chronic persistent hepatitis (n = 2), isolated hemosiderosis (n = 5), reactive hepatitis (n = 6), and others (n = 3). There was a positive correlation between time from the first aminotransferase peak and histologic damage (P = 0.015). However, the severity of liver disease did not correlate with the intensity of RIBA 2 positivity, mean levels or pattern of aminotransferases elevation, or markers of past hepatitis B virus infection. Moreover, aminotransferases were persistently normal in three patients with severe liver disease and were elevated in 10 patients with only mild changes. In 19 biopsied patients, the presence of plasma HCV RNA was examined by the polymerase chain reaction (PCR), which was positive in 15 of the 19 biopsy specimens. The ability of PCR positivity to predict the histologic severity of the disease was insufficient: four patients with minor liver damage had positive PCR and two patients with significant liver damage had negative PCR. No further correlations of PCR positivity were found with the other biochemical or immunologic markers of HCV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver disease patterns in hemodialysis patients with antibodies to hepatitis C virus. 750 4

The diagnosis of homozygous hemochromatosis (HH) should be based on appropriate findings on liver biopsy specimens. In cases with equivocal morphologic features, quantitative tissue iron determination and calculation of the hepatic iron index generally enable one to distinguish HH from other types of hepatic iron overload. In this article, we describe a diagnostic algorithm that is designed to avoid diagnostic errors because of histologic misinterpretation or erroneous, usually false-negative, chemical iron studies. The algorithm also delineates a cost-effective method of using quantitative tissue iron analysis. Diagnostic biopsy features of uncomplicated HH include (1) hemosiderosis that involves primarily hepatocytes, with or without inactive cirrhosis, and (2) a tissue iron index of 1.9 or higher. Findings such as prominent fatty changes or lymphocytic piecemeal necrosis indicate the presence of HH in conjunction with another complicating condition or secondary iron overload in the absence of HH.
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PMID:Liver biopsy diagnosis of homozygous hemochromatosis: a diagnostic algorithm. 847 69

Administration of vitamins or metals may cause severe side effects. Retinoids (derivatives of vitamin A) used for the treatment of various skin disorders are teratogenic, hepatotoxic and may induce a substantial increase in serum lipids. A case report demonstrates that vitamin D supplementation in a patient under total parenteral nutrition can cause hypercalcemia. The isolated administration of vitamin B1, without concomitant vitamin B6 and nicotinamide may precipitate potentially life-threatening pellagra encephalopathy. Repeat blood transfusions may produce clinically overt organ hemosiderosis, e.g. cirrhosis of the liver, diabetes mellitus or myocardiopathy. The literature contains reports on a few cases of sarcoma associated with orthopedic metal implants. The controversial issue of the potential dangers of dental amalgams is briefly mentioned.
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PMID:[Vitamins and metals: possible hazards for humans]. 866 74

Eighty-three patients with chronic end-stage renal failure, including 65 on haemodialysis and 18 on intermittent peritoneal dialysis, were evaluated for hepatitis B virus profile and antibodies to hepatitis C virus (HCV). All those positive for HBsAg were excluded from the study. Nineteen patients were found to be positive for antibodies to HCV by the ELISA II test. Eight cases were already positive for HCV antibody when they started dialysis in our unit, the other 11 became positive during dialysis in our unit. Only one of the patients on peritoneal dialysis was positive for HCV. A liver biopsy was obtained from 17 patients, who consented to the procedure. All the cases were evaluated for the number of blood transfusions received, HIV infection and the approximate time of contracting the HCV infection. Liver enzymes were determined every month. Only three patients had abnormally raised serum aminotransferase at the time of biopsy. The various histopathological lesions detected were chronic active hepatitis (n = 3, including one with changes consistent with cirrhosis), chronic persistent hepatitis (n = 4), non-specific hepatitis (n = 3) and haemosiderosis (n = 3); four biopsy samples were normal. There was no correlation between the biochemical and histopathological changes. Moreover, patients with normal serum aminotransferase levels had abnormal histopathological changes. All were negative for HIV and none of the patients had received a renal graft. Twelve patients had received blood transfusions varying from 2 to 12 units, four had not received any blood, and in one the history of blood transfusion could not be confirmed. The four patients with anti-HCV antibodies who had not received blood transfusion had relatively mild disease--non-specific hepatitis (n = 2) or normal biopsy (n = 2). One patient with cirrhosis died 30 months after liver biopsy from hepatic insufficiency and three received renal transplants. Others are continuing on dialysis and their biochemical tests are within normal limits 12-45 (30 +/- 14) months after biopsy. In conclusion, biochemical tests are poor indicators of liver disease, and liver biopsy is a definitive way of evaluating the patients of dialysis with positive HCV antibodies for prognosis.
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PMID:Liver disease in dialysis patients with antibodies to hepatitis C virus. 894 88

Patients with chronic hepatitis run the risk of developing progressive liver disease during immunosuppressive therapy after kidney transplantation. To determine the impact of chronic hepatitis C on morbidity and mortality we analyzed 162 anti-HCV positive of 1241 renal-grafted patients (prevalence 13.1%; 84.9% HCV RNA positive) regularly surveyed in our outpatient clinic between 1992 and 1994. The mean age at transplantation was 44.5 (6-69) years, and follow-up after grafting was 7.4 (0.1-23.9) years. The immunosuppressive regimen and frequency of rejection episodes in HCV-infected patients were comparable to the total population. Only 4.3% (5/117) of the anti-HCV positive, HBV negative patients living with functioning grafts developed a markedly compromised liver function. Fifteen (9.3%) of the HCV-infected patients died, but none suffered from posthepatitic cirrhosis. An additional retrospective analysis of causes of death after transplantation prior to 1992 revealed that liver disease had only been responsible for 2% of the deaths (7 of 324) in the HBsAg negative population (n= 1901). In contrast, the predominant cause of death in the HBsAg positive population (n=76) was posthepatitic cirrhosis in 58% (15 of 26). Thus, kidney transplantation in patients with replicative hepatitis C and normal liver function appears to be justified because of low early and late morbidity and mortality due to chronic liver disease. HBV infection and hemosiderosis substantially increase the risk of chronic liver disease in renal transplant recipients with hepatitis C.
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PMID:The long-term course of hepatitis C after kidney transplantation. 895 66

Limited information is available regarding the histology of hepatitis C virus infection in children. The aim of this study was to determine the histological pattern of chronic hepatitis C (CHC) in children, and liver biopsy specimens from 109 pediatric patients with CHC were examined. Each biopsy specimen was evaluated based on a numerical scoring system for the stage of fibrosis (1-4), the grade of portal/periportal necroinflammation (0-4), the grade of lobular necroinflammation (0-4), and their sum (final grade). The histological lesions considered to be characteristic of chronic hepatitis were also evaluated. None of the children had liver cirrhosis, and 105 cases (97%) were stage 1 or 2. Only 4 children were stage 3. Two of these 4 cases showed hemosiderosis. A significant correlation was observed between the staging score and the final grade in the pediatric patients (r = .59; P < .0001). The histological characteristics of adult CHC, such as lymphoid aggregate, bile duct injury, and fatty changes, were also observed in the children. In conclusion, the majority of children with CHC presented with mild fibrosis, but a few showed CHC with lobular distortion and hemosiderosis. Frequent blood transfusion may aggravate hepatic lesions in pediatric CHC.
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PMID:Pathology of chronic hepatitis C in children. Child Liver Study Group of Japan. 930 11

Estrogens are known to have mitogenic activities and to influence hematic crasis. A wide literature on this subject allows us to re-evaluate the results of research performed in 1950. Estrogens injected into the peritoneum (estradiol propionate 2.5-5 mg, twice weekly) or into tibial bone marrow (estradiol propionate 1.5 mg weekly) of guinea pigs, after carbon tetrachloride induced cirrhosis (CCI4 inhalation for 7-15 min twice weekly), caused hyperchromic anemia, with erythroblastosis and leucocytosis; hyperplasia of reticulo-hystiocitary cells of bone marrow and lymphoid organs; splenic hemosiderosis; hyperplasia of immature bone marrow cells, with maturative inhibition; and terminal bone marrow hypoplasia. Our results agree with recent literature data concerning the role played by natural estrogens and environmental xenoestrogens that are capable of stimulating bone marrow progenitor cell proliferation and delaying their maturation, by the secretion of growth factors, especially from hyperplastic stromal cells, in solid and hematological tumors.
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PMID:Hematological modifications induced by estrogens in cirrhotic animals. 941 24

Stainable iron in the liver (hemosiderosis) is most commonly seen in individuals with homozygous genetic hemochromatosis, prior transfusion, hemolysis, porphyria cutanea tarda, and chronic alcohol-induced liver disease. In chronic viral hepatitis, however, significant hepatocellular hemosiderosis is uncommon. This report describes unusual foci of hepatocellular hemosiderosis ("iron-rich foci" or IRF) in liver biopsy specimens from three patients with chronic hepatitis with or without cirrhosis (two hepatitis C-related, one hepatitis B-related). IRF present within the lobular parenchyma or cirrhotic nodules contrasted sharply with the immediately adjacent hemosiderin-negative liver tissue. Serum iron indices were abnormal in all three patients, but homozygous hemochromatosis was ruled out based on the hepatic iron concentration and hepatic iron index for each case. These cases highlight the potential for irregular iron storage in chronic viral liver disease and possible confusion with genetic hemochromatosis. The possible pathogenesis of IRF and the relationship of iron storage to the outcome of interferon therapy in chronic viral hepatitis are discussed.
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PMID:Iron-rich foci in chronic viral hepatitis. 949 Feb 68

In a retrospective study of a 12-year period (1981-1992) liver histology was analyzed in 227 autopsied patients infected with the human immunodeficiency virus. Normal histology could only be documented in 29 patients (13%). In the majority of cases (56%) uncharacteristic changes were seen such as steatosis (34%), hemosiderosis (10%) or non-specific reactive hepatitis (7%). The finding of hepatic peliosis obtained in 4 patients was not associated with inflammatory liver changes, especially infections from Rochalimaea. Within a wide range of opportunistic infections recorded in 50 patients (22%), hepatitis caused by Cytomegalovirus (8%), Toxoplasma gondii (5%), Leishmania donovani (1%), Cryptococcus neoformans and Pneumocystis carinii (each 0.5%) was diagnosed. Among 16 cases (7%) of mycobacterial liver infections typical mycobacteria were found in two patients and atypical mycobacteria in 14 patients, respectively. In 23 patients (10%) chronic viral hepatitis, caused by HBV (7%) or HCV infections (3%), respectively, was observed. Hepatitis was typed as mild only in each 5 patients with HBV or HCV infection, whereas the remaining cases showed a transition towards cirrhosis. Two patients with HBV-associated cirrhosis developed hepatocellular carcinoma. The remaining 32 malignant liver tumors represented secondary neoplasms, including 13 cases of non-Hodgkin's lymphomas.
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PMID:[Liver changes in AIDS. Retrospective analysis of 227 autopsies of HIV-positive patients]. 964 44

A 38-year-old woman had a mastectomy for infiltrating ductal carcinoma of the breast 3 years before her last admission and had received chemotherapy for known liver metastases. She developed the rapid onset of liver failure with portal hypertension and died in a hospice. Autopsy revealed macronodular cirrhosis of the liver secondary to metastatic carcinoma of the breast with associated florid fibrosis. This rare lesion, previously called metastatic carcinomatous cirrhosis, was also found, in this case, to have marked hepatic hemosiderosis, and analysis of the patient's DNA showed heterozygosity for the H63D genotype. The possibility of cirrhosis-associated hemosiderosis secondary to an iron metabolism abnormality associated with the H63D mutation of the HFE gene is proposed. Computed tomographic scans showed the development of cirrhosis during the 3-month period before the patient's last admission and suggested the possibility of a postnecrotic type origin.
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PMID:Metastatic carcinomatous cirrhosis and hepatic hemosiderosis in a patient heterozygous for the H63D genotype. 1182 5


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