Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the study was to investigate the frequency of nutritional anemia among western venezuelan indians. Three hundred and ninety nine Yucpa indians from the communities of Aroy, Marewa and Peraya were studied. The concentrations of hemoglobin, serum iron, total iron binding capacity, serum ferritin, serum folate and serum vitamin B12 and the frequency of anemia and nutrient deficiency were determined. Anemia was found in 71.7% of people from Aroy, 52.25 from Marewa and in 74.4% from Peraya. No nutrient deficiencies were found in 48.1% of cases with anemia, while iron deficiency anemia was present in 39% of the population studied, and folate and or vitamin B12 deficiency were associated with anemia in only 12.9% of cases. The high frequency of anemia, unrelated to nutrient deficiency, among the Yucpa indians, is attributed to the prevalence of chronic infectious diseases such as hepatitis and parasitic infections, as well as skin and respiratory infectious processes.
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PMID:[Anemia in indigenous population of the West of Venezuela]. 1053 52

The present study was performed to determine whether excess hepatic iron modulates the cancer-initiating and promoting properties of FB1. Thirty-eight male F344 rats were divided into four dietary treatment groups: (i) control diet (AIN, n = 8); (ii) FB1 250 mg/kg diet (FB1, n = 10); (iii) 1-2% carbonyl iron (CI, n = 10); or (iv) FB1 plus iron loading (FB1/CI, n = 10) for 5 weeks (2 x 2 factorial design). Hepatic iron concentrations in iron-loaded animals at 5 weeks were 444 +/- 56 (CI) and 479 +/- 80 micromol/g dry weight (FB1/CI) (mean +/- SEM). All the FB1-fed rats, in the presence or absence of CI, developed a toxic hepatitis with a 4-fold rise in serum alanine transaminase (ALT) levels. FB1 appeared to augment iron-induced hepatic lipid peroxidation, as measured by the generation of thiobarbituric acid reacting substances (TBARS) in liver homogenates (P < 0.0001). Morphometric analysis showed that FB1 caused a significantly greater mean +/- SEM number of 'enzyme-altered' foci and nodules per cm2 (5.34 +/- 1.42 vs. 1.50 +/- 0.52, P < 0.05), as well as a greater area (%) of liver occupied by foci and nodules (0.33 +/- 0.12% vs. 0.05 +/- 0.03%, P < 0.001), compared with FB1/CI. The addition of FB1 to dietary iron loading caused a shift in distribution of iron from hepatocytes to Kupffer cells, probably due to phagocytosis of necrotic iron-loaded hepatocytes. In conclusion, (i) FB1 appears to cause toxicity in the liver independently from effects on lipid peroxidation; (ii) FB1 has a potentiating effect on iron-induced lipid peroxidation; and (iii) dietary iron loading appears to protect against the cancer promoting properties of FB1, possibly due to a stimulatory effect of iron on hepatocyte regeneration.
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PMID:The effects of dietary iron overload on fumonisin B1-induced cancer promotion in the rat liver. 1065 28

It has been proposed that iron overload may adversely affect liver disease outcome. The recent identification of 2 mutations in the HFE gene related to hereditary haemochromatosis (Cys282Tyr and His63Asp) provided an opportunity to test whether they are associated with hepatic iron accumulation and the activity and severity of liver disease in hepatitis C virus (HCV) infection. We investigated the prevalence of HFE mutations in 135 male patients with chronic HCV hepatitis, and correlated genotype distribution with different parameters of iron status and the activity and severity of liver disease. Of these 135 patients, 6 (4.4%) carried Cys282Tyr and 32 (23.7%) carried His63Asp, frequencies which were similar to those observed in healthy controls. Serum iron levels and transferrin saturation (but not ferritin levels or liver iron content) were significantly higher in carriers than in non-carriers of HFE mutations. No difference was observed in serum ALT, AST and GGT levels between carriers and non-carriers. Finally, scores for necroinflammatory activity and fibrosis in the liver were significantly higher in HFE carriers than in non-carriers. Patients with chronic HCV infection carrying HFE mutations tend to present more evident body iron accumulation and a higher degree of necroinflammatory activity and fibrosis in the liver. HFE gene mutations might be an additional factor to be considered among those implicated in the determination of a worse prognosis of the liver disease in chronic HCV infection.
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PMID:Are haemochromatosis mutations related to the severity of liver disease in hepatitis C virus infection? 1069 80

Thalassemia is a public health problem in Thailand. Progressive iron overload is the life-limiting complication commonly found in thalassemic patients. The assessment of body iron stores is essential for determining the need and efficacy of iron chelation. The parameters of serum iron, total iron binding capacity (TIBC), and serum ferritin were studied in 79 children with thalassemia diseases. The ages ranged from 1 to 17 years with a mean of 7 years and 10 months. Neither of them had clinical symptoms of hepatitis. The correlation between transferrin saturation (TS = serum iron/TIBC x 100) and serum ferritin was shown in the equation of TS = 10.253 In (ferritin) (r = 0.956, p = 0.000). For example, TS = 70.83 per cent indicates serum ferritin of 1,000 ng/ml. Thus, where serum ferritin is not feasible but serum iron and TIBC are available, TS can be used to estimate the level of serum ferritin. Therefore, the assessment of iron stores and monitoring of iron chelation in thalassemic patients can be effectively achieved.
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PMID:The correlation of transferrin saturation and ferritin in non-splenectomized thalassemic children. 1073 May 22

Histologically detectable iron (HDI) and HFE mutations were searched for in liver biopsy specimens from 58 Italian patients with chronic hepatitis C, and morphologic features were compared to examine their reciprocal relation and their contribution to disease progression. HDI was evident in 48% of cases with features of nonhemochromatosis iron overload. Total, sinusoidal, and portal HDI increased with stage; grade was related to all iron scores because of the contribution of portal inflammation and interface hepatitis. HFE mutations were seen in 47% of patients with chronic hepatitis C and in 28% of control subjects; they were related to stage and the His63Asp mutation to portal HDI. On multivariate analysis, grade but not stage or HFE mutations was associated with HDI in all sites. Interface hepatitis with its sequelae (sinusoidal capillarization and microshunting) represents a major factor in iron deposition in chronic hepatitis C and justifies the features of HDI. HFE mutations are not responsible for HDI deposition but could favor the progression of virus-induced damage independently from interference with iron metabolism.
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PMID:Iron deposition and progression of disease in chronic hepatitis C. Role of interface hepatitis, portal inflammation, and HFE missense mutations. 1076 47

Several factors influence the efficacy of the action of human recombinant erythropoietin during treatment of anaemia in haemodialysis patients. We carried out a six-month prospective study of 23 stable patients who had been on haemodialysis for at least one year to attempt to evaluate those factors modifying the dose of the hormone to attain a similar haematocrit, such as use or not of angiotensin converting enzyme inhibitors, hepatitis C virus positive or negative, age older or younger than 60 years, acquired cystic kidney disease or not, and sex. The patients were treated with subcutaneaous erythropoietin for over a year to attain a haematocrit of 35%, intravenous iron to reach plasma ferritin levels > 250 ng/ml and a transferrin saturation index > 20%, folic acid and group B vitamins. Parameters studied included age, time and duration of haemodialysis, Kt/V, albumin, haematocrit, erythropoietin in U/kg/week, intact PTH, hepatitis C virus, PCR of the hepatitis C virus, transaminases, ferritin, transferrin saturation index, folic acid, vitamin B12, and aluminium. No statistically significant differences were seen between the patients with and without hepatitis or in age or acquired cystic kidney disease and sex in the hormone dose given to achieve similar levels of haematocrit. Higher doses of erythropoietin were necessary in those patients treated with antihypertensive agents (71 +/- 25 vs 44 +/- 25 U/kg/week; p < 0.05). There were no differences between groups in factors known to cause resistance to the action of the hormone. The most important conclusions from this study concern the cost-benefit relation of treating hypertensive patients on haemodialysis with angiotensin converting enzyme inhibitors and erythropoietin.
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PMID:[Study of various factors that could have an impact on the treatment with erythropoietin of hemodialysis anemia]. 1085 98

The gut and the liver are the key organs in nutrient absorption and metabolism. Bile acids, drugs, and toxins undergo extensive enterohepatic circulation. Bile acids play a major role in several hepatic and intestinal diseases. Endotoxins deriving from intestinal Gram-negative bacteria are important in the pathogenesis of liver and systemic diseases. Chronic liver diseases can influence gastrointestinal motility, which together with other factors may contribute to bacterial overgrowth and in patients with ascites to an increased risk of spontaneous bacterial peritonitis. Patients with end-stage liver disease frequently develop portal hypertension leading to varices, gastric vascular ectasia, and portal hypertensive gastroenteropathy. Several liver and biliary abnormalities are observed in patients with inflammatory bowel disease (primary sclerosing cholangitis, autoimmune hepatitis, cholelithiasis). The primary defect in hemochromatosis is located in the intestine, causing an inappropriate increase in iron absorption, and the liver is the site of earliest and heaviest iron deposition. Elevated transaminases are observed in many patients with celiac disease, and steatohepatitis frequently develops in patients with jejunoileal bypass and short bowel syndrome. Furthermore, the liver is the primary organ for metastasis of intestinal cancer. Many viral, bacterial, fungal, and parasitic diseases affect the intestine as well as the liver and the biliary tract.
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PMID:Gut-liver axis. 1085 47

The authors report a case of a young woman with adult-onset Still's disease (AOSD) with massive hyperferritinaemia who developed acute florid hepatitis with intraparenchymatous histiocytic infiltration following oral iron substitution for presumed iron deficiency, which settled on withdrawal of the iron. This suggests that the iron exacerbated the macrophage hyperactivity which is presumed to be present in AOSD. Oral iron substitution in the acute phase of this disease may be inadvisable.
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PMID:Acute hepatitis in adult Still's disease apparently resulting from oral iron substitution--a case report. 1087 Jun 59

Iron metabolites were measured in liver homogenates and leukocytes of patients with hereditary hemochromatosis (HHC), chronic viral hepatitis, and secondary iron overloading. Iron and ferritin levels in the liver are increased HHC, while in hepatitis only ferritin level is increased. In the leukocytes ferritin concentrations are increased both in HHC and secondary iron loading and less so in viral hepatitis. The leukocytic ferritin level decreased after a course of bleeding sessions and during maintenance therapy for HHC, which can serve as a diagnostically significant sign for evaluating the treatment efficiency.
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PMID:[Indices of iron metabolism in liver homogenates and leukocytes]. 1087 39

Effects of accumulation of copper and iron on the production of DNA strand breaks were investigated in Long-Evans Cinnamon (LEC) strain rats that spontaneously develop fulminant hepatitis. Copper and iron accumulated in the liver of LEC rats in an age-dependent manner from 4 to 15 weeks. Low-copper food prevented the accumulation of copper in the liver, but did not prevent accumulation of iron. When the amounts of DNA single strand breaks were estimated by comet assay, the number of DNA strand breaks in the liver cells of rats fed standard food increased with age from 4 to 15 weeks. The number of DNA strand breaks in the liver cells from rats fed low-copper food were the same as those of rats at 4 weeks of age. Thus, the copper accumulation in the liver of LEC rats induced DNA strand breaks, but accumulation of iron did not.
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PMID:Hepatic copper accumulation induces DNA strand breaks in the liver cells of Long-Evans Cinnamon strain rats. 1100 2


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