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)

Unravelling the role of interferon (IFN) in the treatment of chronic hepatitis B compliance by many factors. Several mutant forms of hepatitis B virus (HBV) have recently been discovered; the most common of these is the precore mutant, characterized by hepatitis B e antigen (HBeAg) negativity and hepatitis B e antibody (HBeAb) positivity in an individual with an active HBV infection. The aim of this study was to compare the response rate to IFN therapy in patients with wild-type HBV infection and in individuals infected with the precore mutant. A second aim was to evaluate the role of an increased serum ferritin in terms of the IFN response rate in these two different types of HBV infection. IFN therapy was administered at a dose of 5 MU subcutaneously three times weekly for 6 months to 41 individuals with a chronic wild-type hepatitis B infection and 16 individuals with a precore mutant chronic HBV infection. An IFN response was defined as normalization of the serum alanine aminotransferase (ALT) level and an HBeAb to HBeAb seroconversion (in wild-type hepatitis infection), and a normalization of the serum ALT in individuals infected with a precore mutant infection. At entry, the two groups were matched for age, gender, serum ALT, serum iron, total iron binding capacity (TIBC), serum ferritin and liver histology. Forty-six per cent of the subjects with wild-type disease responded to IFN therapy. By contrast, only four of the 16 cases (25%) of the precore mutant cases responded (p < 0.05). Ferritin levels correlated well with the type of IFN response; as the serum ferritin level increased, the response rate to IFN declined. Hapatic infection caused by a precore HBV mutant is more resistant to IFN therapy than wild-type infection. The serum ferritin level appears to influence the type of IFN response achieved. Individuals with a serum ferritin level greater than 300 ng ml-1 failed to respond to IFN in 93% of the cases studied.
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PMID:Relationship between the serum alanine aminotransferase level at the end of interferon treatment and histologic changes in wild-type and precore mutant hepatitis B virus infections. 887 72

Liver transplantation is the treatment of choice for many patients with acute and chronic hepatic failure. Although uncommon, hepatic failure may occur during pregnancy or after delivery, and liver transplantation may be life-saving. We report a case of a liver transplant performed during pregnancy in a patient with decompensated cirrhosis from chronic autoimmune hepatitis. A patient with chronic autoimmune hepatitis developed decompensated cirrhosis at approximately 18 weeks' gestation. Despite attempts at medical stabilization, her condition worsened, and an orthotopic liver transplant was performed at 23 weeks. The procedure was complicated by transient hypotension, and fetal death was diagnosed postoperatively. Her postoperative course was complicated by hypotension, infection, oliguric renal failure, anemia, thrombocytopenia, and rejection. She spontaneously labored on the 6th postoperative day and delivered without difficulty a 560-g stillborn male. The patient recovered and was discharged 31 days after surgery on prednisone, tacrolimus, mycostatin, erythropoietin, and iron. Liver transplantation may be a valuable therapeutic option for treatment of pregnant or puerperal women with hepatic failure.
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PMID:Hepatic transplantation during pregnancy and the puerperium. 902 84

We compared the liver enhancement of two superparamagnetic agents, polycrystalline iron oxide nanoparticles (PION) and PION coated with asialofetuin (ASF), in an experimental model of focal radiation-induced hepatitis. PION, a reticuloendothelial system-directed agent, and PION-ASF, a hepatocellular-directed agent, were compared for time-dependent liver enhancement in an experimental model of radiation-induced liver injury. Using the reticuloendothelial system (RES)-directed PION, the normal, nonirradiated portion of the liver decreased in signal intensity (SI) with a mean negative enhancement of -66% +/- 4, whereas the irradiated portion (60 Gy, 3 days before imaging) of the liver decreased in SI by -24% +/- 2, significantly less (P <.05). SI changes in irradiated liver tissue using PION were dose-dependent, being more pronounced with lower radiation exposure. The difference in SI changes induced by PION-ASF between irradiated and nonirradiated liver was not statistically different, but SI decreased with a mean negative enhancement of -80% +/- 2. The RES-directed PION is more sensitive for the detection of radiation-induced hepatitis than is the hepatocyte-directed PION-ASF. The insensitivity of PION-ASF enhancement for diffuse liver injury may be clinically advantageous for detecting focal lesions in the presence of diffuse hepatic injury.
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PMID:Contrast enhancement in experimental radiation-induced liver injury: comparison of hepatocellular and reticuloendothelial particulate contrast agents. 913 91

Abnormalities in iron metabolism have been reported in patients with acquired immunodeficiency syndrome (AIDS). To assess the frequency of abnormal hepatic iron deposition in these patients and to examine potential causes of iron overload, we analyzed the amount of iron at different cellular sites in liver sections obtained at autopsy of 78 patients with AIDS. Quantitation of serum iron and transferrin levels and estimation of total iron binding capacity was obtained using serum from 63 patients. The number of whole blood/packed red blood cell transfusions and opportunistic infections was recorded. Of the 78 patients, 25 (32%) showed a Grade 3 or 4 (0-4 scale) iron level, distributed in three patterns, i.e., in hepatocytes only, in hepatocytes and Kupffer cells, and in Kupffer cells only. In these 25 livers, 4 had cirrhosis, with no documented cause; the mean number of transfusions was 12.5; and 16 (64%) had Mycobacterium avium-Mycobacterium intracellulare infection. In the 53 livers with little or no iron, 5 had cirrhosis, with 3 of those 5 listing alcoholic liver disease or hepatitis as the cause; the mean number of transfusions was 1.4; and 18 (34%) had Mycobacterium avium-Mycobacterium intracellulare infection. Transferrin saturation was more than 50% in 6 (29%) of 21 cases with increased hepatic iron levels and in 6 (14%) of 42 cases with little or no hepatic iron. These results indicate that hepatic iron overload in patients with AIDS is associated with blood transfusions, an elevated transferrin saturation, and Mycobacterium avium-Mycobacterium intracellulare infection. Significant hepatic iron deposition in patients with AIDS with no other apparent cause of cirrhosis suggests an etiologic role for iron in hepatic injury. The increase in hepatic iron levels in these patients has potentially adverse clinical effects related to the use of transfusions, iron supplements, and iron-containing drugs.
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PMID:Increased hepatic iron in the acquired immunodeficiency syndrome: an autopsy study. 938 70

The aims of this study were to characterize the histological changes observed in 34 accessioned cases of canine chronic hepatitis and to correlate these changes with the clinical pathological data. Cases of chronic hepatitis were subdivided into 6 categories: chronic active hepatitis (10/34), chronic persistent hepatitis (7/32), chronic cholestatic hepatitis (6/34), fibrosing hepatitis with cirrhosis (3/34), chronic cholangiohepatitis (3/34), and miscellaneous secondary hepatitis (5/34). Iron accumulation was a consistent finding in all livers examined. Although all cases of chronic hepatitis had elevated liver enzymes, no correlation was detected between biochemical parameters and the severity of morphologic changes. Similarly, no correlation was detected between rhodanine staining for copper and morphologic or biochemical indicators of cholestasis. However, presence of copper correlated well with reticulo-fibrosis (r = 0.8) and bile duct hyperplasia, suggesting that changes in the hemodynamics of the hepatic acini due to fibrosis could influence storage of copper.
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PMID:Chronic hepatitis: a retrospective study in 34 dogs. 918 2

Anaemia is an almost invariable sign of chronic renal failure [1]. Although many factors have been implicated as causes of this anaemia, it seems probable that deficiency of erythropoietin is the main cause for most patients [2]. Institution of chronic dialysis can improve anaemia in end-stage kidney disease, continuous ambulatory peritoneal dialysis being reported as more successful [3]. The aim of this study was to investigate the influence of haemodialysis and continuous ambulatory peritoneal dialysis on anaemia during the first six months of treatment. We examined 21 persons (14 males and 7 females, aged from 18 to 78 years) on haemodialysis treatment and 13 persons (6 males and 7 females aged from 22 to 64 years) on continuous ambulatory peritoneal dialysis (Table 1). Standard procedures were used for measuring biochemical parameters. Urea and creatinine levels were high, almost incompatible with life, in all tested persons before dialysis treatment. During the first three months of both dialysis techniques urea and creatinine were significantly (p < 0.01) corrected, but remained above the normal ranges (Table 2). Patients on continuous ambulatory peritoneal dialysis have shown significantly (p < 0.01) lower urea and creatinine values compared to patients on haemodialysis (Graph 1). These data suggest better preservation of renal function and better control of the internal environment during continuous ambulatory peritoneal dialysis [6]. All tested patients were severely anaemic before the beginning of dialysis. During the first six months of haemodialysis erythrocyte count, haematocrit and haemoglobin levels were unchanged (Table 3). Transfusions and hepatitis episodes only temporary improved anaemia. Patients on continuous ambulatory peritoneal dialysis exhibited significant correction of anaemia already during the first three months of treatment (Graph 2). Though less significantly, haemoglobin values continued to rise even during the next three months. The reached haemoglobin levels were lower than normal, but significantly higher than values in patients on haemodialysis (p < 0.01), suggesting better control of anaemia during continuous ambulatory peritoneal dialysis. Transfusion requirement was irrelevant, and hepatitis was not noticed, so they cannot be held responsible for the improvement of anaemia. Greater iron consumption, illustrated by higher transferrin saturation, also confirmed increased erythopoitesis in patients undergoing continuous ambulatory peritoneal dialysis. They also had lower blood iron level than those on haemodialysis (who had) numerous blood transfusions. The improvement of anaemia during continuous ambulatory peritoneal dialysis may be the result of reduction in plasma volume [7] as well as an increase in red cell mass and a better clearance of middle molecules in comparison to patients on haemodialysis. The main cause is higher erythropoietin level [8]. All tested patients had low folic acid level. Patients who corrected anaemia showed fall in folat level. This was statistically remarkable during the first three months of continuous ambulatory peritoneal dialysis-from 3.64 ng/ml to 2.09 ng/ml. All these data suggest that both dialysis modalities are effective in the control of protein waste products level, but continuous ambulatory peritoneal dialysis has better influence on the improvement of anaemia that haemodialysis. This can be attributed to better removal of uremic toxins, improved protein metabolism, lower parathyroid hormone level and higher erythropoietin value due to peritoneal macrophage production.
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PMID:[The effect of hemodialysis and continuous ambulatory peritoneal dialysis on renal anemia]. 926 38

Hepatitis C virus (HCV) infection is a common cause of liver disease among polytransfused thalassemics. We treated a cohort of subjects with beta-thalassemia major and chronic hepatitis C with alpha-interferon. The aims of the study were to assess the long-term biochemical and virologic efficacy of alpha-interferon and to evaluate the influence of HCV type and liver siderosis on the outcome of therapy. Seventy subjects (mean age, 14.1 years) with chronic HCV infection and abnormal aminotransferases received recombinant alpha-interferon for 12 months and were observed after therapy for at least 24 months. Sixty-three subjects (90%) were HCV-RNA positive at the start of therapy. HCV type 1b was found in 41 subjects (65.1%), non-1b types in 13 (20.6%), and mixed HCV types in 9 (14.3%). Liver biopsy showed cirrhosis in 11 subjects (15.7%) and siderosis grade 3-4 in 24 patients (34.2%). Three patients stopped therapy due to adverse events. Twenty-eight subjects (40%) had normal aminotransferases and had cleared HCV-RNA when last observed (mean follow-up, 36.5 months; range, 25 to 49 months). Of 41 patients who did not normalize aminotransferases, 9 had become HCV-RNA negative at the end of follow-up. The absence of cirrhosis, low liver iron content, and infection with non-1b HCV type were independently associated to complete sustained response upon multivariable analysis. In conclusion, alpha-interferon may induce a sustained virologic and biochemical remission of hepatitis in beta-thalassemic patients with chronic HCV infection and nonadvanced liver disease.
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PMID:Long-term efficacy of alpha-interferon in beta-thalassemics with chronic hepatitis C. 931 Apr 71

Iron overload develops mainly via two mechanisms, by a defect in the regulation of iron absorption (hereditary hemochromatosis) or by parenteral route (chronic red cell transfusion for anemic patients without blood loss) especially in patients with different categories of refractory anemias, and in anemic patients with chronic infection, alcohol excess, and malignancies. The accurate assessment of body iron is indispensable for the correct diagnosis and for finding the optimal treatment schedule for each individual patient. Liver biopsy with quantitative iron determination and histochemistry is still the reference method for the assessment of body iron status for patients with iron overload. New noninvasive measurements (hepatic magnetic susceptibility, CT, and magnetic resonance imaging) are still investigational procedures. It is important to decrease the need for transfusion by judicious use of red cell concentrates, make more widespread use of erythrocytapheresis, determine the red blood cell phenotype of the patient before the onset of a regular transfusion regimen, treat concomitant hepatitis infections, consider splenectomy to diminish red blood cell requirements, and early on consider allogeneic bone marrow transplantation for thalassemic patients who have HLA-identical siblings. It is advisable to screen for the hereditary hemochromatosis gene before starting any kind or regular red blood cell transfusion therapy, and to avoid if possible, the risk of free radical release by transfusional iron overload during the physiologically hypercoagulable state of pregnancy and its effects on the highly proliferative tissues of the fetus.
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PMID:Transfusion-associated iron overload. 935 2

Because the majority of patients with chronic hepatitis C do not respond to interferon, alternative treatments need to be established. Several lines of evidence suggest that iron depletion is beneficial for such patients. Thus, gastrectomized patients with a reduced capacity for iron absorption might have an advantage in treatment of their liver damage over patients with intact gastrointestinal tracts. Four male gastrectomized patients had post-transfusion chronic hepatitis C. The iron load in three patients was adjusted below 10 ng/ml of serum ferritin level by phlebotomy. Subsequent interferon treatment for the four patients without iron load cleared circulating hepatitis C virus RNA in one patient only. However, serum ferritin concentrations were stabilized at low levels without maintenance phlebotomy, and sustained normalization of serum liver enzyme activities was obtained in all four patients. Similar treatments were done for 10 male patients with intact gastrointestinal tracts. The amount of removed iron from these patients was more than that from gastrectomized patients. Interferon also failed to clear circulating hepatitis C virus RNA except in one case. Low ferritin levels and sustained normalization of liver enzymes were seen in three patients. A transient elevation of ferritin levels with low enzyme activities was seen in two patients. Relapsing hepatitis was seen in five of the seven patients who needed maintenance phlebotomy due to a rebound in serum ferritin levels, probably because of active iron absorption from the intestine. Our data suggest that depletion of cytotoxic iron is a key to managing patients with chronic hepatitis C.
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PMID:The advantage of gastrectomized patients in management of their chronic hepatitis C. 948 Oct 91

Etheno adducts in DNA are formed from the carcinogens vinyl chloride and urethane, and also from products of lipid peroxidation (LPO), such as trans-4-hydroxy-2-nonenal. Using an ultrasensitive detection method, the formation of etheno-DNA adducts in the liver was demonstrated in LEC rats (a strain with hereditary abnormal copper metabolism) that develop hepatitis and hepatocellular carcinoma. Wilson's disease and primary haemochromatosis are human genetic disorders that cause copper or iron accumulation resulting in a high risk for primary liver cancers. Levels of etheno adducts were also significantly elevated in the liver of these patients. In a group of male and female volunteers kept on a controlled diet, the effect of dietary fatty acid composition on the endogenous formation of lipid peroxidation-derived DNA adducts was determined in DNA from white blood cells. Dietary omega-6-polyunsaturated fatty acids greatly increased LPO-derived etheno-DNA adducts in vivo, in females. Thus, exocyclic DNA adducts are promising biomarkers for elucidating the effect of dietary fat intake, oxidative stress and protective dietary antioxidants on endogenous DNA damage and thus may provide a possible mechanistic link with elevated risk for diet-related cancers.
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PMID:Etheno-DNA base adducts as tools in human cancer aetiology and chemoprevention. 949 54


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