Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum hepatitis B surface antigen (HBsAg) status and ferritin levels were measured in 3 groups of subjects: Group A (n = 14) with chronic non-neoplastic liver disease (CNLD), Group B (n = 14) with primary hepatocellular carcinoma (PHC) and Group C (n = 14) comprising healthy matched controls without liver disease. Serum ferritin values were lowest in Group C, intermediate in Group A and highest in the Group B patients (all p < 0.05). About 79% of the patients with PHC, 43% of those with CNLD and none (0%) of the healthy controls, had hyperferritinaemia (serum ferritin > 400 ng/ml). Hyperferritinaemia and HBsAg positivity coexisted in 15% and 73% of the patients with CNLD and PHC, respectively. Hyperferritinaemia and HBsAg were significantly positively related in the patients with PHC (chi 2 5.09, p < 0.05). The predictive indices of hyperferritinaemia in chronic liver disease appeared superior for PHC than for CNLD, and became somewhat enhanced with coexisting HBsAg positivity. These results suggest that serum ferritin could be useful as a tumour marker for PHC in patients with established chronic liver disease.
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PMID:The diagnostic utility of serum ferritin. Estimation in patients with primary hepatocellular carcinoma. 865 Jul 46

Serum hepatitis B surface antigen (HBsAg) status and ferritin levels were measured in three groups of Nigerian subjects: Group A (n = 14) with non-neoplastic disease (CNLD); Group B (n = 14) with primary hepatocellular carcinoma (PHC); and Group C (n = 14) of healthy matched controls. Serum ferritin values were lowest in Group C, intermediate in Group A, and highest in the Group B patients (all p < 0.05). About 79% of the patients with PHC, 43% of those with CNLD, and none (0%) of the healthy controls had hyperferritinemia (serum ferritin > 400 ng/ml). Hyperferritinemia and HBsAg positivity coexisted in 15% and 73% of the patients with CNLD and PHC, respectively. Hyperferritinemia and HBsAg were significantly positively related in the patients with PHC (chi 2 5.09, p < 0.05). The predictive indices of hyperferritinemia in chronic liver disease appeared superior for PHC than for CNLD, and became somewhat enhanced with coexisting HBsAg positivity. These results suggest that serum ferritin could be useful as a tumor marker for PHC in Nigerian patients with established chronic liver disease.
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PMID:The diagnostic utility of serum ferritin estimation in Nigerian patients with primary hepatocellular carcinoma. 874 15

An individual's iron status may affect the response rate achieved with the use of interferon (IFN) as therapy for chronic viral hepatitis. A total of 27 patients with chronic hepatitis B viral infection, who had elevated serum ferritin levels, were randomized to receive either IFN 5 MU, three times weekly by subcutaneous injection alone (n = 14) or in combination with cycles of deferoxamine at a dose od 80 mg kg-1 per cycle (n = 13) administered over 3 consecutive days, to reduce their iron and maintain a serum ferritin level less than 250 ng ml-1. All deferoxamine-treated patients were on a low iron-containing diet. An IFN response was defined as a normalization of the serum alanine aminotransferase (ALT) level and seroconversion from hepatitis B e antigen (HBeAg) positivity to hepatitis B e antibody (HBeAb) positivity. The deferoxamine-treated group experienced a reduction in their serum ferritin level to 226 +/- 73 ng ml-1 as a result of the deferoxamine treatment. Six of the 13 (46%) deferoxamine-treated patients and two of the 14 (14%) control patients normalized their ALT levels. Seven of the 13 (54%) deferoxamine but only 14% of the IFN-treated group seroconverted to HBeAb positivity. A greater rate of histological improvement and loss of hepatitis B virus (HBV) DNA was seen in the deferoxamine-treated group. Two of the deferoxamine-treated patients were treated only once, two were treated twice, seven were treated three times and two were treated four times to achieve a ferritin level below 250 ng ml-1. Based on these data, we conclude that deferoxamine infusion enhances the rate of response to IFN in subjects with chronic hepatitis B. The precise mechanism of this phenomenon is not clear.
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PMID:The use of deferoxamine infusions to enhance the response rate to interferon-alpha treatment of chronic viral hepatitis B. 887 71

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

Although the iron-loading disease, hereditary hemochromatosis, has a strong causal association with hepatocellular carcinoma (HCC), the carcinogenic potential of dietary iron overload in Black Africans is not known. We investigated this potential by evaluating iron status, alcohol consumption, markers for hepatitis B (HBV) and C virus (HCV) infections, and exposure to dietary aflatoxin B1 in 24 rural patients with this tumor, 48 race-, sex-, and age-matched hospital-based controls, and 75 related or unrelated close family members of the cancer patients. Iron overload was defined as a raised serum ferritin concentration in combination with a transferrin saturation > or = 60%, and was confirmed histologically when possible. Among 24 patients and 48 hospital controls, the risk of developing HCC in the iron-loaded subjects was 10.6 (95% confidence limits of 1.5 and 76.8) relative to individuals with normal iron status, after adjusting for alcohol consumption, chronic HBV and HBC infections, and exposure to aflatoxin B1. The risk of HCC in subjects with HBV infection was 33.2 (7.2, 153.4) (odds ratio [95% confidence limits]), HCV infection 6.4 (0.3, 133.5), and alcohol consumption 2.0 (0.5, 8.2). Aflatoxin B1 exposure did not appear to increase the risk of HCC. The population attributable risk of iron overload in the development of HCC was estimated to be 29%. Among 20 cancer patients and 75 family members, the risk of developing HCC with iron overload was 4.1 (0.5, 32.2). We conclude that dietary iron overload may contribute to the development of HCC in Black Africans.
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PMID:Dietary iron overload as a risk factor for hepatocellular carcinoma in Black Africans. 962 Mar 27

The main Fe storage organ in the body is the liver. In patients with chronic liver disease, secondary Fe overload is common. Phlebotomy, often used in the West to reduce Fe overload to improve the efficacy of interferon therapy, is not socially acceptable in India. We assessed the efficacy of a low-Fe diet in reducing serum Fe levels. Nineteen patients with hepatitis B- and C-related chronic liver disease, ten with normal (< 25 mumol/l) baseline serum Fe levels (group A) and nine with high (> 25 mumol/l) serum Fe levels (group B) were included. All the subjects were advised to eat a low-Fe diet. The daily Fe intake was reduced approximately 50% by consumption of the rice-based diet. Haemoglobin, serum Fe, transferrin saturation index (TSI), ferritin and alanine transaminase (EC 2.6.1.2) levels were studied at 1 and 4 months. Dietary Fe intake and body weight were closely monitored. All patients complied with the dietary regimen and at 4 months significant (P < 0.001) reductions from baseline were seen in serum Fe (20 (SD 3) v. 12 (SD 4) mumol/l group A; 30 (SD 3) v. 19 (SD 7) mumol/l group B) and TSI (38 (SD 8) v. 23 (SD 9)% group A; 53 (SD 15) v. 34 (SD 13)%, group B) in both the groups, albeit earlier in group B subjects. Serum ferritin levels, however, reduced only in group A (112 (SD 62) v. 43 (SD 25) ng/ml, P < 0.05) and not in group B. Non-significant reductions in haemoglobin levels were seen in both groups. Alanine transaminase levels reduced significantly (P < 0.05) in both the groups (95 (SD 49) v. 44 (SD 25) IU/l, group A; 82 (SD 16) v. 51 (SD 14) IU/l group B). Thus, a low-Fe diet results in significant reductions in serum Fe and TSI levels, irrespective of baseline Fe levels. This diet should be evaluated to improve the efficacy of interferon therapy in patients with hepatitis B- and C-related chronic liver disease.
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PMID:Beneficial influence of an indigenous low-iron diet on serum indicators of iron status in patients with chronic liver disease. 1088 11

Early erroneous diagnosis of rheumatic disease is common in subjects with arthropathy due to hereditary hemochromatosis. A 71-year-old male with chronic obstructive pulmonary disease and monoclonal gammopathy underwent hip replacement and was referred to our Department because of altered liver function tests. Test results were negative for hepatitis B surface antigen and hepatitis C virus, and positive for rheumatoid factor. A diagnosis of rheumatoid arthritis had been made on the basis of compatible joint involvement and laboratory data and steroid treatment prescribed. Since his serum ferritin was 3249 ng/mL, genetic testing for hereditary hemochromatosis was carried out and revealed homozygosity for Cys282Tyr mutation in the HFE gene. Liver biopsy disclosed cirrhosis compatible with hemochromatosis. Following a review of the patients' radiographs, the diagnosis of hemochromatosis arthropathy was made. Phlebotomies and family screening for hereditary hemochromatosis were done. The most logical explanation for the positive rheumatoid factor result in this subject are his age and the presence of two chronic diseases involving long-standing antigenic stimulation and monoclonal gammopathy of uncertain significance. It is important to distinguish rheumatoid arthritis from hemochromatosis arthropathy for several reasons: patients with hereditary hemochromatosis do not require corticosteroid treatment; in case of erroneous diagnosis of rheumatoid arthritis, phlebotomy is not started early, and familial genetic counseling is not considered. In male subjects with positive rheumatoid factor and joint and liver disease, hereditary hemochromatosis should be considered. More liberal use of genetic testing is justified in such cases.
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PMID:Hereditary hemochromatosis masquerading as rheumatoid arthritis. 1168 50

We report the case of a patient with corticosteroid-responsive giant cell hepatitis associated with typical manifestations and changes of polyarteritis nodosa from the kidney and central nervous system. Initially, the patient presented with transient right hemiparesis, followed by spontaneous remission without any abnormalities on computed tomography scan, magnetic resonance imaging and cerebrospinal fluid examination. A few months later he was admitted to our clinic because of icterus, peripheral oedema and abdominal distension. He was found to have clinical signs of active cirrhosis. Serological tests for hepatitis B, C and HIV virus were negative. Serum ceruloplasmin. a1-AT and ferritin levels were within normal limits. Antinuclear antibodies were positive (1: 160). Liver biopsy showed micronodular cirrhosis with many eosinophils in the portal tracts and giant hepatocytes with multiple nucleoli in the lobule. Fulfilling the diagnostic criteria for autoimmune hepatitis, he was started on treatment with prednisolone and azathioprine, resulting in both clinical and biochemical responses. Four years later he presented with severe pain at the right costovertebral angle. Ultrasonography revealed a haematoma at the right kidney, and selective angiography of the abdominal aorta, renal arteries and hepatic artery documented microaneurysms in both kidney and liver arteries. Because of severe haemorrhage, right nephrectomy was performed. Histology of kidney specimen showed characteristic lesions of polyarteritis nodosa. Several months later, while on treatment with prednisolone and cyclophosphamide, the patient experienced a fatal episode of brain haemorrhage. An association between autoimmune hepatitis, polyarteritis nodosa and postinfantile giant cell hepatitis has not been reported previously.
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PMID:Post-infantile giant cell hepatitis associated with autoimmune hepatitis and polyarteritis nodosa. 1184 28

We investigated the prevalence of positive viral hepatitis titres in sickle cell disease (SCD) and the relationship of abnormal liver function tests (LFTs) to transfusions and ferritin levels. Charts from 141 patients with SCD were reviewed and recent laboratory data on serum ferritin, hepatitis serology, units of packed red blood cells transfused and LFTs were collected. Hepatitis B core antibodies were positive in 14% of patients (12/86) and Hepatitis C viral antibody titres were positive in 16.5% (15/91). There was a relationship of positive serologies to transfusion for hepatitis C virus (HCV), but not for hepatitis B virus (HBV). Hepatitis C antibody negative (HCVAb-) patients had fewer packed red blood cells (pRBC) transfused than Hepatitis C antibody positive (HCVAb+) (6.4 vs. 20.3, P=0.08). Patients with ferritins < 500 ng/ml compared to those with > 1000 ng/ml also showed a difference in units transfused (P < 0.003). Steady state LFTs, with the exception of alkaline phosphatase, had no relationship to serum ferritin or hepatitis serologies. Males were twice as likely to have positive serology as females but more females had elevated ferritin levels. Paired analysis of LFTs in steady state and crisis failed to demonstrate deterioration during crisis. We conclude that: (1) there is a relationship of positive Hepatitis C serology, but not Hepatitis B serology, to transfusion; (2) ferritin levels correlate with transfusion number but not with LFTs; (3) in our population, LFTs in SCD are usually normal and do not increase in vaso-occlusive crises.
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PMID:Liver function tests in sickle cell disease. 1184 94

Primary hepatocellular carcinoma, a major global cause of morbidity and mortality presents a gloomy picture as many patients report late in hospital when routine modalities of therapy are no more applicable. Early diagnosis of the disease is facilitated by half-yearly liver ultrasonography and serological assay of alphafoetoprotein and ferritin in high risk groups. A relief to the scourge of the disease is the new modality radio frequency ablative therapy for both early and advanced diseases as well as recurrences. Prevention of primary hepatocellular carcinoma is by food hygiene, and alleviation of poverty along with governmental disposition to incorporating vaccination against Hepatitis B virus, the commonest aetiological factor, into the National Programme of immunization.
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PMID:Relief to the scourge of primary hepatocellular carcinoma. 1295 91


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