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)

Before establishing the diagnosis of chronic active hepatitis (CAH) non-A-non-B other diseases have to be excluded, like toxic hepatitis (alcohol, drugs), immunological forms (autoimmune hepatitis, primary biliary cirrhosis), and metabolically caused hepatitis (hemochromatosis, Wilson's disease), since for some of these patients specific therapeutic procedures are available. History of the disease and repeated evaluation of control biopsies performed about every 9 to 12 months help in deciding about therapy. Chronic persisting hepatitis non-A-non-B and the mild form of CAH non-A-non-B do not need treatment but only diagnostic follow-up. Patients with apparent clinical disease, increased transaminases and histologically typical findings in at least two biopsies may be looked at as suitable for drug treatment. Since this disease is probably caused by virus, immunosuppressive therapy in this small group of patients described above has to be temporarily limited and should not be used as long term treatment.
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PMID:[Therapy of chronic non-A, non-B hepatitis]. 643 6

33 patients with chronic renal failure were divided into two groups. Group I consisted of 8 non-dialysed patients without any clinical or biochemical sign of liver disturbance nor any iron supplementation. Group II consisted of 25 maintenance hemodialysis (MHD) patients treated from 2 to 13 years. 19 subjects had chronic B hepatitis. Total exogenous iron load parenteral iron and/or blood transfusions) was calculated. Body iron overload (hemosiderosis) was assessed by liver iron concentration (LIC) in needle biopsy specimens according to Barry's method (less than 200 microgram/100 mg dry weight) and serum ferritin levels (less than 360 ng/ml). 4 patients whose serum ferritin was increased with or without hepatic fibrosis and with or without any organ dysfunction due to hemochromatosis received i.v. infusions of desferrioxamine in doses of 2 g at each dialysis. Serum ferritin levels were correlated with LIC (p less than 0.001) and iron load (p less than 0.001). Hemosiderosis was noted in 16 MHD patients (group II) and correlated with iron load. Hemochromatosis was noted in 4 patients (group II). 4 hemodialysed patients with iron overload were treated by desferrioxamine from 6 to 18 months. During this therapy, body iron stores fell and organ dysfunction (heart failure, hepatic cytolysis, anaemia, diabetes mellitus improved. Long-term chelation therapy by desferrioxamine was effective and the chelated iron was readily removed by dialysis. These data show the importance of precise evaluation of iron stores in MHD patients.
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PMID:[Iron-overload in patients on maintenance hemodialysis: diagnostic criteria, indications and treatment by desferrioxamine (author's transl)]. 732 1

The aim of this study was to assess the causes of histologically proven chronic hepatitis in a series of 357 consecutively admitted patients. Patients with chronic alcohol intake above 50 g per day, Wilson's disease, idiopathic hemochromatosis or homozygous alpha-1 antitrypsin deficiency were excluded. Sera of all patients were tested for antibodies to hepatitis C virus with second-generation enzyme-linked immunoassay and recombinant immunoblot assay, for markers of hepatitis B and hepatitis D viruses, and for autoantibodies. Detection of hepatitis C viral RNA by polymerase chain reaction was attempted if recombinant immunoblot assay was indeterminate, or if both viral and autoimmune markers were absent. If no serum markers, including HCV RNA, were found, the cause of chronic hepatitis was considered as unknown. The cause of chronic hepatitis was found in 343 cases (96.4%), including three patients with HCV RNA as the only marker. Chronic hepatitis was related to hepatitis C virus in 51.8%, to hepatitis B virus in 32.8% (including hepatitis D infection in 3.1%), and to autoimmune hepatitis in 5.9% of cases, respectively. No case of drug-induced chronic hepatitis was observed in this series, and in 5.9% of cases, there were probably multiple causes. Finally, in 3.6% of the cases the cause of chronic hepatitis remained unknown despite extensive evaluation suggesting the existence of a non-A, non-B, non-C viral agent.
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PMID:Etiology of chronic hepatitis in France: predominant role of hepatitis C virus. 752 73

Hepatocellular carcinoma (HCC) is among the 10 most common tumors in the world. However, incidence is not evenly distributed across the world. In many instances, the proximate cause for the tumor can be identified. Chronic hepatitis B infection is probably the most common cause, followed by chronic hepatitis C. Other important causes are alcoholic liver disease, hemochromatosis, alpha 1-antitrypsin deficiency, and other chronic liver diseases. Although proximate causes may be identifiable, pathogenesis remains uncertain. Factors that may be important include the presence of Aflatoxin B1 in food, genetic changes induced by the hepatitis B virus, and repeated rounds of necrosis and regeneration, also induced by hepatitis viruses. The genes involved and the mutations necessary for hepatic carcinogenesis are unknown, with the sole exception of the p53 gene, which is probably a late phenomenon. Screening for HCC is widely practiced despite the lack of evidence of improved survival. The screening tests used include alphafetoprotein levels and ultrasonography. Screening can identify small tumors; however, survival may not be improved, because the presence of cirrhosis may limit the number of patients who can undergo resections; recurrences or second primary tumors are common; and the presence of chronic liver disease means that survival may be limited anyway. There are many different forms of therapy available; unfortunately, most have not been compared in randomized controlled trials. Surgery remains the therapy of choice if feasible. All other therapy is palliative, including chemotherapy, chemoembolization, hepatic artery embolization, various forms of radiotherapy, and various forms of ablative therapy.
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PMID:Hepatocellular carcinoma. 753 16

We have recently noted a hitherto undescribed hepatic hemosiderosis confined to endothelial cells of the portal tract in chronic viral hepatitis. In this study, this lesion was surveyed in 156 liver biopsy specimens from patients with chronic hepatitis C and in 21 liver biopsy specimens from patients with chronic hepatitis B. As controls, we examined 110 liver biopsy specimens from patients with primary biliary cirrhosis (PBC), 36 from patients with alcoholic liver injury, nine from patients with autoimmune hepatitis (AIH), and five from patients with primary hemochromatosis. Hemosiderin deposition was found in the endothelial cells of venous vessels in portal tracts regardless of the presence or degree of hemosiderin deposition in hepatic parenchyma. This phenomenon was observed in 65 of 156 cases (42%) of chronic hepatitis C and in eight of 21 (38%) cases of chronic hepatitis B. In controls, this lesion was frequent in AIH (78%), but infrequent in PBC (8.1%) and alcoholic liver injury (11%). The incidence of this lesion showed significant differences between chronic hepatitis C, B, and AIH, and between PBC and alcoholic liver injury. There was a positive correlation between the progression of disease and the incidence of this feature in chronic viral hepatitis; the incidence was 18.3% and 11.1% in milder chronic hepatitis C and B, respectively, and 61.2% and 58.3%, respectively, in more severe cases. However, this correlation was not evident in either PBC or alcoholic liver injury. This hemosiderin deposition was positively correlated with the degree of piecemeal necrosis in chronic hepatitis C, and to a lesser degree, the positive correlation was shown in chronic hepatitis B. These findings suggest that the progression of chronic hepatitis and the piecemeal necrosis in chronic hepatitis C and B, followed by the release of hepatocellular iron to portal and periportal areas, are directly or indirectly responsible for endothelial hemosiderosis. Further studies focusing on this peculiar phenomenon in relation to choice of therapy and evaluation of chronicity of viral hepatitis are encouraged.
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PMID:Hemosiderin deposition in portal endothelial cells: a novel hepatic hemosiderosis frequent in chronic viral hepatitis B and C. 755 40

This is the first reported case, to our knowledge, of hypoparathyroidism and hypothyroidism due to secondary hemochromatosis with onset during childhood. The patient was a boy with refractory aplastic anemia in whom primary hypothyroidism and hypoparathyroidism became apparent at the age of 10 and 11 years old, respectively. He had received a total of 100 L of transfused blood by the age of 10 years. The patient showed poor annual height gain due to primary hypothyroidism, together with hypocalcemia, cataract and intracranial calcification due to hypoparathyroidism. The early appearance of both thyroid and parathyroid dysfunction in this patient may have been due to the delay of initiation of iron-chelating agents and liver dysfunction due to hepatitis type C.
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PMID:Hypothyroidism and hypoparathyroidism in an 11 year old boy with hemochromatosis secondary to aplastic anemia. 757 61

Seventy-two long-surviving liver transplant recipients were evaluated prospectively, including a baseline allograft biopsy for weaning off of immunosuppression. Thirteen were removed from candidacy because of chronic rejection (n = 4), hepatitis (n = 2), patient anxiety (n = 5), or lack of cooperation by the local physician (n = 2). The other 59, aged 12-68 years, had stepwise drug weaning with weekly or biweekly monitoring of liver function tests. Their original diagnoses were PBC (n = 9), HCC (n = 1), Wilson's disease (n = 4), hepatitides (n = 15), Laennec's cirrhosis (n = 1), biliary atresia (n = 16), cystic fibrosis (n = 1), hemochromatosis (n = 1), hepatic trauma (n = 1), alpha-1-antitrypsin deficiency (n = 9), and secondary biliary cirrhosis (n = 1). Most of the patients had complications of long-term immunosuppression, of which the most significant were renal dysfunction (n = 8), squamous cell carcinoma (n = 2) or verruca vulgaris of skin (n = 9), osteoporosis and/or arthritis (n = 12), obesity (n = 3), hypertension (n = 11), and opportunistic infections (n = 2). When azathioprine was a third drug, it was stopped first. Otherwise, weaning began with prednisone, using the results of corticotropin stimulation testing as a guide. If adrenal insufficiency was diagnosed, patients reduced to < 5 mg/day prednisone were considered off of steroids. The baseline agents (azathioprine, cyclosporine, or FK506) were then gradually reduced in monthly decrements. Complete weaning was accomplished in 16 patients (27.1%) with 3-19 months drug-free follow-up, is progressing in 28 (47.4%), and failed in 15 (25.4%) without graft losses or demonstrable loss of graft function from the rejections. This and our previous experience with self-weaned and other patients off of immunosuppression indicate that a significant percentage of appropriately selected long-surviving liver recipients can unknowingly achieve drug-free graft acceptance. Such attempts should not be contemplated until 5-10 years posttransplantation and then only with careful case selection, close monitoring, and prompt reinstitution of immunosuppression when necessary.
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PMID:Weaning of immunosuppression in long-term liver transplant recipients. 783 42

The aim of this study was to evaluate the diagnostic usefulness of percutaneous liver biopsy and screening for hepatitis C virus antibodies with 1st and 2nd generation ELISA in asymptomatic blood donors with persistent (> 1 year) and moderate elevation (> 1.5 times the upper limit of normal) of serum alanine aminotransferase. The diagnosis was established from clinical, biological and ultrasound data before biopsies were obtained, then compared to the histological diagnosis. Thirty one of 56 blood donors who satisfied the preceding criteria accepted liver biopsy and were subsequently included in the study. An accurate diagnosis was proposed before biopsy in 20 cases. This was in agreement with the histological results in 19 cases but in 2 of these, unexpected lobular hepatitis was associated with the expected steatosis. Positive hepatitis C virus tests corresponded to chronic hepatitis in all cases (n = 5). No accurate diagnosis could be proposed in the 11 remaining cases owing to the lack of evidence of any etiology (n = 4) or because several potential etiologies were possible for the same subject (n = 7). Histological diagnoses were: isolated steatosis (n = 12), steatosis associated with lobular hepatitis (n = 7) or with chronic persistent hepatitis (n = 1), chronic active (n = 2) or chronic persistent hepatitis (n = 3), alcoholic hepatitis (n = 2), hemochromatosis (n = 1), and normal liver (n = 3). Liver biopsy is essential to the accurate etiological diagnosis of persistent and moderate elevation of aminotransferases despite hepatitis virus C tests which are associated with the correct diagnosis of chronic hepatitis in 16% of cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Contribution of liver biopsy and serology of hepatitis C virus to the diagnosis of a moderate and prolonged elevation of aminotransferases]. 846 69

In 1986, our institution published the first results of surgical resection of hepatocarcinoma in cirrhotic patients. The aim of this paper is to present long term results of this surgical management. From April 1978 to February 1992, 74 patients were operated on at the surgical clinic of University Medical Center of Rennes (35000) France. There were 60 hepatectomies and 14 transplantations. The mean age was 60.2 years +/- 9 years and the sex ratio: 70 males and 4 females. The etiology was alcoholic in 43 patients (58%), post hepatitis (B and C) in 22 patients (30%) and due to hemochromatosis in 9 patients (12%). According to the Child Pugh classification, 48 patients were Child A, 11 Child B and one Child C in the hepatectomy group and 9 patients Child A and 5 Child B in transplantation group. The operative mortality was 10% in hepatectomy group and 35.7% in liver transplantation group. Overall survival was 61.8% at 1 year, 47.1% at 2 years, 38.2% at 3 years and 20% at 5 years. 5 year survival is 21.4% after transplantation and 18.5% after resection. This difference is not significant. In conclusion, according to 5 years survival and to operative mortality the treatment of choice is hepatectomy in HCC in cirrhotic patients. However the best treatment is the prevention of cirrhosis.
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PMID:[Surgical treatment of hepatocarcinoma in cirrhosis]. 854 50

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23


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