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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

Serum parameters of calcium metabolism were measured in 32 consecutive patients with biopsy-proven cirrhosis due to either hepatitis (n = 13), alcohol abuse (n = 11), Wilson's disease (n = 3), or primary or secondary biliary cirrhosis (n = 5). All measurements were normal in the small group of patients with Wilson's disease. The serum concentrations of albumin, vitamin D-binding protein, total calcium, phosphorus, and 1,25-dihydroxyvitamin D3 (1,25-(OH2)D3) were decreased in the other patients with cirrhosis, but their mean serum concentrations of ionized calcium, 25-hydroxyvitamin D3 (25-OHD3) and free 1,25-(OH2)D3 index were normal. A slight but significant increase in the serum PTH measured using a carboxyl-terminal antiserum was found. A significant correlation was found between the serum concentration of either albumin or vitamin D-binding protein and the serum concentrations of total calcium, 25-OHD3, 1,25-(OH2)D3, and PTH but not with ionized calcium or free 1,25-(OH2)D3 index. The observed abnormalities of calcium metabolism in unselected patients with cirrhosis were mainly due to decreased protein synthesis. Only the patients with severe cirrhosis had decreased concentrations of 25-OHD3 but they were nevertheless able to maintain a normal ionized serum calcium and free 1,25-(OH2)D3 level, possibly by means of compensatory hyperparathyroidism.
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PMID:Serum vitamin D metabolites and their binding protein in patients with liver cirrhosis. 654 47

The necessity is emphasized to perform always a careful anamnesis and a clinical inspection of patients before achieving laboratory examinations (avoiding to demand to a "check up" the diagnosis). This is particularly important in those diseases, like viral hepatitis, which become even more frequent, so that such diagnosis may be supposed basing on unreliable laboratory findings. The possibility is mentioned that different hepato-colangiopathies (Wilson's disease, intolerance to fructose, hepatic congenital fibrosis, hepatic ductal hypoplasia, granulomatous hepatitis, bacterial, micotic and protozoarian cholangitis, liver sufference in onchologic diseases) may simulate viral hepatitis.
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PMID:[Differential diagnostic problems in acute and chronic hepatitis and hepato-cholangiographies of various etiologies in childhood]. 663 43

The entity of chronic hepatitis has long been an enigma, and its treatment confusing. Recent studies have indicated the importance of excluding causes such as drugs, Wilson's disease and alpha 1-antitrypsin deficiency. After excluding such causes, there are 3 major groups--'autoimmune', hepatitis B, and non-A, non-B (NANB) in all of which an immunological basis for pathogenesis exists. The autoimmune group has been subdivided into a milder type (chronic persistent hepatitis) and a more severe type (chronic active hepatitis) on histological grounds. Corticosteroids are indicated in chronic active hepatitis if cirrhosis or bridging necrosis is present. However, corticosteroids are contraindicated in disease due to the hepatitis B virus where chronic active hepatitis correlates with the presence of replicating virus (serum positive for e antigen, DNA polymerase and HBV-DNA), and in such cases antiviral agents and immunomodulation are being studied. Very little is known about NANB hepatitis in the absence of an assay and there may be more than a single agent. In hepatitis B, the development of serological markers, molecular probes (HBV-DNA), natural animal hepatitis with near-identical viruses, and delta antigen (a virus requiring co-infection with hepatitis B) have all extended our knowledge so dramatically that it is hoped that the enigma of chronic hepatitis will be solved when an assay for NANB hepatitis becomes available.
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PMID:Chronic hepatitis. Aetiology and current management. 673 69

A 41/2-year-old asymptomatic girl with persistent elevated serum transaminase levels for eight months was found to have Wilson's disease. The diagnosis was suspected by the presence of fatty liver and nonspecific chronic hepatitis on liver biopsy and was proved by studies of copper metabolism, including determinations of serum ceruloplasmin and hepatic copper concentrations. Unexplained persistent transaminase elevation in children demand investigation by needle liver biopsy. Th presence of fatty liver and hepatitis should raise the possibility of Wilson's disease, which may then be confirmed by more specific tests. Advantages to early diagnosis include the institution of specific therapy and prevention of progressive liver disease.
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PMID:Persistent transaminasemia and fatty liver. Their use in the diagnosis of presymptomatic Wilson's disease. 706 50

A case report is presented of a young woman in whom symptomatic porphyria cutanea tarda (PCT) developed during copper chelation therapy for Wilson's disease. The 22 year old white woman was seen in the summer of 1978 because of development of blisters on the dorsa of the hands associated with focal atrophic hypopigmentation, generalized hyperpigmentation of the skin, and hpertrichosis of the lateral forehead and face. A sibling had died in childhood with Wilson's disease. When the patient developed hepatomegaly, ascites, and an acute hepatitis syndrome at the age of 11, penicillamine therapy was empirically started, with gradual symptomatic improvement. When evaluated at the age of 22, abnormal laboratory values included a total bilirubin of 1.2 mg%; alkaline phosphatase, 96 U; serum glutamic oxaloacetic transaminase (SGOT), 175 U; serum glutamic pyruvic transaminase (SGPT), 122 U; gamma glutamyl trans peptidase (GGTP), 64 U; and Bromsulphalein (BSP) retention, 21% at 45 minutes. Skin biopsy from the hand revealed a noninflammatory subepidermal bulla with prominently PAS positive vessel walls in the festooned dermal papillae at the base of the blister. A fragmented liver biopsy failed to reveal evidence of active hepatitis or cirrhosis, but considerable stainable iron was present in both hepatocytes and Kupffer cells. A rubeanic acid stain for copper was negative. The patient was diagnosed as having Wilson's disease, hepatic hemosiderosis, and PCT. Cessation of all ethanol consumption and discontinuation of the oral contraceptives which she had been taking for 6 years, was recommended. On examination 9 and 22 months after these modifications were instituted, the patient felt asymptomatic and was without evidence of any new blisters or scars of her skin. The hyperpigmentation and hypertrichosis persisted, but she rigidly adhered to a program of penicillamine, topical sunscreen application, and abnegation of alcohol. Liver function studies were normal, and urinary porphyrin levels returned toward normal values. The clinical onset of this patient's blistering disease was temporally associated with ethanol and exogenous estrogen medication.
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PMID:Porphyria cutanea tarda complicating Wilson's disease. 720 91

Urinary copper excretion was found to be increased in patients with cholestasis, hepatitis and cirrhosis, but the penicillamine-induced increment was normal. Wilson's disease patients had increased copper excretion before and after penicillamine, especially in untreated cases. Hepatic copper concentrations correlated with urinary copper excretion in cholestasis and treated Wilson's disease, but not in hepatitis or cirrhosis. In treated Wilson's disease, measurement of urinary copper excretion should be valuable in estimating the degree of removal of copper from the body during therapy. Urinary copper clearances were raised in various liver conditions, maximally in untreated Wilson's disease. It is suggested that only part of the serum non-caeruloplasmin copper is available for excretion into urine.
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PMID:Urinary copper excretion and hepatic copper concentrations in liver disease. 721 19

The term "chronic hepatitis" includes diseases of different etiology, i.e. viral (hepatitis B virus, non-A/non-B hepatitis virus[es]), drug-induced (e.g. oxyphenisatin, alpha-methyldopa), metabolic (Wilson's disease, alpha 1-antitrypsin deficiency) and so-called "autoimmune" hepatitis. In the clinical course, hepatitis running for up to 3 months is considered acute; when lasting for 3-6 months it is termed prolonged, and chronic hepatitis means a duration of more than 6 months by definition. In chronic hepatitis there is international agreement on basing nomenclature on morphologic findings and on distinguishing chronic persistent hepatitis (with a predominantly lymphocytic inflammation restricted to portal tracts) from chronic aggressive (or active) hepatitis. The latter is typified by piecemeal necrosis in the periportal areas (activity a); additional piecemeal necrosis along fibrous septa or bridging hepatic necorsis is the key feature for activity b. In hepatitis B virus infection, the symptomfree carrier of the virus with no inflammation in biopsy, or merely nonspecific reactive hepatitis, must be included under the heading of chronic hepatitis. Cirrhosis, however, although resulting from necrosis, inflammation and fiber formation, refers exclusively to the disturbance of lobular architecture and its microcirculatory consequences. The term "cirrhosis" is thus not included in the definition of chrome hepatitis and should be evaluated separately as an entity in its own right.
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PMID:[Chronic hepatitis]. 742 73

The terms chronic active hepatitis (CAH), chronic persistent hepatitis (CpH), and chronic lobular hepatitis (CLH) have become obsolete, and their use without further specifications should be discontinued. This recommendation has become necessary because these names have changed from descriptive terms, intended for grading, to terms that are used either as morphologic diagnoses or disease designations or both, depending on individual preferences. Because this practice has caused serious misunderstandings, many authors and two international groups have recommended the use of a clear etiologic terminology. For the reporting practice of pathologists, we recommend that the pathologist routinely sign out biopsy samples with features of chronic hepatitis by indicating etiology, grade, and stage. An example would be autoimmune hepatitis, severe, stage 3. The stage in this case would indicate the presence of well-developed septal fibrosis but no nodular regeneration. Obviously, for the etiologic diagnosis, morphologic findings must be integrated with clinical and laboratory data. If this information is not available, clear morphologic diagnoses should be reported. Thus, instead of CPH, the diagnosis should be portal hepatitis, cause undetermined. This reporting practice eliminates ambiguous terminology and avoids the risk of inappropriate treatment as might occur, for example, when a term such as CAH is used to describe Wilson's disease and is misunderstood to mean autoimmune hepatitis. For a transitional period and to facilitate relearning, the terms CAH, CPH, and CLH can be reported in parentheses behind the etiologic diagnosis.
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PMID:Chronic hepatitis. An update on terminology and reporting. 750 62

We reviewed 37 living related liver transplantations (LRLT) performed by our department during the last 27 months on children with end-stage liver disease. The patients were 15 boys and 22 girls aged 7 months to 15 years with biliary atresia (27), cryptogenic cirrhosis (3), Budd-Chiari syndrome (2), progressive intrahepatic cholestasis (2), protoporphyria (1), Wilson's disease (1), and fulminant hepatitis (1). The donors were 14 fathers and 23 mothers. Grafts were made from the left lateral segment (19), left lateral segment with partial S4 (11), left lobe (6), and right lobe (1). After graft harvesting all donors resumed normal liver function and normal life. The recipient underwent total hepatectomy with preservation of the inferior vena cava. FK506 and low-dose steroids were used for immunosuppression. The survival rate was 90% (27/30) in elective cases and 57% (4/7) in emergency cases. Six recipients had functioning grafts but died of extrahepatic complications. Hepatic vein stenosis occurred in 3 cases at 3 months after LRLT and was successfully treated by balloon dilatation. Portal vein stenosis occurred in 1 case at 8 months after LRLT and was also safely dilated. We incurred no hepatic artery thrombosis after introducing microsurgery techniques. Among 12 viral, 5 bacterial, and 3 fungal postoperative infections, 1 Candida pneumonia and 1 EBV-associated lymphoma were lethal. Three patients with ABO-blood group compatible grafts and one with an incompatible graft developed acute rejection, which was controlled in evey case by steroid bolus and/or increasing the dose of FK506. There were no definite episodes of rejection in ABO-identical cases. Children with moderate growth retardation (> or = -1.5 SD of normal growth) caught up in growth soon after LRLT, but those with severe retardation (<-1.5 SD) were slow to attain age-normal height. Appropriate timing, meticulous surgical procedures, and comprehensive management of complications are crucial for successful outcome with LRLT. LRLT is a promising option for alleviating the shortage of livers for pediatric transplantation and may be regarded as an independent modality to supplement cadaver donation.
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PMID:Living related liver transplantation in children. 751 49


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