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

The authors performed 20 liver transplantations from living related donors between June 1990 and July 1991. The 20 pediatric patients (14 biliary atresia, two Budd-Chiari syndrome, one liver cirrhosis after hepatitis C viral infection (HCV hepatitis), 1 progressive intrahepatic cholestasis, 1 liver cirrhosis, 1 protoporphyria) were transplanted with 11 left lobes, eight left lateral segments, and one right lobe. The choice of donors was restricted to the parents of the recipients. The immunosuppressive treatment consisted of FK 506 and steroids. Seventeen recipients are alive, 15 of whom are well and at home. Two recipients, who underwent emergency transplantation, died of postoperative complications. Another recipient died of accidental asphyxia at 6 months after the transplantation. All 20 donors had uneventful postoperative courses and were able to resume their normal social lives. The arterial ketone body ratio (AKBR) increased to above 1.0 within 2 days after the transplantation in all cases. Relatively mild rejection episodes were encountered in only two cases transplanted with ABO-compatible grafts, and these were treated successfully with steroids and FK 506.
 ...
PMID:An appraisal of pediatric liver transplantation from living relatives. Initial clinical experiences in 20 pediatric liver transplantations from living relatives as donors. 128 74

Some complications of liver transplantation appear as aspecific clinical and blood test abnormalities; others--e.g., hepatic artery thrombosis in the immediate postoperative period and stenosis of the biliary anastomosis before T-tube removal--require early diagnosis. These considerations justify the need of frequent radiologic examination in both the complicated course and the follow-up. The authors report their experience in 59 adult patients submitted to liver transplantation for irreversible liver disease in advanced stage (49 with cirrhosis, 10 with HCC; 5 with cholestatic hepatopathy; 3 with fulminant hepatitis; 1 with Budd-Chiari syndrome; 1 with metastatic APUDoma). Two hundred and sixty-three radiological examinations were performed (Doppler US, CT, angiography and cholangiography) which showed numerous early and delayed complications: 13 of them were treated with interventional radiology maneuvers (US-or CT-guided percutaneous drainage of fluid collections, biliary drainage, bilioplasty, arterial transcatheter embolization). Our results demonstrate that diagnostic and operative radiology are essential for the success of liver transplantation; integrated imaging is particularly important in the diagnosis of complications, while interventional radiology techniques can be usefully employed in their treatment.
 ...
PMID:[Liver transplantation: role of the radiologic methods in the postoperative period]. 145 22

The sex-specific and age-specific incidence rates of the major parenchymal liver diseases in a North European population were estimated using a computerized registry of all admissions to somatic hospitals in Denmark. The incidence was calculated by counting all incident cases of these diseases reported to the registry in the 5-yr period 1981 to 1985 and dividing the number of cases by the number of person-years at risk in this period. The incidence rates (per million person-years) were for men and women, respectively: infectious hepatitis, 109 and 71; toxic hepatitis, 19 and 22; chronic hepatitis, 27 and 29; alcoholic cirrhosis, 190 and 85; nonalcoholic nonbiliary cirrhosis, 110 and 82; primary biliary cirrhosis, 4 and 14. The pattern of the age-specific incidence rates was similar in men and women in infectious hepatitis, alcoholic cirrhosis, nonalcoholic nonbiliary cirrhosis and primary biliary cirrhosis. Toxic and chronic hepatitis had a higher incidence in women than in men only in older age groups. The incidence of idiopathic hemochromatosis, Wilson's disease, secondary biliary cirrhosis, portal vein thrombosis and Budd-Chiari's syndrome were less than four in both sexes.
 ...
PMID:Incidence of parenchymal liver diseases in Denmark, 1981 to 1985: analysis of hospitalization registry data. The Danish Association for the Study of the Liver. 201 Jan 59

In a review of literature the presented studies on radiogenic liver injuries are summarized. Whereas in the past the liver tissue was supposed to be radioresistant nearly completely, to newer knowledge this organ has to be classed with most radiosensitive tissues at all. The early picture of a liver injury in man is characterized by the veno-occlusive syndrome. Like in Budd-Chiari-Syndrome a congestion begins in the central veins and the centrolobular sinusoids, that has severest threatening consequences for the patients with extensive liver irradiation. The clinic picture is demonstrated. At present no suitable animal model exists for this disease yet. The presented pathological and electron microscopical findings do not allow any final estimation of the pathogenesis in this disease. The radiogenic late-effects are manifested in the liver in a centrolobular fibrosis, also starting from the Glisson's triangles, with cirrhotic reconstruction of liver architecture. The great compensatory power of the organ does not cause clinical pictures to be effected in radiotherapeutic practice with only partial liver irradiation in most cases. The dose-time-relation of the radiogenic hepatitis shows a very little alpha-/beta-value. With this the liver renders as typical late-effect tissue and should be spared effectively by choice of small single doses.
 ...
PMID:[Radiogenic effects on liver tissue]. 218 82

Liver sinusoids are special capillaries that are limited by fenestrated endothelial cells, without a genuine basement membrane, surrounded by perisinusoidal cells storing vitamin A, and harbouring Kupffer cells and pit cells, resident macrophages, and large granular lymphocytes, respectively. Each nonparenchymal cell and parenchymal cell of the liver interacts with all others and with the extracellular matrix. Therefore, the functional ability of each cell is constantly being modified by the metabolic activity of the others. Human liver biopsies (132), needle or surgical, perfusion-fixed with glutaraldehyde and processed for transmission electron microscopy (TEM), and occasionally for scanning electron microscopy (SEM), were examined. The study included liver diseases (such as alcoholic liver diseases, benign and malignant liver tumors, cholestasis of various origins, fulminant hepatitis, acute rejection after orthotopic liver transplantation, Budd-Chiari syndrome), as well as general or extrahepatic diseases (such as diabetes, hemochromatosis, hypervitaminosis A, various hematological disorders), and normal controls. Ultrastructural abnormalities are described and illustrated under two different headings: 1) elementary lesions of sinusoidal cells (endothelial, Kupffer, perisinusoidal and pit cells), nonsinusoidal cells (in the space of Disse and/or in the lumen), the extracellular matrix; and 2) the major pathological entities including perisinusoidal fibrosis, capillarization of sinusoids, sinusoidal dilatation, and peliosis. In the discussion, an overview of the major abnormalities reported in the literature is presented, and some specific questions regarding 1) perisinusoidal fibrosis in liver with normal histology, 2) the overload of perisinusoidal cells with lipids in non-hypervitaminosis A intoxication and 3) the etiological relationship of sinusoidal dilatation, peliosis, perisinusoidal fibrosis, or sinusoidal tumors with drugs and toxic compounds are discussed. In the event that lesions are not specific to any diagnosis, the knowledge of the ultrastructure of sinusoids is extremely useful from the perspective of the liver as an ecosystem.
 ...
PMID:Fine structure of hepatic sinusoids and sinusoidal cells in disease. 233 89

This is a broad review (140 literature citations) of the possible effects of oral contraceptives on the liver. The oral contraceptives considered consist of combined preparations of estrogens and progestogens although the so-called "minipills" contain only a progestogen. The effects are divided into 1) decrease in excretory liver function; 2) influence on bile acid formation, including cholesterol metabolism; 3) increased synthesis of various transport proteins (ceruloplasmin, transferrin, thyroxine-binding protein, and cortisol-binding protein); 4) the effects of increased tissue circulation caused by sexual hormones and anabolic steroids as a cause for more frequent cavernous angiomas and peliosis hepatis; 5) interference with the metabolism of other drugs by the competitive action of the hepatic metabolites of steroid hormones. This includes the increased formation of delta amino levulinic-acid synthetase, the key enzyme for porphyrin synthesis. The gestagen component of oral contraceptives is responsible for enzyme induction in the smooth endoplasmic reticulum. Morphological liver changes caused by oral contraceptives include parenchyma changes, hepatosis, reactive hepatitis, hepatitis resembling viral hepatitis, vascular changes, sinusoid ectasia, Budd-Chiari syndrome, hyperplasias and neoplasias, focal nodular hyperplasia, adenoma and liver cell carcinoma.
 ...
PMID:[Effects of oral contraceptives on liver function and structure]. 332 30

Two cases of the Budd-Chiari syndrome are described in whom the diagnosis was finally confirmed at necropsy. The presentation was with encephalopathy, occurring within eight weeks of first symptoms and coming therefore within the definition of fulminant hepatic failure. In one, thought to have non-A, non-B hepatitis, encephalopathy progressed to grade 4 coma with death 12 days after presentation. In the other, mistakenly thought to have intra-abdominal malignancy, an exploratory laparotomy exacerbated the encephalopathy with death three weeks later. In neither case were non-invasive investigations, such as ultrasound and isotope scanning, carried out which might have facilitated an earlier diagnosis and consideration for orthotopic liver transplantation, probably the most appropriate form of therapy for these very severe cases.
 ...
PMID:Budd-Chiari syndrome presenting as fulminant hepatic failure. 375 22

Drugs are exogenous substances often requiring metabolic transformation to be therapeutically effective. This occurs primarily in the liver, the most important metabolic organ and a structure able to adapt to this burden. Should its adaptive potential be exceeded, damage can occur, affecting principally the liver parenchyma. Such damage manifests itself as disturbed secretory function and as reversible or irreversible structural alteration of the liver cells. The constellation of toxic-degenerative lesions is referred to as hepatosis (toxic hepatosis, toxic hepatopathy). A variety of patterns of damage (lipidosis, necrosis, cholestasis etc.) occur alone or in combination. Depending on the severity and extent of these alterations a secondary inflammatory reaction may result. These changes are manifest as cellular infiltration and proliferation with formation of reticulo-histiocytic nodules or minifocal epitheloid cell reactions and non-caseous epitheloid cell granulomas. The eosinophilic component is striking. In the face of continued toxic exposures, changes resembling those of chronic aggressive hepatitis may develop following the acute changes. Other drug-related liver damage may present as vascular lesions the afferent or efferent venous systems as well as in the sinusoids (i.e. peliosis hepatis, Budd-Chiari syndrome). Moreover there may be neoplastic alterations such as focal nodular hyperplasia or liver cell adenomas. Pathognomonic histologic criteria for drug-induced liver damage have as yet to be recognized, particularly in the case of facultative toxins. Morphologic indications can only suggest that a prior pharmaceutical agent was the likely cause of the damage. Histologic changes must however be viewed in the context of the medical history, clinical and laboratory findings, as well as results of other studies before the conclusion is drawn that the observed liver changes represent drug-induced injury.
 ...
PMID:[Morphological reaction patterns of the liver induced by drugs]. 383 9

The pathologic specimens (n = 118) and hospital course pertinent to each of 62 adult liver allograft recipients were reviewed. Biopsies and retransplanted organs were obtained at the discretion of the surgical team on the basis of the postoperative clinical course (less than 1 day to greater than 12 years after transplantation), and final interpretation of the pathologic material was based on a correlation of all available data. Most of the specimens (n = 85) were obtained within the first 2 months, and diagnoses in this time period included rejection, biliary obstruction/cholangitis, vascular injury, herpesvirus and cytomegalovirus hepatitis, graft necrosis, and functional cholestasis. Thereafter, rejection and recurrent or primary viral hepatitis were the major causes of graft dysfunction. Histologically, hepatic rejection is manifested by a cellular mediated injury of hepatocytes and bile ductules and a spectrum of vascular lesions in medium-sized hilar arteries. Morphologic changes of biliary duct obstruction and viral liver disease were at times difficult to differentiate from rejection. Two pretransplant disorders, type B viral hepatitis and the Budd-Chiari syndrome, recurred in grafted organs. Although interpretation of pathologic material may be difficult at times, it frequently is helpful in planning an approach to management of liver allograft recipients.
 ...
PMID:Pathology of hepatic transplantation: A review of 62 adult allograft recipients immunosuppressed with a cyclosporine/steroid regimen. 388 Oct 37

Rather rapid and brief over-view of pathology of hepatocellular carcinoma has been made, where the connection between morphology and virology or biochemistry is stressed as the main focus of today's pathology. Thus, existence of some relation between hepatitis virus and hepatocellualr carcinoma seems to be definite for us. However, it is still very difficult to decide whether the relationship is a direct or indirect one. High incidence of hepatocellular carcinoma also in Budd-Chiari's cirrhosis and schistoma-induced cirrhosis seems to suggest existence of the high risk type of cirrhosis for hepatocellular carcinoma development, irrespective of the cause of cirrhosis itself, although HB antigen might be playing some role in these cases especially in the latter.
 ...
PMID:Pathology of hepatocellular carcinoma. 615 15


1 2 3 4 5 Next >>