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)

Two patients with multiple myeloma died in acute liver failure. Both had been treated with the anabolic steroid oxymetholone and both subsequently developed severe cholestatic hepatitis. In one the histological lesion progressed despite cessation of oxymetholone therapy. Myeloma infiltration of the liver and peliosis hepatis were not seen. As a fatal outcome from cholestatic hepatitis due to oxymetholone is rare it is possible that an unknown potentiating factor is present in multiple myeloma that can lead to a fatal outcome. If oxymetholone therapy is to be used in such patients then close clinical and laboratory assessment of liver function should be carried out in an attempt to prevent this unusual and fatal complication.
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PMID:Fatal hepatic coma complicating oxymetholone therapy in multiple myeloma. 26 93

The results of liver biopsies taken from 155 patients, 16-45 years of age, who used oral contraceptives (o.c.s) are reported. In 68.4% of the cases there were morphological changes which could be attributed to o.c. use. In 73 cases, dilation of the sinusoids was found. In many of the cases, a similarity to peliosis hepatis was observed. Proliferation of the endothelium was found regularly, as well as proliferation of Kupffer cells within the sinusoids. In 20 cases hepatitis was determined which could be related to o.c. use. 5 cases of vital hepatitis were found in conjunction with o.c. use. There were 5 cases of cholestatic hepatitis. 1 case of intrahepatic venous thrombosis improved after discontinuation of o.c. use. In 8 cases there were additional uncharacteristic findings besides the sinusoid dilation.
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PMID:[Liver biopsy findings after intake of oral contraceptives (author's transl)]. 47 54

A patient developed disseminated intravascular coagulation with purpura fulminans 1 month after starting Dilantin therapy for a seizure disorder. In addition, the patient developed exfoliative dermatitis, hepatitis, cutaneous vasculitis, and microangiopathic hemolytic anemia. She was successfully treated with adrenal steroids and heparin for her purpura fulminans. The hepatitic dermatologic, along with hemorrhagic, complications of Dilantin are reviewed, and the possible origin of the vasculitis and disseminated intravascular coagulation is discussed.
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PMID:Dilantin-induced disseminated intravascular coagulation with purpura fulminans. A case report. 114 59

The angiographic findings in a patient with peliosis hepatitis are described. Histologically, multiple blood-filled cystic spaces are seen, often communicating with the hepatic sinusoids. There is evidence that steroid therapy may be a causative factor. The differential diagnosis is discussed.
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PMID:Peliosis hepatitis. 120 68

Amongst 17 patients with hepatic focal nodular hyperplasia (FNH) encountered at Westmead Hospital between 1981 and 1990, FNH was found in association with hepatocellular carcinoma (HCC) in three (3/17), one male and two females, one of whom also had peliosis and an hepatic adenoma. FNH was also found in association with other conditions which may affect hepatic function, structure or circulation, including chronic obstructive airways disease (2), congestive cardiomyopathy (1), chronic active hepatitis (1), granulomatous hepatitis (1), coeliac artery stenosis (1) and metastatic malignant melanoma (1). This report, derived from our experience with FNH over 10 years draws attention to a possible link between FNH, hepatic malignancy and conditions which may disturb the hepatic circulation. We suggest that patients with FNH should be investigated thoroughly and an aggressive management policy should be adopted.
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PMID:Hepatic focal nodular hyperplasia: a benign incidentaloma or a marker of serious hepatic disease? 132 5

A healthy 33 year old man presented with a short history of purpura and easy bruising. Investigations showed profound thrombocytopenia with atypical lymphocytes in the peripheral blood. Marrow appearances were consistent with platelet consumption. Biochemical hepatitis was also noted. An infection screen showed the underlying diagnosis to be cytomegalovirus (CMV) infection. He was treated successfully with oral prednisolone. This subsequently tailed off without relapse. Careful examination of a stained blood film is needed in all cases of apparent idiopathic immune thrombocytopenic purpura.
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PMID:Severe thrombocytopenia secondary to asymptomatic cytomegalovirus infection in an immunocompetent host. 133 93

We present pathologic findings for 52 livers (51 autopsy specimens and one wedge biopsy specimen) from patients with systemic lupus erythematosus (SLE). Hepatic congestion was the most common disease (40 livers), followed by fatty liver (38), arteritis (11), cholestasis (nine), peliosis hepatis (six), chronic persistent hepatitis (six), nonspecific reactive hepatitis (five), cholangiolitis (four), nodular regenerative hyperplasia of the liver (three), and hemangioma (three). The data obtained here suggest that arteritis of the SLE liver is more common than has been recognized previously. One patient had hepatic infarction complications induced by arteritis. On the basis of the findings in the present study and a review of the literature, we suggest that hepatic infarction resulting from arteritis is rare in SLE. On the other hand, while occurrence of nodular regenerative hyperplasia of the liver in SLE patients has been considered to be rare, our findings suggest that it may be more common than has been recognized previously. Although congestion and cholestasis may be acute terminal illnesses, fatty change is considered to be specific to the SLE liver. Statistical analysis indicates that exposure to a large dosage of glucocorticoids is a significant factor in the etiology of severe fatty liver. In addition, our review of Japanese autopsy registry data for 1,468 patients with SLE indicates that the incidence of chronic liver diseases in SLE autopsy cases is as follows: chronic hepatitis, 2.4%; cirrhosis, 1.1%; and liver fibrosis, 0.8%.
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PMID:The liver in systemic lupus erythematosus: pathologic analysis of 52 cases and review of Japanese Autopsy Registry Data. 139 43

A distinct peliosis-like lesion arose in the liver allograft of a 51 year old man. This lesion was caused by necrotic, fat-laden hepatocytes that released fat globules into the sinusoids. These then became strikingly distended with cysts, thus mimicking peliosis hepatitis. It is suggested that this lesion be called lipopeliosis.
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PMID:Lipopeliosis: fat induced sinusoidal dilatation in transplanted liver mimicking peliosis hepatis. 147 38

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.
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PMID:Fine structure of hepatic sinusoids and sinusoidal cells in disease. 233 89

Human hypersensitivity angiitis is a disease involving deposition of immune complexes in which patients present with palpable purpuric lesions most often on the lower extremities and sometimes associated with multiple organ involvement. There are numerous potential antigens in the immune complex and the disease may be derived from an infectious organism such as Streptococcus or the hepatitis virus, from a drug, or from a variety of other chemicals which may be ingested or inhaled. In addition, the antigen may be part of another systemic disease. This complex of circulating antigen and antibody may become fixed within the vessel wall activating the complement cascade with elaboration of factors chemotactic for neutrophils. These cells then release lysosomal enzymes which result in destruction of the vessel wall and leakage of red blood cells into the tissue. This produces the typical purpura and palpability seen clinically. A central question in the pathogenesis of this disease is to explain why the immune complex is seemingly so selective in its site of deposition as it may be deposited in postcapillary venules in some patients and medium-sized muscular arteries in other patients. Part of the reason for this must be related to the lattice formation of a particular complex, while other reasons are likely related to alterations in vascular permeability, to the integrity of clearance mechanisms for the complex, or possibly even to a genetically determined defect of the phagocytic system.
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PMID:Human hypersensitivity angiitis. 253 32


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