Search PubMed⌕ Search

Biomedical subjects

H Popper

Publications and source records attributed to H Popper.

At least 145 records · Page 8Linked to original sources
PubMed1979

Hepatic angiosarcoma associated with androgenic-anabolic steroids.

A retrospective epidemiological study of deaths from hepatic angiosarcoma (HAS) in the U.S. showed that during 1964--74 there were 168 such cases, of which 37 (22%) were associated with previously known causes (vinyl chloride, 'Thorotrast', and inorganic arsenic) and 4 (3.1%) of the remaining 131 cases with the use of androgenic-anabolic steroids. It is suggested that the long-term use of androgenic-anabolic steroids is the fourth cause of HAS, the majority of cases still being of unknown aetiology. Moreover, the presented cases serve as a link in a spectrum of hepatic disorders recently recognised to be caused by environmental agents such as vinyl chloride, arsenic, and thorotrast, and by contraceptive and anabolic steroids. Similar precursor stages, usually not recognised by clinical laboratory tests and consisting of areas of hyperplasia of hepatocytes and sinusoidal cells and sinusoidal dilatation, lead potentially to hepatic adenoma, carcinoma, peliosis, and angiosarcoma.

Androstanes↗
PubMed1979

Cytoplasmic copper and its toxic effects. Studies in Indian childhood cirrhosis.

Morphological, histochemical, and chemical study of three necropsy specimens of liver in the terminal stage of Indian Childhood Cirrhosis revealed a strikingly high copper content. it is proposed that excess accumulation of copper in the cytoplasm of hepatocytes disturbs the microtubular system, causing hydropic swelling and the formation of Mallory's hyalin. Copper and copper-binding protein showed topographical association with Mallory's hyalin. Diffuse cytoplasmic staining and the lysosomal copper distribution also suggested that copper had a cytotoxic effect. The pattern of copper distribution in Indian Childhood Cirrhosis differs from that in Wilson's disease and in prolonged cholestasis with excessive hepatic copper deposition, indicating a different mechanism of the copper accumulation.

Child, Preschool↗
PubMed1979

Injury and repair of liver cells.

Alterations in hepatocytes, progressing to necrosis, are the morphologic basis for the main clinical manifestations and aberrations in hepatic test results in acute and chronic liver disease. The light-microscopic manifestations of hepatocellular injury, the mechanisms of necrosis, the light-microscopic features of repair and regeneration, and the applications of histologic alterations to the management and prognosis of liver disease are reviewed.

Biopsy↗
PubMed1979

Veno-occlusive disease of the liver after allogeneic bone marrow transplantation: possible association with graft-versus-host disease.

Acute veno-occlusive disease of the liver developed in seven of 29 patients undergoing bone marrow transplantation for treatment of leukemia, aplastic anemia, or disseminated carcinomatosis. All seven died despite successful marrow engraftment. Hepatic failure was the principal cause of death in four and contributory in three. The veno-occlusive disease did not relate to the nature of the pretransplant immunosuppressive regimen, since it occurred in patients receiving irradiation alone, chemotherapy alone, or both. Twenty-two of the patients were autopsied. Among these, the lesion was found in seven of 11 in whom a graft-versus-host reaction developed but in none of the 11 without such a reaction who had received similar pretransplant immunosuppression (P less than 0.025). Hence, acute veno-occlusive disease of the liver appears to be a complication of allogeneic bone marrow transplantation related to the development of a graft-versus-host reaction.

Acute Disease↗
PubMed1979

Distribution of five antigens in hepatocellular carcinoma.

A variety of antigens may be detected in the serum of patients with hepatocellular carcinoma (HCC). The incidence and distribution of five antigens in 37 HCC and their relation to each other in a given tumor was examined by the peroxidase-antiperoxidase technique using formalin-fixed paraffin-embedded tissues. alpha 1-Antitrypsin was frequently expressed in HCC (73 per cent of cases), whereas alpha-fetoprotein and carcinoembryonic antigen were less common. HBsAg, but not HBcAg, was observed in tumor cells in seven of nine HCC from HBsAg-positive patients. In 20 HCC (54 per cent), two or more antigens, most frequently alpha 1-antitrypsin and alpha-fetoprotein, were detected. Double staining for simultaneous localization of two antigens in the same tissue section revealed that different antigens were usually present in different tumor cells, although some cells displayed two antigens simultaneously. These findings suggest that hepatocellular carcinoma cells are functionally heterogeneous, even if they appear histologically monomorphic.

Antigens, Neoplasm↗
PubMed1978

Transmissible agent in non-A, non-B hepatitis.

Plasma or serum from 4 patients with acute or chronic non-A, non-B post-transfusion hepatitis (P.T.H.) and from a blood-donor implicated in two cases of P.T.H. was inoculated into 5 chimpanzees. Biochemical and histological evidence of hepatitis developed in these 5 chimpanzees but not in a control animal. The mean incubation period in the chimpanzees was 13.4 weeks, compared with 7.7 weeks in the 4 patients with P.T.H. The peak alanine aminotransferase (A.L.T.) levels in the 5 chimpanzees were 265, 212, 219, 70, and 62 I.U./l. Histological changes ranged from mild to conspicuous hepatitis and generally correlated with the degree of A.L.T. elevation. There was no evidence of clinical disease and all animals went on to biochemical and histological recovery. There was no serological evidence of type A or type B hepatitis. Hepatitis was transmitted by serum derived from patients with chronic as well as acute hepatitis, strongly suggesting a chronic carrier state for the agent responsible for non-A, non-B hepatitis. Non-A, non-B hepatitis thus seems to be due to a transmissible agent which can persist and remain infectious for long periods.

Acute Disease↗
PubMed1978

[Hepatic fibrosis--mechanism, dynamics and clinical consequences (author's transl)].

Hepatic fibrosis may result from collapse after hepatocellular necrosis or from new formation of connective tissue. Fibroplasia, particularly within the lobular parenchyma, is a dynamic process. Newer cellular and biochemical investigations clarified its various steps. The process begins with stimulation of cells to connective tissue formation and can be divided into (1) intracellular synthesis, (2) extracellular maturation, and (3) collagen breakdown. The turnover of the connective tissue in the liver is conspicuously increased in chronic hepatitis of any type, as indicated by an elevation of several cellular and metabolic parameters. They are particularly raised in chronic hepatitis and in alcoholic liver injury. Further development of these parameters in the future should facilitate the analysis of the dynamics of fibroplasia. The strongest stimuli for hepatic fibroplasia are hepatocellular necrosis and inflammation, but ethyl alcohol and steatosis are also stimulating, though to a lesser degree. This explains the particular elevation of the fibroplastic parameters in alcoholic hepatitis. It points, however, also to the possibility that cirrhosis might develop without significant hepatocellular necrosis and inflammation. Perihepatocellular, periductular, and septal fibrosis are the functionally most important localizations leading to additional hepatic injury. The initiation of these types of fibrosis by liver injury points to a vicious circle. Specific anti-fibroplastic therapy is still in infancy.

Chronic Disease↗
PubMed1978

Development of hepatic angiosarcoma in man induced by vinyl chloride, thorotrast, and arsenic. Comparison with cases of unknown etiology.

Examples of human angiosarcoma following exposure to vinyl chloride, Thorotrast, or arsenic (medicinal and industrial) and cases, including children, of unknown etiology were studied to establish diagnostic criteria and to study their evolution. The uniform evolution suggests an environmental factor also in the cases of unknown etiology, which may be established by epidemiologic studies. A precursor stage is charaterized by areas of combined hyperlasia of hepatocytes and a variety of sinusoidal and perisinusoidal cells associated with excess of reticulin and with sinusoidal dialation. The diagnostically useful picture in silver impregnations indicated reticulum formation by the perisinusoidal cells, presumably the libocytes. The hepatocytic proliferation suggests a hepatocarcinogenic but usually not fully expressed potential. The mixed hyperplasia of the various sinusoidal cells proceeds to an overgrowth of angiosarcoma cells, presumably derived from endothelial cells. In early stages they are usually in contact with hepatocytes (intralobular growth). A trabecular arrangement results from loosening of the lobular plate arrangement by dilatation of sinusoids, leading to primary peliosis. With disappearance of the hepatocytes, various growth patterns develop, terminating in nodular, solid angiosarcoma composed of either spindle-shaped or polyhedral cells which undergo necrosis or hemorrhage (secondary peliosis). The interaction between hepatocytes and sinusoidal cells requires elucidation.

Adolescent↗