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Biomedical subjects

M Omata

Publications and source records attributed to M Omata.

At least 523 records · Page 29Linked to original sources

Clinical study of eighty-six cases of idiopathic portal hypertension and comparison with cirrhosis with splenomegaly.

The clinical features of 86 cases of idiopathic portal hypertension, the equivalent of hepatoportal sclerosis in the United States and of noncirrhotic portal fibrosis in India, are presented. This disease is characterized by overt splenomegaly with pancytopenia, portal hypertension, and relatively mild abnormalities in liver function tests. Although differential diagnosis from liver cirrhosis is not always easy, liver histology, laparoscopy, portography, hepatic venography, and measurement of wedged hepatic vein pressure are useful in diagnosis. Prognosis is relatively benign if variceal bleeding is controlled or prevented, and the disease does not progress to cirrhosis. The etiology is still undetermined, but the liver pathology characterized by occlusive changes of the intrahepatic portal radicles, portal and periportal fibrosis, and irregularly distributed parenchymal atrophies suggests some sort of portal venopathy that causes decreased portal perfusion of peripheral liver parenchyma. These patients with idiopathic portal hypertension were compared with 63 cases of cirrhosis with splenomegaly and 80 cases of cirrhosis without splenomegaly. There was some similarity in hematologic findings between idiopathic portal hypertension and cirrhosis with splenomegaly, but the basic disease process seemed distinctly different. The cause of marked splenomegaly does not seem to be simply congestion, and remains an enigma.

Adolescent↗

Duck hepatitis B virus and liver diseases.

The presence of duck hepatitis B virus in serum was studied in 61 ducks (24 from Chi-tung county, China, 20 from Changchun, China, and 17 from Chiba, Japan) with relation to liver disease. None of the 37 ducks from Chiba and Changchun was positive for duck hepatitis B virus as assayed by electron microscopy, endogenous deoxyribonucleic acid-polymerase activity, and hybridization with duck hepatitis B virus deoxyribonucleic acid. No liver disease was seen in these ducks. In contrast, viruslike particles were present in the serum of 12 of 24 (50%) ducks from Chi-tung, China. The presence of duck hepatitis B virus in serum was indicated by the hybridization spot test and deoxyribonucleic acid-polymerase activities. A variety of liver diseases including chronic hepatitis and cirrhosis were seen in the livers of a majority of the ducks from Chi-tung. One duck hepatitis B virus-positive duck had multicentric hepatocellular carcinoma with underlying cirrhosis. Comparison of serum duck hepatitis B virus markers and liver disease in the affected flock revealed a tendency for seronegative ducks to have advanced liver diseases. Duck hepatitis B virus infection may be used as an experimental model to test various hypotheses concerning the pathogenesis of hepatitis B virus-associated liver disease in humans.

Animals↗

Hepatitis B virus antigens in liver tissue in hepatocellular carcinoma and advanced chronic liver disease-relationship to liver cell dysplasia.

Hepatitis B surface (HBs) and core (HBc) antigens (Ag) were studied in liver tissue in HBsAg seropositive patients with chronic liver disease complicated (n = 32) and not complicated (n = 36) by hepatocellular carcinoma. Both groups were matched by age, sex and underlying disease. There was no qualitative and quantitative difference in tissue HBsAg between the two groups. However, HBcAg was significantly less in quantity in hepatocytes of patients with hepatocellular carcinoma compared to chronic liver disease without cancer. Serum hepatitis B e antigen tested by radioimmunoassay was also less frequently positive in patients with hepatocellular carcinoma. These findings seem to suggest that hepatitis B virus replication becomes less active in the process of hepatocarcinogenesis. The relationship between intrahepatic hepatitis B antigens and liver cell dysplasia was also studied. In hepatocellular carcinoma, tissue hepatitis B antigens often coexisted in the same liver having liver cell dysplasia, but no such association was observed in chronic liver disease without cancer. However, no indication was obtained that the dysplastic cells harbor HBsAg more frequently than non-dysplastic cells.

Carcinoma, Hepatocellular↗

Liver pathology of idiopathic portal hypertension. Comparison with non-cirrhotic portal fibrosis of India. The Japan idiopathic portal hypertension study.

Morphological changes of the liver were studied in 24 autopsy cases of noncirrhotic portal hypertension of unknown etiology (idiopathic portal hypertension, IPH), and in 123 surgical biopsies from such patients. For comparison, 15 whole-cut liver slices from autopsy cases of noncirrhotic portal fibrosis (NCPF) from India were also studied. Liver pathology was very similar in IPH and NCPF, characterized by phlebosclerotic changes and perivascular fibrosis of the portal vein system, and parenchymal atrophy perhaps secondary to portal circulatory insufficiency. The distribution of lesions was uneven, and despite marked fibrosis and occasional surface nodularity, there was no diffuse pseudonodule formation in the parenchyma. Surgical specimens showed similar changes except for more frequent portal cellular infiltrates, but the changes seen in one biopsy specimen were limited and not always diagnostic. It seems that IPH of Japan and NCPF of India are the same disease, and perhaps hepatoportal sclerosis elsewhere is also the same disease.

Adult↗

Spontaneous reversal of portal blood flow demonstrated by percutaneous transhepatic catheterization: report of two cases.

Two patients are described in whom percutaneous transhepatic catheterization of the portal vein for a hemodynamic study demonstrated a continuous reversed blood flow in the portal vein, entering into a large collateral. The measurements made of blood pressure in the superior mesenteric, splenic, and left gastric veins, and of ammonia, immunoreactive insulin, and C-peptide in blood taken from these and peripheral veins all indicated reversed portal vein blood flow. The evidence for retrograde portal vein blood flow was obtained in only 2 of 203 patients with cirrhosis in whom portal hemodynamics were studied by the same procedure. Thus, spontaneous reversal of portal vein blood flow does occur, but very rarely.

Blood Pressure↗

Sclerosing hepatic carcinoma: relationship to hypercalcemia.

A series of 30 patients is reported whose primary hepatic tumors had a distinctive histologic pattern that we have called "sclerosing hepatic carcinoma" (SHC). Sixty-nine percent of those tested had hypercalcemia and low levels of serum phosphate. As comparison, 38 control patients who had either classical peripheral cholangiocarcinoma or typical hepatocellular carcinoma were studied. In the control group, only two patients, who also had bone metastases, had hypercalcemia. Sclerosing hepatic carcinoma is characterized by intense fibrosis in which the tubular neoplastic structures are embedded. Although the tumor in each patient superficially resembled peripheral cholangiocarcinoma, on close inspection 63% were found to be of apparent hepatocyte origin, 20% were apparently ductal, and 13% were mixed or not distinguishable. One patient's tumor had the pattern of the rare cholangiolocellular carcinoma. The difficulty of histological diagnosis was well illustrated by the fact that none of premortem biopsies in 16 patients was correctly interpreted unequivocally as primary carcinoma of the liver. Many were misinterpreted as metastatic adenocarcinomas, most frequently of pancreatic origin. We believe that, by describing clinicopathological features, more attention will be drawn to this unique carcinoma of liver origin.

Aged↗

Peliosis hepatis as a late and fatal complication of thorotrast liver disease. Report of five cases.

Five autopsy cases of peliosis hepatis occurring as a late complication of thorotrast (ThO2) liver disease are described. The liver contained many blood-filled cystic spaces of various sizes. Marked sinusoidal dilatation, disruption of cell cords and reticulin fiber framework, and cystic dilatation of sinusoids seem to represent the developmental stages of peliosis hepatis in sequence. Of the five cases, two had no other liver disease except for hepatic fibrosis, and the other three had associated neoplasms, such as angiosarcoma, hepatocellular carcinoma, cholangiocarcinoma, benign hemangioma, and their combinations. Peliosis hepatis seemed to have directly contributed to the patient's death in four cases. The most characteristic clinical feature was the fulminant terminal course with massive ascites, deep jaundice, and hepatic failure, often accompanied by hepatorenal syndrome and tendency to hemorrhage. Liver function study suggested progressive hepatic insufficiency with reduction in serum albumin, prothrombin and the clearance rate for test dyes, and increase in bilirubin. Clinical diagnosis was almost impossible without biopsy.

Aged↗

Clinico-pathological study of acute non-A, non-B post-transfusion hepatitis: histological features of liver biopsies in acute phase.

A follow-up study of acute non-A, non-B post-transfusion hepatitis with a mean follow-up period of 30 months was carried out in 24 patients in whom liver biopsy was done within 3 months of onset. Of the 24, 13 patients (54%) developed chronic biochemical liver disease with elevated serum aminotransferases for more than 6 months, and in 11 the elevated liver enzymes were normalized within 6 months. Although there were no statistically significant differences in the mean peak values of liver enzymes, length of incubation period and number of transfusions between the chronic and resolved groups, the former tended to have a slow rise and multiple peaks of serum liver enzymes. Analysis of the liver biopsies made in the acute phase revealed that limiting plate erosion, hepatocellular degeneration, and poor regenerative activities were indicative of subsequent transition to chronicity. Multiple biopsies were taken in five patients who were followed for an average of 29 months, and the subsequent histological diagnosis was chronic persistent hepatitis in two, chronic active hepatitis in two and cirrhosis in one.

Acute Disease↗

Anatomical basis of hepatic venographic alterations in idiopathic portal hypertension.

Hepatic venograms made in 40 authentic cases of idiopathic portal hypertension (Banti's syndrome) were compared with 13 normal venograms and venograms obtained in 88 cases of cirrhosis, and analyzed in the light of the pathological changes seen in 16 postmortem liver specimens. There were frequent anastomoses between hepatic vein radicles, approximation of middle-size branches to the liver surface, reduction in the angles between the main hepatic vein and its tributaries, and difficulty in opacifying portal vein branches in wedged retrograde portography. These angiographic alterations were corroborated by gross pathological findings which comprised displacement of middle-size hepatic vein branches closer to the liver surface and their approximation among themselves, and seem to be accounted for by the disappearance of liver parenchyma secondary to the peripheral portal circulatory failure.

Hepatic Veins↗

Fibrolamellar carcinoma of the liver: a tumor of adolescents and young adults with distinctive clinico-pathologic features.

Clinical and pathologic features of 23 patients with a distinctive histologic and clinical variant of hepatocellular carcinoma are summarized. The variant pattern of hepatocellular carcinoma is most common in the age group 5--35 years and occurs equally in either sex. The distinctive histologic features include 1) deeply eosinophilic neoplastic hepatocytes, many of which contain intracytoplasmic hyaline globules and distinct pale bodies and 2) fibrosis arranged in a lamellar fashion around the neoplastic hepatocytes. The histologic and gross features of the tumor have been confused both with focal nodular hyperplasia and with hepatocellular adenoma. The average survival of 32 months and the high operability rate of 48% far exceed the survival or operability for ordinary hepatocellular carcinoma. Thus, this tumor type must be recognized and considered separately when evaluating therapeutic results in large series of patients with hepatocellular carcinoma.

Adolescent↗

Nonimmunologic binding of horseradish peroxidase to hepatitis B surface antigen. A possible source of error in immunohistochemistry.

In the process of establishing the specificity of direct immunoperoxidase staining of liver tissue for hepatitis B surface antigen (HBsAg), an affinity of free horseradish peroxidase (HRP) for HBsAg in hepatocytes (ground-glass cells) was found. Of 95 patients, the horseradish peroxidase reaction was only positive in the livers of the 35 who were chronically HBsAg seropositive and not in the livers from 60 control patients with alcoholic cirrhosis who were HBsAg seronegative. Comparison studies using the orcein technic and immunoperoxidase methods confirmed the observation that both free horseradish peroxidase (not conjugated to an antibody) and HRP conjugated to an antibody unrelated to HBsAg had an affinity to the cytoplasm of hepatocytes containing HBsAg. The precise nature of this affinity is not known, but it is probably due to a reaction between an activated carbohydrate moiety of horseradish peroxidase and the free amino group of HBsAG.

Hepatitis B Surface Antigens↗

Double-blind controlled trial of prednisolone therapy in patients with severe acute alcoholic hepatitis and spontaneous encephalopathy.

Twenty-eight patients entered a double-blind controlled trial to evaluate the efficacy of prednisolone treatment in severe acute alcoholic hepatitis accompanied by encephalopathy. Fifty-three percent (8 of 15) given prednisolone and 54% (7 of 13) given placebo died during the study. The mean duration of hospitalization was 66 days for the prednisolone-treated group and 56 days for those treated with placebo. Prednisolone treatment produced no important beneficial effect on any of the hepatic biochemical tests. The outcome in any particular case was directly related to the development of specific lethal complications (renal failure, injection, and gastrointestinal bleeding) rather than to the treatment employed. We were unable to show any beneficial effect of prednisolone treatment on morbidity or mortality in patients with severe acute alcoholic hepatitis and encephalopathy.

Adult↗

Hepatocellular carcinoma in the U.S.A., etiologic considerations. Localization of hepatitis B antigens.

The serologic and tissue markers of hepatitis B virus (HBV) were studied in 50 patients in whom hepatocellular carcinoma (HCC) was confirmed at autopsy. Serologic and tissue markers included serum hepatitis B surface antigen (HBsAg), tissue HBsAg, tissue hepatitis core antigen (HBcAg), and serum antibody to HBcAg (anti-HBc). Twenty-two patients had HCC arising in alcoholic cirrhosis; 2 of the 22 (9.1%) had one or more of the HBV tissue and serologic markers. This infection rate is similar to the rate of 7.9% observed in 63 control alcoholic cirrhotic patients without HCC. In contrast, 15 of 20 (75.0%) patients with HCC in nonalcoholic chronic active liver disease showed evidence of active HBV infection. One of 8 patients with HCC in normal liver had serum HBV markers. This result indicates that there is an extremely high prevalence of HBV infection among HCC patients with nonalcoholic chronic liver disease in the U.S.A. The prevalence of HBV infection in these patients is as high as that observed in Asia and Africa. Thus, it can be concluded that the lower prevalence rate of active HBV infection in HCC patients in the U.S.A. is the result of statistical dilution of HCC-B-viral disease by the large numbers of the alcoholic cirrhotic patients with HCC, and that if chronic active hepatitis type B were as common in the United States as it is in Africa and Asia, the frequency of occurrence of HCC might also be as high.

Adult↗