Extra- and intrahepatic portal hypertension without cirrhosis (hepatoportal sclerosis).
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Adolescent↗
Biomedical subjects
R L Peters
Publications and source records attributed to R L Peters.
alpha-1-Antitrypsin phenotypes in hepatocellular carcinoma.
alpha-1-Antitrypsin deficiency due to homozygous Pi ZZ state is reported to be associated with cirrhosis and hepatocellular carcinoma (HCC); however, the role of heterozygous Pi Z state is not definitely known. In order to investigate the possible association, we studied the phenotypic distribution of alpha-1-antitrypsin variants (Pi) in 124 cases of HCC. Two thousand ten normal American Red Cross blood donors were studied as controls. Twelve patients with HCC had aberrant phenotypes, an incidence of 9.67% as compared to 8.36% among normal controls. Nine of 12 patients with HCC with aberrant Pi type had cirrhosis; 5 of the 9 had cirrhosis due to hepatitis B virus; 2 of the 9 had alcoholic liver disease with cirrhosis, and 2 had cryptogenic cirrhosis. The three patients with HCC arising in noncirrhotic livers who also had aberrant Pi phenotypes, had a relatively rare variety of HCC called fibrolamellar type. Z gene was found in five patients: all five were MZ. Incidence of MZ phenotype in HCC was similar to that of the normal control population (4.0% in HCC and 2.9% in the controls). However, 3 of 5 MZ were associated with fibrolamellar HCC. Another aberrant phenotype found among the patients with HCC was MF (fast moving) which occurred with an incidence of 2.41% as compared to none in the control group. In conclusion, we found no significant increase in the incidence of Z gene among 124 patients with HCC as compared to the normal population.
Adult↗
Globular hepatic amyloid--an unusual morphologic presentation.
Hepatic amyloid, when identified, is usually located in the sinusoids, portal tracts, and arterioles. We report 14 cases of hepatic amyloidosis where eosinophilic globules having the histochemical and electron microscopic features of classic amyloid were found. The globules were round to oval, 5 to 40 micrometer in diameter, and were found within the space of Disse as well as aggregated within the portal tracts. There were no distinctive clinical or laboratory features distinguishing this type of amyloidosis from classic hepatic amyloidosis. However, there were no cases of multiple myeloma and only one of benign monoclonal gammopathy. All seven patients who were studied at postmortem examination had systemic (nonglobular) amyloidosis. This form of hepatic amyloidosis is probably not an early form of the disease but is an original but rare presentation of hepatic amyloid deposition.
Aged↗
High-density lipoprotein cholesterol and liver disease.
To establish whether there is any significant relationship between high-density lipoprotein cholesterol (HDLC) concentrations and biopsy-documented liver disease, 169 patients had needle biopsies, serum cholesterol, and HDLC evaluated. Twenty-four patients had serial cholesterol, HDLC, prothrombin, and aminotransferase levels and activities examined. In both men and women, HDLC decreased strikingly and significantly in acute alcoholic hepatitis and in acute viral hepatitis, compared to controls (p less than 0.001). Men and women with inactive alcoholic liver disease and chronic active hepatitis showed moderate decreased in HDLC (p less than 0.001). Patients with primary and metastatic hepatic neoplasms also had strikingly decreased HDLC (p less than 0.001). Serial testing showed an excellent direct correlation between HDLC and prothrombin activity, r values ranging from 0.71 to 0.98. Although alcohol intake is known to correlate positively with HDLC concentrations, our data shows that this association is not absolute, and in most cases is reversed once liver disease becomes apparent.
Biopsy↗
Glomerular tubular reflux--a morphologic renal lesion associated with the hepatorenal syndrome.
The hepatorenal syndrome, a primary cause of death from acute and chronic liver disease, consists of a functional renal failure whereby examination of the kidney has previously shown no distinct or specific morphologic change. We describe an unusual renal lesion consisting of the reflux of proximal convoluted tubular epithelium into Bowman's space. An autopsy series shows this glomerular change to be present in 71.4% of cases with the hepatorenal syndrome, while only present in 0 to 27.3% in other autopsy categories (p less than 0.001). Since this lesion has been previously described with experimental renal ischemic change and terminal hypotension, it is possible that it is caused in part by the decreased or altered renal blood flow known to be associated with the hepatorenal syndrome.
Adult↗
Long-term sequelae of non-A, non-B hepatitis in experimentally infected chimpanzees.
We have observed the development of long-term sequelae in four cases of experimentally induced non-A, non-B (NANB) hepatitis in chimpanzees. These sequelae were characterized by the following manifestations: nonprotection against challenge with autologous infectious plasma following acute disease and subtle histopathological alterations typical of long-lasting viral hepatitis. These manifestations were observed in animals infected with either of two human inocula. Whether or not these inocula represent sources of single or multiple etiologic agents is not known. However, our studies suggest that these inocula share at least one common etiologic agent. Further, these results may represent an atypical chronology of convalescence from viral hepatitis infection. For example, the convalescent stage of a type B hepatitis infection may be expected to occur within 6 to 8 months following exposure, whereas true convalescence in NANB hepatitis may be protracted over several months to several years. Thus, future efforts to identify the causative agent(s) of NANB hepatitis, and efforts to define the immune response in NANB, must take into consideration these studies.
Alanine Transaminase↗
Viral hepatitis: a pathologic spectrum.
Acute viral hepatitis has several identifiable morphologic components but the major categories are (1) cytopathic, (2) inflammatory, and (3) regenerative. Each category has independently variable characteristics. Extreme alterations related to severity of disease, alteration of immune response, or pre-existing liver disease may result in diagnostic difficulties for the pathologist. In contrast to the usual concept, patients who survive fulminant viral hepatitis rarely, if ever, develop cirrhosis and those who have severe hepatic necrosis from hepatitis also do not usually develop serious sequelae of that disease except in the older age group where the difficulty is in impaired regeneration (IR). The usual criteria for the diagnosis of chronic active hepatitis or chronic aggressive hepatitis need a thorough review since many of the variations of acute viral hepatitis result in histologic patterns that might be considered to be chronic aggressive hepatitis using the previous definitions; yet such patients recover without developing chronic liver disease. Chronic active hepatitis, a progressive hepatic disorder, is characterized by changes in the distribution of necrosis and regeneration within the lobule from that usually observed in acute viral hepatitis. Persistent viral hepatitis, a development in 10 to 12 per cent of adult patients after icteric acute disease, is characterized by a "cobblestone" hepatocellular change that resembles continued regeneration, focal hepatocytolysis, and often portal lymphoid hyperplasia. Apparently with time, these histologic features fade and the incidence, in type B PVH, of "ground glass" HBs Ag laden cells increases. This may reflect a continued adaptation of host and virus to one another.
Acute Disease↗
Nodular regenerative hyperplasia of the liver with and without portal hypertension: a comparison.
The clinical and the pathologic features of seven patients with nodular regenerative hyperplasia of the liver are analyzed and compared with those of 37 patients reported in the literature in an attempt to distinguish the features of those with portal hypertension from those without. Severe degrees of obliterative portal venopathy usually associated with the portal hypertension were found among the various pathological features. The association of nodular regenerative hyperplasia with a variety of chronic diseases suggests a heterogeneous group of pathogenic mechanisms. Our study reveals that only some of these mechanisms lead to the hepatic changes that cause portal hypertension.
Adult↗