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Biomedical subjects

M Ashcavai

Publications and source records attributed to M Ashcavai.

At least 19 recordsLinked to original sources
PubMed1989

Alpha-fetoprotein and its concanavalin A affinity in acute exacerbation of chronic hepatitis B.

Serum samples from 20 patients with acute exacerbation of chronic hepatitis due to hepatitis B virus and 20 patients with hepatocellular carcinoma arising from B viral cirrhosis with elevated levels of alpha-fetoprotein (AFP) were analyzed by affinity column chromatography for concanavalin A binding. Serum AFP was tested at regular intervals in all of these patients. Acute exacerbation was defined as elevation of serum transaminase greater than 300 IU/L in patients with chronic hepatitis B. In hepatocellular carcinoma, serum AFP levels fluctuated but remained higher than 92 ng/ml, whereas, in acute exacerbation of chronic hepatitis B, serum AFP levels returned to normal within 3-12 months of follow-up. The results of concanavalin A-binding assay revealed that AFP from both these groups had a high affinity for concanavalin A, and this assay could not be used to discriminate between the two conditions.

Adult↗
PubMed1987

Concanavalin A affinity of alpha-fetoprotein. Its use in differentiating tumors.

Using affinity chromatography on concanavalin A Sepharose, the authors studied the molecular heterogeneity of the serum alpha-fetoprotein of 53 patients with hepatocellular carcinoma, 16 patients with metastatic tumors to the liver, and 16 patients with germ cell tumors. Mean concanavalin binding of alpha-fetoprotein in the sera of patients with hepatocellular carcinoma was 79%, whereas the mean binding in metastatic tumors was 52% and that of germ cell tumors was 45%. This striking molecular variation of the alpha-fetoprotein produced by these different tumors is helpful in the clinical distinction of these tumors.

Carcinoma, Hepatocellular↗
PubMed1986

HBsAg clearance in chronic active hepatitis B. A possible cause of cryptogenic cirrhosis.

Three patients with chronic hepatitis B infection, two with chronic active hepatitis and cirrhosis, and the third with quiescent cirrhosis, cleared HBsAg from their serum and eventually developed anti-HBs. All three were asymptomatic and had nearly normal serum aminotransferases following loss of HBsAg. Liver biopsy revealed cirrhosis in each patient. With the development of anti-HBs, these patients became serologically indistinguishable from patients with a cryptogenic cirrhosis who had prior unrelated exposure to hepatitis B. Remote chronic hepatitis B infection may be a more common cause of cryptogenic cirrhosis than is commonly appreciated.

Adult↗
PubMed1984

Evaluation of enzyme immunoassay for anti-HBc IgM in the diagnosis of acute hepatitis B virus infection.

Corzyme-MTM (Abbott Laboratories, North Chicago, IL), a newly introduced kit for the measurement of serum IgM antihepatitis B core antigen by enzyme immunoassay, was evaluated for the diagnosis of acute B-viral hepatitis (AVH-B). The study included 175 acute viral hepatitis patients with transient hepatitis B surface antigen (HBsAg). Sera from 160 were tested on multiple occasions until their HBsAg cleared. IgM anti-HBc was found in 171 of 175 patients (98.4%) during the acute phase. The serum samples from 42 patients with liver biopsy-proven chronic active hepatitis, type B (CAH-B), and 18 patients with persistent hepatitis, type B (PH-B), were analyzed for the presence of IgM anti-HBc, using the same technic. None of the sera from 42 patients with CAH-B and only 2 of the 18 patients with PHB had IgM anti-HBc. Thus, the measuring IgM anti-HBc using Corzyme-M kit is helpful in the diagnosis of AVH-B and in the discrimination of acute from chronic HBV infections.

Acute Disease↗
PubMed1980

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↗
PubMed1979

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↗
PubMed1977

Liver replacement for alpha1-antitrypsin deficiency.

A 16-year-old girl with advanced cirrhosis and severe alpha 1-antitrypsin deficiency of the homozygous Pi ZZ phenotype was treated by orthotopic liver transplantation. After replacement of the liver with a homograft from a donor with the normal Pi MM phenotype, the alpha 1-antitrypsin concentration in the recipient's serum rose to normal; it had the Pi MM phenotype. Two and a third years later, chronic rejection necessitated retransplantation. Insertion of a homograft from a heterozygous Pi MZ donor was followed by the identification of that phenotype in the recipient's serum. Neither liver graft developed the alpha 1-antitrypsin glycoprotein deposits seen with the deficiency state. These observations confirm that this hepatic-based inborn error of metabolism is metabolically cured by liver replacement.

Adolescent↗
PubMedDate not supplied

Delayed HBsAg clearance in chronic hepatitis B viral infection.

Seven patients are described in whom HBsAg persisted for 13 to 98 months after acute viral hepatitis B and then became nondetectable. All patients subsequently developed anti-HBs. During the period of HBs-antigenemia, liver biopsies in five patients showed persistent viral hepatitis. Retrospectively, impending negativity of HBsAg was predictable in five patients by a decrease in HBsAg titer, and in four patients by persistent normalization of serum alanine aminotransferase. Although delayed clearance of HBsAg in patients with chronic hepatitis B virus infection is uncommon, it appears to be predictable.

Acute Disease↗
PubMedDate not supplied

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↗