PubMed Health⌕ Search

Biomedical subjects

L R Mathiesen

Publications and source records attributed to L R Mathiesen.

66 records · Page 4Linked to original sources
PubMed1979

Detection of immunoglobulin M antibodies to hepatitis A virus by enzyme-linked immunosorbent assay.

An enzyme-linked immunosorbent assay for the detection of immunoglobulin M (IgM) antibodies to hepatitis A virus is described. The test uses the principle of binding of IgM antibodies to anti-IgM-coated microtiter plates to determine whether the IgM antibodies attached have specificities for hepatitis A virus. In three patients with hepatitis type A followed up to 12 months, IgM antibodies to hepatitis A virus could be demonstrated from the onset of illness and during the following 2 to 3 months. When acute-phase sera from 48 patients with acute hepatitis were tested, IgM antibodies to hepatitis A virus could only be demonstrated in 18 patients previously classified as type A, whereas 30 patients with type B and non-A non-B hepatitis were negative. IgM antibodies to hepatitis A virus could not be demonstrated in 108 normal sera nor in 55 sera containing rheumatoid factor. These results indicate that the enzyme-linked immunosorbent assay for IgM antibodies to hepatitis A virus is useful in the serodiagnosis of acute hepatitis type A on a single serum sample taken during the acute phase of illness.

Acute Disease↗
PubMed1979

Epidemiology and clinical characteristics of acute hepatitis types A, B, and non-A non-B.

A consecutive series of 115 patients hospitalized with acute viral hepatitis in Copenhagen was studied for serological markers for hepatitis A and B virus. Thirty-nine patients had type B, 66 had type A, 3 had both type A and B, and 7 had type non-A non-B. Of the patients 81% were between 15 and 40 years of age, and there was a dominance of males due to an overrepresentation of homosexual males (30%) in both the A and B group. The main type of exposure to hepatitis type A was travel to foreign countries (53%), and for type B it was drug addiction (41%). In types A and B the duration of jaundice was positively correlated to the age of the patients but did not vary with sex or type of exposure. There was no difference in maximum alanine aminotransferase levels between the groups, but maximum bilirubin levels were lower for the type A group. Patients with hepatitis type A had a higher level of IgM than those with type B and with type non-A and non-B. We conclude that both clinically acute hepatitis type A and type B occur mainly in young adults and that foreign travel, drug addiction, and homosexuality increase the risk of getting acute hepatitis.

Acute Disease↗
PubMed1979

Fulminant hepatitis A.

During a small epidemic of infectious hepatitis, a fulminant infection with fatal outcome occurred in a 54-year-old woman. IgM antibody to hepatitis A virus was demonstrated in the serum and large amounts of hepatitis A virus were found in the liver. It is suggested that the pathogenesis may be different for fulminant hepatitis A and B infection.

Female↗
PubMed1979

Immunofluorescence studies for hepatitis A virus and hepatitis B surface and core antigen in liver biopsies from patients with acute viral hepatitis.

Immunofluorescence studies for hepatitis A virus and hepatitis B surface and core antigen were performed on liver biopsies from 48 patients with acute viral hepatitis. Hepatitis A virus was detected in 11 out of 17 patients with type A hepatitis and was not found in patients with type B or non-A non-B hepatitis. Hepatitis B surface and core antigens were detected in 2, hepatitis B core antigen alone in 1, and hepatitis B surface antigen alone in 4 out of 24 patients with type B hepatitis. Neither hepatitis B surface nor core antigen were found in patients with type A or non-A non-B hepatitis. One patient with both type A and B hepatitis were all negative for hepatitis A virus, and hepatitis B surface and core antigens. Immunofluorescence examination for hepatitis A virus in human liver biopsies appears to be a sensitive and specific technique and might be valuable in the search for possible chronic carriers of hepatitis A virus.

Adult↗
PubMed1978

Localization of hepatitis A antigen in marmoset organs during acute infection with hepatitis A virus.

Twelve marmosets (Saguinus mystax) were inoculated intravenously (iv) with hepatitis A virus (HAV). One died early (day 12); seven were sacrificed at the time of elevation in level of alanine aminotransferase (serum glutamic-pyruvic transaminase), and four without elevation were not sacrificed but seroconverted. In the seven marmosets sacrificed during the acute stage of illness, hepatitis A antigen (HA Ag) was detected in the liver by immunofluorescence in all cases, by immune electron microscopy in four, and by enzyme-linked immunosorbent assay (ELISA) in three. The HA Ag appeared by immunofluorescence as very fine granules in the cytoplasm of hepatocytes and Kupffer cells. The HA Ag could not be detected by immunofluorescence in biopsy specimens taken from the duodenum, jejunum, ileum, or transverse colon in any of eight marmosets in which necropsy was performed during the acute or preacute stage of illness. These findings suggest that the gut is not involved during the acute phase of HAV infection following iv inoculation into marmosets. The ELISA results showed that only three of 12 marmoset livers obtained during the acute phase of HAV infection could be used as an antigen source in serologic testing for antibody to HA Ag. Thus, marmoset livers were no better as a source of HA Ag than acute-phase stools from patients with type A hepatitis.

Acute Disease↗
PubMed1978

Enzyme-linked immunosorbent assay for detection of hepatitis A antigen in stool and antibody to hepatitis A antigen in sera: comparison with solid-phase radioimmunoassay, immune electron microscopy, and immune adherence hemagglutination assay.

Previously described techniques for detection of hepatitis A antigen (HA Ag) and antibody (anti-HA) have required purified HA Ag and expensive equipment. Herein is described an enzyme-linked immunosorbent assay (ELISA) for specific detection of HA Ag in human stool filtrates and of anti-HA in sera by using selected HA Ag-containing human stool filtrates as the antigen source. Because human stools often react nonspecifically in serological tests for HA Ag, blocking with preexposure and hyperimmune anti-HA sera from a chimpanzee inoculated with hepatitis A virus was used to confirm specific detection of HA Ag. The sensitivity of ELISA was found to be comparable to that of solid-phase radioimmunoassay (SPRIA) and immune electron microscopy (IEM). Of 37 acute-phase stools collected from nine patients, 16 were positive for HA Ag by ELISA. In 13 of these, HA Ag particles were found by IEM, and an additional 3 stools negative by ELISA contained HA Ag particles by IEM. Eight control stools were negative by both ELISA and IEM. Anti-HA was measured in sera by demonstrating its ability to block binding of the enzyme conjugate to HA Ag in a stool without detectable nonspecificity. This test (blocking ELISA) was as sensitive and specific as blocking SPIRA, IEM, and immune adherence hemagglutination and, like SPRIA and IEM, detected early-developing antibody. The ELISA is simple to perform and requires only a minimum of equipment. It is useful for screening stools for HA Ag and for monitoring HA Ag during purification, as well as for detecting early and late anti-HA in sera.

Acute Disease↗
PubMed1978

Localization of hepatitis A antigen in liver tissue by peroxidase-conjugated antibody method: light and electron microscopic studies.

Hepatitis A antigen (HAAG) was localized in liver tissue from marmosets inoculated with human hepatitis A virus (HAV) by light and electron microscopy by using a peroxidase-conjugated antibody method. The fine granular peroxidase staining was scattered throughout the cytoplasm of liver cells when viewed with the light microscope. The distribution of HAAg-positive cells was focal. Virus-like particles, 24 to 27 nm in diameter, were observed in the cytoplasm of hepatocytes and smaller cells, resembling Kupffer cells, by standard thin-section electron microscopy (thin section EM). By immunoperoxidase electron microscopy (immunoperoxidase EM), HAAg was detected on the particles, which were aggregated within cytoplasmic vesicles of the hepatocyte. The surrounding membrane of the vesicles was also HAAg- positive. Similar HAAg particles were observed in the cytoplasm of smaller cells adjacent to hepatocytes as well. Thus, immunoperoxidase EM revealed that the 24- to 27-nm virus-like particles in the cytoplasm of liver cells obtained from marmosets were infected with HAV contained HAAg.

Animals↗
PubMed1977

Detection of hepatitis A antigen by immunofluorescence.

Hepatitis A antigen (HA Ag) was demonstrated by immunofluorescence (IF) in liver biopsies from chimpanzees with experimental hepatitis A virus infection. Blocking experiments with paired sera from patients with hepatitis types A, B, or non-A, non-B, as well as with purified HA Ag, showed that the fluorescence was specific for HA Ag. HA Ag could be demonstrated only in biopsies from chimpanzees inoculated with hepatitis A virus. In two of four chimpanzees biopsied weekly, HA Ag could be detected by IF before stool shedding of HA Ag, elevation in serum alanine aminotransferase (SGPT), or histopathological evidence of liver disease was seen. The HA Ag was detected for 4 to 5 weeks; the last IF-positive biopsy was obtained after SGPT activity had returned to normal. In the two other chimpanzees, HA Ag could be detected only in the biopsy taken at the time of SGPT elevation. In the early IF-positive biopsies, HA Ag was diffusely distributed in the cytoplasm of many cells, but it later accumulated in a focal distribution in the cytoplasm of a few of the hepatocytes and Kupffer cells. This cytoplasmic distribution agrees with previous electron microscopic data.

Alanine Transaminase↗
PubMedDate not supplied

Presence and meaning of anti-HBc IgM as determined by ELISA in patients with acute type B hepatitis and healthy HBsAg carriers.

To evaluate the clinical implication of IgM antibody against hepatitis B core antigen (anti-HBc IgM), a consecutive series of 87 patients with acute type B hepatitis and 16 healthy carriers of hepatitis B surface antigen (HBsAg) were studied by a newly developed reverse ELISA technique. Anti-HBc IgM was present for at least 2 months in 81 of the 82 patients with HBsAg at the time of admission. Seroconversion from HBsAg to anti-HBs was observed in 38 patients during the time of observation, and in all patients, anti-HBc IgM was present until clearance of HBsAg. Thirty-three of the 38 patients remained anti-HBc IgM positive, at least until the appearance of anti-HBs. Quantitation of anti-HBc IgM by ratio unit (RU) values revealed that 3 of 8 patients with RU values greater than or equal to 5 for more than 6 months subsequently developed chronic liver disease, as compared to 1 of 72 patients with anti-HBc IgM above this level for less than 6 months. Anti-HBc IgM was demonstrated in 3% of 5 patients with total anti-HBc titer above 1:100 despite the presence of anti-HBs. In these patients, anti-HBc IgM steadily decreased after the onset of illness indicating a recent acute hepatitis B infection. Anti-HBc IgM was present in 12 of 16 healthy HBsAg carriers (75%). However, these 12 carriers had RU values between 2.5 to 5.5, compared with RU values above 5 (mean RU value 11.3) at the onset of illness in 80 of 82 HBsAg-positive patients with acute hepatitis. Anti-HBc IgM seems to be a specific serological marker for recent or ongoing hepatitis B infection which may be useful in differentiation between hepatitis B infection with or without HbsAg and acute non-A, non-B hepatitis.

Acute Disease↗
PubMedDate not supplied

Acute type B hepatitis among HBsAg negative patients detected by anti-HBc IgM.

A consecutive group of 169 patients with acute hepatitis found negative for hepatitis B surface antigen (HBsAg) and negative for IgM antibody against hepatitis A (anti-HAV IgM) was studied for presence of IgM antibody against hepatitis B core antigen (anti-HBc IgM) by ELISA. Anti-HBc IgM was found in a total of 34 of 60 patients with detectable total anti-HBc. One hundred and nine patients had no detectable anti-HBc IgM and no total anti-HBc and were thus considered as having acute non-A, non-B hepatitis. Among the 34 patients with anti-HBc IgM in their first serum sample, 23 were anti-HBs negative and all had high and steadily decreasing ratio unit (RU) values for anti-HBc IgM (mean RU value 17.1). Twelve of the 23 patients showed seroconversion to anti-HBs during the follow-up, indicating an actual hepatitis B virus infection. Eleven of the 34 anti-HBc IgM positive patients had anti-HBs in their first serum sample. In this group, the RU values for anti-HBc IgM were high and steadily declining and the initial values were significantly lower (mean RU value 9.9) (p less than 0.05) than in the anti-HBs negative group. Evidence is provided that anti-HBc IgM in serum from patients with HBsAg negative hepatitis with or without anti-HBs indicates an actual hepatitis B virus infection. According to generally accepted criteria, the demonstration of anti-HBc IgM identified 20% of the 169 patients with acute non-A, non-B hepatitis as having an actual hepatitis B infection.

Acute Disease↗
PubMedDate not supplied

Chronic persistent hepatitis: serological classification and meaning of the hepatitis B e system.

In order to evaluate the prognostic implications of the hepatitis B e system in patients with chronic persistent hepatitis (CPH), 53 consecutive patients were studied. Fourteen of 16 patients with HBsAg and HBeAg were followed from 12 to 120 months (mean, 38 months). Eleven of the 14 patients were persistently HBeAg positive and five of these developed chronic active hepatitis (CAH) or cirrhosis. A further nine patients were HBsAg positive but HBeAg negative at time of CPH diagnosis (mean follow-up, 47 months). One of these nine patients developed CAH during follow-up. The remaining 28 patients were all HBsAg negative, and only 2 or the 28 patients progressed to CAH or cirrhosis during the time of follow-up (mean, 43 months). It is concluded that the persistence of HBeAg in patients with CPH indicates a serious prognosis with a frequent transition to CAH or cirrhosis.

Adult↗