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Biomedical subjects

M A Gerber

Publications and source records attributed to M A Gerber.

At least 253 records · Page 14Linked to original sources
PubMed1977

The lack of nurse-infant transmission of type B hepatitis in a special care nursery.

Twenty-four infants cared for by a nurse who developed acute B hepatitis with HBsAg present in her serum and saliva were examined for serologic evidence of hepatitis B virus transmission. None of the infants had HBsAg by radioimmunoassay or anti-HBc by complement fixation. One infant had anti-HBs whose transient presence was consistent with passive acquisition. Using sensitive serologic tests, no identifiable risk to newborn infants in a special care nursery could be documented as a result of exposure to a nurse who developed acute type B hepatitis during their period of care.

Cross Infection↗
PubMed1977

Antibodies to hepatitis B core antigen in hepatitis B surface antigen-positive and -negative chronic hepatitis.

Antibody to hepatitis B core antigen (anti-HBc) is a sensitive indicator of hepatitis B virus (HBV) infection. However, anti-HBc has been found in only a few patients with chronic hepatitis. Therefore, we tested for anti-HBc in 124 sera from 67 patients with histologically proven chronic hepatitis by the indirect fluorescent antibody technique. All patients, except for one with chronic hepatitis who was seropositive for hepatitis B surface antigen (HBs Ag), had anti-HBc that persisted throughout the follow-up period (three months to three years). Of 33 HBs Ag-seronegative patients, anti-HBc was detected in seven patients and persisted for six months to two years. These findings suggest that in this study 21% of patients with chronic hepatitis with undetectable amounts of HBs Ag in the serum had evidence of recent or continued HBV replication.

Adolescent↗
PubMed1977

Immune response to hepatitis B virus in children with papular acrodermatitis.

Papular acrodermatitis of childhood (PAC) is characterized by papular eruption of skin, lymphadenopathy, and acute hepatitis B surface antigen (HBsAg)-positive anicteric hepatitis. To study the course of hepatitis B virus infection we followed 16 patients with PAC, 2 to 7 years of age, for periods ranging from 6 to 46 months. All patients tested developed hepatitis B surface antigenemia subtype ay, and produced antibody to hepatitis B core antigen with the highest incidence after 3 to 5 months. Half of the children investigated developed antibody to hepatitis B surface antigen 4 to 18 months (mean, 6.5) after the onset of PAC. At the end of the investigation, 31% of the children were still HBsAg-positive, 50% were antibody to hepatitis B core antigen-positive, and in 43% the activity of serum aminotransferases was abnormal. Liver biopsy repeated in 2 children showed chronic aggressive hepatitis. The pattern of antibody response to hepatitis B virus is similar in both HBsAg-positive hepatitis and PAC. The frequent development of HBSAg carrier state and the high proportion of children with liver abnormalities at the end of the investigation suggest an impaired clearance of hepatitis B virus and a tendency to chronicity.

Acrodermatitis↗
PubMed1976

Immune complexes in hepatocytic nuclei of HB ag-positive chronic hepatitis.

To localize immune complexes in viral hepatitis Type B and to assess their pathogenic role, we examined by the direct fluorescent-antibody technic 21 liver specimens with hepatitis B core antigen (HBc Ag) in hepatocytic nuclei from 10 patients with HBs Ag-seropositive acute viral hepatitis and from 11 patients with HBs Ag-seropositive chronic active hepatitis. IgG with in vitro fixation of complement was demonstrated in HBc Ag-containing hepatocytic nuclei of all patients with chronic active, but not in those with acute viral hepatitis. All patients except for one had antibody to HBc Ag in the serum as determined by indirect immunofluorescence. The evidence suggests that intranuclear IgG in chronic active hepatitis has anti-HBc specificity and forms immune complexes with HBc Ag. The binding of IgG to intranuclear HBc Ag might have pathogenic importance in chronic active hepatitis.

Acute Disease↗
PubMed1975

Immunohistochemical findings in the renal vascular lesions of progressive systemic sclerosis.

Four selected patients with progressive systemic sclerosis showed deposition of immunoglobulins and complement in diseased renal arteries and arterioles. Although three patients had hypertension, in two of these malignant, the third patient did not have hypertension over a four year period. These findings suggest that immune complexes may be involved in the pathogenesis of some cases of progressive systemic sclerosis, the primary target being the vascular system.

Adult↗
PubMed1975

Incidence and nature of cytoplasmic hepatitis B antigen in hepatocytes.

Hepatitis B antigen (HB Ag) in the hepatocytic cytoplasm is detected by immunofluorescence after reaction with fluoresceinated antiserum to HB Ag or by electron microscopy as numerous 20- to 30-nm. tubular and circular structures in dilated cisternae of excess endoplasmic reticulum. On light microscopy, these hepatocytes can be recognized because their cytoplasm has a ground-glass appearance and stains with Gomori's aldehyde fuchsin. Aldehyde fuchsin-positive ground-glass hepatocytes were detected in all 14 asymptomatic carriers of HB Ag and in 16 of 60 HB Ag-seropositive patients with chronic hepatitis, but not in HB Ag-seropositive acute viral hepatitis or in various other HB Ag-seronegative liver diseases. These cells are helpful in identifying on light microscopy HB Ag carriers and a portion of patients with HB Ag-positive chronic hepatitis. Nuclear HB Ag did not stain with aldehyde fuchsin. Nucleic acids were not detected in the ground-glass cytoplasm by special stains at the light or electron microscopic level. We suggest that the tubular and circular structures in the hepatocytic cytoplasm are coat material of the hepatitis B virus or virally coded host cell reaction product rather than the complete hepatitis B virus.

Acute Disease↗
PubMed1974

Electron microscopy and immunoelectronmicroscopy of cytoplasmic hepatitis B antigen in hepatocytes.

The localization of hepatitis B antigen (HB Ag) and the nature of the virus-like particles in hepatocytes of patients with HB antigenemia are controversial. In many reports, numerous virus-like particles have been demonstrated in hepatocytic nuclei; the few reported in the cytoplasm are insufficient in number to explain the intense cytoplasmic fluorescence after staining with fluoresceinated antibody to HB Ag (HB Ab). We found numerous tubular and circular structures, measuring 20 to 30 nm in diameter, in the cisternae of the excess smooth endoplasmic reticulum (ER) of varying numbers of hepatocytes in 13 of 16 HB Ag carriers and in 4 of 9 patients with HB Ag-positive chronic hepatitis corresponding to cytoplasmic HB Ag-specific fluorescence. Direct immunoelectronmicroscopy using peroxidase-labeled HB Ab revealed that the intracisternal bodies and the surrounding membranes contain HB antigenic determinants. These bodies are an ultrastructural correlate of cytoplasmic HB Ag. It is suggested that they are virally coded coat material rather than the mature hepatitis B virus or its core.

Antigens, Viral↗