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Biomedical subjects

F Gudat

Publications and source records attributed to F Gudat.

At least 145 records · Page 8Linked to original sources
PubMed1979

[Hepatitis B markers in paediatric patients (author's transl)].

372 children with suspected liver disease were examined for serum HBsAg. Six (three boys, three girls) were found to be positive (1.6%). Further studies of these patients for up to three and a half years revealed elimination of HBsAg in one case only. Biopsies were performed in five patients. Three showed mild chronic hepatitis (two chronic persistent hepatitis, one unspecific reactive hepatitis). Chronic aggressive hepatitis was diagnosed in one patient. One child seemed to be normal on light microscopy, but the findings on electron microscopy were abnormal, the liver cell nuclei being filled with core particles. Two thirds of the family contacts of these children showed hepatitis B marker. Two pregnancies were observed in HBsAg-positive mothers. An infection of the babies was not demonstrable.

Carrier State↗
PubMed1979

Pathological cell aggregates in bone marrow cultures from patients with various hematological diseases.

Non-clonal growth of macroscopic cell aggregates in methylcellulose cultures of abnormal marrow is described. They were seen in all patients with Graft-versus-Host Disease, graft rejection, and autoimmune disease presumably directed against hemopoietic cells, we found them in 35% of patients with primary hematological neoplasias and rarely in patients with solid tumors. They were never encountered in 80 healthy controls. The aggregates originated from small cell clumps which sedimented with the "buffy coat" in contrast to normal bone marrow particles. They contained tumor cells, grafted myeloid cells, or target cells of autoimmune disease in association with a widely varying amount of macrophages. Preliminary results suggest that the frequency of macrophages within the aggregates correlates inversely with the aggressiveness of the clinical condition. We propose that appearance of such aggregates in an indicator of immune activation; we expect that further quantitation of the phenomenon will reveal important clinical correlations and provide a model for the study of host defense to "foreign" cells.

Anemia, Hemolytic, Autoimmune↗
PubMed1979

Systemic karyomegaly associated with chronic interstitial nephritis. A new disease entity?

In 3 patients, two 26 and one 29 years of age, a nephropathy was accidentally discovered which progressed to end stage renal failure within 4 to 6 years. Renal biopsy revealed an unusually marked karyomegaly particularly of the tubular epithelium. These cytopathological changes were associated with chronic interstitial nephritis. Biopsies of other organs, i.e. liver, colon, bronchus and lungs indicated in 2 patients a systemic distribution of the karyomegaly, particularly in mesenchymal cells. Neither the chronic interstitial nephritis nor the karyomegaly could be ascribed to a recognized etiology. This suggests, therefore, that there is a relationship between these changes. The karyomegaly could be the result of the action of some antimitotic agent such as chemical toxins or virus infections.

Adult↗
PubMed1979

[Angio-immunoblastic lymphadenopathy (author's transl)].

The general clinical and pathological findings of angio-immunoblastic lymphadenopathy are reviewed and illustrated by a case-report with involvement of the tonsils. Our patient showed all the characteristic signs of this disease, including fever, pruritus, rash, generalized lymphadenopathy and hepatosplenomegaly. Histologically the wellknown triad of arborizing postcapillary vessels, proliferation of immunoblasts and plasma-cells, as well as deposition of PAS-positive interstitial material was found. Laboratory findings included a polyclonal hyperglobulinemia and a hemolytic anemia. Treatment consisted of corticosteroids and supportive medications. The prognosis is generally poor, with a median survival of 13 months. At present, the cause is unknown.

Adrenal Cortex Hormones↗
PubMed1978

[Chronic hepatitis B. Relationships between virus in the liver and immune response (author's transl)].

A combined histological examination with detection of virus antigens in liver tissue and blood and the corresponding antibodies in blood can give information on the following problems: Standardization of a hepatitis virus B infection, with diagnostic and prognostic information; determination of infectivity; effects of therapy can be monitored, possibly glimpses may be obtained into the mechanism of cancerization.

Antibodies, Viral↗
PubMed1978

[Specific characteristics of hairy cell leukemia].

Report on a now 58-year-old female patient who presented in 1969 with the following objective findings: anemia, thrombocytopenia, lymphocytosis and hepatosplenomegaly. The first first diagnosis was lymphosarcoma, but up to 1976 nearly ten other diagnoses were established, e.g. reticulum sarcoma, leukemic lymphosarcoma, CML, ALL, CLL and Waldenström's disease. The patient did not respond to combined chemotherapy, but splenectomy brought about significant improvement in anemia and thrombocytopenia. She is now doing well without cytotoxic treatment. Hairy cell leukemia was diagnosed on the basis of electron microscopic findings in peripheral lymphocytes and histologic findings in bone marrow and spleen. The tartrate-resistant acid phosphatase was positive. Immunologic tests in the hairy cells showed surface immunoglobulins of monoclonal origina and the T-cells were shown to be decreased. The tests for phagocytosis and nonspecific esterase were negative. The hairy cells in this patient exhibited no colony stimulating activity in culture studies with bone marrow from 4 normal donors, as compared with the stimulating activity of normal monocytes in the same assay. In the light of this case report the question is discussed whether the hairy cells are mainly cells with lymphocytic (B-lymphocytes) or monocytic characteristics. On this question the findings in our patient support the hypothesis of a B-cell nature for the hairy cells.

Acid Phosphatase↗
PubMed1978

Long-term cultivation of plasma cell leukemia cells and autologous lymphoblasts (LCL) in vitro: a comparative study.

Two long-term cell lines were established in vitro from the peripheral blood of a patient with plasma cell leukemia: one line with plasma cell proliferation, the other with lymphoblastoid cell proliferation (LCL). The 9-month-old plasma cell line showed the typical morphology of plasmoblasts. The cells neither had B- nor T-lymphocyte characterisitics, were EBV negative, and showed aneuploidy with various marker chromosomes, including the 14 q+ marker. The cytogenetic findings indicate a monoclonal proliferation of the plasmacells. No tumor growth in thymusless nude mice could be induced upon intracranial inoculation with these cells. In contrast, the autologous LCL, cultured after addition of exogenous EBV, showed the characteristic markers of lymphoblastoid cells, with the typical morphology of pear- and handmirror-shaped lymphoblasts, growing in clumps. They had C3- and Fc-receptors, surface-Ig, E-rosette-negativity, a diploid karyotype, and EBV dependent macromolecule synthesis. They lymphoblastoid cells produced intracranial tumors in nude mice in 8 out of 8 attempts.

Adult↗
PubMed1978

[Microangiopathic hemolytic anemia in malignant tumors. 2 cases].

Two cases of microangiopathic hemolytic anemia in disseminated carcinoma are reported. Both showed the classical features of this illness, namely acute generalized hemorrhagic diathesis, severe hemolytic anemia, thrombocytopenia, fragmentation of erythrocytes in the peripheral blood smear, increased erythropoiesis and megakaryopoiesis or tumor cell invasion in the bone marrow, tumor cell emboli in venules and disseminated intravascular coagulation. In both cases the microangiopathic hemolytic anemia was the first sign of the disseminated carcinoma. Differential diagnosis, pathogenesis and therapy are discussed.

Aged↗
PubMed1978

[Anti-HBc within the framework of hepatitis B virus infection: correlation to the form of inflammation and to the viral expression].

168 HBAg seropositive and 105 HBAg seronegative liver biopsies were studied for correlations between anti-HBc titers (indirect immunofluorescence method) and tissue expression of HBsAg and HBcAg (immunofluorescence), Dane particles in blood (immune electron microscopy) and inflammatory reaction. 98.8% of the HBAg seropositive patients were positive for anti-HBc. The mean titers showed statistically significant differences mainly between chronic aggressive hepatitis (1:2(11.3)) versus lobular hepatitis (1:2(10.1)), chronic persistent hepatitis (1:2(9.9)) and nonspecific reactive hepatitis (1:2(7.6)). Due to the considerable deviation of titers within the histological groups, however, titers below 1:2(11) are of low diagnostic relevance, whereas titers above 1:2(12) are mainly indicative of chronic aggressive hepatitis, although acute lobular hepatitis with signs of possible transition to chronicity or chronic persistent hepatitis with strong inflammatory activity may occur. Among HBAg seronegative patients 20% were positive for anti-HBc (mean titer = 1:2(7.7)). Among 78 patients also tested for anti-HBs, 10.2% were positive for both anti-HBc and anti-HBs. In an additional 12.8%, anti-HBc was the only marker of past hepatitis B virus infection. Anti-HBs was the only marker in a further 33%. In none of the HBAg seronegative patients and in only 59% of all HBAg seropositive patients, there was an association of anti-HBc with complete virus synthesis as measured by the demonstration of HBcAg in tissue or Dane particles in blood. It is concluded that anti-HBc is not a criterion of infectiosity but a specific, although non-characteristic, marker for HBAg seropositive acute and chronic hepatitis as well as for terminated HBV infection of all possible inflammatory and HBAg expression types.

Antibodies, Viral↗
PubMed1977

[Immunological aspects of acute viral hepatitis treated with corticosteroids].

Acute viral B-hepatitis is the consequence of an effective specific immune response against the hepatitis B-virus with elimination of the virus. Corticosteroids decrease this immune reaction and thereby inhibit virus elimination. In principle, therefore, corticosteroid therapy promotes a transition to chronicity. This theoretical concept is documented practically by 8 patients treated with steroids in the early phase of acute viral hepatitis. Transition to some form of chronic liver disease is documented by serial liver biopsies in all 8 patients. The immunohistological findings showed the presence of HBsAg and HBcAg, as theoretically expected. These 8 selected cases, although uncontrolled, together with the theoretical concept of B-virus elimination, provide evidence against the use of corticosteroids in acute B-hepatitis.

Acute Disease↗
PubMed1977

Nuclear fluorescence of liver cells for IgG in viral hepatitis B: significance and relation to hepatitis B-core and anti-hepatitis B-core formation.

The occurrence of anti-HBcAg antibodies in the blood as determined by indirect immunofluorescence and its relation to the occurrence of HBsAg in the cytoplasm and of HBcAg and IgG in the nuclei of hepatocytes were studied in the following groups of patients (total of 123 biopsies): I. 64 HBAg-negative patients with various liver diseases; II. 51 HBAg-positive patients without therapeutical immunosuppression (6 acute hepatitis, 10 nonspecific reactive and 10 chronic persistent hepatitis, 19 chronic aggressive hepatitis, 6 "Hippie"-hepatitis); III. 8 kidney transplant recipients. It could be shown that nuclear IgG is found only if both parameters can be demonstrated at the same time: HBcAg in liver cell nuclei and anti-HBcAg antibodies in the serum in titers higher than 1:64. Accordingly, all types of hepatitis with excess formation of nuclear HBcAg (early phase of acute hepatitis, chronic aggressive hepatitis and chronic non-aggressive forms with generalized core formation, i.e. carrier state or chronic persistent hepatitis of the HBc type) may show nuclear fluorescence for IgG. All forms of hepatitis B without detectable core formation (acute hepatitis in the elimination phase, chronic non-aggressive hepatitis with isolated HBsAg expression, i.e. carrier state or chronic persistent hepatitis of the HBs type, posthepatitic phase) do not present nuclear IgG despite eventual anti-HBcAg formation. Finally, lack of anti-HBcAg or very low titers associated with lack of IgG in hepatocytic nuclei do not exclude generalized core formation in liver cell nuclei in chronic persistent hepatitis of effectively immunosuppressed patients. Although the demonstration of nuclear IgG has several diagnostic and prognostic consequences in common with the demonstration of HBcAg, a specific search for the core antigen in the tissue is needed for the correct appraisal of the HBcAg- and HBsAg tissue expression pattern and the associated disease.

Antigen-Antibody Complex↗
PubMed1977

Evidence for phasic sequences in nuclear HBcAg formation and cell membrane-directed flow of core particles in chronic hepatitis B.

Seven liver biopsies (6 chronic aggressive hepatitis B, 1 kidney transplant recipient with chronic persistent hepatitis B) are described showing differential distribution patterns of HBcAg in liver cells (with gradual transitions): pure nuclear, mixed nuclear/cytoplasmic, and pure cytoplasmic (diffuse and/or submembraneous). This was combined with spotty expression of HBsAg (cytoplasm and liver cell membrane) and with Dane particles (DP) in blood. A phasic nuclear formation and release of cores from the nucleus and of DP from the cell, respectively, is suggested. Electron microscopy (EM) of one biopsy indicates a secretory disturbance as a possible cause for HBcAg accumulation in liver cells the tolerance of which is attributed to immunosuppression therapeutically induced in 4 patients and suspected in 3 (2 dialysis patients, 1 spontaneous chronic aggressive hepatitis B).

Cell Membrane↗