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Biomedical subjects

J Hastrup

Publications and source records attributed to J Hastrup.

At least 19 recordsLinked to original sources
PubMed1991

Clinicopathological features and prognostic factors in extranodal non-Hodgkin lymphomas. Danish LYFO Study Group.

In a Danish population-based non-Hodgkin lymphoma (NHL) registry, 1257 newly diagnosed NHL cases were registered over a 5-year period. Of these, 463 (37%) were extranodal. The gastrointestinal tract was the most common site of extranodal involvement (30% of the cases). Histologically, 44% of all extranodal NHL cases had high-grade, 17% intermediate and 27% low-grade features, while 12% were unclassified. The most common histological subtype (Kiel) was the centroblastic diffuse (23% of cases). 50% of all extranodal NHL were localised (stage IE or IIE) and 27% had B symptoms. Site-specific features included a strong age-correlation for thyroid and testes lymphoma (greater than 50 years) and a high prevalence of female cases in thyroid and salivary glands lymphomas (M/F 0.14 and 0.30, respectively). Overall 7-year survival for extranodal NHL was 46% (median 4.9 years). Poor prognosis patients could be identified by the presence of one or more of the following presentation characteristics: age greater than 65 years, B symptoms, high-grade histology, disseminated disease, elevated s-IgA and hyperuricaemia. Relative risk values ranged from 2.1 for age and B symptoms to 1.7 for hyperuricaemia.

Adolescent↗
PubMed1989

Immunohistochemistry and cytochemistry of experimental rat bladder cancer: binding of the lectins PNA and WGA and of a Le(Y) mouse monoclonal antibody.

Two lectins, peanut agglutinin (PNA) and wheat germ agglutinin (WGA), and a mouse monoclonal antibody against blood group Le(Y) were used to study the distribution of carbohydrate antigens in an experimental rat bladder cancer model. Neoplasia was induced in 28 rats by intravesical installation of N-nitroso-N-methyl-urea (NMU). Fifteen rats were installed with the NMU solvent and served as controls. Urothelial samples were taken from all animals, the atypia were graded and detailed data on the location of the lectin-binding structures and the binding of the monoclonal antibody were obtained by immunohistochemical methods. Urine samples were collected at different times during tumor development and data on the cytological location of the lectin-binding structures and the binding of the monoclonal antibody were obtained by immunocytochemical methods. Examination of the histological distribution of lectin binding structures and Le(Y) antigen showed a characteristic change in carbohydrate antigen expression associated with the development of urothelial atypia. In normal urothelium carbohydrate antigens were present in cytoplasm, whereas they became expressed on cell membranes in non-invasive carcinomas. Immunocytochemistry of urine specimens revealed a lack of correlation between the antigen expression found in exfoliated cells and that found in tissue. Morphologically normal cells from NMU-treated animals were found to express a carcinoma associated antigen pattern.

Animals↗
PubMed1983

Treatment of dysplasia of the cervical epithelium with an interferon gel.

Human leukocyte interferon was incorporated into a hydrophilic gel and applied to the cervix of six patients suffering from moderate to severe dysplasia or carcinoma in situ of the cervix. Only patients showing no spontaneous regression during at least 27 consecutive weeks were admitted to the trial. The diagnoses were established by Papanicolaou smears and biopsy specimens of the cervix. The gel was applied directly on the cervix twice weekly for six weeks, and only minor clinical improvements were seen. However, after an additional six weeks, six of six patients responded positively; three of them regressed completely. No side effects were noted.

Administration, Topical↗
PubMed1981

Large-cell T-lymphoma with hypersegmented nuclei.

Clinical, morphological, cytochemical and immunological features in a case of T-lymphoma in a 67-year-old man are presented. Clinically, a predilection for lymph nodes was observed with a subsequent tumour-like spread to the liver, lungs and, to a minor extent, to the bone marrow. The skin, the spleen and the thymus were spared. Morphologically, the neoplastic lymphoid cells were characterized by their large size and particularly by their hypersegmented nuclei with a relatively coarse chromatin and large nucleoli. Cytochemically, a T-cell-like staining pattern in the acid phosphatase and in the acid alpha-naphthyl acetate esterase stains was absent. The neoplastic lymphocytes demonstrated a strong binding with sheep erythrocytes in suspension and in cryostat tissue sections. The morphological features of this lymphoma appear distinct from other non-Hodgkin's lymphomas. The similarities and the differences of our case in relation to some recently described cases of peripheral T-lymphomas comprising large cells with hyperlobated nuclei, are discussed.

Aged↗
PubMed1980

Epstein-Barr-virus-induced lymphoproliferative disorder converting to fatal Burkitt-like lymphoma in a boy with interferon-inducible chromosomal defect.

A 6-year-old boy presenting with swelling of cervical and axillary lymph-nodes was diagnosed as having an Epstein-Barr virus infection because of EBV-nuclear-antigen-positive B-lymphocytes in blood and lymph nodes and high antibody titres to EBV antigens. The natural killer activity of blood-lymphocytes was low, and so was the percentage of T-lymphocytes with Fc receptors for IgG (T-gamma cells). Chromosomal studies revealed a defect in the long arms of one of the chromosomes in pair no. 16 (16q22). The defect only appeared after addition of interferon to the lymphocyte cultures and preferentially in T-gamma lymphocytes. The disease progressed despite attempts to restore the patient's immune reactivity by interferon, transfer factor, and blood transfusions. Necropsy showed that the severe hyperplasia of lymph nodes found during life had become a Burkitt-like lymphoma. The possible connection between an interferon-induced chromosomal defect (break at 16q22) and reduced level of natural killer activity, reduced T-gamma lymphocytes, and proliferation of EBV-positive B-lymphocytes is discussed.

Burkitt Lymphoma↗
PubMed1980

The effect of quinidine on digoxin kinetics in cardiac patients.

The pharmacokinetics of digoxin was studied in 11 subjects before and during quinidine treatment. Renal clearances of digoxin and creatinine were calculated from plasma concentrations and urinary excretions of digoxin and creatinine in subjects on long-term digoxin treatment. The investigations were repeated in the same subjects during administration of quinidine. Renal clearance of digoxin decreased, while plasma concentration of digoxin and renal excretion of digoxin increased in the presence of quididine, indicating substantial changes of digoxin kinetics, induced by quinidine. The reduction in renal clearance of digoxin may be due to a specific inhibition of tubular secretion of digoxin. The considerable rise of the plasma digoxin level and the increased excretion of digoxin support the assumption of a major extrarenal mechanism of interaction.

Aged↗
PubMed1980

Histological and immunopathological studies in a case of chronic Epstein-Barr virus infection terminating in a Burkitt-like lymphoma.

A 6-year-old boy suffered from a severe lymphadenopathy, characterized histologically by a fulminant polyclonal immunoblast proliferation simulating malignant lymphoma with many immunoblasts resembling Reed-Sternberg cells. He had no history of infectious mononucleosis but Epstein-Barr virus (EBV) infection was evident from serological findings, and EBV-associated nuclear antigen (EBNA) was demonstrated in a high percentage of lymphocytes of blood and lymph nodes. An adequate humoral response to EBV ruled out the possibility of an X-linked recessive lymphoproliferative syndrome as the underlying cause of chronic EBV infection. A chromosomal defect in a subpopulation of lymphocytes was induced by interferon and might somehow be associated with a subtle immunodeficiency of our patient. After exacerbation of the disease chemotherapy was included in the treatment but the patient died 9 months after the onset of the disease. At autopsy the lymphoblastic cell proliferation had changed from that of immunoblasts to cells resembling the Burkitt's lymphoma cells. A change of the proliferating cell type was supported by means of cytochemical and immunological cell markers. The presence of EBV in these cells was demonstrated with the EBNA technique. It is concluded that our case may well support the hypothesis, that EBV may induce lymphoma-like polyclonal immunoblast proliferation in immunodeficient individuals, and that occasionally a monoclonal proliferation of the Burkitt's lymphoma type may supervene.

Biopsy↗