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Biomedical subjects

C Nissen

Publications and source records attributed to C Nissen.

At least 181 records · Page 10Linked to original sources
PubMed1979

The Basel experience with total body irradiation for conditioning patients with acute leukemia for allogeneic bone marrow transplantation.

We are reporting our experience with 13 patients suffering from end stage acute leukemia that were prepared for allogeneic bone marrow transplantation by combined chemotherapy followed by high dose cyclophosphamide (Cy) and total body irradiation (TBI). Only one patient became a long term survivor. Of the evaluable 12 patients, 6 died of interstitial pneumonia, 4 of GvH and 1 of recurrent leukemia. We conclude that adding combined chemotherapy to the standard conditioning program with Cy and TBI probably increases the risk of developing fatal interstitial pneumonia without eliminating the risk of recurrent leukemia. We suggest that allogenic marrow grafts should be performed earlier in the course of refractory acute leukemias, because in patients with end stage disease its chances of being curative are small.

Adolescent↗
PubMed1978

[Differential diagnosis of primary and secondary erythrocytosis by means of in vitro culture of hematopoietic stem cells].

Peripheral blood precursor cells from all of 12 patients with polycythaemia vera (PV) formed hemoglobinized colonies in vitro without addition os was strictly epo-dependent in 30 normals and 8 patients with erythrocytosis of other origin. By addition of 1 U epo/ml to the cultures, colony formation was increased up to 5-fold in PV. Untreated patients with a short history had the highest numbers of such epo-responsive precursor cells. In 3 patients with concomitant myelofibrosis, erythroid in vitro growth was abundant, but scattered, single colonies could hardly be identified and their hemoglobinization was poor. This picture did not change with addition of epo, and hemoglobinization did not improve. In vitro grown colonies in PV had morphological abnormalities as compared to colonies grown from normal precursor cells: all stages of erythroid differentiation and up to 50% necrotic cells were found within single colonies. Scattered colonies contained an excess of large, immature, vacuolated erythroblasts. It is concluded that these functionaland morphological abnormalities of in-vitro erythropoiesis are a reliable indicator of PV. Further, transition to myelofibrosis is recognized by a characteristic growth pattern with decreased epo-responsiveness.

Cells, Cultured↗
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↗
PubMed1977

[Allogenic bone marrow transplantation in severe aplastic anemia and refractory acute leukemia. 35 cases].

23 patients with severe aplastic anemia have been treated. 10 marrow grafts between HLA matched siblings were performed after conditioning with cyclophosphamide. 5 are still alive at over 7 months to over 2 1/2 years after grafting. 3 are hemopoietic chimeras and 2 show autologous marrow reconstitution. 13 patients were treated by ALG with or without transfusion of allogeneic marrow. 9 are still alive with partial to complete autologous hemopoietic reconstitution at over 1 month to over 4 years. It is concluded that in many instances aplastic anemia is an autoimmune disease rather than a primary failure of the hemopoietic stem cells. In acute leukemia allogeneic marrow grafts still pose enormous problems and only one of our 12 grafts has become a longterm survivor.

Acute Disease↗
PubMed1976

Failure of isogeneic marrow engraftment in a patient with acute leukemia.

Marrow transplantation was carried out in a patient with acute myelogenous leukemia using a healthy identical twin as donor. The patient was prepared for grafting with combination chemotherapy, high dose cyclophosphamide, and 1,000 rad total body irradiation. Repopulation of marrow did not occur despite a second marrow infusion 21 days following the first attempt. The patient died 44 days after the initial marrow infusion. To our knowledge this is the first patient transplanted from an identical twin who did not achieve engraftment after high dose chemotherapy and supralethal irradiation. The survival time was well in excess of that required for evaluation of engraftment. The possible mechanisms for graft failure are discussed. The use of prophylactic interferon against viral infections is considered as the most likely cause of failure of engraftment.

Bone Marrow Cells↗
PubMed1976

[Graft versus host disease, a little known complication of blood transfusion].

A case of fatal graft-versus-host disease (GvHD) following blood transfusions is reported. This relatively rare complication of blood and bloodcomponent replacement therapy may occur in recipients with decreased cellular immunity, which may be due to the underlying disease, chemotherapy or radiation therapy, or a combination of both. GvHD is a result of active proliferation of transfused immunologically competent cells which attack host organs. This complication can be prevented by irradiating transfusions with 1500 rads in vitro.

Adult↗