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Biomedical subjects

P Stavem

Publications and source records attributed to P Stavem.

At least 19 recordsLinked to original sources
PubMed1979

Why do crystalline precipitates in plasma cells always coalesce with parallel light and dark lines strictly end-to-end and side-to-side?

During transmission electron microscopy of plasma cells from two patients with plasma cell proliferative disorders, we observed a large number of small crystals, most of which showed a striation with alternating light and dark parallel lines. Ultraphotos strongly suggested that smaller crystals often coalesced to larger ones. The coalescence occurred in such a way that the parallel lines of the respective smaller crystals always met each other end-to-end and hardly ever end-to-side. A similar pattern can be seen on previously published ultraphotos from other patients with plasma cell proliferative disorders and intracellular crystals, although not commented upon by the respective authors. The parallel lines of the smaller crystals certainly must correspond to defined structures of the crystal. The stability of a certain configuration is therefore in all likelihood due to electrical potentials created by the crystal structure.

Crystallization↗
PubMed1978

Smouldering acute myelogenous leukemia.

Among 195 patients with variants of acute myelogenous leukemia (AML), a minimum of 11 met our criteria of smouldering AML: patients with less than 30% of blast cells plus promyelocytes in the bone marrow at the time of diagnosis who were observed without specific antileukemic therapy for a period of at least 6 months without entering a fulminant stage of the disease. These patients were older than other patients with AML, they had initially relatively few infections, bled rarely, and did not enter the fullblown clinical picture typical of acute leukemia until the last months of life. For these 11 patients the median survival time was 29 months from the time of diagnosis. Patients with smouldering leukemia shall be observed carefully and not be given specific antileukemic therapy, at least not before they flare into a blast crisis. Transfusions, antibiotics and a small dose of prednisone should be given when necessary.

Adolescent↗
PubMed1978

Acute eosinophilo-myelomonocytic leukaemia, one of the 'in between leukaemias'.

A patient is reported to have an in between type of acute myeloid leukaemia, namely acute eosinophilomyelomonocytic leukaemia. The blasts in the peripheral blood showed a definite transition towards immature monocytes. The bone marrow contained 65% blasts and 13% eosinophil promyelocytes. The large number of immature eosinophils in the bone marrow strongly support the view that they were part of the leukaemic process and not merely a reactive eosinophilia.

Acute Disease↗
PubMed1978

Acute myelogenous leukaemia occurring at the same time in husband and wife.

Acute myelogenous leukaemia was diagnosed within a 1 week's interval in a married couple without consanguinity. The husband had acute myelomonocytic leukaemia whereas the wife had acute myelogenous leukaemia of the classical type. Neither the histories nor findings contributed to an understanding of leukaemogenesis. The calculated risk that a husband and wife should develop acute myelogenous leukaemia within the same year is approximately 1:400 millions.

Adult↗
PubMed1977

Leukaemia-associated antigen (LAA) in proliferative blood disorders.

Serum leukaemia associated antigen (LAA) was found in 41-75% of patients with acute leukaemia or chronic myelogenous leukaemia, but in only 12% of persons suffering from chronic lymphocytic leukaemia. LAA was present in detectable amounts in 1% of healthy blood donors. Thus LAA is truly leukaemia associated rather than leukaemia specific. Occurrence of LAA in the serum of a leukaemia patient may signal a serious turn of the disease.

Adolescent↗
PubMed1977

Light green crystals in May-Grünwald and Giemsa-stained bone marrow macrophages in patients with myeloid leukaemia.

A patient in a terminal stage of myelomocytic leukaemia had a number of elongated crystals in many bone marrow macrophages. The crystals were up to 20 micron long, showed a characteristic light green colour with May-Grünwald & Giemsa, but did not stain with Sudan Black B or PAS. Electron microscopy showed that many of the crystals had a rhomboid form, but failed to show periodicity with the magnification used. A search was made for similar light green crystalline inclusions in patients with different types of leukaemia. Identical inclusions were found in 2 out of 5 other cases of myelomonocytic leukaemia, and in 3 out of 5 cases of chronic myeloid leukaemia. In contrast, such inclusions were not found in any of 6 patients with acute lymphoblastic leukaemia, nor in 4 patients with chronic lymphocytic leukaemia.

Bone Marrow↗
PubMed1977

Complement activation and phagocytosis of cryoglobulin particles in a patient with plasma cell proliferative disease.

The serum of a patient with a non-aggressive plasma cell proliferative disorder contained two monoclonal immunoglobulins: IgG3 lambda in moderate concentration and having cryoglobulin features, and IgA kappa in low concentration and without cryoprecipitability. The patient's serum had low complement concentration and C3 was partly converted into split products in vivo. Complement (C3) together with cryoglobulin and fibrinogen was found by immunofluorescence in sections from skin showing vasculitis. The cryoglobulin particles which formed at room temp. were vividly phagocytized in vitro by neutrophile granulocytes from the patient and from normal individuals as demonstrated in light microscopy and ultramicroscopy.

Biopsy↗
PubMed1977

Human leukaemia associated antigen (LAA): occurrence and characteristics.

Serum leukaemia-associated antigen (LAA) is identified as an oncofetal antigen (or antigens) since it is present in fetal liver and in amniotic fluid. Although it is mainly found in patients with proliferative haematological disorders, particularly acute leukaemias and chronic myelogenous leukaemia, LAA is occasionally present in sera from healthy people. In protein fractionation experiments, LAA behaves as a distinct population of molecules and has the characteristics of an alpha2-beta-globulin, not carrying any lipids. The origin of LAA in haematological disorders is unknown. Its presence does not correlate with high white blood cell count, although antibody to LAA has been raised in animals injected with blast cells from leukaemia patients. LAA is distinct from alpha-fetoprotein, and we have observed a reaction of immunological non-identity between LAA and ferritin. This is of considerable interest since ferritin has been reported to be immunologically closely related to alpha2H-globulin which may occur in the same categories of patients as LAA. It is preliminary concluded that LAA as defined by our antisera may be different from alpha2H-globulin and ferritin.

Amniotic Fluid↗
PubMed1977

In vitro platelet stain preventing (degranulating) effect of various substances, Study of mechanism of action.

A few years ago a patients, T.L., with metastatic leiomyosarcoma found to have a serum and tumor factor which caused the granulomere of normal platelets to disappear as seen using light microscopy. The present report describes the effect on platelet granules of several different substances using various anticoagulants. Ultramicroscopy showed in all instances that the platelet stain preventing effect as seen in May-Grünwald & Giemsa stained films reflected a degranulation. Ultramicroscopy was little better than light microscopy in the differentiation between the mechanisms of the various degranulating substances. Different conditions such as variation in anticoagulant or combination of anticoagulants, storage at room temperature for 24h, heating to 56 degrees C for 1 h on the other hand were very useful methods for differentiating between the various degranulating substances. These methods failed, however, to differentiate between patient T.L.-serum and patient T.L.-tumour fraction SSS, probably because the active factor was the same in both.

Adenosine Diphosphate↗