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Biomedical subjects

W Fereberger

Publications and source records attributed to W Fereberger.

30 records · Page 2Linked to original sources

[A contribution to the cytostatic long-term chemotherapy of polycythemia vera (author's transl)].

From 1967 to 1978 38 patients with polycythemia vera received a long term cytostatic chemotherapy. The results of 14 patients who were given Procarbacin (Natulan) during a mean treatment time of 9 1/2 years are communicated. Two patients showed secondary tumors after 9 or 11 years respectively. The advantages and disadvantages of the various therapeutic approaches in the management of polycythemia in the literature are discussed together with our own experiences.

Female↗

[Dyserythropoietic anemia].

The leading symptom of dyserythropoiesis is an increased, ineffective erythropoiesis with characteristic morphological and functional features. The molecular background of the disturbances is unknown. There are similar structural and biochemical characteristics with different etiologic factors. In addition to rare, congenital forms acquired forms are observed frequently. A causal therapy is only known in deficiency and toxic states. There is an increased risk of transfusion hypersiderosis for the rest of patients with dyserythropoiesis. Among the acquired forms frequently premalignant diseases and tumours are found.

Aged↗

[Transferrin and serum ferritin in tumor patients].

Serum iron, an iron absorption test, transferrin and serumferritin were investigated in patients with malignant disease. A positive correlation was found between increased serumferritin and decreased transferrin and the clinical tumor staging in single cases of acute leukemia and in advanced tumor stages.

Acute Disease↗

[Serum ferritin and cytochemical storage iron in erythropoiesis and the R.E.S. in iron deficiency and faulty iron metabolism].

In 60 patients with iron deficiency anemia of chronic disorders serum iron, an iron absorption test, serum transferrin, serumferritin and stainable non-heme iron in erythropoiesis and reticuloendothelial system, were evaluated. Intercorrelations of these parameters were studied in different diagnostic groups. Pathogenetic principles and the clinical value of the applied diagnostic methods are discussed.

Adult↗

[A method for the evaluation of nitroblue tetrazolium reduction in human platelets (author's transl)].

A long term incubation in NBT-solution leads not only to NBT-reduction by polymorphnuclear leukocytes and monocytes, but also in washed human platelets. The reaction is enhanced by ADP and to a smaller and very variable extent also by Thrombin and Ristocetin. It is inhibited by incubation in plasma environment as well by DBcAMP and PGE1. After a detailed demonstration of the applied method, some possible biochemical mechanisms of the NBT-reduction in human platelets are discussed.

Adenosine Diphosphate↗

[67Ga-whole-body-scanning for non-invasive diagnosis and observation of the course of Hodgkin's disease].

Whole body scanning with 67-Ga citrate, could stand the test as a valuable non-invasive agent for the diagnosis and course study of Hodgkin's disease. It shows a differential accuracy in various nodal and extranodal manifestations, as well as in treated and non-treated cases. The method is not capable of replacing the common diagnostic methods which has been thus far used, but it can complete and occasionally correct them. The best diagnostic information can be gained in the thorax and in extranodal manifestations, which are difficult to evaluate by conventional studies. Our own results, which were obtained by means of studies in 18 cases, are discussed in comparison with reported results in the literature.

Adult↗

[Monoclonal gammopathy in chronic polyarthritis].

Disturbances of immunoglobulin production have often been observed in preclinical multiple myeloma and have led to the question of a pattern of reactive formation of monoclonal gammopathies. In the documented rare case of coincidental Ig-G-myeloma and rheumatoid arthritis some possible similar pathogenetic mechanisms in both diseases are discussed.

Arthritis, Rheumatoid↗