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Biomedical subjects

D Urbanitz

Publications and source records attributed to D Urbanitz.

49 records · Page 3Linked to original sources
PubMed1975

Reduced monocyte phagocytosis in patients with advanced Hodgkin's disease and lymphosarcoma.

The monocytes of 7 patients with advanced Hdgkin's disease (stages III and IV) and of two patients with generalized lymphosarcoma exhibited a highly significant impairment of the phagocytosis of IgG-coated red cells, regardless of receiving therapy or not. In contrast three patients with M. Hodgkin, stage II B, and one with lymphosarcoma in complete remission showed a rather elevated monocyte phagocytic acitivity. The nitroblue tetrazolium reduction by monocytes in the mean was significantly enhanced in all patients investigated, compared with normal persons, although only in one patient a bacterial infection was apparent at the time of the test. The possible implication of the findings in the well known immunodeficiency present in M. Hodgkin and lymphosarcoma is discussed.

Centrifugation, Density Gradient↗
PubMed1975

[Monocyte function in chronic uremia (author's transl)].

Monocyte function studies in vitro have been performed in 21 patients with terminal, dialysis-treated uremia and, in parallel, in 21 healthy normal subjects. In uremia the attachment, spreading activity, and reduction of nitroblue tetrazolium were shown to be significantly enhanced, indicating a metabolic activation of the monocytes. The phagocytosis of IgG-coated red cells, however, was significantly impaired. A modification of the monocyte IgG-receptor in uremic conditions is supposed; its relevance for the immunosuppression in uremic states is discussed.

Adult↗
PubMed1975

[Nitroblue-tetrazolium test in isolated human monocytes].

Depending upon the NBT charge 50 to 80% of isolated non stimulated human monocytes reduce NBT ro morphologically demonstrable Formazan. Similar to neutrophils two different patterns of reaction are exhibited: discrete load with finely distributed Formazan granula surrounding the nucleus; massive reaction with large distributed Formazan granula surrounding the nucleus; massive reaction with large Formazan deposits throughout the cytoplasma. In a low percentage morphologically desintegrated, massive loaden cells appear. After an additional incubation in medium without NBT the number of these necrotic cells increases. The phagocytosis of IgG-coated red cells is impaired after incubation of the monocytes in NBT. In the presence of an alkylating agent not only the NBT-reaction is inhibited; the number of necrotic cells is also diminished. Apparently the Formazan is cytotoxic. The significance of these results in particular in cases of enhanced NBT reduction is discussed. Compared with the findings of other authors concerning the neutrophils the monocytes possess a markedly stronger NBT reducing activity. Considering the lower bactericidal capacity of the monocytes NBT reduction does not in every case parallel bactericidal activity.

Antineoplastic Agents↗
PubMed1975

Impaired phagocytic activity of human monocytes in respect to reduced antibacterial resistance in uremia.

Resistance to bacterial infection, particularly septicemia and pneumonia, is decreased in patients with uremia. Tests of monocyte function in 21 patients with chronic uremia and in 21 normal healthy subjects showed an increase in attachment rate, spreading activity and Nirtoblue-tetrazolium reduction in the uremic subjects. In contrast, phagocytosis of IgG-coated red cells was impaired.

Adult↗
PubMedDate not supplied

Treatment of refractory acute myeloid leukemia with mAMSA and VP 16-213 in combination: results of a clinical phase I/II study.

Twenty patients with refractory AML were treated with mAMSA and VP 16-213 in combination to assess the toxicity and anti-leukemic activity of the two-drug regimen. Refractoriness was defined according to the response to induction therapy consisting of 6-thioguanine, cytosine arabinoside and daunorubicin (TAD9) and the duration of the preceding remission. Patients were eligible for AMSA/VP 16-213 if they were primary non-responders against two TAD9 induction courses, had early relapses within the first six months, were nonresponders to one additional TAD9 course at later relapses or were at second or subsequent relapses. Therapy consisted of a five-day course of mAMSA 210 mg/m2/d on days 2, 3 and 4. VP 16-213 was applied on days 1 and 5 by a 1-h infusion of 100 mg/m2 followed by a 23 h infusion, the dosage of which was escalated in three steps from 110 mg/m2 over 200 mg/m2 to 230 mg/m2 in subsequent patients. Even at the highest dose of VP 16-213, toxicity was mild to moderate except for mucositis of grade III after two cycles and severe intrahepatic cholestasis in one case. Four of the 20 patients died within the first three weeks after the onset of treatment and were not evaluable for the assessment of antileukemic efficacy. From the remaining 16 patients five achieved partial remissions while no complete remission was obtained. Four of the five PR occurred in the eight patients with primary TAD9 resistance. These data indicate that AMSA/VP 16-213 reveals a moderate toxicity only, and that the combination may not be completely cross-resistant with TAD9. The overall anti-leukemic activity is limited however, and seems inferior compared to other presently available salvage regimens in refractory AML.

Adult↗
PubMedDate not supplied

Phase II evaluation of 5-fluourouracil plus folinic acid and alpha 2b-interferon in metastatic colorectal cancer.

Biochemical modulation of 5-fluorouracil (5-FU) by folinic acid (FA) increases the response rate in patients with metastatic colorectal cancer compared to 5-FU alone. Phase II trials also demonstrated increased efficacy when interferon was added to 5-FU. In two consecutive trials, 76 patients were treated on days 1-5 with FA 200 mg/m2 plus interferon 5 x 10(6) U/m2 and 5-FU 350 mg/m2 as intravenous bolus injection (n = 33, regimen A) or 5-FU 500 mg/m2 as 2-hour infusion (n = 43, regimen B), repeated every 3 weeks with individual 5-FU dose escalation in steps of 50 (regimen A) or 100 mg/m2 (regimen B). In regimen A 5-FU dose reduction to 300 mg/m2 due to toxicity was necessary in 49% of the patients; in regimen B a 5-FU dose of 600 mg/m2 or above was tolerated by 70% of the patients. Dose-limiting toxicity was severe mucositis and/or diarrhea. Objective responses were observed in 5 of 33 patients (15%) in regimen A (3-28%, 95% confidence interval) and 7 of 41 patients (17%) in regimen B (5-29%, 95% confidence interval). Median time to progression was 4.7 and 4.8 months, and median survival 9.9 and 11.4 months for regimens A and B, respectively. Prolonged 5-FU administration over 2 h allows the administration of a higher 5-FU dose compared to bolus injection with no apparent improvement in antineoplastic efficacy. The addition of interferon to the combination of 5-FU plus FA in this dose and schedule does not seem to improve the response rate but appears to increase treatment toxicity.

Adult↗