Conventional-dose Ara-C (200 mg/m(2) d 1-5) combined with idarubicin (12 mg/m(2) d 1-3) was employed as remission induction and consolidation therapy in 23 elderly AML patients with a median age of 66 years (range, 60-75) with AML according to the FAB criteria (M1 n = 3, M2 n = 10, M4 n = 6, M5 n = 2, M6 n = 2), eligible for the study. In seven patients earlier MDS had been documented by previous bone marrow aspirates. The CR rate after one induction course was 65% (15/23). Toxicity was acceptable, with four patients dying during the chemotherapy-induced hypoplasia (4/23). Although 80% of the CR patients received two additional cycles of Ara-C and idarubicin as consolidation therapy, only two patients are still in continuous complete remission more than 12 months after achieving CR. The median disease-free survival of the CR patients was 11.5 months and the median survival of the entire group was 10 months. We conclude that conventional dose Ara-C/idarubicin is an effective protocol for inducing complete remission in elderly patients with AML, but that consolidation therapy consisting of two courses of the same regimen does not produce a relevant rate of long-term disease-free survival.

Background: The thioether phospholipid analogue ilmofosine has demonstrated antineoplastic activity in several experimental tumor systems. In a clinical phase I study tumor response was observed in malignant melanoma, so that a disease-oriented phase II study was started.Material and Methods: 43 patients with advanced and progressive malignant melanoma were treated with the alkyllysophospholipid ilmofosine. Patients with and without pretreatment received 75 mg ilmofosine tablets t.i.d. Response evaluation was performed after an 8-week treatment period.Results: 35 patients were evaluable for response, 15 non-pretreated and 20 pretreated. Disease stabilization was achieved in 11 patients (7 pretreated), 4 had an early progression within the first 8 weeks of treatment and 20 had progressive disease thereafter. In 2 patients a documented tumor progression before study entry was stopped during the treatment period. Gastrointestinal side effects were predominant and dose-limiting.Conclusion: In conclusion, oral ilmofosine has shown limited efficacy in this trial.

In a prospective randomized multicentric trial, 61 patients from six hospitals with resectable pancreatic cancer were recruited between 1987 and 1989. All patients underwent a Whipple resection. Two weeks after surgery, the patients were randomized to be given either intravenous (IV) treatment with 370 mg (100 mg loading dose, 9 x 30 mg continuing within 10 days) of monoclonal antibody (MoAb) 494/32 (Behringwerke AG, Marsburg, Germany) or no additional anti-cancer treatment. This murine immunoglobulin (Ig) G1 antibody has been shown to strongly bind to human pancreatic cancer cells and to induce an antibody-dependent cellular cytotoxicity (ADCC). Both study groups were well matched with respect to age, sex, tumor staging, and grading. Six patients suffered from minor toxicity (vomiting and abdominal pain) after immunotherapy. Ten months after the end of the recruitment period, 65% and 53% of the patients in the treatment and control groups, respectively, had died. Of the living patients, 60% and 53% are alive with recurrent or progressive cancer disease. Median survival time was 428 days (range, 248 to 510 days) and 386 days (range, 296 to 509 days) in the treatment and control groups, respectively. The authors concluded that repeated IV treatment with the antibody 494/32 is not helpful in resectable pancreatic cancer. This study provides the first controlled data on passive immunotherapy in solid cancer.

Polyploidy — the doubling of chromosome sets of cells caused by a stop of mitosis at different levels of the mitotic cycle — is a phenomenon widely observed in plants, protozoa, metazoa, and animals. In man obligate polyploid tissues are found in liver parenchyma, heart muscle cells, and bone marrow megakaryocytes. Polyploidy occurs mostly in stable and highly differentiated cells and tissues. Besides age, stimulation of proliferation and increased metabolic function lead to polyploidization in these organs. Aneuploidy, however, is exclusively found in tumor cells.

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study

In a 45-year-old woman with severe normochromic anemia (Hb 2.8 g%) an extensive myelofibrosis and infiltration of the bone marrow with small blasts was observed histologically. Cytochemical examination of the blasts showed a negative peroxidase and a strongly positive alpha-NE reaction. PAS reaction was slightly granular positive in the cytoplasmic protuberances of the blasts and in the platelets. Marker analysis yielded no evidence of lymphatic origin of the blasts. In flow-cytometric studies of 230,000 cells a homogeneous 2c blast population could be identified. Cytogenetic analysis revealed an abnormal pseudo-diploid karyotype characterized by 2 acrocentric marker chromosomes caused by a translocation of chromosomes 8 and 14, as usually seen in Burkitt type lymphoma. Finally the reaction product of platelet-specific peroxidase could be demonstrated in the perinuclear cisternae of the endoplasmic reticulum by electron microscopy. Highly elevated β-thromboglobulin and platelet factor 4 plasma levels were also measured.

Though it has been generally accepted that uremic serum contains substances which impair platelet function and inhibit erythropoiesis, the mechanism of uremic thrombocytopathy and bleeding tendency is still not clearly understood. By measuring the nuclear DNA content of the megakaryocytes of 20 patients with end-stage renal failure, we demonstrated that ploidy levels correlate with parameters of uremia. High creatinine and BUN levels as well as low hemoglobin or creatinine clearance values correlate with low average ploidy of megakaryocytes. In explaining this phenomenon, uremic inhibition of DNA replication seems to be more important than dialysis or the type of renal disease. As megakaryocytes of higher ploidy are thought to produce more reactive platelets than megakaryocytes of lower DNA content, this could be another reason for uremic thrombocytopathy and bleeding tendency.

ZusammenfassungWir bevorzugen folgendes therapeutisches Vorgehen: Bei Patienten mit gesicherter ITP ist ein Abwarten gerechtfertigt, solange die Thrombozytenwerte mehr als 30000/µl betragen und keine manifesten Blutungen bestehen. Bei Thrombozyten werten unter 30000/µ1 sowie manifesten Blutungen beginnen wir eine PrednisolonTherapie mit initial mindestens 100 mg Prednisolon/die, gefolgt von einer ausschleichenden Dosierung über 6-8 Wochen nach Eintritt der Remission. Beim ersten Rezidiv wird individuell unterschiedlich entweder ein zweiter Therapieversuch mit Prednisolon unternommen oder eine Splenektomie durchgeführt.