Cisplatin and melphalan given ip exert a synergistic therapeutic effect against ascitic P388 leukemia in mice and have different dose-limiting toxic effects as well as favorable pharmacokinetic characteristics in ip phase I studies. We gave a total of 98 courses of cisplatin (escalated from 40 to 120 mg/m2) and melphalan (escalated from 12 to 30 mg/m2) to 30 patients with ip tumors, most of whom had residual ovarian cancer following iv cisplatin-containing regimens. Treatment was delivered in 2 L of 0.9% NaCl through a Tenckhoff catheter with or without a Port-a-Cath system every 28 days for one to nine cycles. Myelosuppression was dose-related and leukopenia was dose-limiting. The maximum tolerated dose was 120 mg of cisplatin/m2 and 20 mg of melphalan/m2. With the exception of treatment-induced nausea and vomiting, nonhematologic toxic effects were mild and no (or very little) local toxicity occurred. Pharmacokinetic analyses showed that the areas under the peritoneal concentration versus time curve averaged 16-fold and 17-fold more than the area under the plasma curve for cisplatin and melphalan, respectively. Objective responses were documented by third-look laparotomy in ovarian cancer patients with minimal (less than 2 cm) residual disease.
The marrow myeloid precursor cells of a haematologically normal patient were labelled by intravenous injection of tritiated thymidine. Young labdled segmented neutrophils were then released from the marrow into the blood by an injection of cortisol. These PMN had a significantly lower LAP activity than the older blood neutrophils. It is shown that within the morphologic boundaries of the segmented PMN, the cells are still in different stages of cytoplasmic maturation. In addition, labelled and unlabelled neutrophils showed a linear and parallel increase of LAP activity during the 24 h following cortisol injection. This observation suggests that the neutrophil prematurely released in the blood can mature into normal LAP-PMN and more generally that LAP activity of a blood neutrophil increases with time.
This paper describes clinical findings in subjects heterozygous for hemoglobin C and in compound heterozygotes SC. Most of our patients were coming from lands bordering the Guinea Gulf, on the inside of the loop made by the river Niger and from Haiti, which was populated by African slaves coming mainly from the Golden Coast (actually Ghana). Heterozygotes are asymptomatic and do not suffer from anemia. Age at diagnosis is higher than for SCA, although one of our cases was diagnosed at age one. Overwhelming infections or major anemia were not observed. Basal hemolysis remained moderate. HbF levels were not increased as they may be in sickle cell anemia. Splenomegaly was observed in 2/5 patients. Among severe complications we encountered, we must mention one case of foetal death, one tibial infarct, one case of pure red cell aplasia caused by parvovirus B19 infection, and one case of proliferative retinopathy.
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