In a prospective study 50 febrile episodes in severely neutropenic patients (neutrophils less than 500/mm3) were empirically treated with ceftazidime monotherapy. If no response was seen after 48 h, vancomycin was added. After another 72 h period, patients with persisting fever additionally received amphotericin B. In 29 episodes (58%) patients became afebrile with ceftazidime monotherapy. Another seven patients (14%) responded to the addition of vancomycin and five patients (10%) needed amphotericin B to become afebrile. A success of the study drugs without modification was seen in 40 episodes (80%), success with modification in three episodes (6%) and failure in six episodes (12%). One patient died of myocardial infarction. No other death occurred during the two-week observation period after entering the study. Though there were two gram-negative isolates resistant to ceftazidime, these patients were successfully treated with modification. It is concluded that the response-adapted additive sequence of ceftazidime, vancomycin and amphotericin B is an effective approach towards febrile episodes in severely neutropenic patients.

Adolescent↗

PubMedDate not supplied

Tissue factor is the only activator of coagulation in cultured human lung cancer cells.

It is a long-known principle that tumour cells tend to exploit the host's physiologic systems in order to get support in terms of, for example, nutrition, growth or metastasis. One of these physiologic systems is the blood coagulation cascade, which has been found activated in many tumour patients. The mechanisms of the activation of coagulation have been assessed in numerous animal and in vitro experiments, and the results appeared to point to several distinct activators. The present study used a large panel of different cultivated human lung cancer cell lines and experimental systems involving normal plasma, plasmas deficient of factors V, VII or X, purified coagulation factors II and X, recombinant tissue factor (TF), and specific inhibitory antibodies against factor VII and TF. The results provide strong evidence that there is no activator of coagulation besides TF in the wide array of lung cancer cells examined. However, this work reveals a striking variability of TF content among the cell lines. This might explain ambiguous results of clinical trials of anticoagulation as an adjunct to antineoplastic therapy in lung cancer. By sensitive diagnostic tools like the plasma thrombin-antithrombin complex levels it might be possible to select patients with activated coagulation, who might benefit from anticoagulation.

Antibodies↗