Intraventricular etoposide safety and toxicity profile in children and young adults with refractory or recurrent malignant brain tumors.

Systemic administration of etoposide is effective in treating metastatic, recurrent or refractory brain tumors, but penetration into the cerebrospinal fluid is extremely poor. This study was designed to determine the safety and toxicity profile of intraventricular etoposide administration and was affiliated with the prospective, multicenter, nonblinded, nonrandomized, multi-armed HIT-REZ-97 trial. The study enrolled 68 patients, aged 1.1-34.6 (median age 11 years). Adverse events that could possibly be related to intraventricular etoposide therapy were documented and analyzed. Intraventricular etoposide was simultaneously administered with either oral or intravenous chemotherapy in 426 courses according to three major schedules varying in dosing (0.25-1 mg), frequency of administration (bolus injection, every 12 or 24 h), course duration (5-10 days) and length of interval between courses (2-5 weeks). Potential treatment-related adverse effects included transient headache, seizures, infection of the reservoir, nausea and neuropsychological symptoms. Hematological side effects were not observed. One patient, with history of multiple prior therapies, who received long-term intraventricular and oral etoposide treatment developed acute myeloid leukemia as a secondary malignancy. Overall intraventricular etoposide is well tolerated. The results of this study have warranted a phase II trial to determine the effectiveness of this regimen in disease stages with very limited therapeutic options.

Pleural effusion: beta-trace protein in diagnosing ventriculoperitoneal shunt complications.

Catheter dysfunction is a common complication with ventriculoperitoneal shunts. Apart from infection, obstruction, and leakage, migration of the shunt tip may cause particular problems. Pleural effusion is easily classified as a shunt complication if a transdiaphragmatic migration of a shunt can be demonstrated. If, however, the tip of the shunt is found adjacent to the diaphragm, it is difficult to decide if the effusion is caused by the ventriculoperitoneal shunt. Different diagnostic methods can be used in this situation. Below we report a case of pleural effusion-without shunt migration-which was revealed to be a shunt complication by quantifying beta-trace protein in the effusion.