[A Case of Encapsulated Peritoneal Sclerosis Associated with a Ventriculo-Peritoneal Shunt].

We experienced a case of encapsulated peritoneal sclerosis(EPS)that developed as a result of peritoneal deterioration induced by ventriculo-peritoneal(VP)shunting. The patient was a 48-year-old man who underwent VP shunting five times since 1 month of age. Six months after the last operation, abdominal symptoms developed and the patient was hospitalized. A localized cyst was recognized in the left upper abdomen, and we diagnosed him with a cerebrospinal fluid pseudocyst. Soon, a shunt tube translocation was performed to another portion of the abdominal cavity, but a new short-term cyst appeared. During laparotomy, the inner surface of the abdominal cavity was very strong due to adhesions and the peritoneum was thickened. A large portion of the intestines and the mesentery was covered with a translucent film-like substance. Afterward, an ileus developed and he was diagnosed with EPS intraoperatively. We judged that an additional VP shunt was impossible, so a ventriculo-atrial shunt was placed. Afterward, his symptoms disappeared and the EPS improved. Although a few similar reports exist, this condition is thought to be extremely rare. Clinicians should recognize EPS as a complication of VP shunting.

In vitro growth suppression of human glioma cells by a 16-mer oligopeptide: a potential new treatment modality for malignant glioma.

Fibroblast growth factor-2 (FGF-2) is involved as an autocrine growth factor in the autonomous proliferation of glioma cells. To develop a new strategy for treating patients with glioma, we studied the effect on human glioma cells of a 16-mer oligopeptide with conformational similarity to the putative receptor-binding domain of FGF-2. A synthesized oligonucleotide was assessed its receptor-binding activity by BIAcore instrument. Its biological effect on glioma cell lines was examined in vitro by MTT assay. The peptide suppressed the in vitro growth of human glioma cells U87MG, T98G and U251MG cells, but not of A431 cells whose growth is not dependent on FGF-2. Apoptotic bodies were noted after 24-h incubation in the presence of the peptide; Ac-YVAD-CHO, a caspase-3 inhibitor, suppressed apoptosis. Furthermore, we examined the modulation of the cytotoxic effect of anticancer drugs by the oligopeptide. The addition of this oligopeptide to the chemotherapeutic agents CDDP, ACNU and VP16 had additive effects in vitro. These results suggest that the pathway of the FGF-2 autocrine loop through the FGF receptor plays an important role in the proliferation of glioma cells. New drugs targeting this loop may be highly effective in treating FGF-2-dependent tumors. Our results suggest that its addition to the therapeutic arsenal may lead to improved treatment regimens for patients with FGF-2-dependent tumors.

Effects of combination chemotherapy with biscoclaurine-derived alkaloid (Cepharanthine) and nimustine hydrochloride on malignant glioma cell lines.

In the treatment of malignant glioma, chemotherapy plays a critical role as do surgical resection and irradiation. Cepharanthine (CEP), a biscoclaurine-derived alkaloid, reportedly potentiates the effects of antitumor agents and induces apoptosis in some cancer cells. Here, we examined the effects of CEP, alone and in combination with nimustine hydrochloride (ACNU), on the in vitro proliferation of malignant glioma cells. The cell lines used were U87MG, U251MG, and T98G. At concentrations from 1 to 10 microg/ml, CEP-promoted cell proliferation somewhat; growth inhibition was noted at concentrations of 15 microg/ml and higher. Phase-contrast microscopy showed that cells tended to detach from the culture dishes and that cell density became sparse at the higher concentrations. DAPI fluorescence nuclear staining revealed condensation and fragmentation of nuclei, indicating the induction of apoptosis. To examine the cascade of apoptosis, the caspase inhibitors YVAD and DEVD were added. They inhibited CEP-induced apoptosis in U251MG cells (a p53-mutant cell line), but not in U87MG cells (a p53 wild-type cell line), suggesting that in CEP-induced apoptosis two possible cascades are in play. In combination with ACNU, the effects of the higher concentrations of CEP were enhanced.