Brachytherapy as an Adjuvant for Recurrent Atypical and Malignant Meningiomas.

BACKGROUND: Recurrent atypical and malignant meningiomas have poor outcomes with surgical therapy alone. Neither adjuvant chemotherapy nor postoperative radiation therapy remedies this problem. OBJECTIVE: To evaluate our experience with the treatment of 15 patients treated with I-125 or Cs-131 brachytherapy radiation seeds as an adjuvant in these difficult cases. METHODS: Patients with high-grade recurrent meningioma who underwent resection and intraoperative placement of brachytherapy seeds at our institution from 2002 to 2014 were identified and studied by retrospective chart review. RESULTS: Fifteen patients with median age of 68.8 yr were treated with I-125 (n = 13) or Cs-131 (n = 2) brachytherapy seeds for cases of recurrent, grade II (n = 8), or grade III (n = 7) meningioma at our institution from 2002 to 2014. These lesions originated from a variety of locations including, convexity (3), falcine (3), frontal (2), occipital (1), parietal (2), 2 sphenoid wing (2), and temporal (2), based recurrent meningiomas. Patients had a median of 2 prior open surgical interventions and received local radiation therapy with a median dose of 55 Gy prior to brachytherapy. Survival at 2.5 yr was 56% for grade II and 17% for grade III lesions. Survival was significantly associated with patient age but not tumoral pathology. Forty percent of patients required reoperations for wound complications following brachytherapy. CONCLUSION: Brachytherapy with implantation of permanent radiation seeds provides a viable alternative treatment for recurrent meningioma while carrying a significant clinical risk of wound infection and need for reoperation.

Left Thalamus Arteriovenous Malformation Secondary to Radiation Therapy of Original Vermian Arteriovenous Malformation: Case Report.

A 70-year-old gentleman with history of hypothyroidism, hyperlipidemia, hypertension, and right superior cerebellar aneurysm presented to the neurosurgery service in 2008 with vertigo. Diagnostic cerebral angiography performed that year demonstrated a vermian arteriovenous malformations (AVM). The patient underwent stereotactic proton beam radiosurgery, which resulted in a decrease in flow and size of the lesion, and the patient was lost to follow-up. Now at the age of 80, the patient presented with acute gait instability. Cerebral angiogram demonstrated his stable vermian AVM and a new 1.1 cm AVM nidus in the region of the left posterior thalamus. Although AVMs are often described as congenital lesions, there is a growing body of literature suggesting that AVMs can grow, spontaneously regress, and even arise de novo in response to some insult. Understanding what leads to the growth, remodeling, regression, and hemorrhage of AVMs is crucial in order to better direct therapeutic endeavors. We would argue that this patient's AVM is secondary to endothelial cell damage from radiation therapy. Radiation can cause endothelial cell injury and upregulation of factors, such as vascular endothelial growth factor and transforming growth factor beta expression, which are implicated in AVM development pathways. We believe that this patient's new AVM is secondary to entrance radiation dosing affecting the thalamus during radiation therapy for the original vermian AVM.

Oral feeding acutely down-regulates serum PTH in hemodialysis patients.

BACKGROUND: Changes in serum parathyroid hormone (PTH) within minutes are known only to be mediated by changes in ionized calcium. Recent animal studies show ingestion of a low phosphorus meal can lower serum PTH within 15 min, before changes in serum ionized calcium or phosphorus occur, suggesting a rapid gastrointestinal signal may regulate PTH. METHODS: Eight hemodialysis patients with secondary hyperparathyroidism were admitted twice to a metabolic unit and ate a high and low phosphorus meal after an overnight fast. Serum PTH, total and ionized calcium, phosphorus, pH, and glucose were measured at 0, 15, 30, 60, 120 and 240 min. In the second protocol, we examined the possible role of volume or glucose changes in rapid PTH suppression by administering intravenous saline and glucose after an overnight fast to 6 patients, with similar testing. RESULTS: Intact PTH decreased 24% from 419 +/- 331 at baseline to 312 +/- 221 pg/ml (p = 0.002) 15 min after a meal. Total and ionized calcium and pH did not change, glucose rose by 15 min, and phosphorus changed only after 60-90 min. During the second protocol, saline and glucose infusions failed to change PTH. CONCLUSIONS: In dialysis patients, a glucose-containing meal, with or without phosphorus, rapidly suppresses serum PTH approximately 25% within 15 min. This effect is not mediated by changes in ionized calcium, phosphorus, pH, glucose, or insulin. These data suggest there may be an as yet unknown enteral signal that rapidly suppresses PTH.