Hyponatremia is often seen after transsphenoidal surgery and is a source of considerable economic burden and patient-related morbidity and mortality. We performed a retrospective review of 344 patients who underwent transsphenoidal surgery at our institution between 2006 and 2012. Postoperative hyponatremia was seen in 18.0% of patients at a mean of 3.9 days postoperatively. Hyponatremia was most commonly mild (51.6%) and clinically asymptomatic (93.8%). SIADH was the primary cause of hyponatremia in the majority of cases (n = 44, 71.0%), followed by cerebral salt wasting (n = 15, 24.2%) and desmopressin over-administration (n = 3, 4.8%). The incidence of postoperative hyponatremia was significantly higher in patients with cardiac, renal and/or thyroid disease (p = 0.0034, Objective Risk (OR) = 2.60) and in female patients (p = 0.011, OR = 2.18) or patients undergoing post-operative cerebrospinal fluid drainage (p = 0.0006). Treatment with hypertonic saline (OR = −2.4, p = 0.10) and sodium chloride tablets (OR = −1.57, p = 0.45) was associated with a non-significant trend toward faster resolution of hyponatremia. The use of fluid restriction and diuretics should be de-emphasized in the treatment of post-transsphenoidal hyponatremia, as they have not been shown to significantly alter the time-course to the restoration of sodium balance.

Pituitary dysfunction following traumatic brain injury (TBI) is significant and rarely considered by clinicians. This topic has received much more attention in the last decade. The incidence of post TBI anterior pituitary dysfunction is around 30% acutely, and declines to around 20% by one year. Growth hormone and gonadotrophic hormones are the most common deficiencies seen after traumatic brain injury, but also the most likely to spontaneously recover. The majority of deficiencies present within the first year, but extreme delayed presentation has been reported. Information on posterior pituitary dysfunction is less reliable ranging from 3%–40% incidence but prospective data suggests a rate around 5%. The mechanism, risk factors, natural history, and long-term effect of treatment are poorly defined in the literature and limited by a lack of standardization. Post TBI pituitary dysfunction is an entity to recognize with significant clinical relevance. Secondary hypoadrenalism, hypothyroidism and central diabetes insipidus should be treated acutely while deficiencies in growth and gonadotrophic hormones should be initially observed.

Background: Glioblastoma (GBM) can use metabolic fuels other than glucose (Glc). The ability of GBM to use galactose (Gal) as a fuel via the Leloir pathway is investigated. Methods: Gene transcript data were accessed to determine the association between expression of genes of the Leloir pathway and patient outcomes. Growth studies were performed on five primary patient-derived GBM cultures using Glc-free media supplemented with Gal. The role of Glut3/Glut14 in sugar import was investigated using antibody inhibition of hexose transport. A specific inhibitor of GALK1 (Cpd36) was used to inhibit Gal catabolism. Gal metabolism was examined using proton, carbon and phosphorous NMR spectroscopy, with ¹³C-labeled Glc and Gal as tracers. Results: Data analysis from published databases revealed that elevated levels of mRNA transcripts of SLC2A3 (Glut3), SLC2A14 (Glut14) and key Leloir pathway enzymes correlate with poor patient outcomes. GBM cultures proliferated when grown solely on Gal in Glc-free media and switching Glc-grown GBM cells into Gal-enriched/Glc-free media produced elevated levels of Glut3 and/or Glut14 enzymes. The ¹³C NMR-based metabolic flux analysis demonstrated a fully functional Leloir pathway and elevated pentose phosphate pathway activity for efficient Gal metabolism in GBM cells. Conclusion: Expression of Glut3 and/or Glut14 together with the enzymes of the Leloir pathway allows GBM to transport and metabolize Gal at physiological glucose concentrations, providing GBM cells with an alternate energy source. The presence of this pathway in GBM and its selective targeting may provide new treatment strategies.

Alternating electric field therapy has been approved for glioblastoma (GBM). We have preclinical evidence for anticancer effects in GBM cell cultures and mouse xenografts with an oscillating magnetic field (OMF) generating device. Here we report OMF treatment of end-stage recurrent glioblastoma in a 53-year-old man who had undergone radical surgical excision and chemoradiotherapy, and experimental gene therapy for a left frontal tumor. He experienced tumor recurrence and progressive enlargement with leptomeningeal involvement. OMF for 5 weeks was well tolerated, with 31% reduction of contrast-enhanced tumor volume and reduction in abnormal T2-weighted Fluid-Attenuated Inversion Recovery volume. Tumor shrinkage appeared to correlate with treatment dose. These findings suggest a powerful new noninvasive therapy for glioblastoma.

BACKGROUND. Early results of postoperative fractionated stereotactic radiotherapy (FSRT) for functional and nonfunctional pituitary adenomas appear prom