Polidocanol sclerotherapy for multiple gastrointestinal hemangiomas: A case report.

BACKGROUND: Gastrointestinal (GI) hemangioma has a low incidence among systemic hemangiomas, and some GI hemangiomas occur in the intestine, stomach, and esophagus. Polidocanol has been increasingly used in sclerotherapy. However, this paper reports that minimally invasive treatment of multiple hemangiomas with large diameters can achieve satisfactory results by multipoint injection. CASE SUMMARY: A 46-year-old female patient was hospitalized in another hospital for cough. We accidentally found thickening of the lower esophagus by chest computed tomography. The patient was eventually diagnosed with multiple GI hemangiomas and underwent a series of examinations including esophagogastroduodenoscopy (EGD), endoscopic ultrasound, and magnetic resonance imaging. We calculated the dose of polidocanol according to the volumes of the hemangiomas, fixed the target vein with the help of a transparent cap, and then administered polidocanol via multipoint injection into the hemangiomas under endoscopic guidance. EGD and endoscopic ultrasound showed that the hemangiomas disappeared. The color of the esophageal mucosa returned to normal 1 mo after sclerotherapy. CONCLUSION: Sclerotherapy may be a safe and effective method for treating multiple hemangiomas of the alimentary canal.

Influence of glibenclamide on outcome in patients with type 2 diabetes and traumatic brain injury.

BACKGROUND AND PURPOSE: The influence of sulfonylurea receptor 1 (SUR1) and its inhibitor glibenclamide on progressive secondary hemorrhage (PSH), progressive hemorrhagic necrosis (PHN), and brain edema has been studied in rat models of traumatic brain injury (TBI) and ischemia. These studies indicate that blocking SUR1 may exert protective effects in terms of outcome. METHODS: We discuss the effects of glibenclamide on outcome in patients with type 2 diabetes mellitus and TBI. We collected demographic, clinical, and imaging data from the clinical records of TBI patients with type 2 diabetes who were admitted to the neurosurgery department at Shanghai 6th People's Hospital between 2001 and 2012. Data from patients who met the inclusion criteria were analyzed. Patients were divided into glibenclamide group and insulin group. RESULTS: Of 70 patients fit criteria for inclusion, no significant difference was observed except for age and fasting plasma glucose between the two groups. Outcome indicators, including GCS discharge, GOS discharge, length of study in hospital (LOS-H), and the presence of PSH showed no significant difference too (p>0.05), except for length of stay in neuro-intensive care unit (LOS-NICU) (p<0.05). Age, hours between the initial CT scan and the injury (HCT1) and GCS at admission were observed as factors associated with PSH after logistic regression. CONCLUSIONS: In general, the use of glibenclamide to control plasma glucose after TBI had no significant effect on patient outcome at discharge but it could reduce the LOS-NICU (p<0.05). Glibenclamide also had no apparent effect on the presence of PSH in TBI patients with type 2 diabetes mellitus.

Dose-dependent protective effect of bisperoxovanadium against acute cerebral ischemia in a rat model of ischemia/reperfusion injury.

PTEN (phosphatase and tensin homologue deleted on chromosome 10) is a dual-specificity lipid and protein phosphatase. The loss of PTEN was originally discovered in numerous human cancers. PTEN inhibition by bisperoxovanadium (bpV) reduces neurological damage after ischemic brain injury. The purpose of this study was to identify the optimal neuroprotective dose of bpV when administrated after focal ischemia/reperfusion (I/R) injury in rats. Focal I/R injury was induced using the middle cerebral artery occlusion method. bpV at doses of 0.25, 0.50 and 1.0 mg/kg were injected intraperitoneally just after reperfusion, with saline serving as a vehicle control. A maximal reduction in brain injury was observed with 1.0 mg/kg bpV. This dose of bpV also significantly blocked apoptosis in the penumbral cortex of rats. This beneficial effect was associated with the increasing levels of Akt phosphorylation in the penumbral cortex. These results demonstrate that the pharmacological inhibition of PTEN protects against I/R injury in a dose-dependent manner and the protective effect might be induced through upregulation of the phosphoinositide-3 kinase/Akt pro-survival pathway, suggesting a new therapeutic strategy to combat ischemic brain injury.