ported in 4 (5%) and 8 (10%) patients, respectively. Reason for drug discontinuation was not specified in 11 (14%) patients.Discussion. Aripiprazole was generally well tolerated, with a treatment continuation rate of 71% in this inpatient psychiatric setting. Adverse effects were reported as the reason for drug discontinuation in only 5% of patients. This reported rate may be an underestimate since the reason for drug discontinuation was not recorded in the discharge summaries of 11 patients. Despite this shortcoming, it is important to determine whether continuation rates observed in controlled clinical trials can be achieved in real-world settings. The rate of drug discontinuation due to adverse effects observed in this naturalistic setting was consistent with that described in prospective studies (7-11%). 3,4This evaluation provides some additional insight on dosing of aripiprazole in a real-world setting. In general, lower doses are being prescribed for children in our setting. Appropriate dosing in children has not been clearly delineated, and weight-based dosing has been proposed. In a case report by Davenport et al., 5 treatment initiation with a standard adult dose of 15 mg caused excessive sedation in a 9-year-old patient. It is evident that more research should be conducted to determine optimal dosing in children.

Cisplatin, an effective antineoplastic agent, frequently induces acute renal failure in animals and humans. Hyperbaric oxygen (HBO) has been shown to prevent cisplatin-induced nephrotoxicity in rats. This study investigated the effect of two different HBO regimes on renal functions, oxidative stress, and histopathological changes in rat kidneys after cisplatin treatment. Wistar rats were divided into five groups: control, HBO, cisplatin, cisplatin plus once daily HBO, and cisplatin plus twice daily HBO. Cisplatin was given as a single intraperitoneal dose of 6 mg/kg, and HBO was applied for 60 min at 2.5 atm for six days. HBO alone did not alter any biochemical parameters or histopathological findings compared with the control group. Cisplatin increased serum urea and creatinine levels and caused severe histopathological injury. In addition, cisplatin increased lipid peroxidation and impaired superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in kidney tissue. Once daily HBO after cisplatin treatment slightly reduced serum urea and creatinine levels and attenuated histopathological injury. HBO also reduced lipid peroxidation and increased SOD and GSH-Px activities significantly. Although twice daily HBO was determined to be more effective than once daily HBO on oxidative stress parameters, it increased serum creatinine levels and histopathological injury compared with the cisplatin group. It was concluded that HBO alone does not induce nephrotoxicity and oxidative stress in rat kidneys; once daily HBO may prevent cisplatin-induced nephrotoxicity, an effect that is partially mediated by the modification

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The explosive RDX (hexogen, cyclonite) is usually used for the production of C-4 explosive. The rare occurrence of accidental and intentional RDX intoxications has been reported during manufacturing process or in wartime. In this article, the authors report 5 cases of accidental oral RDX poisoning. On admission, observed signs and symptoms included repetitive generalized tonic-clonic convulsions, postictal coma, lethargy, confusion, hyperreflexia, postictal amnesia, nausea, vomiting, abdominal tenderness, sinusal tachycardia, dysrhythmia with frequent ventricular premature beats, generalized muscle spasms, and myoclonus. Leukocytosis, mild anemia, methemoglobinemia, elevated levels of blood glucose, serum aspartate transaminase, alanine transaminase, lactic dehydrogenase, creatine phosphokinase, amilase, hypokalemia, metabolic acidosis, proteinuria, glucosuria, and myoglobinuria were also noted. Plasma RDX concentrations were 268 to 969 ng/mL at 3 hours of ingestion. For management, supportive and symptomatic measures were taken. Whole-bowel irrigation might have been an effective therapeutic procedure due to probable slow gastrointestinal absorption of RDX. Three patients who developed severe metabolic acidosis underwent urgent hemodialysis. All patients were discharged 7 to 21 days after admission without any sequelae. Plasma RDX levels were strongly correlated with the clinical and laboratory manifestations. The available toxicological data on this rare accidental poisoning are reviewed in light of the literature.

Objective: Renal ischemia/reperfusion (I/R) injury occurs in both native and transplanted kidneys. Hyperbaric oxygen (HBO) has been shown to prevent I/R injury in different tissues. The aim of this study was to evaluate the effect of HBO on renal I/R injury in rats. Materials and Methods: Sprague-Dawley rats were randomly assigned to one of three groups. The Control group (n = 6) received right nephrectomy. The I/R (n = 6) and I/R+HBO groups (n = 6) received 30 min left renal ischemia followed by 24 h of reperfusion after right nephrectomy. The I/R+HBO group (n = 6) received additional HBO therapy for 60 min at 2.5 absolute atmospheres starting at the initial 15th minute of reperfusion. Results: In the I/R group, blood urea nitrogen (BUN) and creatinine levels increased significantly compared with the Control and I/R+HBO groups (p < 0.05). BUN and creatinine levels were similar in the Control and I/R+HBO groups. Kidney samples from I/R group rats revealed severe tubular damage and neutrophil infiltration at histopathological examination. The animals treated with HBO showed markedly improved lesions and less neutrophil infiltration compared with the I/R group (p < 0.05). Conclusions: HBO exhibited marked protection against I/R injury in this study as measured using BUN and creatinine levels and renal histopathology. However, further studies are needed to clarify the renoprotective effect of HBO on I/R injury.