Interventional oncology in the elderly: complications and early response in liver and kidney malignancies.

OBJECTIVES: The complication rate, loco-regional responses and length of hospital stay were analyzed in patients with liver and kidney cancer older than 70years treated with interventional oncology procedures. The findings from the older population were compared with the younger patients (<70years) to detect any difference not related to chance. MATERIALS AND METHODS: Prospectively collected data on patients who underwent hepatic artery embolization (with or without radiofrequency ablation) and kidney radiofrequency ablation were retrospectively analyzed. Complication rates, loco-regional responses and length of hospital stay for patients older and younger than 70 were compared. RESULTS: 163 patients were treated, 66 (40.5%) older and 97 (59.5%) younger than 70years. The complication rate in patients older than 70 was 4.5% (3/66 pts) versus 3.1% (3/97 pts) (p=0.69) in the younger age-group. The complication rates for the liver embolization group, liver embolization plus radiofrequency and kidney radiofrequency group were 2/90 pts (2.2%), 2/42 pts (4.8%) and 2/31 pts (6.5%), respectively (p=0.46). Median hospital stay was three nights in both older and younger patients. Response rates were not significantly influenced by age. CONCLUSION: Liver embolization with or without radiofrequency and renal radiofrequency are safe and effective in older patients. Age alone should not be considered a contraindication to treatment in carefully selected patients.

Surgical 'damage control' treatment of a large retroperitoneal liposarcoma encasing a horseshoe kidney.

Damage control is a surgical strategy for severely compromised trauma patients based on speed control of life-threatening injuries that aims to rapidly resuscitate patients in an intensive care unit (ICU). We report on the use of such therapeutic strategy in a patient affected by a retroperitoneal sarcoma concomitant to a horseshoe kidney, a relatively rare anatomical malformation.

Norepinephrine modulates seizures induced by quinolinic acid in rats: selective and distinct roles of alpha-adrenoceptor subtypes.

We investigated in rats whether alterations in noradrenergic function caused by 6-hydroxydopamine or alpha- and beta-adrenoceptor agonists and antagonists would modify the susceptibility of the brain to electroencephalographic seizures induced by intrahippocampal infusion of quinolinic acid. 6-Hydroxydopamine depletion of norepinephrine facilitated the expression of seizures while alpha-adrenoceptor stimulation by clonidine had either proconvulsant (0.1 mg/kg) or anticonvulsant (from 0.5 to 2 mg/kg) effects. Clonidine's anticonvulsant activity (0.5 mg/kg) was mimicked by methoxamine given intrahippocampally (10 micrograms), and antagonized by prazosin (1 mg/kg), whereas both yohimbine (5 and 10 mg/kg) and piperoxane (5 mg/kg) had no significant effect. Seizure facilitation induced by clonidine (0.1 mg/kg) was blocked by yohimbine (10 mg/kg). Systemic (0.25 and 0.5 mg/kg) or intrahippocampal (10 and 20 micrograms) isoproterenol and propranolol (10 mg/kg) had no effect. Spiking activity and neurotoxicity induced by quinolinic acid were unaltered by treatments which protected against convulsions. Modulation of quinolinic acid-convulsive activity by alpha-adrenoceptor subtypes appears to be selective and complex, since alpha 1-type activation reduces seizures while alpha 2-type stimulation has proconvulsant effects.

Anticonvulsant drugs effective against human temporal lobe epilepsy prevent seizures but not neurotoxicity induced in rats by quinolinic acid: electroencephalographic, behavioral and histological assessments.

Intrahippocampal injection of quinolinic acid (QUIN) in rats caused an epileptic-like syndrome reminiscent of human temporal lobe epilepsy. By electroencephalographic (EEG) analysis, the authors assessed whether QUIN seizures were responsive to anticonvulsants effective in the treatment of the human disease. Anticonvulsants used in clinical practice to control partial seizures, such as carbamazepine, diphenylhydantoin, sodium phenobarbital, sodium valproate and diazepam, prevented QUIN-induced EEG seizures, whereas ethosuximide, which is specifically used to control absence attacks, and chlorpromazine, a sedative with no anticonvulsant properties, were ineffective. QUIN seizures showed particular sensitivity to carbamazepine (5 mg/kg) but were resistant to diphenylhydantoin unless a relatively high dose was used (100 mg/kg). None of the effective anticonvulsants completely suppressed EEG paroxysmal events like spikes and fast activity. Animals injected with QUIN displayed chewing, sniffing and rearing; no clear correlation was found between the ability of drugs to prevent QUIN-induced EEG seizures and effects on stereotypies, suggesting that these behavioral signs are not sensitive measures of anticonvulsant activity in this model. The anticonvulsants that protected animals from QUIN seizures did not prevent nerve cell degeneration induced by the excitotoxin, thus indicating that nerve cell death can occur even in the absence of sustained seizure activity. The data show that, in this animal model of epilepsy, the EEG seizure activity is specifically sensitive to anticonvulsants effective in partial epilepsy, thus suggesting that it could be used to test potential new drugs for this human disorder.