A simple, rapid and highly sensitive high-performance liquid chromatographic method with fluorescence detection for determining the enantiomers of methamphetamine and its major metabolites, amphetamine and p-hydroxymethamphetamine, in urine samples was developed. Using a newly developed reagent for amines, namely, 4-(4,5-diphenyl-1H-imidazol-2-yl)benzoyl chloride, six enantiomers were derivatized under mild conditions (i.e., 10 min at room temperature, pH 9.0) and separated isocratically on a cellulose tris(3,5-dimethylphenylcarbamate) coated silica gel column following a pre-separation on an ODS column within 42 min, and the effluent was monitored at 440 nm (lambda ex 330 nm). Calibration curves for these derivatives using spiked human urine were linear in the range 0.05-100 mumol dm-3 with correlation coefficients > or = 0.999. The detection limits at a signal-to-noise ratio of 3 were 2.8-8.8 fmol per 5 microliters injection. The relative standard deviations of within- (n = 6) and between-day (n = 5) variations were < or = 7.4%. The method was successfully applied to discriminate between (S)-(+)-methamphetamine and its corresponding metabolites found in abusers' urine and their antipodes in a sample taken from a Parkinsonian patient on selegiline (Deprenyl) therapy.
lucinations that consisted of vivid recollections of his old jobs. He described transient episodes in which he saw and dyed clothes, talked of town affairs with his friends, and obeyed his employer's instructions. He had experienced similar events about 50 years ago in his first job. Other scenes were related to his last job. He felt that each episode lasted about five minutes and was convinced the hallucinations were real while they were happening. The hallucinations arose involuntarily in objective space. They were normally coloured and encompassed the whole visual field. There were no diurnal fluctuations in the appearance of the hallucinations.The following laboratory investigations and analysis of CSF were normal: CBC, routine blood chemistry, antinuclear antibody, VDRL, triglycerides, cholesterol, vitamin B1,, T4 and T, resin uptake, thyroid-stimulating hormone (TSH), and arterial blood gases. An EEG when the patient was hallucinating demonstrated diffuse slow waves at 5 to 7 Hz with bifrontal intermittent delta waves. An EEG when the spells were not occurring showed similar findings.CT three days after onset showed a small, low density area in the central part of the right thalamus. CT 14 days after onset showed no lesion, but one month after onset the small, low density area reappeared in the same position, indicating a CT fogging effect.6The hallucinations slowly resolved over a two week period, although morphine sulphate (60 mg/day) was continued. At the end of this time, hallucinations were shorter and simpler. He frequently reported that he saw a dish of sweet potatoes on the table near his bedside or a cigarette between his fingers: they disappeared in a few seconds. He had often eaten sweet potatoes one month before the occurrence of hallucinosis and was a heavy smoker. These hallucinations developed when he was sitting on a chair or resting in bed without falling asleep. He was left without memory impairment or any other neurological deficits.Two months later, the patient died. Postmortem examination disclosed widespread carcinomatosis with involvement of both lungs, mediastinal nodes, liver, and left kidney. Small polypoidal growths were found on the mitral valve. The tumour histology revealed squamous carcinoma. The brain showed mild atherosclerosis. It was fixed in formalin and sliced serially.
The patient (case 1) was a 72 year old female with multiinfarct dementia. Four months before our examination she had been started on a regimen of calcium hopantenate therapy (37 mg/kg/&). One day before the examination, with no prodromal symptoms, she developed severe nausea and vomiting, and then became stuporous. On examination her vital signs were as follows: temperature 35 6°C; pulse, 96 beats/min, respiration, 36/min, and BP, 160/70mmHg. She was deeply comatose and unresponsive to noxious stimuli. Pupils were small and reactive to light. Her upper limbs were flaccid and her lower limbs were spastic in flexion, a condition present since the age of 70 years. Deep tendon reflexes were brisk in all four extremities. Hepatosplenomegaly was not observed.Laboratory values at the time of coma included: arterial pH, 704; PaCO2, 12 mmHg; PaO2, 152 mmHg; HC03 , 5 mmol/l; base excess, -22 mmol/l; blood glucose,
ABSTRACT— In Japan, acute encephalopathy with hepatic steatosis resembling Reye's syndrome has been reported to occur after treatment with the pantothenic acid antagonist, calcium hopantenate. We studied the causal relationship and the pathogenesis in dogs. The agent was administered to seven dogs at increasing doses over a period of 8 weeks. Anorexia, vomiting, and diarrhea were common clinical findings. In four dogs, coma suddenly developed after the appearance of gastrointestinal signs. Three animals died during periods when they were not under direct observation. The effects of the agent appear to be related to dose. Laboratory findings representing significant changes at the time of coma included hypoglycemia, leukocytosis, hyperammonemia, hyperlactatemia, and elevated levels of serum transaminases. Microvesicular hepatic steatosis and mitochondrial abnormalities were consistent pathological findings. The hepatic mitochondria were enlarged and characterized by an increased number of cristae and the presence of crystalloid inclusions. In a second group of four dogs, pantothenic acid was given in addition to and in the same amount as calcium hopantenate at increasing doses over a period of 8 weeks. All four dogs survived the 8 weeks and only one developed mild anorexia. No significant biochemical changes were found and neither hepatic steatosis nor mitochondrial abnormalities were observed. The addition of pantothenic acid prevented the development of the disorder in the four animals. These results show that calcium hopantenate produces acute encephalopathy with hepatic steatosis in dogs, by inducing a deficiency of pantothenic acid. The hepatic mitochondrial changes of this reaction differ from those of Reye's syndrome.
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