Usefulness of serum concentration measurement for acute pentobarbital intoxication in patients.

Toxicokinetic parameters were analyzed in 25 patients who were acutely intoxicated with pentobarbital. The serum pentobarbital concentrations were at hypnotic / therapeutic levels (1- 10 microg/mL) in 11 patients, at toxic levels (10-24 microg/mL) in 10 patients, and at lethal levels (>24 microg/mL) in 4 patients. One fatal case was encountered with a serum pentobarbital concentration of 37.27 microg/ mL. The relationships between serum pentobarbital concentrations and the drug, the induced toxic symptoms, such as respiratory / cardiac depression and hypotension, were in good correlation. The therapy of direct hemoperfusion carried out for many pentobarbital-intoxicated patients was highly effective.

[Serum fenitrothion concentration and toxic symptom in acute intoxication patients].

The serum drug concentrations were measured by HPLC or GC/MS in 15 patients of acute fenitrothion (MEP), an organophosphorus insecticide, intoxication. There was no fatal case. The patients were admitted 0.5 approximately 12 hours after the ingestion of 5 approximately 50g MEP. The range of serum MEP concentrations were from undetectable level (< 0.01 microg/mL) to 9.73 microg/mL. Toxic symptoms were correlated with the serum MEP levels. About < 7 microg/mL of the serum MEP levels associated with mild cases and about > 7 microg/mL associated with serious cases. The elimination curves in mild cases were successfully simulated by the one-compartment model and the elimination half-lives (T1/2) were 9.9 +/- 7.7hr (mean +/- S.D.). The serum MEP concentrations declined below the detectable level in 48hr. The elimination curves in two serious cases were successfully simulated by the two-compartment model. The T1/2 in the alpha phase were 5.3hr and 6.7hr (under the direct hemoperfusion), and the T1/2 in the beta phase were 35hr and 52hr. The serum MEP concentrations declined below the detectable level in 300hr.

[Pharmacokinetics of bromazepam in 57 patients with acute drug intoxication].

Pharmacokinetic parameters of bromazepam were analyzed by 57 cases. The patients were admitted 7.3 +/- 8.9 hours (mean +/- S.D.) after ingestion of 88 +/- 127 mg bromazepam. Most patients had taken several drugs other than bromazepam and the number was 5.5 +/- 2.6 drugs. The serum bromazepam levels were 1,871 +/- 2,428 ng/ml and the elimination half-lives were 29 +/- 4 hours. Increased serum bromazepam levels were followed by extended elimination half-lives. There was no bromazepam toxic sign under 2,300 ng/ml. One case was treated with direct hemoperfusion and the therapy was effective.

[Serum and urine total arsenic concentration in a case of acute arsenic intoxication].

The 68-year-old man took arsenic pasta 1 g (arsenic trioxide 0.45 g) to commit suicide and was admitted 16 hours after ingestion. He developed vomiting and coma, followed by pancytopenia. He was treated with activated charcoal, laxative, dimercaprol, sodium thiosulfate and direct hemoperfusion with good recovery. Total arsenic concentrations in serum and urine were 39 ng/ml and 89 ng/ml on admission, respectively. Urine arsenic concentration showed the second peak around 48 hours after admission.

[A case of fluvoxamine overdose].

Selective serotonin reuptake inhibitors (SSRI) are newly developed-antidepressants authorized in 1999 in Japan. We experienced a case of drug poisoning including fluvoxamine, one of SSRI. A comatose nineteen-year-old girl was transported to our ER in the morning on July 25, 2000. There remained many empty packages of fluvoxamine and several sorts of tranquilizers in the room. Her consciousness became alert over the next morning. HPLC analysis revealed fluvoxamine, chlorpromazine, promethazine, biperiden, phenobarbital, and zopiclone in her blood and that serum concentrations of the first three were above the therapeutic ranges. The peak values of fluvoxamine, chlorpromazine, and promethazine were 1,343 ng/ml (6.7 times of the upper limit), 861 ng/ml (2 times), and 529 ng/ml (1.3 times), respectively. Fluvoxamine must be a main cause of her toxic symptoms although other CNS-depressing drugs might work jointly.