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Ethylene glycol (EG), in addition to its neurotoxic and nephrotoxic effects, evokes oxidative stress. The aim of this study was to assess the influence of the ethylene glycol on the biochemical indicators and oxidoreductive balance of patients treated for acute poisoning. The total study group consisted of 56 persons including 26 alcoholics who took EG as a substitute for ethyl alcohol in the course of alcohol dependence syndrome and 30 controls. Severity of poisoning, results of acid-base parameters, biochemical, and toxicological tests as well as biomarkers of the oxidative stress in blood were analyzed during the patients’ hospitalization. The key issue was to assess the oxidative stress and biochemical disturbances caused by EG and the type of treatment applied in the course of poisoning. Significant changes in some parameters were found both at time of diagnosis and after treatment initiation (ethanol as an antidote and hemodialysis). The most important differences included the activity of hepatic parameters (aspartate aminotransferase, AST) and oxidative stress markers like catalase (CAT); correlation of the lipid peroxidation products level (TBARS) with urea concentration has been shown. On the last day of the hospitalization, in some cases, the mutual correlation between the evaluated markers were observed, for example, between alanine transaminase (ALT) and glutathione reductase (GR), and urea concentration and glutathione level (GSH/GSSG). The concentration of ions (H+) had a major impact on the oxidoreductive balance, correlating with the elevated GR and GSH/GSSG levels.

Toxic effects of ethylene glycol (EG) and its metabolites are mainly related to metabolic acidosis and kidney damage. EG biotransformation involving CYP2E1 affects the oxidant-antioxidant balance. The study assessed the effect of repeated administration of 4-methylpyrazole (4MP, 15mg/kg b.w. after 2h, followed by 10mg/kg b.w. every 12h) on renal function (creatinine, urea and urinary protein levels) as well as products of kidney's lipid peroxidation (MDA and TBARS levels) in rats poisoned with EG (5745mg/kg b.w.). Serum EG and glycolic acid (GA) concentrations were measured throughout the experiment. Repeated administration of 4MP reduced the rate of EG elimination, extended the period of EG persistence in serum and significantly limited formation of GA. The study showed the temporary intensification of kidney oxidative processes that correlated with changes in kidney function. It was found that the use of 4MP in EG poisoning inhibited its biotransformation to toxic metabolites, but simultaneously intensified oxidative damages in kidneys.

In addition to designer benzodiazepines such as etizolam, deschloroetizolam, pyrazolam, diclazepam, nifoxipam, or clonazolam, a new psychoactive substance like flubromazolam, triazole of flubromazepam has become available. Flubromazolam is currently not marketed as a medication but rather as a research chemical and recreational drug. It mostly causes sedative effects but also has moderate anti-anxiety and muscle relaxant effects. A case of a severe intoxication of flubromazolam has been reported.A 27-year-old man, presented with deep coma, bilateral pinpoint unreactive pupils, acute respiratory failure and hypotension, complicated by hypoxic ischemic changes in the central nervous system. A positive result of a urine screening test confirmed the presence of benzodiazepines, which resulted in administration of flumazenil and improved patient consciousness. Quantitative method of liquid chromatography indicated flubromazolam in the patient's serum at 59 ng/mL and urine at 105 ng/mL about 19 h after ingestion of 3 mg dose. On admission, serum creatine kinase was 15,960 U/L. The patient was treated with mechanical ventilation, intravenous fluids, flumazenil and continuous infusion of norepinephrine at a dose of 0.12 µg/kg/min. The patient survived and on the ninth day of hospitalization he was transferred to the Department of Neurology.Flubromazolam is a new designer drug. Recreational use may be a cause of prolonged, severe intoxication associated with coma, hypotension, and rhabdomyolysis.

A serious case of barium intoxication from suicidal ingestion is reported. Oral barium chloride poisoning with hypokalemia, neuromuscular and cardiac toxicity, treated with intravenous potassium supplementation and hemodialysis, was confirmed by the determination of barium concentrations in gastric contents, blood, serum and urine using the inductively coupled plasma mass spectrometry method. Barium concentrations in the analyzed specimens were 20.45 µg/L in serum, 150 µg/L in blood, 10,500 µg/L in urine and 63,500 µg/L in gastric contents. Results were compared with barium levels obtained from a non-intoxicated person.

The post-injection olanzapine delirium/sedation syndrome (PDSS) was observed in a 60-year-old Caucasian, schizophrenic, non-smoker and underweight [body mass index (BMI), 18.2 kg/m(2) ] women after the fourth intramuscular injection of 405 mg olanzapine pamoate. Clinical symptoms of PDSS were similar to those of acute oral olanzapine intoxication. The patient received supportive treatment and recovered fully. High olanzapine concentrations in serum, with maximum level of 698 ng/mL, were confirmed by liquid chromatography with tandem mass spectrometry (LC-MS/MS). The authors wonder whether a low BMI and advanced age may predispose patients to PDSS occurrence.