sodium-oxybate and Acidosis

Gammabutyrolactone is included in the solvent such as wheel cleaners, pesticides, cosmetics, drugs. After ingestion GBL is converted to gamma-hydroxybutyrate. Both substances are classified as so called "club drugs" and their action is characterized by euphoria, sedation, and induction of retrograde amnesia of events. These activities were basis for the use of GHB and its lactone as rape pill. Acute poisoning with these compounds causes confusion, agitation, ataxia, nausea, vomiting, nystagmus, dyskinesia, hallucinations, coma, irregular breathing, hypothermia, bradycardia, hypotension, convulsions, respiratory paralysis and thus respiratory arrest. These substances carry a risk of development of physical addiction of the hard proceeding of abstinence syndrome. In the USA there is a ban on the sale and promotion of these compounds. In Poland despite the fact that GHB is a controlled substance, there is no regulation of GBL trading. The aim of this paper is to summarize current knowledge regarding the pharmacology, impact on the human body, toxicity, and the effects of chronic abuse of these substances.

Topics: 4-Butyrolactone; Acidosis; Amnesia, Retrograde; Drug Overdose; Euphoria; Humans; Sodium Oxybate; Solvents; Substance Abuse Detection; Substance-Related Disorders

A young woman with a history of several suicide attempts was admitted to the hospital after suspicion of a new intoxication without definite identification of the causing agent. The patient had a high anion gap metabolic acidosis (HAGMA) with respiratory compensation, a lactate gap and an osmolar gap at admission. Initial toxicological screening showed no abnormalities except for a weak positive gamma-hydroxy butyric acid (GHB) enzymatic screen in urine. This finding could not be confirmed using chromatographic analysis nor be explained by the presence of known cross-reacting substances like ethanol. In this case, falsely elevated urinary GHB screening was caused by the ingestion of ethylene glycol. To confirm that the interference was due to ethylene glycol or its metabolites, we performed a spiking experiment. Cross reactivity was linked to ethylene glycol and was low in our experiments (0.1-0.2%). Substantial amounts of ethylene glycol are required to slightly elevated GHB results, depending on the endogenous cutoff used. We can conclude that ethylene glycol can give rise to falsely elevated urinary GHB levels at ethylene glycol concentrations that are typically found in intoxications.

Topics: Acid-Base Equilibrium; Acidosis; Butyric Acid; Ethanol; Ethylene Glycol; Female; Humans; Poisoning; Sodium Oxybate

Topics: Acidosis; Continuous Renal Replacement Therapy; Drug Overdose; Humans; Sodium Oxybate

The causes of high anion gap metabolic acidosis (HAGMA) are well described in the literature. However, sometimes more frequent causes of HAGMA cannot explain its occurrence.In the case of HAGMA and severe neurological depression in the absence of other causes of HAGMA, clinicians should consider an intoxication with gamma-hydroxybutyrate (GHB) as a possible cause.GHB is endogenous to the mammalian central nervous system (CNS). Synthetic GHB was initially used as an anesthetic but is now only licensed for medical use in a limited number of indications such as the treatment of narcolepsy. Because of its euphoric effects, it became popular for recreational use under the street names: Liquid Ecstasy, Georgia Home Boy, and Liquid G.We describe the clinical case of a patient who suffered from severe neurological depression and HAGMA.

Topics: Acidosis; Alcoholism; Gas Chromatography-Mass Spectrometry; Glasgow Coma Scale; Humans; Male; Middle Aged; Narcotics; Sodium Oxybate

A quantitative assay for 4-hydroxybutyric acid was developed using D6-4-hydroxybutyric acid as an internal standard. 4-Hydroxybutyric acid was isolated by liquid chromatography and the amount quantified by selected ion monitoring, ammonia chemical ionization gas chromatography/mass spectrometry of the trimethylsilyl derivatives. The concentrations of 4-hydroxybutyric in control physiological fluids were: 2.64 +/- 3.46 mmol mol-1 creatinine in urine, 1.09 +/- 2.87 mumol l-1 in plasma, 0.98 +/- 1.17 mumol l-1 in cerebrospinal fluid and 1.28 +/- 0.47 mumol l-1 in amniotic fluid. The concentration of 4-hydroxybutyric acid in the amniotic fluid from a pregnancy at risk for 4-hydroxybutyric aciduria was 2.30 mumol l-1, indicating an unaffected fetus. The stable isotope dilution assay of 4-hydroxybutyric acid in physiological fluid samples is a rapid, sensitive and accurate method for quantification, as well as a valuable technique for the prenatal diagnosis of 4-hydroxybutyric aciduria.

Topics: Acidosis; Adult; Amniocentesis; Child; Child, Preschool; Chromatography, Liquid; Female; Gas Chromatography-Mass Spectrometry; Humans; Hydroxybutyrates; Indicators and Reagents; Infant; Pregnancy; Prenatal Diagnosis; Radioisotope Dilution Technique; Sodium Oxybate

The effect of DL-sodium beta-hydroxybutyrate (Na BOHB) on urinary ammonia excretion was studied in seven chronically acidemic human subjects. Metabolic acidosis was induced by the ingestion of 0.1 g/kg body weight of ammonium chloride for three days. On the morning of day 4, baseline blood and urine samples were collected during three 30-minute periods. Na BOHB (1 mmol/kg, pH = 7.4) was then infused over 20 minutes, and this was followed by a continuous infusion at the rate of 10 mumol/kg min for 160 minutes. Urinary ammonia excretion decreased by 35% (P less than 0.001) while urine pH rose slightly from 5.49 to 5.82 (P less than 0.002). Venous pH increased from 7.31 to 7.38 (P less than 0.005) and bicarbonate concentration from 19 to 25 mEq/L (P less than 0.002). Four subjects were restudied with an infusion of Na beta-OHB (pH adjusted to 4.4 with the addition of HCI). Venous pH and bicarbonate concentration did not change significantly while urine pH decreased from 5.25 to 4.90 (P less than 0.001). Urinary ammonia excretion fell by 34% (P less than 0.01) despite the decline in urine pH and the absence of change in blood pH and bicarbonate concentration. Three subjects were restudied with sodium bicarbonate (0.52 to 0.85 mEq/min) infusion. Despite similar increases in blood pH and plasma bicarbonate concentration as observed with Na beta-OHB at pH = 7.4, urinary ammonia excretion did not fall significantly. In an attempt to simulate the change in redox potential and NAD+ to NADH ratio that occurred during the metabolism of beta-hydroxybutyrate to acetoacetate, sodium lactate was given to four subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acidosis; Adult; Ammonia; Ammonium Chloride; Electrolytes; Female; Humans; Hydrogen-Ion Concentration; Hydroxybutyrates; Ketones; Kidney; Male; Oxidation-Reduction; Sodium Oxybate