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Background: Gamma-hydroxybutyrate (GHB) is used at disproportionately high rates within sexuality and gender diverse communities and carries a high risk of overdose. GHB overdose can result in death. Internationally, recent increases in GHB overdoses have been observed. Coronial reviews of GHB-related death highlight the pivotal roles that bystanders to GHB overdose play in preventing fatality. No research has examined, in detail, how bystanders respond to GHB overdose. This qualitative study was conducted among people who use GHB and explored how they responded upon witnessing a GHB overdose experienced by someone else. Methods: Interviews were conducted with 31 sexuality and gender diverse Australian residents reporting three or more occasions of GHB use in the previous 12 months. Participants were asked questions about witnessed GHB overdose, their actions and decision-making processes throughout overdose. Data were analysed thematically. Results: Participants described witnessing GHB overdose, commonly in private settings involving sexualized GHB use. Variable definitions of GHB overdose were reported, ranging from GHB-induced symptoms of distress to comatose intoxication. Drastic actions to keep someone alert and responsive post-GHB ingestion were reported; these included the administration of stimulant substances and citrus. Decisions to call or not call for emergency medical services (EMS) were influenced by many circumstantial variables. In most instances, an EMS call was resisted and response practices deviated from established first aid protocols. Conclusions: GHB overdose prevention and response training programs targeting people who use GHB are urgently required. These education interventions ought to address inaccuracies that inform street remedies for GHB overdose, teach people how to safely check breathing and response, promote basic first aid principles and address barriers to contacting EMS. [ABSTRACT FROM AUTHOR]

Background: The recreational use of gamma hydroxybutyrate (GHB) is associated with frequent overdoses, coma and the risk of developing GHB use disorder (GUD). Several studies suggest negative effects of GHB use or related comas on cognition. Since relapse rates are high in GUD and cognitive impairment has been associated with relapse in other substance use disorders, we aimed to (1) investigate the prevalence of cognitive impairment before and after detoxification, (2) analyse the relationship between GHB use, comas, and cognitive impairment, and (3) explore the association between cognitive impairment and relapse after detoxification in GUD patients. Methods: In these secondary analyses of a prospective cohort study, a consecutive series of patients with GUD (n = 103) admitted for detoxification were recruited at six addiction care facilities in the Netherlands. The Montreal Cognitive Assessment (MoCA) was used to screen for cognitive impairments before and after detoxification. The follow-up duration for the assessment of relapse in GHB use was 3 months. Results: A substantial number of patients with GUD screened positive for cognitive impairment before (56.3%) and after (30.6%) detoxification. Impairment on the MoCA memory domain was most frequent (58.8%). Cognitive impairment was not related to the severity of GUD or number of GHB-induced comas. Logistic regression analysis showed that only the memory score independently predicted relapse. Discussion: Cognitive impairment seems highly prevalent among patients with GUD, possibly related to the risk of relapse. The absence of a relationship between the severity of GUD, level of GHB use, the number of GHB-induced comas, and cognitive impairment suggest that other factors may also contribute to the observed cognitive impairment. [ABSTRACT FROM AUTHOR]

Gamma Hydroxybutyrate (GHB) is a central nervous system depressant effecting GABA-B receptors. GHB is taken along with other psychoactive substances like alcohol, cocaine, ecstasy, and amphetamines especially during parties. Due to the fact that it has been linked to sexual assault, GHB has drawn attention in recent years. This substance is often taken by youngsters and results in euphoric states of mind, signs of relief, easiness in communication, increases in sexual appetite, and experiences of different states of mind. Dizziness, hypotension, bradycardia, nauseation, and vomiting are typical toxication symptoms of GHB. Also, epileptic seizures, respirotary depression, and deaths have been reported as a result of taking GHB. It is widely known that the use of GHB in our country has increased gradually. This case report is important as it summarizes the anamnesis, penetration, and clinical symptoms of GHB. In order to prevent the use of GHB, it would be appropriate to develop psycho-education methodologies, establish legislative regulations, and include GHB tests in substance screening analyses. [ABSTRACT FROM AUTHOR]

Background: Many patients present to emergency departments (EDs) with an altered state of consciousness. Fast exclusion of gamma hydroxybutyrate (GHB)-associated intoxication in these patients may optimize diagnostic and therapeutic algorithms and decisions in the ED. Methods: Between January and March 2014, a novel enzymatic test system was used to quantify GHB in blood and urine samples of suspected intoxicated patients in the ED of the University Hospital. The underlying causes for suspected intoxication and the diagnostic and therapeutic measures were documented and analysed retrospectively. Results: GHB measurements were performed in 13 patients with suspected ingestion during a 3-month study period. GHB was positive in six patients showing serum levels between 61.8 mg/l and 254.8 mg/l, and GHB was tested negative in seven patients with a range of 0.3–6.2 mg/l (upper reference limit 6.1 mg/l). Additional intoxication was found in five of six GHB positive (83%, alcohol n = 2 and other drugs n = 5) and in six of seven negative-tested patients (86%, alcohol n = 5 and other drugs n = 1). Conclusion: GHB quantification in the ED provides specific additional information for intoxication, which can lead to more precise diagnostic and therapeutic decisions and may also be important for legal aspects. We believe that GHB analysis in unconscious patients with suspected intoxication may improve the efficient treatment of intoxicated patients. [ABSTRACT FROM AUTHOR]

Gamma hydroxybutyrate (GHB) is a recreational and date-rape drug, for which the detection following ingestion is hampered by rapid metabolism and its endogenous presence. GHB catabolism occurs mainly by its oxidation to succinic semialdehyde (SSA), which converts to succinate and enters the tricarboxylic acid cycle. A high Km aldehyde reductase has previously been reported to catalyse the NADP-dependent oxidation of GHB at high concentrations. It is assumed that this enzyme is identical to the aldo-keto reductase AKR1A1, but its role in GHB oxidation has not been fully evaluated. In this study, the extent of AKR1A1 in GHB metabolism has been determined in HepG2 cells using RNA-interference technology. The gene encoding AKR1A1 was targeted by siRNA. Results demonstrate a successful knock-down of the AKR1A1 gene with 92% reduction in total mRNA and 93% reduction in protein expression. Demolishing AKR1A1 expression in HepG2 cells leads to significant 82% decrease in NADP-dependent GHB-dehydrogenase activity at high concentration (10 mM) of GHB. Moreover, when exposing the cells to 50 μM of GHB for 24 h, and measuring intracellular and extracellular GHB levels by GC/MS, a significant two-fold increase was observed on GHB intracellular level in silenced cells. In contrast, measuring SSA-reductase activity in silenced cells indicated that AKR1A1 is not involved in endogenous GHB production. These findings describe a pathway for GHB metabolism in the liver which should be useful in GHB exposure cases, and will enable a better understanding of the enzymes participating in its metabolism at natural and overexposed levels. [ABSTRACT FROM AUTHOR]

Gamma hydroxybutyrate (GHB) is a central nervous system depressant with euphoric and relaxant effects. Documentation of GHB prevalence and the underreporting of abuse remains problematic, given the availability of GHB and its precursors γ-butyrolactone (GBL) and 1,4-butanediol (1,4-BD) and the ease of synthesis from kits available on the Internet. The continued abuse of and dependence on GHB, and associated fatalities, present an on-going public health problem. As the drug GHB remains an underresearched topic, a scoping review was chosen as a technique to map the available literature into a descriptive summarized account. PRISMA was used to assist in data retrieval, with subsequent data charting into three key themes (pharmacology and toxicology, outcomes, and user groups). Administered orally, GHB is dose-dependent and popular for certain uses (therapeutic, body enhancement, sexual assault) and amongst user sub groups (recreational party drug users, homosexual men). Despite the low prevalence of use in comparison to other club drugs, rising abuse of the drug is associated with dependence, withdrawal, acute toxicity, and fatal overdose. Clinical diagnosis and treatment is complicated by the co-ingestion of alcohol and other drugs. Limitations of the scoping review and potential for further research and harm reduction initiatives are discussed. [ABSTRACT FROM PUBLISHER]

Gamma hydroxybutyrate (GHB) levels in biological fluids are known to be increased after death. To date, there have been studies on sample storage conditions and preservatives on the postmortem in vitro formation of GHB. However, only few studies explored the effects of body storage conditions on GHB formation after death. In this study, we determined the effect of body refrigeration during body storage in mortuary refrigerators on postmortem formation of GHB in whole blood samples. A total of 41 fatalities were divided into two groups: Group A with a total refrigeration time less than 10 h and Group B with a total body refrigeration time more than 10 h. Femoral blood was collected 3 times: upon arrival at the mortuary, after 4 h of refrigeration, and at autopsy. Rectal temperatures were recorded at the time of specimen collection. Blood GHB concentration was analyzed by LC-MS/MS. The rate of change in GHB levels was calculated. The study revealed that in the later phase of refrigeration, no difference was observed in the blood GHB levels between the two groups despite differences in the postmortem interval (PMI) and refrigeration time. Moreover, the rate of change in the GHB levels was lower in the group with a longer refrigeration time. Hence, we concluded that once the plateau of postmortem GHB formation is reached in a refrigerated body, further formation is not expected even with prolonged PMI. Early body refrigeration can minimize postmortem GHB production, thereby preventing the incorrect interpretation of analytical results. [ABSTRACT FROM AUTHOR]

Abstract: Background: The number of admissions to addiction treatment centers in the Netherlands for gamma hydroxybutyrate (GHB) dependence is rapidly growing. Until now, treatment seeking GHB users have hardly been studied. This study characterizes inpatients in treatment for GHB dependence in terms of sociodemographics, motives for substance use and reasons for seeking treatment. In addition, variables associated with dependence severity are identified. Methods: Patients were recruited by their therapists at 4 different addiction treatment centers dispersed throughout the Netherlands. They were asked to fill out the questionnaire, including sociodemographic and clinical characteristics, GHB and other drug use, and a modified version of the Drug Use Disorders Identification Test (DUDIT) to screen for GHB dependence. The associations of relevant variables with dependence severity were determined using multiple regression analysis. Results: A total of 75 inpatients (response rate 90.4%) participated in the study. Most patients were young (mean 26.8±9.1) males (73%) with low education (78%) and not employed (48%). Most of them (75%) had started using GHB the year before treatment admission, 42 (56%) frequently combined GHB with sedatives and 26 (35%) frequently combined GHB with stimulants. Dependence severity was strongly associated with sleep problems and the combined use of GHB and stimulants. Conclusion: This study shows that sociodemographic characteristics of GHB inpatients are similar to those of problematic users of other club drugs. Sleep problems and combined use of GHB and stimulants were strongly associated with GHB dependence. Together, these factors might help to better identify people at risk for GHB dependence. [Copyright &y& Elsevier]

Introduction. Gamma-hydroxybutyrate (GHB) and its precursors, gamma-butyrolactone (GBL) and 1,4-butanediol (1,4-BD), are drugs of abuse which act primarily as central nervous system (CNS) depressants. In recent years, the rising recreational use of these drugs has led to an increasing burden upon health care providers. Understanding their toxicity is therefore essential for the successful management of intoxicated patients. We review the epidemiology, mechanisms of toxicity, toxicokinetics, clinical features, diagnosis, and management of poisoning due to GHB and its analogs and discuss the features and management of GHB withdrawal. Methods. OVID MEDLINE and ISI Web of Science databases were searched using the terms 'GHB,' 'gamma-hydroxybutyrate,' 'gamma-hydroxybutyric acid,' '4-hydroxybutanoic acid,' 'sodium oxybate,' 'gamma-butyrolactone,' 'GBL,' '1,4-butanediol,' and '1,4-BD' alone and in combination with the keywords 'pharmacokinetics,' 'kinetics,' 'poisoning,' 'poison,' 'toxicity,' 'ingestion,' 'adverse effects,' 'overdose,' and 'intoxication.' In addition, bibliographies of identified articles were screened for additional relevant studies including nonindexed reports. Non-peer-reviewed sources were also included: books, relevant newspaper reports, and applicable Internet resources. These searches produced 2059 nonduplicate citations of which 219 were considered relevant. Epidemiology. There is limited information regarding statistical trends on world-wide use of GHB and its analogs. European data suggests that the use of GHB is generally low; however, there is some evidence of higher use among some sub-populations, settings, and geographical areas. In the United States of America, poison control center data have shown that enquiries regarding GHB have decreased between 2002 and 2010 suggesting a decline in use over this timeframe. Mechanisms of action. GHB is an endogenous neurotransmitter synthesized from glutamate with a high affinity for GHB-receptors, present on both on pre- and postsynaptic neurons, thereby inhibiting GABA release. In overdose, GHB acts both directly as a partial GABAb receptor agonist and indirectly through its metabolism to form GABA. Toxicokinetics. GHB is rapidly absorbed by the oral route with peak blood concentrations typically occurring within 1 hour. It has a relatively small volume of distribution and is rapidly distributed across the blood-brain barrier. GHB is metabolized primarily in the liver and is eliminated rapidly with a reported 20-60 minute half-life. The majority of a dose is eliminated completely within 4-8 hours. The related chemicals, 1,4-butanediol and gamma butyrolactone, are metabolized endogenously to GHB. Clinical features of poisoning. GHB produces CNS and respiratory depression of relatively short duration. Other commonly reported features include gastrointestinal upset, bradycardia, myoclonus, and hypothermia. Fatalities have been reported. Management of poisoning. Supportive care is the mainstay of management with primary emphasis on respiratory and cardiovascular support. Airway protection, intubation, and/or assisted ventilation may be indicated for severe respiratory depression. Gastrointestinal decontamination is unlikely to be beneficial. Pharmacological intervention is rarely required for bradycardia; however, atropine administration may occasionally be warranted. Withdrawal syndrome. Abstinence after chronic use may result in a withdrawal syndrome, which may persist for days in severe cases. Features include auditory and visual hallucinations, tremors, tachycardia, hypertension, sweating, anxiety, agitation, paranoia, insomnia, disorientation, confusion, and aggression/combativeness. Benzodiazepine administration appears to be the treatment of choice, with barbiturates, baclofen, or propofol as second line management options. Conclusions. GHB poisoning can cause potentially life-threatening CNS and respiratory depression, requiring appropriate, symptom-directed supportive care to ensure complete recovery. Withdrawal from GHB may continue for up to 21 days and can be life-threatening, though treatment with benzodiazepines is usually effective. [ABSTRACT FROM AUTHOR]

Abstract: Gamma butyrolactone (GBL) is metabolized to gamma hydroxybutyrate (GHB) in the body. GHB is a DEA Schedule 1 compound; GBL is a DEA List 1 chemical. Gamma valerolactone (GVL) is the 4-methyl analog of GBL; GVL is metabolized to 4-methyl-GHB; GVL is NOT metabolized to GBL or GHB. The effects of GBL (18.75–150mg/kg), GVL (200–1600mg/kg) or vehicle on the acoustic startle reflex (ASR), and the classically-conditioned enhancement of startle, the Startle Anticipated Potentiation of Startle (SAPS) response were studied in male rats. Both compounds produced a dose-dependent reduction of ASR, with GBL 5–7 times more potent than GVL. In contrast, GBL treatment significantly reduced SAPS at doses that exerted only moderate effects on ASR, whereas GVL exerted little or no effect on the SAPS, except at doses that produced pronounced reductions in Noise Alone ASR. In a second experiment, rats were tested for Noise Alone ASR behavior following treatment with a single mid-range dose of GBL (75mg/kg), GVL (400mg/kg) or vehicle; immediately following startle testing the animals were sacrificed and their brains and blood were collected for determination of GHB, 4-methyl-GHB, GBL and GVL. GHB was found in measurable concentrations in all of the blood specimens and 6 (of 8) of the brain specimens from the GBL-treated subjects. 4-Methyl-GHB was found in measurable concentrations in all of the blood and brain specimens of the GVL-treated subjects; the change in startle amplitude was inversely correlated to the brain concentrations of these compounds. These findings confirm the differences in the metabolic fate of GBL and GVL as pro-drugs for the formation of GHB and 4-methyl-GHB, respectively. Moreover, the dissimilarity in effect profile for GBL and GVL on ASR versus SAPS behaviors suggests that different receptor(s) may be involved in mediating these behavioral effects. [Copyright &y& Elsevier]

Abstract: Purpose: Hypothermia is a promising neuroprotective therapy. We studied the feasibility and safety of very prolonged moderate hypothermia for severe acute ischemic stroke. Methods: Moderate hypothermia was induced within 24h after a severe ischemic stroke involving the middle cerebral artery. Hypothermia, with cooling blankets, reduced body-core temperature to 32–33°C, and was prolonged for up to 22days until cerebral edema had significantly decreased (assessed by serial cerebral computed tomography) before slow rewarming (<1.5°C/day). Patients were mechanically ventilated and sedated with gamma-hydroxybutyrate (GHB), a naturally occurring metabolite of gamma-aminobutyric acid (GABA), which acts on the GABAB receptors. Outcomes and side effects at 12months were recorded. Results: Nineteen patients (mean age: 52.6years, mean National Institute of Health Stroke Scale (NIHSS) score 21) were enrolled. Cooling was achieved in all patients. The mean time to reach target temperature was 11.4±8.6h and the mean duration of rewarming was 4.0±1.1days. For the 10 survivors (53%), the mean duration of hypothermia and rewarming was 22.6±4.9days. Five patients underwent a hemicraniectomy. All patients presented with hypotension, bradycardia, and hematological side effects. Eight patients had pneumonia (42%). At 12months, the mean NIHSS score was 8.3±2.7, the Barthel Index was 67±18, and the modified Rankin scale was 3.2±0.9. Conclusions: This study shows the feasibility of very prolonged hypothermia beyond 3weeks using GHB sedation in severe hemispheric infarcts. [Copyright &y& Elsevier]

Abstract: Fatalities resulting from popular use of gamma hydroxybutyrate (GHB) have previously been reported. We report three deaths associated with use of Xyrem® (sodium oxybate), a pharmaceutical preparation of GHB initially approved for treatment of narcolepsy with cataplexy. One death appears associated with Xyrem® abuse, with extremely high postmortem blood GHB levels documented. Although postmortem blood GHB levels in two other deaths are consistent with therapeutic levels, cause and effect cannot be established. We discuss these cases and factors which may have exerted contributory respiratory depressant effects, singly or in combination, including concurrent use of sedative hypnotics, obstructive sleep apnea, and obesity. [Copyright &y& Elsevier]

Gamma hydroxybutyrate (GHB) is a psychoactive substance with complex neurophysiological activity and significant potential for abuse, addiction, and dangerous toxicity. In this study, a semistructured interview was administered to 17 subjects to investigate GHB use, including: manner of use; setting; positive and negative consequences; other drug history; and sexual practices. Respondents were overwhelmingly male, but otherwise had a broad demographic background. Settings varied from nightclubs to private use at home. There was significant variability in the drug obtained, which subjects found problematic because of the narrow therapeutic window and ease of accidental overdose. Common positive experiences included increased sexual desire, decreased sexual inhibitions, and decreased anxiety. Common negative consequences included oversedation, loss of consciousness, motor incoordination, and mental confusion. Nine subjects reported that they would use GHB again, some despite severe negative consequences. Although most subjects reported negative experiences, only three felt their use was problematic, and none sought treatment for GHB abuse or addiction. Subjects were highly drug-experienced, most commonly using MDMA, ketamine, cocaine, alcohol, and methamphetamine. Some reported that GHB could cause poor decision making in sexual situations. This effect has significant ramifications for issues such as date rape and control of sexually transmitted diseases, such as HIV. [ABSTRACT FROM AUTHOR]

Succinate-semialdehyde dehydrogenase (SSADH) deficiency is a rare neurometabolic disorder of v-amino butiric acid catabolism with autosomal recessive inheritance. Accumulation of g-hydroxybutyrate in urine and plasma is biochemically key finding. SSADH deficiency can be demonstrated by measuring level of SSADH enzyme in lymphocytes or leukocytes. In a child with mental retardation and speech disorder the isolated pallidal brain magnetic resonance pattern with absent white-matter changes should raise the suspicion of SSADH deficiency and prompt biochemical analysis of hydroxybutyrate. [ABSTRACT FROM AUTHOR]

Focus group discussions elicited descriptive experiences of driving under the influence of gamma hydroxybutyrate (GHB), and uncovered motivations that led participants to decide whether to get behind the wheel after ingesting this illegal psychoactive substance. Of the 51 current and past users interviewed, average age 31.1 ± 7.7 years, 40% were female. All were recruited from the San Francisco Bay Area, in 2004. Factors making users vulnerable to adverse complications of driving while under the influence of GHB are also examined. Study limitations were noted. Implications for various law enforcement agencies and health professionals are derived from the data. [ABSTRACT FROM AUTHOR]

GHB (gamma hydroxybutyrate) is a significant new drug of abuse added to the United States Controlled Substance Act in 2000. The majority of the published literature on GHB consists of clinical case reports, mainly from emergency departments, and a collection of laboratory-based studies, focused mainly on anesthesia. While comments about the various experiences and behaviors of human users are often included in such studies or reports, these aspects of GHB are only just beginning to be systematically investigated or detailed. Reported here are data from a qualitative study using focus group methods on the consumption habits, experiences, and beliefs of GHB users. A total of 51 people, 30 men and 21 women, mean age of 31.1+/-7.6 years (range 18 to 52 years), who report having used GHB for an average of 4.3+/-2.5 years (range one to 11 years), were interviewed in 10 separate groups held in 2004. This article discusses broadly the general experience of the GHB high, major perceived benefits including sexual responses to the drug, perceived risks and dangers of ingestion, co-ingestion, and various contexts of use. It concludes with a discussion of the implications drawn from this information for clinicians treating patients who use GHB. [ABSTRACT FROM AUTHOR]

Introduction: Little is known about behaviors linked to gamma hydroxybutyrate (GHB) morbidity.Methods: We surveyed 131 GHB users, using logistic regression to test the associations between the high risk behaviors and hospital treatment for GHB (26 [20%] of subjects).Results: Increased risk of GHB hospital treatment was associated with: co-ingestion of ethanol (OR 5.2; 95% CI 1.7-16), driving under the influence of GHB (OR 3.2; 95%, CI 1.3-7.8),use of GHB to treat withdrawal symptoms (OR 2.9; 95% CI 1.1-7.9), and co-ingestion of ketamine (OR 2.7; 95% CI 1.1-6.7).Conclusion: Targeted prevention activities could focus on selected high-risk behaviors. [ABSTRACT FROM AUTHOR]

Physostigmine has been proposed as an antidote for gamma hydroxybutyrate (GHB) intoxication, based on associated awakenings in 1) patients anesthetized with GHB and 2) five of six patients administered physostigmine for GHB intoxication. However, there are neither well-supported mechanisms for physostigmine reversal of GHB effects, supportive animal studies, nor randomized, placebo-controlled trials demonstrating safety, efficacy, or improved outcomes. We sought to determine the outcomes of patients with GHB-induced coma after a physostigmine treatment protocol was instituted in an urban Emergency Department and ambulance service. Our search of medical records located five cases of GHB toxicity, all with co-intoxicants, who received physostigmine. None demonstrated response and, further, there were associated adverse events, including atrial fibrillation (2), pulmonary infiltrates (1) and significant bradycardia (1), and hypotension (1). We also reviewed 18 published GHB toxicity case series for incidence of adverse effects, stimulant co-intoxicants (which may heighten risk of physostigmine), complications, and outcomes of supportive care for GHB toxicity. We conclude that physostigmine is not indicated for reversal of GHB-induced alteration of consciousness; it is not efficacious, it may be unsafe, particularly in the setting of recreational polydrug use; and supportive care results in universally good outcomes. [ABSTRACT FROM AUTHOR]

Critical care physicians are frequently confronted with intoxicated patients who have used street drugs. In the last decade there has been an upward trend in the use of these substances, particularly amongst adolescents and young adults in large urban areas. In excess quantities all street drugs can lead to critical illness. Early and appropriate medical attention by emergency medicine physicians and intensivists can improve outcomes. In this review article we intend to familiarize critical care physicians with the most common street drugs such as amphetamines, ecstasy, cocaine, gamma hydroxybutyrate, opioids, and phencyclidine. [ABSTRACT FROM AUTHOR]

The endogenous nature of the drug of abuse gamma hydroxybutyric acid (GHB) has caused various interpretative problems for toxicologists. In order to obtain data for the presence of endogenous GHB in humans and to investigate any factors that may affect this, a volunteer study was undertaken. The GHB concentrations in 119 urine specimens from GHB-free subjects and 25 urine specimens submitted for toxicological analysis showed maximal urinary GHB concentrations of 3 mg/l. Analysis of 15 plasma specimens submitted for toxicological analysis detected no measurable GHB (less than 2.5 mg/l). Studies in a male and female volunteer in which different dietary food groups were ingested at weekly intervals, showed significant creatinine-independent intra-individual fluctuation with overall urine GHB concentrations between 0 and 2.55, and 0 and 2.74 mg/l, respectively. Urinary concentrations did not appear to be affected by the particular dietary groups studied.The concentrations measured by gas chromatography with flame ionisation detection (GC–FID) and gas chromatography with mass spectrometry (GC–MS) lend further support to the proposed urinary and plasma interpretative cut-offs of 10 and 4 mg/l, respectively, where below this it is not possible to determine whether any GHB detected is endogenous or exogenous in nature. [Copyright &y& Elsevier]

Abstract This paper describes two group presentations of intoxicated patients to the Emergency Department of Gold Coast Hospital in October 1996 and July 1997 respectively. A total of 14 patients received treatment. The clinical features, investigation findings and clinical course of each patient are outlined. A discussion is undertaken of the literature surrounding the emergence of gamma hydroxybutyrate (GHB) as a drug of abuse, and of the major issues involved in the emergency department management of such patients. [ABSTRACT FROM AUTHOR]