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GHB (as Title word) - Medline search, 74 references

Last updated: 11/2001

UI - 18
TI - More on gamma-butyrolactone (GBL/GHB) toxicity
NT - UI - 0DA - 20010214IS - 0099-1767LA - ENGPT - JOURNAL ARTICLEJC - UR - PM:11174256
SO - J Emerg Nurs 2001 Feb ;27(1):7-8

UI - 17
TI - GHB: its use and misuse
UR - PM:11276153
SO - Harv Ment Health Lett 2001 Mar ;17(9):7-8

UI - 19
AU - Addolorato G
AU - Caputo F
AU - Capristo E
AU - Gasbarrini G
TI - Diazepam in the treatment of GHB dependence
UR - PM:11157447
SO - Br J Psychiatry 2001 Feb ;178():183

UI - 1
AU - Ciolino LA
AU - Mesmer MZ
AU - Satzger RD
AU - Machal AC
AU - McCauley HA
AU - Mohrhaus AS
AD - U.S. Food and Drug Administration Forensic Chemistry, Cincinnati, OH 45237, USA
TI - The chemical interconversion of GHB and GBL: forensic issues and implications
AB - In this work, the interconversion of GHB and GBL in a variety of aqueous media was studied. The effects of solution pH and time were determined by spiking GHB or GBL into pure water and buffered aqueous solutions, and determining the GHB and GBL contents at various time intervals. The degree of GBL hydrolysis to GHB was determined for several commercial aqueous-based GBL products, and further studied as a function of time. The effects of temperature and time were also determined for five commercial beverages spiked with GHB or GBL. GHB and GBL contents were determined using high performance liquid chromatography (HPLC). GHB and/or GBL confirmations were made using gas chromatography-mass spectrometry (GC-MS) and/or infrared spectroscopy (IR). Solution pH, time, and storage temperature were determined to be important factors affecting the rate and extent of GBL hydrolysis to GHB. Under strongly alkaline conditions (pH 12.0), GBL was completely converted to GHB within minutes. In pure water, GBL reacted to form an equilibrium mixture comprising ca. 2:1 GBL:GHB over a period of months. This same equilibrium mixture was established from either GHB or GBL in strongly acidic solution (pH 2.0) within days. A substantial portion of GBL (ca. 1/3) was hydrolyzed to GHB in aqueous-based GBL products, and in spiked commercial beverages, after ambient storage for a period ranging from several weeks to several months. Heat increased and refrigeration decreased the rate of GBL hydrolysis relative to ambient conditions. These studies show that hydrolysis of GBL to GHB does occur in aqueous-based solutions, with samples and time frames that are relevant to forensic testing. Implications for forensic testing and recommendations are discussed
UR - PM:11714141
SO - J Forensic Sci 2001 Nov ;46(6):1315-1323

UI - 12
AU - Colombo G
AU - Lobina C
AU - Agabio R
AU - Brunetti G
AU - Diaz G
AU - Littera M
AU - Melis S
AU - Pani M
AU - Reali R
AU - Serra S
AU - Vacca G
AU - Carai MA
AU - Gessa GL
AD - C.N.R. Center for Neuropharmacology, c/o 'Bernard B. Brodie' Department of Neuroscience, University of Cagliari, SS 554, Km. 4.5, I-09042, Monserrato (CA), Italy. colomb@unica.it
TI - Selective breeding of two rat lines differing in sensitivity to GHB and baclofen
AB - Two Wistar-derived rat lines, one sensitive (GHB-S) and the other resistant (GHB-R) to the anesthetic effect of gamma-hydroxybutyric acid (GHB), have been selectively bred. GHB-S and GHB-R rats were also sensitive and resistant, respectively, to the anesthetic effect of baclofen, the prototype GABA(B) receptor agonist, suggesting that they may be useful to elucidate not only the role of endogenous GHB but also that of GABA(B) receptors in sleep and anesthesia
UR - PM:11376602
SO - Brain Res 2001 May 25 ;902(1):127-130

UI - 8
AU - Couper FJ
AU - Logan BK
AD - Washington State Toxicology Laboratory, University of Washington, Seattle 89134, USA. fcouper@wsp.wa.gov
TI - GHB and driving impairment
AB - Gamma hydroxybutyrate (GHB) was identified in the blood of 13 subjects arrested for impaired driving. GHB concentrations ranged from 26 to 155 mg/L (mean 87 mg/L, median 95 mg/L). In eight cases, GHB was the only drug detected, and signs of impairment were consistent with those of a CNS depressant, including erratic driving (weaving, swerving, ignoring road signs), confusion, incoherent speech, unresponsiveness, lack of balance, unsteady coordination, poor performances on field sobriety tests, and varying states of wakefulness. Given the ability of GHB to induce sleep and unconsciousness, it is evident from these cases that recreational use of the drug has the potential to impair a person's driving ability
UR - PM:11451079
SO - J Forensic Sci 2001 Jul ;46(4):919-923

UI - 2
AU - Elian AA
AD - Commonwealth of Massachusetts, Slate Police Crime Laboratory, Forensic Toxicology Unit, 59 Horsepond Road, 01776, Sudbury, MA, USA
TI - GC-MS determination of gamma-hydroxybutyric acid (GHB) in blood
AB - A sensitive and specific gas chromatography-mass spectrometer (GC-MS) method using selective ion monitoring (SIM) has been developed for the quantification of gamma-hydroxybutyric acid (GHB) in blood. This method uses liquid-liquid extraction and disilyl-derivatization, without conversion to the gamma-butyrolactone (GBL), followed by GC-MS analysis using GHB-d(6) as the internal standard. The method was linear from 0.1 to 20mg/dl, and the limit of quantification using 50&mgr;l of blood was determined to be 0.1mg/dl
UR - PM:11587864
SO - Forensic Sci Int 2001 Oct 15 ;122(1):43-47

UI - 15
AU - Elliot S
TI - The presence of gamma-hydroxybutyric acid (GHB) in postmortem biological fluids
UR - PM:11300509
SO - J Anal Toxicol 2001 Mar ;25(2):152

UI - 9
AU - Goss J
TI - Designer drugs. Assess & manage patients intoxicated with ecstasy, GHB or rohypnol--the three most commonly abused designer drugs
UR - PM:11409205
SO - J Emerg Med Serv JEMS 2001 Jun ;26(6):84-3

UI - 14
AU - Jensen K
AU - Mody I
AD - Department of Neurology, UCLA School of Medicine, Los Angeles, CA 90095, USA
TI - GHB depresses fast excitatory and inhibitory synaptic transmission via GABA(B) receptors in mouse neocortical neurons
AB - Gamma-hydroxybutyrate (GHB) is a drug of abuse which induces sedation and euphoria. However, overdoses can severely depress the level of consciousness or can be fatal especially when combined with other substances. Studies have suggested that the GHB-effects are mediated via actions on thalamocortical pathways and local neocortical circuits, although the effect of GHB at the level of single neocortical neurons is not clear. Using whole-cell patch-clamp recordings, we studied the effects of GHB on neocortical neurons in brain slices from 12- to 33-day-old mice. We found that GHB depressed the frequency and amplitude of GABAergic and glutamatergic spontaneous inhibitory and excitatory post-synaptic currents (IPSCs and EPSCs) driven by presynaptic action potential firing, while the amplitude and frequency of Ca(2+) entry-independent miniature IPSCs were not affected. Using minimal stimulation, GHB reduced the probability of release at inhibitory synapses onto neocortical layer 2/3 pyramidal cells. Also, GHB directly hyperpolarized layer 2/3 non-pyramidal cells by up to 11 mV and inhibited action potential firing. All these effects of GHB were mediated via GABA(B)-receptors. In conclusion, GHB activates both pre- and postsynaptic GABA(B)-receptors in neocortical neurons participating in fast synaptic transmission, leading to a powerful depression of neocortical network activity. We propose that GABA(B)-receptor antagonists may be useful in the treatment of acute GHB intoxication
UR - PM:11313294
SO - Cereb Cortex 2001 May ;11(5):424-429

UI - 13
AU - Kalasinsky KS
AU - Dixon MM
AU - Schmunk GA
AU - Kish SJ
AD - Office of the Armed Forces Medical Examiner, Armed Forces Institute of Pathology, Rockville, MD 20850, USA. kalasink@afip.osd.mil
TI - Blood, brain, and hair GHB concentrations following fatal ingestion
AB - Despite the increasing incidence of illicit use of gamma-hydroxybutyrate (GHB), little information is available documenting levels of the drug in GHB fatalities. We measured GHB levels in postmortem blood, brain and hair specimens from a suspected overdose case by gas chromatography/mass spectrometry (GC/MS) following solid phase extraction (SPE) and derivatization with bis(trimethyl-silyl) trifluoroacetamide (BSTFA). Examination found 330 microg/mL GHB in femoral blood and 221 ng/mg GHB in frontal cortex brain tissue, values higher than those typically reported in the literature. The hair shaft was negative for GHB whereas the plucked root bulbs with outer root sheath attached (2,221 ng/mg) and root bulbs after washing and removal of the outer root sheath (47 ng/mg) contained the drug. Our results are consistent with an acute single dose of GHB and, as the toxicology screen was negative for other drugs of abuse, emphasize the significant danger of this drug
UR - PM:11373018
SO - J Forensic Sci 2001 May ;46(3):728-730

UI - 3
AU - Karch SB
AU - Stephens BG
AU - Nazareno GV
AD - Assistant Medical Examiners, City and County of San Francisco, CA 94103, USA. fdaa@batnet.com
TI - GHB. Club drug or confusing artifact?
AB - GHB can be produced either as a pre- or postmortem artifact. The authors describe two cases in which GHB was detected and discuss the problem of determining the role of GHB in each case. In both cases, NaF-preserved blood and urine were analyzed using gas chromatography. The first decedent, a known methamphetamine abuser, had GHB concentrations similar to those observed with subanesthetic doses (femoral blood, 159 microg/ml; urine, 1100 microg/ml). Myocardial fibrosis, in the pattern associated with stimulant abuse, was also evident. The second decedent had a normal heart but higher concentrations of GHB (femoral blood, 1.4 mg/ml; right heart, 1.1 mg/ml; urine, 6.0 mg/ml). Blood cocaine and MDMA levels were 420 and 730 ng/ml, respectively. Both decedents had been drinking and were in a postabsorptive state, with blood to vitreous ratios of less than 0.90. If NaF is not used as a preservative, GHB is produced as an artifact. Therefore, the mere demonstration of GHB does not prove causality or even necessarily that GHB was ingested. Blood and urine GHB concentrations in case 1 can be produced by a therapeutic dose of 100 mg, and myocardial fibrosis may have had more to do with the cause of death than GHB. The history in case 2 is consistent with the substantial GHB ingestion, but other drugs, including ethanol, were also detected. Ethanol interferes with GHB metabolism, preventing GHB breakdown, raising blood concentrations, and making respiratory arrest more likely. Combined investigational, autopsy, and toxicology data suggest that GHB was the cause of death in case 2 but not case 1. Given the recent discovery that postmortem GHB production occurs even in stored antemortem blood samples (provided they were preserved with citrate) and the earlier observations that de novo GHB production in urine does not occur, it is unwise to draw any inferences about causality unless (1) blood and urine are both analyzed and found to be elevated; (2) blood is collected in NaF-containing tubes; and (3) a detailed case history is obtained
UR - PM:11563737
SO - Am J Forensic Med Pathol 2001 Sep ;22(3):266-269

UI - 11
AU - LeBeau MA
AU - Miller ML
AU - Levine B
AD - Federal Bureau of Investigation, FBI Laboratory, 935 Pennsylvania Avenue, Washington, DC, USA
TI - Effect of storage temperature on endogenous GHB levels in urine
AB - Because gamma-hydroxybutyrate (GHB) is an endogenous substance present in the body and is rapidly eliminated after ingestion, toxicologists investigating drug-facilitated sexual assault cases are often asked to differentiate between endogenous and exogenous levels of GHB in urine samples.This study was designed to determine the effects of storage temperature on endogenous GHB levels in urine. Specifically, it was designed to ascertain whether endogenous levels can be elevated to a range considered indicative of GHB ingestion.Urine specimens from two subjects that had not been administered exogenous GHB were collected during a 24h period and individually pooled. The pooled specimens were separated into standard sample cups and divided into three storage groups: room temperature ( approximately 25 degrees C), refrigerated (5 degrees C), and frozen (-10 degrees C). Additionally, some specimens were put through numerous freeze/thaw cycles to mimic situations that may occur if multiple laboratories analyze the same specimen. Periodic analysis of the samples revealed increases in the levels of endogenous GHB over a 6-month period. The greatest increase (up to 404%) was observed in the samples maintained at room temperature. The refrigerated specimens showed increases of 140-208%, while the frozen specimens showed smaller changes (88-116%). The specimens subjected to multiple freeze/thaw cycles mirrored specimens that had been thawed only once. None of the stored urine specimens demonstrated increases in GHB concentrations that would be consistent with exogenous GHB ingestion
UR - PM:11376982
SO - Forensic Sci Int 2001 Jun 15 ;119(2):161-167

UI - 6
AU - Maremmani I
AU - Lamanna F
AU - Tagliamonte A
AD - Department of Psychiatry, Neurobiology, Pharmacology and Biotechnology, University of Pisa, Italy
TI - Long-term therapy using GHB (sodium gamma hydroxybutyrate) for treatment-resistant chronic alcoholics
AB - Thirty-five alcohol-dependent patients according to DSM-IV criteria who also met criteria for treatment resistance were treated with doses of gamma hydroxybutyrate (GHB) ranging between 25 and 100 mg/kg/die in an open one-year study. The results show that no patients discontinued the program during the first month of treatment. Sixty percent of these patients successfully completed the protocol; 11.4% showed complete abstinence (full responder patients); 14.3% strongly reduced their alcohol intake (partial responder patients) and 34.3% of the patients were still under treatment after one year. Forty percent of the patients were nonresponders. The retention rate under treatment of the studied sample was statistically higher than that found during the last treatment of the same subjects. No significant differences were found between full responder and partial responder patients regarding changes in clinical features, alcohol intake or social adjustment. Patients still in treatment after one year significantly differed from nonresponder patients on all the variables investigated. A six-times/daily fractionated administration of the GHB dose was the only significant predictor of the retention rate
UR - PM:11476260
SO - J Psychoactive Drugs 2001 Apr ;33(2):135-142

UI - 4
AU - Marinetti LJ
AU - Isenschmid DS
AU - Hepler BR
AU - Commissaris RL
TI - Response to the presence of gamma-hydroxybutyric acid (GHB) in postmortem biological fluids
UR - PM:11499892
SO - J Anal Toxicol 2001 Jul ;25(5):356-357

UI - 5
AU - McDaniel CH
AU - Miotto KA
AD - ULCA Department of Psychiatry and Biobehavioral Sciences, Los Angeles, California 90024, USA
TI - Gamma hydroxybutyrate (GHB) and gamma butyrolactone (GBL) withdrawal: five case studies
AB - There is little medical information available about gamma-hydroxybutyrate (GHB) or gamma-butyrolactone (GBL) dependence or withdrawal. In this study the authors treated and reviewed multiple cases of GHB and GBL withdrawal in high-dose users. Five patients during nine hospitalizations were treated for GHB or GBL withdrawal. The authors describe a spectrum of GHB or GBL withdrawal from mild to severe and discuss medications used for treatment. They conclude that patients with GHB or GBL withdrawal may present with agitated psychosis, delirium, and autonomic instability. In this sample, relapse to GHB or GBL use occurred soon after treatment of withdrawal
UR - PM:11476261
SO - J Psychoactive Drugs 2001 Apr ;33(2):143-149

UI - 16
AU - Nicholson KL
AU - Balster RL
AD - Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0613, USA. klnichol@hsc.vcu.edu
TI - GHB: a new and novel drug of abuse
AB - There has been increasing attention in the United States to problems of abuse of gamma-hydroxybutyrate (GHB), with some evidence for problems in other parts of the world as well. In vitro and animal research show that, while GHB shares some properties with abused central nervous system depressant drugs, it has unique aspects of its pharmacology as well, including actions at a specific neural receptor which probably mediates many of its effects. Abuse potential assessment of GHB using standard animal models has not yielded a picture of a highly abusable substance, but little human testing has yet been done. Very little systematic data exist on tolerance and dependence with GHB, but both have been seen in human users. Quantitative data on the prevalence of GHB abuse is incomplete, but various qualitative measures indicate that a mini-epidemic of abuse began in the late 1980s and continues to the present. GHB is often included with the group of 'club drugs', and can be used as an intoxicant. It also has been used as a growth promoter and sleep aid and has been implicated in cases of 'date rape', usually in combination with alcohol. Undoubtedly the easy availability of GHB and some of its precursors has contributed to its popularity. Recent changes in the control status of GHB in the US may reduce its availability with as yet unknown consequences for the scope of the public health problem. Drug abuse experts need to familiarize themselves with GHB as possibly representing a new type of drug abuse problem with some unique properties
UR - PM:11297827
SO - Drug Alcohol Depend 2001 Jun 1 ;63(1):1-22

UI - 7
AU - Okun MS
AU - Boothby LA
AU - Bartfield RB
AU - Doering PI
AD - Emory University, Department of Neurology, Atlanta, Georgia, USA and University of Florida, Department of Neurology, The Brain Institute, Gainesville, Florida, USA
TI - Ghb: an important pharmacologic and clinical update
AB - Gamma-hydroxybutyrate (GHB) intoxication is a significant cause of morbidity and mortality in patients taking the drug for recreational purposes. Due to the recent increase in emergency room visits, hospital admissions, and deaths, it has become necessary to re-examine the pharmacology, pharmacokinetics, pharmacodynamics, clinical manifestations, and potential adverse effects associated with GHB use. We present an important pharmacologic and clinical update on GHB
UR - PM:11466174
SO - J Pharm Pharm Sci 2001 May ;4(2):167-175

UI - 10
AU - Schneir AB
AU - Ly BT
AU - Clark RF
AD - Division of Medical Toxicology, Department of Emergency Medicine, UCSD Medical Center, California Poison Control System-San Diego Division, 200 West Arbor Drive, San Diego, CA 92103-8925, USA
TI - A case of withdrawal from the GHB precursors gamma-butyrolactone and 1,4-butanediol
AB - We describe a case of withdrawal from the gamma hydroxybutyric acid (GHB) precursors gamma butyrolactone and 1,4-butanediol. Symptoms included visual hallucinations, tachycardia, tremor, nystagmus, and diaphoresis. Administration of benzodiazepines and phenobarbital successfully treated the withdrawal symptoms. As predicted from the metabolism of gamma butyrolactone and 1,4-butanediol to GHB, the symptoms were nearly identical to those reported from GHB withdrawal. Because GHB is now illegal in the United States, individuals have begun abusing the legal and easier to acquire GHB precursors. More frequent cases of both abuse and withdrawal from these GHB precursors can be expected
UR - PM:11399385
SO - J Emerg Med 2001 Jul ;21(1):31-33

UI - 30
AU - Andera KM
AU - Evans HK
AU - Wojcik CM
AD - San Bernardino County Sheriff's Department, Rancho Cucamonga, CA 91739-6979, USA
TI - Microchemical identification of gamma-hydroxybutyrate (GHB)
AB - A new microcrystal test for the detection of gamma-hydroxybutyrate (GHB) is described. The silver/copper reagent consists of an aqueous solution of 0.1 g of cupric nitrate and 0.1 g of silver nitrate in 10.0 mL water. While some crystals form upon evaporation of the reagent, the test forms distinctive crystals for GHB and does not form crystals with some commonly encountered controlled substances. The reagent was also tested against some controlled substances that have similar biological activity to GHB, including flunitrazepam, and some barbiturates. No crystals were observed with these compounds. A blind test was performed to determine if GHB could be discriminated from the other compounds. Two of ten unknowns were correctly identified as GHB--one solid, one liquid. One GHB sample was not identified as GHB and the remaining seven non-GHB samples were not identified as GHB. The reagent is therefore selective for GHB, but not extremely sensitive
UR - PM:10855974
SO - J Forensic Sci 2000 May ;45(3):665-668

UI - 20
AU - Boyce SH
AU - Padgham K
AU - Miller LD
AU - Stevenson J
AD - Accident and Emergency Department, Crosshouse Hospital, Kilmarnock, UK
TI - Gamma hydroxybutyric acid (GHB): an increasing trend in drug abuse
AB - The use of recreational drugs in society is becoming a widespread problem increasing the workload of all the emergency services. Gamma hydroxybutyric acid (GHB) is one of these, a drug used primarily for its euphoric effect. Toxic effects of ingestion include bradycardia, slow respiration or apnoea, coma and death. We present seven cases, all of which had consumed GHB either alone or in conjunction with other drugs and alcohol. The presentation, clinical features and management of these cases are described. All health care personnel involved in the emergency setting need to know of its existence, toxic effects and initial management with particular reference to airway control and possible assisted ventilation
UR - PM:11142268
SO - Eur J Emerg Med 2000 Sep ;7(3):177-181

UI - 34
AU - Couper FJ
AU - Logan BK
AD - Washington State Toxicology Laboratory, University of Washington and Bureau of Forensic Laboratory Services, Washington State Patrol, Seattle 98134, USA
TI - Determination of gamma-hydroxybutyrate (GHB) in biological specimens by gas chromatography--mass spectrometry
AB - A simple liquid-liquid extraction procedure for the analysis of gamma-hydroxybutyrate (GHB) in biological fluids without conversion to its lactone, gamma-butyrolactone, is described. Following derivatization to its di-TMS derivative, GHB was detected using gas chromatography-electron impact mass spectrometry. Diethylene glycol was used as the internal standard. The limit of quantitation in 1 mL of blood was 1 mg/L, and a linear response was observed over the concentration range 1 to 100 mg/L. Coefficients of variation for both intra-assay precision and interassay reproducibility ranged between 3.9 and 12.0%. GHB was detected in the blood of a sexual assault victim (3.2 mg/L), in the blood of two driving (DUI) cases (33 and 34 mg/L), and in the blood and urine of two nonfatal GHB-overdose cases (blood 130 and 221 mg/L; urine 1.6 and 2.2 g/L). The observed clinical symptoms ranged from confusion, disorientation, vomiting, and nystagmus to ataxia, sinus bradycardia, unconsciousness, and apnea
UR - PM:10654561
SO - J Anal Toxicol 2000 Jan ;24(1):1-7

UI - 32
AU - Elian AA
AD - Commonwealth of Massachusetts, State Police Crime Laboratory, Forensic Toxicology Unit, 59 Horsepond Road, Sudbury, MA 01776, USA. albert/elian@pol.state.ma.us
TI - A novel method for GHB detection in urine and its application in drug-facilitated sexual assaults
AB - A confirmation procedure for the identification and quantification of gamma-hydroxybutyric acid (GHB) in urine is presented. This method is unique in that it does not involve the conversion of GHB to the gamma-butyrolactone (GBL). The urine samples were extracted using ethyl acetate, evaporated and derivatized with N, O-bis(trimethylsilyl)trifluoroacetamide (BSTFA) with 1% trimethylchlorosilane (TMCS), and analyzed by gas chromatography-mass spectrometry. Quantification was performed using selective ion monitoring (SIM), using GHB-d(6) as the internal standard. This method is simple and provides excellent linearity and sensitivity for GHB in urine
UR - PM:10725654
SO - Forensic Sci Int 2000 Apr 10 ;109(3):183-187

UI - 22
AU - Frison G
AU - Tedeschi L
AU - Maietti S
AU - Ferrara SD
AD - Forensic Toxicology and Antidoping, University Hospital of Padova, Via Falloppio 50, I-35121 Padova, Italy
TI - Determination of gamma-hydroxybutyric acid (GHB) in plasma and urine by headspace solid-phase microextraction and gas chromatography/positive ion chemical ionization mass spectrometry
AB - A new method for the qualitative and quantitative analysis of gamma-hydroxybutyric acid (GHB) in plasma and urine samples is described. It involves the conversion of GHB to gamma-butyrolactone (GBL), its subsequent headspace solid-phase microextraction (SPME), and detection by gas chromatography/positive ion chemical ionization mass spectrometry (GC/PICI-MS), using D(6)-GBL as internal standard. The assay is linear over a plasma GHB range of 1-100 &mgr;g/mL (n = 5, r = 0.999) and a urine GHB range of 5-150 &mgr;g/mL (n = 5, r = 0. 998). Relative intra- and inter-assay standard deviations, determined for plasma and urine samples at 5 and 50 &mgr;g/mL, are all below 5%. The method is simple, specific and reasonably fast. It may be applied for clinical and forensic toxicology as well as for purposes of therapeutic drug monitoring
UR - PM:11114057
SO - Rapid Commun Mass Spectrom 2000 ;14(24):2401-2407

UI - 33
AU - Hu RQ
AU - Banerjee PK
AU - Snead OC
AD - Department of Pediatrics, Faculty of Medicine, Hospital for Sick Children, University of Toronto, Ontario, Canada. ruo.hu@sickkids.on.ca
TI - Regulation of gamma-aminobutyric acid (GABA) release in cerebral cortex in the gamma-hydroxybutyric acid (GHB) model of absence seizures in rat
AB - Gamma-hydroxybutyric acid (GHB) has the ability to induce absence seizures. The precise way in which GHB causes seizures remains unclear, but GABA(B)- and/or GHB-mediated presynaptic mechanisms within thalamocortical circuitry may play a role. In the present study, we determined the basal and K+-evoked release of GABA and glutamate in the superficial laminae of frontal cortex during GHB-induced absence seizures. Our data indicate that both the basal and K+-evoked release of GABA were significantly decreased in laminae I-III of frontal cortex at the onset of GHB-induced absence seizures. The appearance and disappearance of the observed changes in basal and K+-evoked extracellular levels of GABA correlated with the onset and offset of absence seizures. In contrast, neither the basal nor the K+-evoked release of glutamate was altered in superficial laminae of cerebral cortex at any time during the absence seizures. Intracortical perfusion of the GABA(B) receptor antagonists, CGP 35348 and phaclofen as well as the GHB receptor antagonist, NCS 382 attenuated GHB-mediated changes in the basal and K+-evoked release of GABA. These data suggest that GHB induces a selective decrease in the basal and depolarization-induced release of GABA in cerebral cortex, and further, that this action of GHB may play a role in the mechanism by which GHB induces absence seizures
UR - PM:10698009
SO - Neuropharmacology 2000 Jan 28 ;39(3):427-439

UI - 29
AU - Ingels M
AU - Rangan C
AU - Bellezzo J
AU - Clark RF
AD - Department of Emergency Medicine, University of California San Diego Medical Center, 92103-8925, USA
TI - Coma and respiratory depression following the ingestion of GHB and its precursors: three cases
AB - Gamma hydroxybutyrate (GHB) is a product of the metabolism of both gamma butyrolactone (GBL) and 1,4-butanediol (1,4-BD). Gamma hydroxybutyrate (GHB) is an illegal agent that causes central nervous system depression. Chemical precursors of GHB, such as GBL and 1,4-BD, have been available for purchase from many health food stores and Internet websites for mood-enhancement, sleep-induction, and stimulation of growth hormone release. We report three cases of ingestion of products containing GHB and chemical precursors of GHB. All three patients had severe presentations followed by full recoveries. Some products containing GBL were withdrawn from the market after the FDA issued a warning regarding these products. Products containing 1,4-butanediol remain on the market today
UR - PM:10863118
SO - J Emerg Med 2000 Jul ;19(1):47-50

UI - 31
AU - Nordenberg T
TI - The death of the party. All the rave, GHB's hazards go unheeded
MH - Adult
MH - Case Report
MH - Human
MH - Male
MH - Overdose
MH - Rape
MH - Recreation
MH - Sodium Oxybate
MH - adverse effects
MH - poisoning
MH - Substance-Related Disorders
UR - PM:10783685
SO - FDA Consum 2000 Mar ;34(2):14-19

UI - 21
AU - O'Connell T
AU - Kaye L
AU - Plosay JJ
AD - Santa Monica-UCLA Medical Center, California, USA. toconnel@mednet.ucla.edu
TI - Gamma-hydroxybutyrate (GHB): a newer drug of abuse
AB - Gamma-hydroxybutyrate (GHB) is an illicitly marketed substance that has recently gained popularity among body builders and party attendees as a drug of abuse. GHB is a depressant that acts on the central nervous system. It is purported as a strength enhancer, euphoriant and aphrodisiac and is one of several agents reported as being used as a "date rape" drug. Because of its central nervous system depressant effects, GHB can be lethal when combined with alcohol or other depressants. Currently, there is no accepted medical use for GHB, and the U.S. Food and Drug Administration has prohibited its manufacture and sale. Clinicians should be familiar with the typical clinical presentation of GHB and its adverse effects. In addition, patients should be warned of its potential toxicity and be cautioned to avoid the use of GHB
UR - PM:11130233
SO - Am Fam Physician 2000 Dec 1 ;62(11):2478-2483

UI - 23
AU - Price G
TI - In-patient detoxification after GHB dependence
MH - Adjuvants,Anesthesia
MH - adverse effects
MH - Adult
MH - Case Report
MH - Hospitalization
MH - Human
MH - Male
MH - Metabolic Detoxication,Drug
MH - Sodium Oxybate
MH - Substance Withdrawal Syndrome
MH - etiology
MH - Substance-Related Disorders
MH - rehabilitation
UR - PM:11026962
SO - Br J Psychiatry 2000 Aug ;177():181

UI - 35
AU - Addolorato G
AU - Balducci G
AU - Capristo E
AU - Attilia ML
AU - Taggi F
AU - Gasbarrini G
AU - Ceccanti M
AD - Institute of Internal Medicine, Universita' Cattolica del Sacro Cuore, Rome, Italy. ecapristo@pelagus.it
TI - Gamma-hydroxybutyric acid (GHB) in the treatment of alcohol withdrawal syndrome: a randomized comparative study versus benzodiazepine
AB - BACKGROUND: Benzodiazepine has been shown to be one of the most effective class of drugs in the management of alcohol withdrawal syndrome (AWS). Gamma-hydroxybutyric acid (GHB) has recently been introduced in the treatment of alcohol problems, including AWS. At present there are no comparative studies between benzodiazepines and GHB in AWS treatment. The aim of the present randomized, controlled, single-blind study was to evaluate the efficacy and safety of GHB compared with diazepam in the treatment of AWS. METHODS: Sixty alcoholics affected by AWS were enrolled in the study. Diazepam (0.5-0.75 mg/kg body weight for 6 days, tapering the dose 25% daily until day 10) was administered orally to 30 patients (25 males, 5 females; mean age 44.3 +/- 10.9 years); GHB (50 mg/kg body weight for 10 days) was administered orally to 30 patients (26 males,4 females; mean age 41.7 +/- 10.4 years).The Clinical Institute Withdrawal Assessment for Alcohol-revised scale (CIWA-Ar) was used to evaluate the AWS physical symptoms. The State Anxiety Inventory test for current anxiety assessment and the Zung self-rating Depression Scale for current depression assessment were performed. RESULTS: Eight patients (26.6%) in the diazepam group and 4 patients (13.3%) in the GHB group dropped out. Both treatments were effective in reducing AWS. No significant difference was found between the groups in CIWA-Ar total score at baseline and at the different times of observation. Considering the CIWA-Ar subscore and Zung scale, a significant reduction of anxiety on day 4 (p < 0.02), agitation on day 5 (p < 0.02) and time of recovery of depression on day 5 (p < 0.02) was observed in the GHB group with respect to the diazepam group. Drowsiness and vertigo developed after initial drug administration in the GHB (19.2%) and diazepam (36.4%) groups and quickly resolved in both groups. CONCLUSIONS: GHB is as effective in the management of AWS as benzodiazepine and it seems to be quicker in reducing anxiety, agitation, and depression. Both drugs are safe and well-tolerated in AWS management
UR - PM:10549990
SO - Alcohol Clin Exp Res 1999 Oct ;23(10):1596-1604

UI - 38
AU - Addolorato G
AU - Capristo E
AU - Gessa GL
AU - Caputo F
AU - Stefanini GF
AU - Gasbarrini G
AD - Institute of Internal Medicine, Catholic University, Rome, Italy
TI - Long-term administration of GHB does not affect muscular mass in alcoholics
AB - Gamma-hydroxybutyric acid (GHB) is a drug recently utilized for alcoholism management. It has been shown that GHB has anabolic effects since it can increase growth hormone (GH) release in healthy subjects. At present, there are no studies investigating body composition in alcoholics during long-term GHB treatment. In this study body composition and GH secretion in alcohol dependent subjects was evaluated during addiction and at different time of GHB administration and alcohol abstinence. A total of 45 male alcohol dependent patients (mean age 39.7+/-9.8 yrs, mean height: 171+/-6.8 cm, body mass index--BMI--22.1+/-1.6 kg/m(-2)) were consecutively enrolled. Body composition was assessed by anthropometry, bioimpedance analysis and tritiated water method. A 7-day food diary was collected. Plasma GH levels were determined by radioimmunoassay. A 6-month total abstinence was obtained in 22 patients, by means of psychological support counseling and self-help groups in 9 subjects and also by 50 mg/kg/day of GHB in 13 subjects. At 1, 2, 3 and 6 months of abstinence, the biochemical assessment and metabolic variables were re-examined. Fat-free mass (FFM) and basal GH secretion were similar at the different times of follow-up in both groups of patients. GHB treated patients and those receiving psychological support alone showed similar values in FFM and GH. Both groups of patients did not differ in FFM and plasma GH level from healthy controls at any of the times evaluated. Waist-to-hip ratio did not differ between patient groups, while higher values were shown in alcoholics with respect to control subjects. The present study shows that long-term administration of GHB did not affect muscular mass and did not determine an increase of GH release in chronic alcoholics. This findings could be due to an impairment of the hypothalamic-limbic system and of GABAergic neurotransmission in alcoholics' brain
UR - PM:10530806
SO - Life Sci 1999 ;65(14):L191-L196

UI - 42
AU - Badcock NR
AU - Zotti R
TI - Rapid screening test for gamma-hydroxybutyric acid (GHB, Fantasy) in urine
MH - Human
MH - Hydroxybutyrates
MH - urine
MH - Mass Screening
MH - methods
MH - Time Factors
UR - PM:10365656
SO - Ther Drug Monit 1999 Jun ;21(3):376

UI - 36
AU - Davis LG
TI - Fatalities attributed to GHB and related compounds
MH - 4-Butyrolactone
MH - blood
MH - poisoning
MH - Adult
MH - Case Report
MH - Ethanol
MH - Fatal Outcome
MH - Female
MH - GABA Modulators
MH - Human
MH - Hydroxybutyrates
MH - Male
MH - Respiration
MH - drug effects
UR - PM:10548184
SO - South Med J 1999 Oct ;92(10):1037

UI - 37
AU - Eckstein M
AU - Henderson SO
AU - DelaCruz P
AU - Newton E
AD - Los Angeles City Fire Department, California, USA. eckstein@hsc.usc.edu
TI - Gamma hydroxybutyrate (GHB): report of a mass intoxication and review of the literature
UR - PM:10534040
SO - Prehosp Emerg Care 1999 Oct ;3(4):357-361

UI - 40
AU - Li J
AD - Division of Emergency Medicine, Harvard Medical School, USA
TI - The new "Mickey Finn specials"--should GHB and ketamine be banned?
UR - PM:10467808
SO - J Am Pharm Assoc (Wash ) 1999 Jul ;39(4):442-443

UI - 39
AU - McCusker RR
AU - Paget-Wilkes H
AU - Chronister CW
AU - Goldberger BA
AD - Department of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville 32610-0275, USA
TI - Analysis of gamma-hydroxybutyrate (GHB) in urine by gas chromatography-mass spectrometry
AB - A simple method for the direct analysis of gamma-hydroxybutyrate (GHB) from human urine is described. The method uses solid-phase extraction, liquid-liquid extraction, and silyl-derivatization, then gas chromatographic-mass spectrometric analysis using GHB-d6 as the internal standard. The method was linear from 5 to 500 mg/L, and coefficients of variation were less than 10%. Twenty-six urine specimens previously analyzed by an existing method were analyzed and yielded GHB concentrations ranging from 0 to 6100 mg/L; the results correlated between the two methods. Compared with existing methods, the method described here is superior because it is specific to GHB and can discriminate between GHB and gamma-butyrolactone
UR - PM:10488915
SO - J Anal Toxicol 1999 Sep ;23(5):301-305

UI - 43
AU - Banerjee PK
AU - Liu CC
AU - Snead OC
AD - Division of Neurology and The Brain and Behavior Program, Hospital for Sick Children, Department of Pediatrics, Faculty of Medicine, University of Toronto, 555 University Ave., Toronto, Ontario, Canada. pradeep.banerjee@mailhub.sickkids.on.ca
TI - Steroid-inhibition of [3H]gamma-hydroxybutyric acid (GHB) binding in thalamic relay nuclei increases during absence seizures
AB - gamma-Hydroxybutyric acid (GHB), a naturally occurring analog of GABA, induces absence-like seizures in rats. We characterized the interaction of 3alpha-hydroxy steroids, alphaxalone and tetrahydrodeoxycorticosterone (which are potent modulators of GABAA receptors) with GHB binding sites in rat brain cortical membranes. The steroids inhibited [3H]GHB binding in a dose-dependent fashion (IC50 approximately 1 microM). Neither bicuculline nor GABA altered the dose-response of steroids in the [3H]GHB assay, suggesting that there was no GABAA component involved in the steroid-inhibition of [3H]GHB binding. Also, non 3alpha-hydroxy steroids were inactive in displacing [3H]GHB. Because GHB-induced absence seizures evolve most readily from layers I-IV of frontoparietal cortex and thalamic relay nuclei, we determined if the interaction of steroids with GHB binding sites in layers I-IV of frontoparietal cortex and thalamic relay nuclei was altered during GHB-induced absence seizures. We found that during GHB-seizures steroid-inhibition of [3H]GHB binding was increased selectively in thalamic relay nuclei but not in the layers I-IV of frontoparietal cortex or any other brain regions tested. This increase in steroid-inhibition of [3H]GHB binding in thalamus was apparent about 30 min after the onset of seizures, but not at the seizure-onset. As the seizures dissipated, the IC50 values for steroids rose to the pre-seizure level. These data suggest that the enhancement in steroid-inhibition of [3H]GHB binding in thalamic relay nuclei observed during GHB-seizures was caused by absence seizures
UR - PM:9838187
SO - Brain Res 1998 Dec 7 ;813(2):343-350

UI - 48
AU - Gillery P
AU - Dumont G
AU - Vassault A
AD - Central Laboratory of Biochemistry, Robert Debre Hospital, Centre Hospitalier Universitaire, Reims, France. gillery@infobiogen.fr
TI - Evaluation of GHb assays in France by national quality control surveys
AB - OBJECTIVE: To evaluate the state of the art concerning GHb assays through analysis of a large-scale quality control survey and to compare the results with those of previous surveys. RESEARCH DESIGN AND METHODS: A lyophilized hemolyzate prepared from human erythrocytes containing a physiological HbA1c level (5.5%) was sent to 3,500 French laboratories in February of 1995 and assayed as a patient's sample under routine conditions. Distribution of values was analyzed from the reported results for each method. The results were compared with the assigned value (acceptable range: +/- 20%) and with the upper value of the reference range currently used. RESULTS: Results were obtained from 2,674 laboratories, among which 39% used cation-exchange chromatography methods, 37.5% affinity chromatography, 16% immunological methods, and 7.5% electrophoresis. The number of laboratories using immunological methods increased from 100 to 400 between 1993 and 1995. The overall interlaboratory coefficient of variation (CV) was 20.2%, with within-method CVs ranging between 3.2 and 29.5%. Method-to-method accuracy varied dramatically, with mean HbA1c values ranging from 4.4 to 8.2%. Results from 75% of the laboratories were comprised in the acceptable range; 88% of them reported a value within the normal range of the method used. CONCLUSIONS: The interlaboratory variability of results illustrates the difficulties encountered by diabetologists in the follow-up of diabetic patients using results obtained from different laboratories. It demonstrates the usefulness of the internationally developed standardization process of GHb measurements and points out the need for laboratories to fulfill good practices
UR - PM:9539994
SO - Diabetes Care 1998 Feb ;21(2):265-270

UI - 49
AU - Hernandez M
AU - McDaniel CH
AU - Costanza CD
AU - Hernandez OJ
AD - University of Southern California School of Medicine, Los Angeles, California, USA
TI - GHB-induced delirium: a case report and review of the literature of gamma hydroxybutyric acid
AB - We describe what we believe is the first psychiatric hospitalization due to GHB-induced delirium reported in the medical literature. We examine the use of the substance gamma hydroxybutyric acid (GHB) and describe the clinical findings in a patient who presented to an acute inpatient psychiatric unit with a chief complaint of feeling suicidal and a 1-year history of GHB use. A review of the literature and GHB's availability through the Internet are discussed
UR - PM:9513637
SO - Am J Drug Alcohol Abuse 1998 Feb ;24(1):179-183

UI - 44
AU - Kleinschmidt S
AU - Grundmann U
AU - Knocke T
AU - Silomon M
AU - Bach F
AU - Larsen R
AD - Department of Anaesthesiology and Critical Care Medicine, University of Saarland, Homburg, Saar, Germany
TI - Total intravenous anaesthesia with gamma-hydroxybutyrate (GHB) and sufentanil in patients undergoing coronary artery bypass graft surgery: a comparison in patients with unimpaired and impaired left ventricular function
AB - The haemodynamic effects of anaesthesia with gamma-hydroxybutyrate (GHB)/sufentanil for elective coronary artery bypass grafting (CABG) were investigated and compared in patients with unimpaired left ventricular function (ejection fraction > or = 45%, left ventricular end diastolic pressure < or = 16 mmHg) and patients with impaired left ventricular function. In 38 consecutive patients scheduled for CABG (21 with unimpaired and 17 with impaired left ventricular function), anaesthesia was induced with etomidate, sufentanil and pancuronium. After tracheal intubation, the lungs were normoventilated (end tidal Pco2 4.9-5.6 kPa) with an oxygen-air mixture (Fio2 0.5). Total intravenous anaesthesia was maintained with GHB (20 mg kg-1 h-1 after a 'priming dose' of 40 mg kg-1) and sufentanil (2 micrograms kg-1 h-1). Haemodynamic measurements were made after induction of anaesthesia and at various times in the prebypass period. Patients in both groups showed similar haemodynamic trends. Mean arterial pressure showed a maximum reduction of 10%, whereas heart rate and right- and left-sided filling pressures remained unchanged within the groups after the induction of anaesthesia. Cardiac index remained unchanged in both groups, although values differed between the groups. A total of 14 out of 21 patients (67%) with unimpaired and 10 out of 17 patients (59%) with impaired ventricular function required supplementary administration of opioids to control temporary hypertension after sternotomy. No episodes of myocardial ischaemia were detected during the study period using ST segment analysis (leads II and V5). The results of this study suggest that GHB provides adequate haemodynamic conditions in the prebypass period and may be a suitable agent for TIVA also in patients with impaired left ventricular function undergoing CABG
UR - PM:9785071
SO - Eur J Anaesthesiol 1998 Sep ;15(5):559-564

UI - 46
AU - Scharf MB
AU - Lai AA
AU - Branigan B
AU - Stover R
AU - Berkowitz DB
AD - Center For Research In Sleep Disorders, Cincinnati, Ohio, USA
TI - Pharmacokinetics of gammahydroxybutyrate (GHB) in narcoleptic patients
AB - Sodium gammahydroxybutyrate (GHB) is an endogenous compound that has been under investigation in the management of narcolepsy for about two decades. The data confirm that GHB treatment decreases daytime sleepiness and episodes of cataplexy, sleep paralysis, and hypnagogic hallucinations. The current study evaluated the pharmacokinetics of GHB, given twice in one night to six narcoleptic patients who had been chronically taking GHB nightly on a similar basis. Results confirmed earlier reports and showed nonlinear pharmacokinetics. Maximum concentrations were reached in 40 +/- 6.2 and 35.7 +/- 7 minutes after the first and second dose respectively. Mean AUCinf was 17731.6 +/- 4867 mg/mL/m. Mean GHB T1/2 was 53 +/- 19 minutes. GHB elimination appears to be capacity-limited in some patients when administered at a fixed dose of 3 g twice nightly at a 4-hour interval
UR - PM:9703591
SO - Sleep 1998 Aug 1 ;21(5):507-514

UI - 47
AU - Williams H
AU - Taylor R
AU - Roberts M
AD - United Medical School, Guy's Hospital (UMDS), London
TI - Gamma-hydroxybutyrate (GHB): a new drug of misuse
AB - Accident and Emergency Departments offer a unique opportunity for identifying and monitoring new drugs of misuse. This series of six case reports describes the potentially serious medical complications associated with the use of gamma-hydroxybutyrate (GHB) a new drug of misuse on the UK scene. Profound unconsciousness occurred in all cases and despite full (and often rapid) recovery all patients required medical intervention. Adverse effects occurred both when GHB was used alone or in combination with other illicit drugs and alcohol
UR - PM:9617031
SO - Ir Med J 1998 Mar ;91(2):56-57

UI - 52
AU - Bismuth C
AU - Dally S
AU - Borron SW
AD - Hopital Fernand Widal Paris University, France
TI - Chemical submission: GHB, benzodiazepines, and other knock out drops
MH - Adjuvants,Anesthesia
MH - poisoning
MH - Adult
MH - Benzodiazepines
MH - Case Report
MH - Crime Victims
MH - legislation & jurisprudence
MH - Fatal Outcome
MH - Female
MH - Forensic Medicine
MH - Human
MH - Male
MH - Middle Age
MH - Sodium Oxybate
MH - Street Drugs
MH - Substance Abuse Detection
MH - Substance-Related Disorders
MH - prevention & control
UR - PM:9365425
SO - J Toxicol Clin Toxicol 1997 ;35(6):595-598

UI - 55
AU - Hoshino T
AU - Okahashi M
AU - Arai H
AU - Hoshine T
AD - Pharmaceutical Institute, Keio University, Tokyo, Japan
TI - Survey and assessment of the actual state of routine measurement of glycohaemoglobin/GHb by commercial methods: warning to the users and the providers
AB - As the clinical availability of glycohaemoglobin/GHb measurement increases, so does the need for comparable and accurate values among different laboratories and different methods. At least there should be comparability, i.e., commutability or feasibility of providing comparable results from different assays in different laboratories. A clinical joint study on insulin therapy, a survey of the actual inter-laboratory differences in GHb measurement among 41 institutions and an assessment of 11 assay methods for the determination of GHb were performed using commercial calibrators and fresh blood samples. Data on the actual state of inter-laboratory and inter-assay differences of observed values were useful for comparing results among facilities. The recommendation of the Japan Diabetes Society to measure only the stable GHb component and to correct the GHb percentage by two-point calibration with assigned values, was effective but not sufficient. Even after correction, 8 out of 11 methods still remained of little practical use because of their large relative errors. Inter-method differences among 11 available assay methods were great even after correction and depended on not only the methods but the samples used for the determination. The performance of some methods or instruments used are only poor at distinguishing the stable glycated haemoglobin itself. Some alternative measurement system with comparability, commutability and precision should be established. An urgent and worldwide problem to remove inter-laboratory differences in the measurement of GHb needs to be solved. Users in clinical practice must recognize these problems, and, before supply, the providers should check their method and keep records that are readily traceable
UR - PM:9226589
SO - J Pharm Biomed Anal 1997 Jun ;15(9-10):1551-1562

UI - 50
AU - King MA
AU - Thinschmidt JS
AU - Walker DW
AD - VA Medical Center, University of Florida College of Medicine, Gainesville, USA
TI - Gammahydroxybutyrate (GHB) receptor ligand effects on evoked synaptic field potentials in CA1 of the rat hippocampal slice
AB - GHB produced a concentration-dependent depression of evoked synaptic field potentials (EFPs) recorded extracellularly in the CA1 region of the in vitro rat hippocampal slice. The concentration/response function revealed a threshold near 1 mM, with IC50 of 10.85 mM and a Hill coefficient of 1.29. The gamma-aminobutyric acid B-receptor (GABA-B) agonist baclofen also depressed the EFP, but even maximally effective concentrations of the GABA-B antagonist 2-hydroxy-saclofen (800 microM) could not completely block the GHB-induced EFP depression. Nor was GHB-induced EFP depression blocked by the GHB receptor "antagonist" NCS-382, which does not displace GABA-B receptor ligands. However, NCS-382 produced a concentration-dependent increase in EFP slope. The threshold concentration was about 100 microM but the maximally effective concentration, and thus the IC50, could not be determined in the perfusion slice system. NCS-382 may be an inverse agonist at hippocampal GHB receptors, or else endogenous hippocampal GHB receptor ligands medicate a tonic inhibition in CA1. At concentrations sufficient to induce EFP depression GHB did not alter pH. Although isosmotic sucrose did depress CA1 EFPs it was essentially ineffective at the IC50 for GHB. Gamma-butyrolactone, a prodrug of GHB, was only 1/20th as effective as GHB. This is consistent with previous data suggesting that GBL is freely permeable (does not substantially disturb tonicity) and that brain has very little capacity to either enzymatically convert the lactone to GHB or respond to the lactone itself
UR - PM:9503264
SO - J Neural Transm 1997 ;104(11-12):1177-1193

UI - 53
AU - Louagie HK
AU - Verstraete AG
AU - De Soete CJ
AU - Baetens DG
AU - Calle PA
AD - Department of Clinical Biology, University Hospital, Ghent, Belgium. Henk.Louagie@rug.ac.be
TI - A sudden awakening from a near coma after combined intake of gamma-hydroxybutyric acid (GHB) and ethanol
AB - OBJECTIVE: A case of a sudden awakening from a near coma after combined intake or gamma-hydroxybutyric acid (GHB) (125 micrograms/mL), ethanol (134 mg/dL), and cannabinoids is described. METHODS: GHB was determined by gas chromatography-mass spectrometry after acetonitrile precipitation and derivation with N-methyl-N-trimethylsilyltrifluoroacetamide, using valproic acid as the internal standard. CONCLUSION: The described case illustrates the consequences of GHB overdose. GHB overdose should be considered in every case of unexplained sudden coma, i.e., without any evidence of head injury, intake of coma-inducing drugs, or increasing intracranial pressure. GHB overdose will be missed by routine toxicological screening
UR - PM:9365424
SO - J Toxicol Clin Toxicol 1997 ;35(6):591-594

UI - 56
AU - Marwick C
TI - Coma-inducing drug GHB may be reclassified
MH - Coma
MH - chemically induced
MH - Drug and Narcotic Control
MH - Human
MH - Overdose
MH - Sodium Oxybate
MH - adverse effects
MH - Substance-Related Disorders
MH - epidemiology
MH - United States
UR - PM:9153353
SO - JAMA 1997 May 21 ;277(19):1505-1506

UI - 58
AU - Rosen MI
AU - Pearsall HR
AU - Woods SW
AU - Kosten TR
AD - Yale University School of Medicine, Department of Psychiatry, New Haven, CT, USA
TI - Effects of gamma-hydroxybutyric acid (GHB) in opioid-dependent patients
AB - Gamma-hydroxybutyric acid (GHB) is a GABA metabolite used clinically for sleep induction. The abuse liability of GHB is controversial. As part of a study of the effect of GHB pretreatment on naloxone-precipitated opiate withdrawal, eight opioid-stabilized subjects received a balanced, randomized, double-blind sequence of oral placebo, GHB 15 mg/kg and 30 mg/kg. GHB had no consistent physiological effects. After GHB and prior to naloxone, subjects rated "sluggish," "spaced," "carefree," and "good-mood" higher after GHB 30 mg/kg than after placebo. Subjects identified the 30 mg/kg dose as most similar to placebo (n = 3), benzodiazepine (n = 2), opiate (n = 2), and alcohol (n = 1)
UR - PM:9258859
SO - J Subst Abuse Treat 1997 Mar ;14(2):149-154

UI - 51
AU - Sanguineti VR
AU - Angelo A
AU - Frank MR
AD - Department of Psychiatry and Human Behavior, Thomas Jefferson Medical College, Philadelphia, Pennsylvania, USA
TI - GHB: a home brew
AB - Gamma-hydroxybutyric acid is an allegedly benign illicit substance that is gaining increasing recognition and attention among substance abusers and athletes. Alongside foreign-made brands, the compound is also easily available, at low cost because of the facility with which it can be produced in one's kitchen. Named by some "Nature's Quaalude" or sold as a health product, it is often used with a false sense of security as it may cause serious and disabling complications, as illustrated by this clinical vignette
UR - PM:9366979
SO - Am J Drug Alcohol Abuse 1997 Nov ;23(4):637-642

UI - 54
AU - Tunnicliff G
AD - Indiana University, School of Medicine, Evansville 47712, USA. gtunnic@indyvax.iupui.edu
TI - Sites of action of gamma-hydroxybutyrate (GHB)--a neuroactive drug with abuse potential
AB - OBJECTIVE: This review highlights the biochemistry, pharmacology, and toxicology of the naturally-occurring fatty acid derivative, gamma-hydroxybutyrate (GHB). GHB is derived from gamma-aminobutyric acid (GABA) and is proposed to function as an inhibitory chemical transmitter in the central nervous system. CONTENT: When administered in pharmacological doses, its powerful central nervous system depressant effects are readily observed. Although some of the neurophysiological actions of GHB could involve alterations in dopaminergic transmission in the basal ganglia, both its physiological and pharmacological actions are probably mediated through specific brain receptors for GHB. In addition, GHB might mediate some of its effects through interaction with the GABA(B) receptor. Experimentally, GHB has been used as a model for petit mal epilepsy; clinically, it has been used as a general anesthetic and as a drug to treat certain sleep disorders and related conditions. Owing to the purported ability of GHB to induce a state of euphoria, recreational use of this substance is popular. Although no deaths or long-term problems have been associated with GHB abuse, symptoms of GHB intoxication can be severe. The continued potential for GHB abuse makes it imperative for clinical toxicologists to be aware of the effects of this agent. Future research on the mechanism of action of GHB is needed to elucidate both its central nervous system depressant properties and its ability to effect a state of well-being
UR - PM:9365423
SO - J Toxicol Clin Toxicol 1997 ;35(6):581-590

UI - 61
AU - Addolorato G
AU - Castelli E
AU - Stefanini GF
AU - Casella G
AU - Caputo F
AU - Marsigli L
AU - Bernardi M
AU - Gasbarrini G
AD - Internal Medicine II Chair, Catholic University Sacro Cuore, Rome, Italy
TI - An open multicentric study evaluating 4-hydroxybutyric acid sodium salt in the medium-term treatment of 179 alcohol dependent subjects. GHB Study Group
AB - We report the results of an "open' multicentre study evaluating the use, tolerability and therapeutic efficacy of the sodium salt of 4-hydroxybutyric acid (GHB) for the medium-term treatment of withdrawal symptoms in 179 patients with alcohol dependence followed up as outpatients. The follow-up of patients was 6 and 12 months after drug discontinuation. Following a daily oral administration of 50 mg/kg for approximately 6 months, no serious systemic or single-organ consequences leading to drug discontinuation were reported, and tolerability was fair in all patients. Eleven subjects (10.1%) showed craving for the drug and voluntarily increased their doses (6-7 times the recommended levels). GHB led to complete abstinence during drug administration in 78.0% of the patients. A significant reduction of compulsive desire ("craving') was observed in parallel, as deduced from evaluation of a specific questionnaire, the Alcohol Craving Scale. At follow-up examination, 43 of the treated subjects remained abstinent at 6 months, and 30 subjects were abstinent for 1 year after drug discontinuation
UR - PM:8879280
SO - Alcohol Alcohol 1996 Jul ;31(4):341-345

UI - 60
AU - Beardsley PM
AU - Balster RL
AU - Harris LS
AD - Medical College of Virginia, Department of Pharmacology & Toxicology, Richmond 23298-0613, USA
TI - Evaluation of the discriminative stimulus and reinforcing effects of gammahydroxybutyrate (GHB)
AB - Gammahydroxybutyrate (GHB) satisfies many of the criteria for consideration as a neuro-transmitter including having specific receptor sites, endogenous synthesis, and heterogeneous CNS distribution. GHB has been reported to be illicitly used, to induce physical dependence, and to relieve effects from alcohol and heroin withdrawal. GHB has also been shown to have antidopaminergic activity to displace 3H[MK-801] binding in brain membranes, and to have some in vivo effects similar to the typical antipsychotics. To characterize the behavioral pharmacology of GHB further, we evaluated it for its reinforcing effects upon IV administration in rhesus monkeys with PCP self-administration histories, its ability to produce heroin- and PCP-like discriminative stimulus effects, and for its ability to antagonize cocaine discrimination in rats. The results indicated that GHB (300-7500 micrograms/kg per infusion) was not self-administered above vehicle control rates, although self-infusions occurred at levels sufficient to produce signs indicative of sedation. Also, neither heroin nor PCP discriminative stimulus effects generalized to injections of GHB up to 300 mg/kg IP, and GHB did not effectively antagonize the cocaine discriminative stimulus when tested up to 300 mg/kg IP. These data indicate that GHB is unlike PCP as a reinforcer and that neither PCP nor heroin generalize to injections of GHB, nor can injections of GHB attenuate the discriminative stimulus effects of cocaine
UR - PM:8923566
SO - Psychopharmacology (Berl) 1996 Oct ;127(4):315-322

UI - 62
AU - Gilbert RE
AU - Goodall I
AU - Young V
AU - Jerums G
AD - Endocrinology Unit, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia. barbara@pet1.austin.unimelb.edu.au
TI - Interlaboratory variation of GHb assays in Victoria, Australia
AB - OBJECTIVE: To determine the extent of interlaboratory variation and accuracy in the measurement of glycated hemoglobin (GHb). RESEARCH DESIGN AND METHODS: All laboratories that measure glycated hemoglobin in the State of Victoria, Australia, were invited to participate, and positive responses were received from 27 to 30 laboratories. An aliquot of blood drawn from three patients with diabetes and varied glycemia and from one nondiabetic subject was sent to each participating laboratory. Distribution of results was analyzed according to the reported results and their variance from an assigned reference value and were expressed as differing from this latter value as percentage bias and in absolute terms. A bias > or = 10% or an absolute difference of > or = 1% HbA1c from the reference value was considered significant. RESULTS: Reported results for the same blood sample ranged from 4.1 to 5.8%, 5.1 to 8.2%, 6.7 to 9.3%, and 10.1 to 14.7% for the specimens from the nondiabetic subject and the diabetic patients with good, moderate, and poor glycemic control, respectively. The proportion of laboratories with results that differed by > or = 10% bias from the reference value were 39% (12 of 30), 29% (9 of 30), 16% (5 of 30), and 32% (10 of 30), and the proportion reporting results that differed by > or = 1% HbA1c in absolute terms from the reference values were 3% (1 of 30), 6% (2 of 30), 16% (5 of 30), and 23% (7 of 30) for the specimens from the nondiabetic subject and the diabetic patients with good, moderate, and poor glycemic control, respectively. CONCLUSIONS: A substantial degree of interlaboratory variation for GHb measurement exists in Victoria, Australia. This may lead to difficulties in interpretation when GHb is assayed by different laboratories in the same patient over time. Interlaboratory standardization may be achievable by calibration to a standard assigned by a reference laboratory and distributed to all laboratories measuring GHb
UR - PM:8799628
SO - Diabetes Care 1996 Jul ;19(7):730-734

UI - 65
AU - James C
TI - Another case of gamma hydroxybutyrate (GHB) overdose
MH - Case Report
MH - Coma
MH - chemically induced
MH - Emergency Service,Hospital
MH - Fatal Outcome
MH - Human
MH - Seizures
MH - Sodium Oxybate
MH - poisoning
NT - UI - 96344939DA - 19960919IS - 0099-1767LA - engPT - CommentPT - LetterCY - UNITED STATESJC - KRURN - 502-85-2 (Sodium Oxybate)SB - N
UR - PM:8716296
SO - J Emerg Nurs 1996 Apr ;22(2):97

UI - 63
AU - Kullberg CE
AU - Bergstrom A
AU - Dinesen B
AU - Larsson L
AU - Little RR
AU - Goldstein DE
AU - Arnqvist HJ
AD - Department of Internal Medicine, Faculty of Health Sciences, Linkoping, Sweden
TI - Comparisons of studies on diabetic complications hampered by differences in GHb measurements
AB - OBJECTIVE: To compare glycated hemoglobin (GHb) values of the relationship between glycemic control and complications of diabetes from laboratories involved in long-term studies (Steno, Oslo, Stockholm, Diabetes Control and Complications Trial, and Linkoping.) RESEARCH DESIGN AND METHODS: Blood samples were collected from 25 subjects selected to represent the clinically relevant measurement range. Fresh whole-blood samples were distributed and analyzed within 4 days of sample collection. Pretreatment of samples and analyses of GHb were performed according to the routine method of each study's central or reference laboratory. Results from each laboratory were compared with the group mean, i.e., the mean of all results for each sample. RESULTS: Regression analyses with the group mean values as independent variables and results from each laboratory as dependent variables showed that Oslo's result had a slope significantly different from the group mean. Laboratories used by the DCCT, Oslo, and Steno studies gave, on average, 0.4, 0.4, and 0.7% higher HbA1c readings than the group mean, respectively, while HbA1c results from Linkoping and Stockholm were, on average, 0.6 and 1.0% lower, respectively. CONCLUSIONS: There were large differences in GHb values among laboratories participating in studies of diabetic complications. The present data offer a guide to the comparison of results from the studies and underscores the need for standardization of GHb measurements
UR - PM:8799627
SO - Diabetes Care 1996 Jul ;19(7):726-729

UI - 59
AU - Snead OC
AD - Department of Neurology and Pediatrics, University of Southern California, School of Medicine, Los Angeles, USA
TI - Relation of the [3H] gamma-hydroxybutyric acid (GHB) binding site to the gamma-aminobutyric acidB (GABAB) receptor in rat brain
AB - gamma-Hydroxybutyric acid (GHB) is a naturally occurring compound that has the ability to induce generalized absence seizures when given to animals. GHB has been hypothesized to induce this effect via the postsynaptic gamma-aminobutyric acidB (GABAB) receptor. We sought to test this hypothesis by examining the affinity of GABAB agonists and antagonists for the [3H]GHB binding site, the affinity of GHB and a GHB antagonist for the [3H]GABAB binding site, and the effect of guanine nucleotides and pertussis toxin on both, using autoradiographic binding assays. GHB and its antagonist, NCS 382, did not compete for [3H]GABAB binding, nor did (-)-baclofen or the [3H]GABAB antagonists, CGP 35348 or SCH 50911, compete for [3H]GHB binding; however, the GABAB agonist 3-amino-propylphosphinic acid (3-APPA), and the GABAB antagonists phaclofen and 2-hydroxysaclofen (2-OH saclofen) did show a weak affinity for [3H]GHB binding in frontal cortex. GTP and the nonhydrolyzable GTP analogues, GTP gamma S and Gpp(NH)p, depressed [3H]GABAB binding throughout the brain, but increased [3H]GHB binding in frontal cortex and thalamus, those regions involved in GHB-induced absence seizures. Pertussis toxin significantly depressed [3H]GABAB binding throughout the brain, but attenuated [3H]GHB binding only in frontal cortex, and to a lesser degree than [3H]GABAB binding. The guanine nucleotide-induced changes in [3H]GHB and [3H]GABAB binding were due to a change in KD for both. Moreover, GTP gamma S reversed the ability of 3-APPA, phaclofen, and 2-OH saclofen to compete for [3H]GHB binding. These data do not support the hypothesis that GHB acts through the postsynaptic GABAB receptor to produce absence seizures. Rather, they raise the possibility either that the [3H]GHB binding site may be an isoform of the presynaptic GABAB receptor or that an independent GHB site is operative in the GHB model of absence seizures
UR - PM:8937431
SO - Biochem Pharmacol 1996 Oct 25 ;52(8):1235-1243

UI - 68
AU - Banerjee PK
AU - Snead OC
AD - Department of Neurology, University of Southern California School of Medicine, Los Angeles, USA
TI - Presynaptic gamma-hydroxybutyric acid (GHB) and gamma-aminobutyric acidB (GABAB) receptor-mediated release of GABA and glutamate (GLU) in rat thalamic ventrobasal nucleus (VB): a possible mechanism for the generation of absence-like seizures induced by GHB
AB - The ventrobasal nucleus of thalamus (VB) is considered to be intimately involved in the genesis of experimental absence-like seizures. Bilateral microinfusion of gamma-hydroxybutyric acid (GHB) into VB or systemic administration of gamma-butyrolactone, the pro-drug of GHB, induces generalized absence-like seizures in rats. In the present study, the basal and K(+)-evoked extracellular output of endogenous gamma-aminobutyric acid (GABA) and glutamate (GLU) in behaving rat VB nucleus was characterized 1) during unilateral GHB perfusion into VB and 2) during the course of generalized absence-like seizures induced by GHB. Although the basal extracellular release of GABA was inhibited by GHB (250-1500 microM) in a concentration-dependent manner, basal GLU levels remained unaltered. However, K(+)-evoked release of both GABA and GLU was significantly attenuated by GHB. During GHB-induced absence-like seizures, a similar decrease in basal GABA or K(+)-evoked GABA and GLU levels was observed. These effects of GHB were partially reversed by the specific GHB receptor antagonist NCS 382. (-)-Baclofen (10-50 microM) also produced a concentration-dependent decrease in basal and K(+)-evoked levels of GABA and GLU in this thalamic nucleus. The effects of either (-)-baclofen or GHB on the release of GABA and GLU were selectively antagonized by the GABAB receptor antagonists phaclofen (0.75-2 mM) and CGP 35348 (50-200 microM), respectively. These results suggest that by selectively modulating the basal and K(+)-evoked release of GABA and GLU, GHB induces, in the thalamic ventrobasal relay nucleus, an optimal "excitatory" environment conducive to the generation of absence seizures. Moreover, the data raise the possibility that a presynaptic GHB/GABAB receptor complex occurs in VB
UR - PM:7791129
SO - J Pharmacol Exp Ther 1995 Jun ;273(3):1534-1543

UI - 66
AU - Colombo G
AU - Agabio R
AU - Bourguignon J
AU - Fadda F
AU - Lobina C
AU - Maitre M
AU - Reali R
AU - Schmitt M
AU - Gessa GL
AD - Dipartimento di Neuroscienze "Bernard B. Brodie", Universita di Cagliari, Italy
TI - Blockade of the discriminative stimulus effects of gamma-hydroxybutyric acid (GHB) by the GHB receptor antagonist NCS-382
AB - The present study was designed to assess the ability of the newly synthetized, selective gamma-hydroxybutyric acid (GHB) receptor antagonist, NCS-382, in blocking the discriminative stimulus effects of GHB in a T-maze, food-reinforced drug discrimination procedure. Two groups of rats were trained to run the left arm of the maze 30 min after the i.g. administration of either 300 or 700 mg/kg GHB and the right arm after water. Once discrimination was acquired, combination of different doses of NCS-382 (0, 12.5, 25.0 and 50.0 mg/kg, IP) and GHB training doses were tested for blockade of GHB discrimination. NCS-382 dose-dependently blocked GHB-appropriate responding in both the 300 and 700 mg/kg GHB rat groups. The results of the present study indicate that the discriminative stimulus properties of GHB are mediated via stimulation of GHB receptors
UR - PM:8587968
SO - Physiol Behav 1995 Sep ;58(3):587-590

UI - 69
AU - Ferrara SD
AU - Tedeschi L
AU - Frison G
AU - Rossi A
AD - Centre of Behavioural and Forensic Toxicology, University of Padova, Italy
TI - Fatality due to gamma-hydroxybutyric acid (GHB) and heroin intoxication
AB - The first case of fatal intoxication due to ingestion of gamma-hydroxybutyric acid (GHB) and intravenous use of heroin is reported. A 42-year-old man, known to have been a heroin addict and to have taken other psychoactive substances, who had been in treatment with GHB for several months, was found dead. Anatomohistopathologic examination showed generalized visceral congestion, edema and pulmonary anthracosis, chronic bronchitis and chronic active hepatitis. Toxicological findings included fluid and tissue distributions of GHB, morphine and 6-monoacetylmorphine. GHB and morphine concentrations were respectively 11.5 and 0.77 micrograms/mL (blood), 84.3 and 0.3 micrograms/mL (vitreous humor), 258.3 and 1.35 micrograms/mL (urine), 57.0 and 14.3 micrograms/mL (bile), 40.0 and 0.43 micrograms/g (brain), 43.0 and 0.60 micrograms/g (liver), 47.0 and 0.68 micrograms/g (kidney). Blood and urine levels of 6-monoacetylmorphine were 28.5 and 12.1 ng/mL respectively. The presumed mechanism of action and pharmacokinetics of GHB are briefly reviewed, with reference to its therapeutic use and to reports of non-fatal GHB intoxication
UR - PM:7782758
SO - J Forensic Sci 1995 May ;40(3):501-504

UI - 70
AU - Frau M
AU - Colombo G
AU - Marchese G
AU - Stefanini E
AU - Gessa GL
AD - Bernard B. Brodie Department of Neuroscience, University of Cagliari, Italy
TI - Different affinity of cortical GHB binding sites in sardinian alcohol-preferring (sP) and -non preferring (sNP) rats
AB - Specific gamma-hydroxybutyric acid (GHB) binding sites in cortical membranes of selectively bred alcohol-preferring sP and alcohol-non preferring sNP rats were compared using [2,3(-3)H]GHB ligand. The sP rat line showed an increased affinity (approximately 40% lower Kd) of both the high- and low-affinity sites in comparison with the sNP line. No significant difference in GHB receptor density (Bmax) was detected between the two rat lines. The results raise the possibility that differences in GHB binding sites may play a role in the genetic predisposition to ethanol preference in our rat line
UR - PM:7748271
SO - Alcohol Alcohol 1995 Jan ;30(1):133-137

UI - 67
AU - Steele MT
AU - Watson WA
AD - Department of Emergency Medicine, Truman Medical Center, University of Missouri-Kansas City School of Medicine, USA
TI - Acute poisoning from gamma hydroxybutyrate (GHB)
AB - Gamma hydroxybutyrate (GHB) is an illicitly marketed substance promoted by body builders as a growth hormone releaser. Poisoning can produce seizures and coma. Acute poisonings from GHB have primarily been reported on the West coast and the Southeast. We report two cases from Kansas City where the patients presented in, or developed profound coma. Physicians should suspect GHB poisoning in patients who present with unexplained seizures and/or coma, particularly if they are body builders, health food fanatics or dieters
UR - PM:7651315
SO - Mo Med 1995 Jul ;92(7):354-357

UI - 71
AU - Stephens BG
AU - Baselt RC
AD - Chemical Toxicology Institute, Foster City, CA 94404
TI - Driving under the influence of GHB?
AB - A driver was found asleep behind the steering wheel of his car, and the vehicle was at rest in a traffic lane with the engine running. His manifestations included horizontal and vertical gaze nystagmus, muscle flaccidity, and severe ataxia. He admitted ingesting a white powder, which he identified as an amino acid, about 1 hour prior to discovery by police. A urine specimen collected approximately 1 hour after the traffic stop contained 1975 mg/L of gamma-hydroxybutyrate (GHB). We tentatively conclude that GHB may cause impairment of the psychomotor skills required for safe operation of a motor vehicle
UR - PM:7823545
SO - J Anal Toxicol 1994 Oct ;18(6):357-358

UI - 75
AU - Luby S
AU - Jones J
AU - Zalewski A
TI - GHB use in South Carolina
UR - PM:1536324
SO - Am J Public Health 1992 Jan ;82(1):128

UI - 77
AU - Kolin A
AU - Brezina A
AU - Mamelak M
AD - Department of Anatomical Pathology, Sunnybrook Health Science Centre, University of Toronto, Ontario, Canada
TI - Cardioprotective effects of sodium gamma-hydroxybutyrate (GHB) on brain induced myocardial injury
AB - Gamma-hydroxybutyrate (GHB) was evaluated as a protective agent in a gerbil model of non-lethal myocardial injury that follows brain ischaemia. The accumulation of fat droplets in myocardial fibers following brain infarction was measured by electron microscopic morphometry and expressed as a percentage of the area of the sarcoplasm. GHB treatment significantly reduced the area occupied by lipid droplets compared with that found in saline treated controls measured both 10 hours (p less than .005) and 24 hours (p less than 0.05) after unilateral carotid ligation. GHB did not affect the ischaemic swelling of the brain
UR - PM:1810434
SO - In Vivo 1991 Jul ;5(4):429-431

UI - 78
AU - Lane RB
TI - Gamma hydroxy butyrate (GHB)
UR - PM:2033762
SO - JAMA 1991 Jun 12 ;265(22):2959

UI - 76
AU - Zhang X
AU - Ju G
AU - Le Gal LS
AD - Department of Neurobiology, Fourth Military Medical University, Xian, P.R. China
TI - Fos expression in GHB-induced generalized absence epilepsy in the thalamus of the rat
AB - Using the model of gamma-hydroxybutyrate (GHB)-induced generalized absence epilepsy, the present work investigated the distribution of fos oncoprotein expression in the rat thalamus with fos antibody immunohistochemistry. Thirty minutes after absence-like seizures, some fos-immunoreactive cell nuclei were found in bilateral thalamic paraventricular nuclei (PV). After a further 30 min, a massive bilateral induction of fos was observed in the lateral habenular nucleus (LHb), the PV, the rhomboid thalamic nucleus, and the intralaminar nuclei of the thalamus. These results suggest that the LHb and the midline and intralaminar thalamic nuclei may very likely be involved in the pathophysiology of absence seizures
UR - PM:1912482
SO - Neuroreport 1991 Aug ;2(8):469-472

UI - 79
AU - Scharf MB
AU - Fletcher KA
TI - GHB--new hope for narcoleptics?
MH - Arousal
MH - drug effects
MH - Cataplexy
MH - drug therapy
MH - Human
MH - Hydroxybutyrates
MH - therapeutic use
MH - Narcolepsy
MH - Sleep Stages
MH - Sodium Oxybate
UR - PM:2765597
SO - Biol Psychiatry 1989 Aug ;26(4):329-330

UI - 80
AU - Little RR
AU - Goldstein DE
TI - Reassessment of GHb measurement from blood dried on filter paper
UR - PM:3383737
SO - Diabetes Care 1988 Feb ;11(2):222-223

UI - 81
AU - Snead OC
AU - Liu CC
AU - Bearden LJ
TI - Studies on the relation of gamma-hydroxybutyric acid (GHB) to gamma-aminobutyric acid (GABA). Evidence that GABA is not the sole source for GHB in rat brain
AB - The effects of gamma-aminobutyric acid (GABA)-alpha-oxoglutarate aminotransferase (GABA-T) inhibitors, L-glutamic acid decarboxylase (GAD) inhibitors, and antipetit mal anticonvulsants on gamma-hydroxybutyric acid (GHB) and GABA were studied. Treatment with anticonvulsants and GABA-T inhibitors resulted in an increase in steady-state brain levels of both GHB and GABA. GAD inhibitors produced markedly decreased levels of brain GABA but no change in GHB concentrations. Studies of GHB derived exclusively from GABA showed that GABA-T inhibitors which produced an elevation of steady-state levels of GHB in brain also resulted in a decrease in GABA-derived GHB. Intracerebroventricular (i.c.v.) administration of GABA, putrescine, and 1,4-butanediol all produced significant elevations in brain GHB, but GABA-T inhibitors blocked this effect of GABA and putrescine. These data suggest that there may be another source for GHB in brain in addition to GABA and raise the possibility that 1,4-butanediol may be that source
UR - PM:7159469
SO - Biochem Pharmacol 1982 Dec 1 ;31(23):3917-3923

UI - 84
AU - Plantey F
UR - PM:900292
SO - Am J Psychiatry 1977 Sep ;134(9):1045-1046

UI - 85
AU - Bant T
AU - Hojo M
TI - The central action of gamma-butyrolactone and gamma-hydroxybutyrate. II. The effect of GHB and related agents on the cortical dendritic responses
UR - PM:5306224
SO - Jpn J Pharmacol 1969 Mar ;19(1):89-101

UI - 86
AU - Leaver FW
TI - Separation of human growth hormone into two components--GHA and GHB
UR - PM:5944872
SO - Proc Soc Exp Biol Med 1966 May ;122(1):196-200



Alexander DeLuca, M.D., FASAM.
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