Sodium Oxybate in Alcohol-Responsive Essential Tremor of Voice: An Open-Label Phase II Study.

BACKGROUND: Essential tremor of voice (ETv) is characterized by involuntary oscillations of laryngeal and upper airway muscles, causing rhythmic alterations in pitch and loudness during both passive breathing and active laryngeal tasks, such as speaking and singing. Treatment of ETv is challenging and typically less effective compared with treatment of ET affecting extremities. OBJECTIVE: We conducted a proof-of-concept, open-label phase II study to examine the efficacy and central effects of sodium oxybate in patients with alcohol-responsive ETv. METHODS: All subjects received 1.0 to 1.5 g of oral sodium oxybate and underwent brain functional magnetic resonance imaging. The primary endpoint was the number of patients (% from total) with reduced ETv symptoms by at least 10% at about 40 to 45 minutes after sodium oxybate intake based on the combined visual analog scale score of ETv symptom severity. The secondary endpoint included changes in brain activity after sodium oxybate intake compared to baseline. RESULTS: Sodium oxybate reduced ETv symptoms on average by 40.8% in 92.9% of patients. Drug effects were observed about 40 to 45 minutes after intake, lasting about 3.5 hours, and gradually wearing off by the end of the fifth hour. The central effects of sodium oxybate were associated with normalized activity in the cerebellum, inferior/superior parietal lobules, inferior frontal gyrus, and insula and re-established functional relationships between these regions. CONCLUSIONS: Sodium oxybate showed high efficacy in ETv patients, with a likely central action on disorder pathophysiology. Sodium oxybate may be an effective novel oral drug for treatment of alcohol-responsive ETv patients. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Sodium Oxybate for Alcohol Dependence: A Network Meta-Regression Analysis Considering Population Severity at Baseline and Treatment Duration.

AIMS: The estimated effect of sodium oxybate (SMO) in the treatment of alcohol dependence is heterogeneous. Population severity and treatment duration have been identified as potential effect modifiers. Population severity distinguishes heavy drinking patients with <14 days of abstinence before treatment initiation (high-severity population) from other patients (mild-severity population). Treatment duration reflects the planned treatment duration. This study aimed to systematically investigate the effect of these potential effect moderators on SMO efficacy in alcohol-dependent patients. METHODS: Network meta-regression allows for testing potential effect modifiers. It was selected to investigate the effect of the above factors on SMO efficacy defined as continuous abstinence (abstinence rate) and the percentage of days abstinent (PDA). Randomized controlled trials for alcohol dependence with at least one SMO group conducted in high-severity and mild-severity populations were assigned to a high-severity and mild-severity group of studies, respectively. RESULTS: Eight studies (1082 patients) were retained: four in the high-severity group and four in the mild-severity group. The high-severity group was associated with larger SMO effect sizes than the mild-severity group: abstinence rate risk ratio (RR) 3.16, P = 0.004; PDA +26.9%, P < 0.001. For PDA, longer treatment duration was associated with larger SMO effect size: +11.3% per extra month, P < 0.001. In the high-severity group, SMO showed benefit: abstinence rate RR 2.91, P = 0.03; PDA +16.9%, P < 0.001. In the mild-severity group, SMO showed benefit only in PDA for longer treatment duration: +23.9%, P < 0.001. CONCLUSIONS: In the retained studies with alcohol-dependent patients, high-severity population and longer treatment duration were associated with larger SMO effect sizes.

[Withdrawal syndrome following chronic use of gamma-hydroxybutyric acid (GHB)]. / Syndrome de sevrage lors d'une consommation chronique d'acide gamma-hydroxybutyrique (GHB).

Chronic use of gamma-hydroxybutyric acid (GHB) and its precursors can rapidly lead to physical dependence with the emergence of a withdrawal syndrome. This complication is similar to the one linked to alcohol or benzodiazepines. The onset of symptoms and specially neuro-psychiatric symptoms is, however, more rapid in the case of the GHB and precursors. There is currently no consensus on the therapeutic management of GHB withdrawal syndrome. High-dose benzodiazepines are the most commonly used treatment. The use of GHB by titration and tapering could show fewer side effects and withdrawal symptoms. It appears necessary to reflect on and pursue research on the use of GHB and its precursors, which remains poorly understood, on the management of withdrawal syndrome due to the lack of protocol and on its probably underestimated impact on public health.

La consommation chronique d'acide gamma-hydroxybutyrique (GHB) et de ses précurseurs peut rapidement entraîner une dépendance physique avec l'émergence d'un syndrome de sevrage à l'arrêt des consommations. Ce syndrome de sevrage présente des similitudes avec celui lié à l'alcool ou aux benzodiazépines. On retrouvera, cependant, une apparition et une évolution plus brutales ainsi que l'émergence, plus précoce, de symptômes neuropsychiatriques. Il n'y a actuellement pas de consensus concernant la prise en charge thérapeutique de ce syndrome de sevrage. Dès lors, le recours aux benzodiazépines à hautes doses constitue le traitement le plus régulièrement utilisé. L'utilisation de GHB médical, titré et avec une posologie progressivement diminuée, pourrait démontrer moins d'effets secondaires et de symptômes de sevrage. Il apparaît nécessaire de réfléchir et de poursuivre les recherches sur la consommation du GHB et ses précurseurs, qui reste largement méconnue, ainsi que sur la prise en charge du sevrage, au vu de l'absence de protocole et de son impact en santé publique, probablement sous-estimé.

Cognitive Impairments in Patients with GHB Use Disorder Predict Relapse in GHB Use.

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.

Characteristics of patients with analytically confirmed γ-hydroxybutyric acid/γ-butyrolactone (GHB/GBL)-related emergency department visits in Taiwan.

The recreational drug γ-hydroxybutyric acid (GHB) is a central nervous system depressant, and can produce euphoria at low doses. GHB is a controlled substance in Taiwan. However, the organic solvents γ-butyrolactone (GBL) and 1,4-butanediol (BD), which are unregulated, may be used as an alternative source of GHB. There is no clinical report of analytically confirmed GHB use in Taiwan. We retrospective reviewed the clinical characteristics from the medical charts between May 2017 and April 2020. The urine samples of patients presented to the emergency departments with drug-related complaints were sent for toxicological analysis. Patients with urine samples detected GHB >10 µg/mL by liquid chromatography/tandem mass spectrometry were included. Overall, 11 men and one woman with an average age of 35.3 ± 8.7 years were included. Most patients co-ingested amphetamine (n = 6) and initially presented with depressed consciousness levels (n = 7). One patient presented with out-of-hospital cardiac arrest and one with respiratory depression. All patients regained consciousness within 6 h of admission. All patients used GBL to evade conviction. Although patients recovered with supportive care, respiratory failure and cardiac arrest occurred after GHB/GBL use. It is important to legislate GBL and BD as controlled chemical substances in Taiwan.

Can emergency department clinicians diagnose gamma-hydroxybutyrate (GHB) intoxication based on clinical observations alone?

OBJECTIVES: Gamma-hydroxybutyrate (GHB) is a drug of abuse with central depressing effects, which may cause coma with a GCS score as low as 3. A rapid diagnosis 'GHB intoxication' may prevent unnecessary diagnostic work-up and may lead to guided, less invasive, treatment. The aim of this study was to evaluate if ED physicians' clinical evaluation were sufficient for diagnosis in patients with suspected GHB-intoxication. METHODS: Patients presenting at the ED with a GCS<15 and a potential intoxication with drugs of abuse for whom urine toxicology screen was performed were included consecutively. After a first assessment, the ED physician registered the most likely initial diagnosis in the hospital information system. Urine of these patients was tested with a validated gas chromatography analytical method for GHB (confirmation test). The initial diagnoses were compared for agreement with the results of the confirmation test. RESULTS: A total of 506 patients were included, 100 patients tested positive for GHB and 406 patients tested negative for GHB. Sensitivity and specificity of the ED physicians compared with the confirmation test to diagnose GHB intoxications were 63% (95% CI 52 to 73) and 93% (95% CI 90 to 95), respectively. The positive predictive value was 67% (95% CI 60 to 77) and the negative predictive value was 92% (95% CI 88 to 94). CONCLUSION: Physicians underestimate the presence of GHB intoxication and can fail to diagnose GHB intoxication based on clinical observations alone. In the future, a rapid reliable initial analytical GHB test in addition to clinical judgement could be valuable to reduce false negative diagnosis.

Demographic and Clinical Characteristics of Regular GHB-Users with and without GHB-Induced Comas.

BACKGROUND: Gamma hydroxybutyric acid (GHB) has been used recreationally for nearly three decades and its chronic use is frequently associated with serious adverse events including GHB-intoxication with GHB-induced comas. Moreover, despite its low prevalence, the number of individuals with GHB-use disorders is steadily increasing. However, the risk-factors associated with chronic GHB-use or the development of a GHB-use disorders remain poorly understood. Purpose: This study aims to profile two types of GHB-users, those with and those without GHB-induced comas. Methods: We included 27 GHB users with ≥4 GHB-induced comas (GHB-Coma), 27 GHB users without a coma (GHB-NoComa), and 27 polydrug users who never used GHB (No-GHB). Participants completed self-reported questionnaires in order to assess their demographic and clinical features, and their use profile of GHB and other drugs. Results: The typical GHB user in our sample was young, single, living alone, well-educated, and a student. The GHB-Coma group had lower self-control and reported higher negative affect than the GHB-NoComa group. GHB-Coma participants were heavier GHB users and mostly used GHB alone at home, whereas the GHB-NoComa group mostly used GHB with friends and in nightclubs. Remarkably, the majority of participants were not concerned about potential neurocognitive impairments induced by GHB-intoxication and/or GHB-induced comas. Conclusion: In this assessment, different profiles for recreational users with and without GHB-induced comas were well expressed. Their description contributes to a better understanding of the risk factors associated with recreational GHB-use, GHB-induced coma, and the development of GHB-use disorders.

Severe delirium after GHB abuse. / Alvorlig delir etter GHB-misbruk.

BACKGROUND: The management of benzodiazepine-resistant GHB withdrawal requires careful consideration of GHB pharmacodynamics. CASE PRESENTATION: A young woman was admitted with tachycardia, confusion, agitation and delusions the day after attempting to quit a daily, high-dose GHB habit. A total of 225 mg of diazepam had no effect. She was sedated with propofol and intubated. An extubation attempt after 24 hours was followed by recurrence of delirium. After reintubation she required high doses of propofol, alfentanil and dexmedetomidine to maintain sedation for two days. Baclofen and diazepam were introduced on the third day, allowing dose reductions in anaesthetic agents the fourth day and extubation on the fifth day with resolution of the delirium. INTERPRETATION: GHB targets the GABAB receptor and downregulates it with abuse. Most anaesthetic agents affect the GABAA receptor. Our report suggests that baclofen, a GABAB receptor agonist, may reduce the need for anaesthetic agents and facilitate recovery.

Recreational use of GHB is associated with alterations of resting state functional connectivity of the central executive and default mode networks.

Gamma-hydroxybutyrate acid (GHB) is a recreational drug with a high addictive potential. Severe side effects such as GHB-induced coma are common and linked to increased emergency room attendances. Task-based functional-imaging studies have revealed an association between the regular use of GHB and multiple GHB-induced comas, and altered neurocognitive function. However the effects of multiple GHB-induced comas and regular GHB-use on intrinsic brain connectivity during rest remain unknown. The study population consisted of 23 GHB-users with ≥4 GHB-induced comas (GHB-Coma), 22 GHB-users who never experienced a GHB-induced coma (GHB-NoComa) and 24 polydrug users who never used GHB (No-GHB). Resting-state scans were collected to assess resting-state functional-connectivity within and between the default mode network (DMN), the bilateral central executive network (CEN) and the salience network (SN). The GHB-NoComa group showed decreased rsFC of the right CEN with a region in the anterior cingulate cortex (pFWE = 0.048) and decreased rsFC between the right CEN and the DMN (pFWE = 0.048) when compared with the No-GHB group. These results suggest that regular GHB-use is associated with decreased rsFC within the right CEN and between the right CEN and the DMN. The presence of multiple GHB-induced comas is not associated with (additional) alterations in rsFC.

Inpatient management of gamma-hydroxybutyrate withdrawal.

OBJECTIVES: To describe the baseline characteristics, treatment and retention in patients electively admitted for gamma-hydroxybutyrate (GHB) withdrawal management. METHODS: All patients admitted between July 2010 to June 2016 who used GHB two or more times per week with a minimum duration of 3 months were identified and data extracted by file review. RESULTS: Twelve cases satisfied the inclusion criteria, of whom 50% were female; 75% were using GHB daily, with an average daily amount of 16 ml. Average duration of use was 60 months. All subjects were using amphetamine type stimulants and nicotine. Psychiatric comorbidity and unintentional overdose were common; 50% completed treatment. Medications used included diazepam and neuroleptic. Two patients completed withdrawal with no medications. No subject using greater than 90 ml GHB in the preceding week completed treatment. Pattern of GHB use did not predict medication requirements during withdrawal management. CONCLUSIONS: There were low numbers attending for elective treatment for GHB use. Heavier GHB use predicted poor treatment retention. Polysubstance use and psychiatric co-morbidities need consideration in treatment planning.

Inpatient management of GHB/GBL withdrawal.

BACKGROUND: Gamma-hydroxybutyrate (GHB) and its precursor gamma-butyrolactone (GBL) are popular drugs of abuse used for their euphoric, (potential) anabolic, sedative, and amnestic properties. Daily use of GHB/GBL can lead to addiction and the possibility of withdrawal syndrome on cessation which results in tremor, tachycardia, insomnia, anxiety, hypertension, delirium, coma. AIM: To describe the baseline characteristics, treatment and retention in patients admitted for GHB/GBL withdrawal management. METHODS: A retrospective review of 4 consecutive cases of patients reporting GHB/GBL addiction who were admitted for inpatient management of withdrawal syndrome. RESULTS: All patients were using GHB/GBL daily, 1-1.5 ml per hour. One of them was using cannabis additionally, others were using alcohol, cocaine and amphetamine type stimulants. Psychiatric comorbidities as personality disorders, depression, anxiety and bigorexia were recognized. Patients were treated with benzodiazepines and/or clomethiazole, atypical and typical antipsychotics and beta-blockers. Delirium was developed in two patients. One patient completed detoxification and finished the treatment program. One patient completed detoxification but stopped his treatment earlier, two patients did not completed detoxification and left the program. CONCLUSION: GHB/GBL withdrawal can be severe and retention in program is poor. Polysubstance use, psychiatric co-morbidities and heavier GHB/GBL use as possible predictors of poor treatment outcome need consideration in treatment planning.

[Party drugs†: when «â€ recreation†¼ rhymes with «â€ consultation†¼]. / Drogues festives†: quand «â€ récréation†¼ rime avec «â€ consultation†¼.

Since the nineties, we note a diversification of recreational drugs and an increase in intoxications requiring medical care. From cannabis to cocaine through the New Psychoactive Substances, the aim of this article is to focus on Gamma-hydroxybutyrate (GHB), lysergic diethylamid acid (LSD) and 3,4-methylenedioxymethamphetamin (MDMA), three substances that we are confronted with in our emergency rooms and review the effective care to provide in case of intoxication.

Nous observons depuis les années 90 une diversification des drogues dites festives ou récréatives associée à une augmentation des intoxications admises dans les services d'urgences. Du cannabis à la cocaïne, en passant par les drogues émergentes, ou détournées de leur utilisation médicale, le but de cet article est de se concentrer sur le Gamma-hydroxybutyrate (GHB), l'acide lysergique diéthylamide (LSD) et la 3,4-méthylènedioxyméthamphétamine (MDMA), trois molécules déjà connues ayant fait leur réapparition ces dernières années dans les services d'urgences, et de revoir leur présentation clinique et leur prise en charge.

Clinical management of gamma-hydroxybutyrate (GHB) withdrawal delirium with CIWA-Ar protocol.

Gamma-hydroxybutyrate (GHB) is a synthetic drug used mainly for recreational purpose. Although the prevalence of GHB abuse is low in Taiwan, GHB has become increasingly popular in certain subpopulations such as clubbers and men who have sex with men (MSM). GHB dependence could be associated with severe withdrawal syndrome including hallucinations and delirium. Despite systematic studies on detoxification and management of GHB withdrawal have been performed, no validated measurement for severity of GHB withdrawal syndrome is available. Here we present a case of GHB withdrawal delirium that was treated successfully with fixed and symptom-triggered benzodiazepine dosing regimen based on Clinical Institute Withdrawal Assessment for Alcohol-Revised (CIWA-Ar) scale. The utilization of CIWA-Ar in such cases could offer useful guidance for benzodiazepine dosing. To the best of our knowledge, this is the first case report of GHB withdrawal delirium in Taiwan.

Impact of concomitant medications on obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) is characterized by repeated episodes of apnoea and hypopnoea during sleep. Little is known about the potential impact of therapy drugs on the underlying respiratory disorder. Any influence should be taken into account and appropriate action taken, including drug withdrawal if necessary. Here, we review drugs in terms of their possible impact on OSA; drugs which (1) may worsen OSA; (2) are unlikely to have an impact on OSA; (3) those for which data are scarce or contradictory; and (4) drugs with a potentially improving effect. The level of evidence is ranked according to three grades: A - randomized controlled trials (RCTs) with high statistical power; B - RCTs with lower power, non-randomized comparative studies and observational studies; C - retrospective studies and case reports. Our review enabled us to propose clinical recommendations. Briefly, agents worsening OSA or inducing weight gain, that must be avoided, are clearly identified. Drugs such as 'Z drugs' and sodium oxybate should be used with caution as the literature contains conflicting results. Finally, larger trials are needed to clarify the potential positive impact of certain drugs on OSA. In the meantime, some, such as diuretics or other antihypertensive medications, are helpful in reducing OSA-associated cardiovascular morbidity.

Melatonin successfully rescues hippocampal bioenergetics and improves cognitive function following drug intoxication by promoting Nrf2-ARE signaling activity.

Prolonged exposure to gamma-hydroxybutyric acid (GHB) would cause drug intoxication in which impaired cognitive function results from enhanced hippocampal oxidative stress may serve as a major symptom in this deficiency. Considering melatonin possesses significant anti-oxidative efficacy, this study aimed to determine whether melatonin would successfully promote the nuclear factor erythroid 2-related factor 2 and antioxidant responsive element (Nrf2-ARE) signaling, depress oxidative stress, and rescue hippocampal bioenergetics and cognitive function following drug intoxication injury. Adolescent rats subjected to 10 days of GHB were received melatonin at doses of either 10 or 100 mg/kg. Time-of-flight secondary ion mass spectrometry, biochemical assay, quantitative histochemistry, [14 C]-2-deoxyglucose analysis, together with Morris water maze were employed to detect the molecular signaling, oxidative status, bioenergetic level, as well as the cognitive performances, respectively. Results indicated that in GHB-intoxicated rats, enhanced oxidative stress, increased cholesterol level, and decreased anti-oxidative enzymes activities were detected in hippocampal regions. Intense oxidative stress paralleled well with reduced bioenergetics and poor performance in behavioral testing. However, in rats treated with melatonin following GHB intoxication, all above parameters and cognitive function were gradually returned to nearly normal levels. Melatonin also remarkably promoted the translocation of Nrf2 from cytoplasm to nucleus in a dose-dependent manner, thereby increased the Nrf2-ARE signaling-related downstream anti-oxidative enzymes activities. As melatonin effectively rescues hippocampal bioenergetics through depressing the oxidative stress by promoting Nrf2-ARE molecular machinery, this study thus highlights for the first time that clinical use of melatonin may serve as a therapeutic strategy to improve the cognitive function in unsuspecting victims suffered from GHB intoxication injury.

Effect of chronic γ-hydroxybutyrate (GHB) administration on GHB toxicokinetics and GHB-induced respiratory depression.

BACKGROUND: γ-hydroxybutyrate (GHB) has a high potential for illicit use; overdose of this compound results in sedation, respiratory depression and death. Tolerance to the hypnotic/sedative and electroencephalogram effects of GHB occurs with chronic GHB administration; however, tolerance to respiratory depression has not been evaluated. GHB toxicodynamic effects are mediated predominantly by GABAB receptors. Chronic treatment may affect monocarboxylate transporters (MCTs) and alter the absorption, renal clearance and brain uptake of GHB. OBJECTIVES: To determine effects of chronic GHB dosing on GHB toxicokinetics, GHB-induced respiratory depression, and MCT expression. METHODS: Rats were administered GHB 600 mg/kg intravenously daily for 5 days. Plasma, urine and tissue samples and respiratory measurements were obtained on days 1 and 5. Plasma and urine were analyzed for GHB by LC/MS/MS and tissue samples for expression of MCT1, 2 and 4 and their accessory proteins by QRT-PCR. RESULTS: No differences in GHB pharmacokinetics or respiratory depression were observed between days 1 and 5. Opposing changes in MCT1 and MCT4 mRNA expression were observed in kidney samples on day 5 compared to GHB-naïve animals, and MCT4 expression was increased in the intestine. CONCLUSIONS: The lack of tolerance observed with GHB-induced respiratory depression, in contrast to the tolerance reported for the sedative/hypnotic and electroencephalogram effects, suggests that different GABAB receptor subtypes may be involved in different GABAB-mediated toxicodynamic effects of GHB. Chronic or binge users of GHB may be at no less risk for fatality from respiratory arrest with a GHB overdose than with a single dose of GHB.

[Treatment of fibromyalgia syndrome with gamma-hydroxybutyrate : A randomized controlled study]. / Die Behandlung des Fibromyalgiesyndroms mit Gamma-Hydroxybuttersäure : Eine randomisierte, kontrollierte Studie.

BACKGROUND: The etiology of fibromyalgia syndrome is not yet fully understood. Current hypotheses suggest a potential role of gamma-hydroxybutyrate (GHB) in influencing endocrinological abnormalities in patients with fibromyalgia. OBJECTIVE: The aim of the study was to investigate whether low dose GHB as a growth-hormone releasing substance reduces pain intensity and improves depressive mood, physical impairment and sleep quality in outpatients with fibromyalgia. Additionally, adverse events were recorded. MATERIAL AND METHODS: The pilot study was conducted in the outpatient clinic for pain at the clinic for anesthesiology and surgical intensive care of the Charité Universitätsmedizin Berlin. In the study 25 female patients with fibromyalgia according to the criteria of the American College of Rheumatology were randomized into 2 groups. Over 15 weeks patients of the intervention group received 25 mg/kg body weight oral GHB before going to bed and were compared with a placebo control group. In addition, all patients participated in operant behavioral pain treatment in a group setting. Dependent variables were pain intensity, depressive mood, physical impairment and quality of sleep. RESULTS: There were no group differences in the course of pain intensity (p = 0.61), depressive mood (p = 0.16), physical impairment (p = 0.25) and quality of sleep (p = 0.44); however, all symptoms improved across the groups from pretherapy to posttherapy. Low dose GHB did not increase growth hormone blood concentrations. The number of adverse events that were reported more than two times was similar in both groups. DISCUSSION: Administration of low dose GHB did not yield clinical improvements in female outpatients with fibromyalgia. General improvement in the course of treatment may have resulted from operant behavioral pain therapy. Future studies on GHB should control hypothetical risk factors for identification of non-responders.

[Hypernatremia caused by treatment with GHB obtained via a doctor's prescription]. / Hypernatriëmie door GHB op doktersrecept.

In the last few years, gamma hydroxybutyric acid (GHB) has been used increasingly as a party drug; this has led to a marked increase in the number of requests for professional help with the treatment of GHB addiction. Pharmaceutical GHB (sodium oxybate, the sodium-salt of GHB), registered for cataplexia in narcolepsy patients, is used off-label to treat the withdrawal symptoms associated with GHB addiction. Pharmaceutical GHB has a high sodium load. In this report we present the cases of two patients who developed symptomatic hypernatremia following treatment with pharmaceutical GHB and who thereafter needed intensive care for the severe withdrawal symptoms that they experienced.