DecaDent*
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For anyone who uses GHB for sleep this article has some very useful and potentially lifesaving information. It focuses on whithdrawl syndrome,similar to what happens in chronic alcoholics or people hooked on Valium/benzo's. The stricking fact that 63% of the reported cases of GHB withdrawl were found in bodybuilders caught my attention........be careful with G ...not just short term OD problems but low dose long term use can lead to this....
Early symptoms of insomnia, tremor, confusion, nausea, and vomiting are mild, and medical admission to a health care facility is often delayed until more severe symptoms of agitation and hallucinations are experienced. The withdrawal syndrome progresses over the initial 2 to 3 days with mild autonomic instability manifested by tachycardia, hypertension, tremor, and diaphoresis. Central nervous system symptoms include vivid hallucinations and anxiety. Confusion, disorientation, and delirium with agitation and combative behavior occur as the syndrome progresses, often requiring 4-point leather restraints and sedation. These symptoms become episodic in nature as the syndrome wanes
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. Manifestations of withdrawal from GHB.
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Symptoms Early
(1–24 h) Progressive
(1–6 d) Episodic When Waning
(7–14 d)
Anxiety/restlessness +++ +++ ++
Insomnia +++ +++ ++
Tremor + ++ +
Confusion +++ ++
Delirium +++
Auditory, tactile, and visual hallucinations +++ ++
Tachycardia + ++ +
Hypertension + ++ +
Nausea ++ +
Vomiting ++ +
Diaphoresis + ++ +
+, Mild; ++, moderate; +++, severe.
NOTE: Symptoms did not always progress from mild to severe in a predictable fashion.
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The patients ranged from 22 to 38 years of age, and most (88%) were employed. Bodybuilding was frequently (63%) the motivation for GHB use. . All patients reported frequent ingestion of GHB, every 1 to 3 hours around-the-clock with nighttime awakening to take doses. The duration of GHB use was 2 months to 3 years. Some patients had recently escalated their dosing frequency.
The patients exhibited a consistent abuse pattern of large frequent amounts of GHB documented by family and friends. A similar withdrawal toxidrome rapidly followed the last dose of GHB. The denial of concurrent alcohol and drug abuse accompanied by the lack of social or laboratory evidence of alcoholism makes delirium tremens in the setting of alcohol withdrawal an unlikely explanation for this syndrome.
GHB overdose has become a significant cause of patients with drug-induced coma presenting to EDs6; however, reports of a withdrawal syndrome are rare.2 The low incidence of dependence and the rapid onset of withdrawal symptoms are probably related to the rapid absorption and elimination kinetics of GHB. After ingestion, GHB effects can begin within 10 to 15 minutes. Absorption of GHB is capacity limited, resulting in increased time to peak levels with increased dose. A therapeutic dose (50 mg/kg) produced peak levels in 45 minutes. The elimination of GHB is rapid but saturable, culminating in a terminal half-life of 23 minutes after a 50-mg/kg dose.9 Consequently, frequent dosing is expected to be required to maintain levels sufficient for physiologic adaptation and dependence. Our patients reported physiologic adaptation with dosing every 3 hours around-the-clock.
After dependence develops, GHB use is maintained as withdrawal symptoms threaten whenever GHB is discontinued. The approximate daily dose estimated in cases 1 and 2, where the concentration of GHB was known, ranged from 43 to 144 g/d. In contrast, evaluations of GHB for narcolepsy reported neither tolerance to GHB during experimental courses of 6 months to 9 years nor withdrawal symptoms at their completion (reference 3 and Mamelak M, Baycrest Hospital Toronto Canada; personal communication, July 1998). These narcolepsy studies used total daily doses of 4.5 to 9 g per night administered as two or three 30-mg/kg doses 3 hours apart, leaving a GHB-free period of more than 12 hours. The balance between dose and dosing interval necessary to produce GHB dependence is not known, but around-the-clock dosing is a feature of our cases.
GHB exerts a distinct effect at specific GHB receptors. The close structural and metabolic relationship of GHB and -aminobutyric acid (GABA) may also play an important role in the withdrawal syndrome. In vivo conversion of radioactive GHB into GABA has been described, and current research has proposed that GHB modulates both GABAA and GABAB receptors.10,11 The end result, acutely, is neuroinhibition with physiologic tolerance developing over time.
Early symptoms of insomnia, tremor, confusion, nausea, and vomiting are mild, and medical admission to a health care facility is often delayed until more severe symptoms of agitation and hallucinations are experienced. The withdrawal syndrome progresses over the initial 2 to 3 days with mild autonomic instability manifested by tachycardia, hypertension, tremor, and diaphoresis. Central nervous system symptoms include vivid hallucinations and anxiety. Confusion, disorientation, and delirium with agitation and combative behavior occur as the syndrome progresses, often requiring 4-point leather restraints and sedation. These symptoms become episodic in nature as the syndrome wanes
--------------------------------------------------------------------------------
. Manifestations of withdrawal from GHB.
--------------------------------------------------------------------------------
Symptoms Early
(1–24 h) Progressive
(1–6 d) Episodic When Waning
(7–14 d)
Anxiety/restlessness +++ +++ ++
Insomnia +++ +++ ++
Tremor + ++ +
Confusion +++ ++
Delirium +++
Auditory, tactile, and visual hallucinations +++ ++
Tachycardia + ++ +
Hypertension + ++ +
Nausea ++ +
Vomiting ++ +
Diaphoresis + ++ +
+, Mild; ++, moderate; +++, severe.
NOTE: Symptoms did not always progress from mild to severe in a predictable fashion.
--------------------------------------------------------------------------------
The patients ranged from 22 to 38 years of age, and most (88%) were employed. Bodybuilding was frequently (63%) the motivation for GHB use. . All patients reported frequent ingestion of GHB, every 1 to 3 hours around-the-clock with nighttime awakening to take doses. The duration of GHB use was 2 months to 3 years. Some patients had recently escalated their dosing frequency.
The patients exhibited a consistent abuse pattern of large frequent amounts of GHB documented by family and friends. A similar withdrawal toxidrome rapidly followed the last dose of GHB. The denial of concurrent alcohol and drug abuse accompanied by the lack of social or laboratory evidence of alcoholism makes delirium tremens in the setting of alcohol withdrawal an unlikely explanation for this syndrome.
GHB overdose has become a significant cause of patients with drug-induced coma presenting to EDs6; however, reports of a withdrawal syndrome are rare.2 The low incidence of dependence and the rapid onset of withdrawal symptoms are probably related to the rapid absorption and elimination kinetics of GHB. After ingestion, GHB effects can begin within 10 to 15 minutes. Absorption of GHB is capacity limited, resulting in increased time to peak levels with increased dose. A therapeutic dose (50 mg/kg) produced peak levels in 45 minutes. The elimination of GHB is rapid but saturable, culminating in a terminal half-life of 23 minutes after a 50-mg/kg dose.9 Consequently, frequent dosing is expected to be required to maintain levels sufficient for physiologic adaptation and dependence. Our patients reported physiologic adaptation with dosing every 3 hours around-the-clock.
After dependence develops, GHB use is maintained as withdrawal symptoms threaten whenever GHB is discontinued. The approximate daily dose estimated in cases 1 and 2, where the concentration of GHB was known, ranged from 43 to 144 g/d. In contrast, evaluations of GHB for narcolepsy reported neither tolerance to GHB during experimental courses of 6 months to 9 years nor withdrawal symptoms at their completion (reference 3 and Mamelak M, Baycrest Hospital Toronto Canada; personal communication, July 1998). These narcolepsy studies used total daily doses of 4.5 to 9 g per night administered as two or three 30-mg/kg doses 3 hours apart, leaving a GHB-free period of more than 12 hours. The balance between dose and dosing interval necessary to produce GHB dependence is not known, but around-the-clock dosing is a feature of our cases.
GHB exerts a distinct effect at specific GHB receptors. The close structural and metabolic relationship of GHB and -aminobutyric acid (GABA) may also play an important role in the withdrawal syndrome. In vivo conversion of radioactive GHB into GABA has been described, and current research has proposed that GHB modulates both GABAA and GABAB receptors.10,11 The end result, acutely, is neuroinhibition with physiologic tolerance developing over time.