INTRODUCTION — MDMA (3,4-methylenedioxymethamphetamine; commonly called "ecstasy") is a synthetic compound with structural and pharmacologic similarities to both amphetamines and mescaline. First developed in 1914 as an appetite suppressant, MDMA found use as a psychotherapeutic agent during the 1970s [1,2]. However, its potential for abuse was quickly recognized, leading government agencies to place tight restrictions on its use .
MDMA is a commonly abused drug, particularly among young party-goers at electronic dance music venues, including dance clubs and festivals. Typical effects include feelings of euphoria, wakefulness, intimacy, excitement, and disinhibition .
The clinical features and management of acute MDMA intoxication are reviewed here. A summary table to facilitate emergency management is provided (table 1). Detailed discussions of related issues, such as serotonin syndrome, severe hyperthermia, and a general discussion of the poisoned patient are found separately. (See "Serotonin syndrome (serotonin toxicity)" and "Severe nonexertional hyperthermia (classic heat stroke) in adults" and "General approach to drug poisoning in adults" and "Approach to the child with occult toxic exposure".)
EPIDEMIOLOGY — Abuse of MDMA fluctuates [5,6]. Most new MDMA users in the United States are adults. Both adult and teenage use there is less prevalent than in the previous 10 years. This includes decrease in use prior to and during the coronavirus disease 2019 (COVID-19) pandemic. The number of younger MDMA users may be due in part to the erroneous belief that MDMA provides a “safe” high. In fact, MDMA shares toxicities with amphetamine, in addition to unique adverse effects, and adverse events including deaths associated with its use have increased since 2013. MDMA users are most commonly polysubstance users . Multiple dance festivals in the United States have experienced partygoer deaths from MDMA use [7,8]. Most of these have onsite medical staff to provide medical attention for attendees, which regularly includes adverse events from drug use .
Experimental use of MDMA to treat a number of psychiatric disorders (eg, posttraumatic stress) continues to increase dramatically . Based on efficacy in phase II and III clinical trials of resistant post-traumatic stress disorder (PTSD), it is anticipated that the U.S. Food and Drug Administration (FDA) may grant limited approval for use of MDMA in 2023 . If MDMA becomes an FDA-approved medication, more persons will likely be exposed to MDMA.
PHARMACOLOGY AND CELLULAR TOXICOLOGY — MDMA (3,4-methylenedioxymethamphetamine, also commonly called “Molly” or “ecstasy”) is a sympathomimetic amphetamine that causes release of endogenous catecholamines (particularly norepinephrine and dopamine) and blocks their reuptake into presynaptic vesicles.
MDMA differs somewhat from traditional amphetamines in that it is structurally similar to serotonin. This difference likely accounts for an increased release of serotonin and inhibition of serotonin reuptake [3,12].
This results in a toxicity profile for MDMA that is different from that of traditional amphetamines. Although typical findings of amphetamine toxicity (hypertension, tachycardia, hyperthermia, CNS stimulation) are often seen in MDMA toxicity, serotonergic toxicity (serotonin syndrome, SIADH) may be seen as well.
Over 100 congeners of MDMA exist. Tablets purported to contain MDMA may contain highly toxic MDMA analogs or completely different drugs altogether. Hair testing of individuals who take illicit drugs they believe to be MDMA demonstrate that these persons have actually been exposed to MDPV (methylenedioxypyrovalerone, one of the compounds known as “bath salts”) and numerous other similar novel psychoactive substances . In addition to amphetamine derivatives, numerous other compounds are abused in a manner similar to MDMA. Many are sold illicitly by internet vendors, and these substances are often misrepresented as MDMA and sold to unknowing users. Such substances include phenylethylamines 2CB, 2CT2, 2CT7, DOM, Bromo-dragonfly, and the tryptamines DMT, 5 Meo-DMT, and “Foxy.” The effects of these agents may be similar to MDMA, but they may have greater potency, causing more severe hallucinations, greater serotonergic activity, and more severe overall toxicity [14,15]. Management is similar to that described below for MDMA.
Fentanyl derivatives are the most lethal and concerning contents of substances illicitly sold as MDMA. Fentanyl or other opioid contaminants cause opioid toxicity, which is vastly different than typical toxicity resulting from MDMA . (See "Acute opioid intoxication in adults".)
KINETICS — MDMA is typically ingested as a tablet in dosages ranging from 50 mg to 200 mg, and it is readily absorbed from the gastrointestinal tract. Peak effects occur within two hours of ingestion and typically last four to six hours . Up to 75 percent of MDMA is excreted in the urine unchanged, while the remainder is primarily metabolized by the hepatic enzyme CYP2D6 [17,18].
The concentrations of MDMA contained in illicitly produced pills vary widely . Major toxicity and death may occur after ingestion of a single tablet; ingestion of larger quantities carries greater risk of toxicity.
CLINICAL FEATURES — MDMA increases alertness, reduces fatigue, and leads to feelings of increased physical and mental powers, and euphoria. Users typically begin to experience the desired effects of MDMA approximately one hour following oral administration. Minor adverse reactions, such as agitation, nausea, bruxism (grinding teeth), ataxia, diaphoresis, blurry vision, tachycardia, and hypertension, can also occur at typical MDMA doses. These effects are usually self-limited and resolve within hours . More serious effects are uncommon and described below.
Vital signs — MDMA can cause hypertension, tachycardia, and hyperthermia.
Cardiovascular stimulation — Life-threatening increases in heart rate and blood pressure may occur. Cardiovascular toxicity can include hypertensive emergencies, myocardial infarction, aortic dissection, and dysrhythmia [20-26]. In addition, catastrophic central neurologic hemorrhage, including intracranial hemorrhage and posterior spinal artery aneurysm, has been reported [27,28].
Hyperthermia and related effects — Hyperthermia may result from drug effects on the central nervous system (CNS), prolonged physical exertion (eg, prolonged dancing) and environmental conditions (eg, dancing in a warm or hot environment). Both the stimulant effect of amphetamines and serotonin syndrome may contribute to severe hyperthermia in these patients [24,29]. Hyperthermia can lead to disseminated intravascular coagulation and rhabdomyolysis. (See 'Hyperthermia' below.)
Manifestations of hyponatremia — MDMA use can lead to hyponatremia due to increased fluid intake and persistent secretion of antidiuretic hormone that slows the rate of water excretion. The belief among some MDMA users that they can avoid hyperthermia by drinking large amounts of water is one reason for increased fluid intake. The mechanisms that lead to hyponatremia are described separately.
Marked, acute reductions in serum sodium can lead to serious neurologic manifestations including confusion, seizures, cerebral edema, cerebral herniation, and death. The serum sodium in such patients is usually below 120 meq/L (120 mmol/L). Young women appear to be at increased risk for both symptomatic hyponatremia and residual neurologic injury. (See "Manifestations of hyponatremia and hypernatremia in adults", section on 'Susceptibility of premenopausal females'.)
Neurologic — Stimulation of the CNS is common and can manifest as agitation, hyperactivity, anxiety, and even delirium . Seizures and status epilepticus can occur. Psychomotor agitation may be associated with hyperthermia as well as rhabdomyolysis.
Hepatotoxicity — Hepatotoxicity caused by MDMA poisoning is well recognized. Even in the absence of severe hyperthermia or disseminated intravascular coagulation, hepatitis, centrilobular necrosis, and hepatic fibrosis may result from MDMA abuse [30,31]. Clinical findings are similar to other forms of toxin-induced hepatic injury and may include jaundice, abdominal pain, and vomiting. Elevations of bilirubin, aspartate transaminase (AST), and alanine transaminase (ALT) may be present.
Serotonin syndrome findings — Serotonin syndrome is a potentially life-threatening condition characterized by the triad of autonomic dysfunction, abnormal neuromuscular activity, and altered mental status. MDMA use can cause serotonin syndrome, presumably via stimulation of massive serotonin release. Individuals who use MDMA in combination with selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs), or other drugs that increase 5-HT1A receptor activity (such as meperidine, tryptophan, or lithium) are at greater risk of developing serotonin syndrome [32,33]. (See "Serotonin syndrome (serotonin toxicity)".)
DIFFERENTIAL DIAGNOSIS — Other sympathomimetic drugs of abuse, such as cocaine, amphetamine, and methamphetamine, may present with a clinical syndrome that is indistinguishable from MDMA toxicity. (See "Cocaine: Acute intoxication" and "Methamphetamine: Acute intoxication" and "Acute amphetamine and synthetic cathinone ("bath salt") intoxication".)
Anticholinergic toxicity can present with delirium, dilated pupils, hyperthermia, tachycardia, and hypertension. Skin findings may be helpful in distinguishing the two syndromes: patients with anticholinergic toxicity generally present with reduced or absent sweating, whereas patients with MDMA toxicity are usually diaphoretic. The typical pattern of speech is also different for the two poisonings, frequently being clear but pressured for MDMA and resembling a "mouthful of marbles" with anticholinergic toxicity. (See "Anticholinergic poisoning".)
Other causes of altered mental status, such as hypoglycemia, electrolyte disorders, intracranial hemorrhage, and infection should be considered. In particular, patients with hyperthermia and alteration in mental status who do not have a history strongly suggestive of MDMA or other drug intoxication should undergo lumbar puncture to rule out a CNS infection. (See "Diagnosis of delirium and confusional states".)
LABORATORY EVALUATION — Routine laboratory evaluation of the poisoned patient should include the following:
●Point-of-care glucose measurement, to rule out hypoglycemia as the cause of any alteration in mental status
●Acetaminophen and salicylate levels, to rule out these common coingestions
●Electrocardiogram (ECG), to rule out conduction system poisoning by drugs that affect the QRS or QTc intervals
●Pregnancy test in female patients of childbearing age
For patients in whom significant toxicity related to use of MDMA is suspected, the clinician should also obtain the following [3,12]:
●Basic serum electrolytes; if hyponatremia is present, a serum osmolality is recommended
●Creatine kinase and urine myoglobin, to evaluate for rhabdomyolysis (see "Rhabdomyolysis: Clinical manifestations and diagnosis")
●Serum creatinine, to assess for renal injury
●Serum aminotransferase concentrations, to assess for hepatic injury
●Coagulation studies (ie, aPTT, PT, INR, platelet count, d-dimer), to assess for disseminated intravascular coagulation (see "Evaluation and management of disseminated intravascular coagulation (DIC) in adults")
Although serum and urine assays specific for MDMA are available, we strongly advise against using them to guide clinical management. A positive MDMA screening test cannot confirm that a patient's symptoms are the result of MDMA toxicity. A negative test can occur despite the presence of MDMA congeners, of which there are over 100. Such congeners may cause clinical symptoms that are indistinguishable from MDMA toxicity. Regardless of whether the inciting agent is MDMA or a related drug, management is identical and based solely on the patient's clinical status.
MANAGEMENT — The general approach to any poisoned patient must always begin with stabilization of the airway, breathing, and circulation. General discussions of the basic facets of the management of poisonings are found separately. Detailed management of MDMA intoxication and similar agents is discussed immediately below. A summary table to facilitate emergent management is provided (table 1). (See "General approach to drug poisoning in adults" and "Gastrointestinal decontamination of the poisoned patient" and "Enhanced elimination of poisons".)
Airway — MDMA-associated hyponatremia may produce obtundation to a degree that necessitates endotracheal intubation [29,34]. Standard agents for rapid sequence intubation (RSI) may be used. Prophylactic agents to prevent elevations in intracranial pressure during RSI are unnecessary.
Breathing — Abnormalities of oxygenation are not expected with MDMA toxicity and should prompt consideration of another diagnosis or a separate concurrent problem (such as aspiration pneumonia).
Circulation — Severe hypertension from sympathomimetic use typically has a central and peripheral component. Treatment of the central component is accomplished with sedatives; benzodiazepines (eg, lorazepam, 1 to 2 mg IV push; may repeat until hypertension is controlled or patient is sedated) are appropriate first line agents. Hypertension refractory to aggressive benzodiazepine therapy is not typical, but can be treated with peripheral agents, such as sodium nitroprusside (standard doses) or the alpha-adrenergic blocking agent phentolamine (1 to 5 mg IV).
Although nitroprusside and phentolamine are standard initial therapies for stimulant-induced hypertension, these medications are not routinely available in some settings. In such cases, the calcium channel blockers nicardipine or the dopamine antagonist fenoldopam can decrease systemic vascular resistance without affecting the cardiac conduction system. Where other antihypertensive medications are not available, closely monitored use of labetalol, a mixed alpha-beta adrenergic antagonist, is reasonable.
The use of beta-blocking agents to control pulse or blood pressure in sympathomimetic poisoning is controversial. Pure beta-blocking agents, such as metoprolol, esmolol, or propranolol, may lead to unopposed alpha-adrenergic stimulation, may exacerbate coronary artery vasospasm, and increase lethality in animal studies [35-37]. Data relating to the use of labetalol is less clear. Labetalol appears to be the safest beta-blocking agent to treat stimulant-induced hypertension [38-42]. Opponents emphasize that intravenous labetalol acts almost entirely as a beta blocking agent (ratio of beta to alpha blockade is 7:1).
Given the availability of other antihypertensive agents and the controversy that surrounds this issue, we suggest against the use of pure beta blocking agents in the treatment of hypertension associated with MDMA poisoning, and support cautious use of labetalol in circumstances where other options are unavailable.
Indiscriminate fluid resuscitation should be avoided, as it may cause or exacerbate MDMA-associated hyponatremia. In the event the patient truly appears hypovolemic (as demonstrated by poor skin turgor or dry mucous membranes), normal saline may be administered until euvolemia is obtained. Tachycardia is not an appropriate surrogate endpoint for dehydration, as many patients with MDMA toxicity are tachycardic due to the sympathomimetic effects of the drug.
Isolated tachycardia not associated with hypertension rarely requires treatment. In the unlikely event of a supraventricular tachycardia, adenosine or calcium channel blockers may be used. Otherwise, cardiac arrhythmias are managed according to current advanced cardiac life support (ACLS) protocols. (See "Advanced cardiac life support (ACLS) in adults".)
Gastrointestinal decontamination — For a recent ingestion (ie, less than one hour) of MDMA, a single dose of activated charcoal (AC) (1 g/kg; maximum dose 50 g) should be administered. Beyond one hour, drug absorption is usually complete and decontamination is not indicated. However, if a coingestant is suspected, decontamination after one hour may be beneficial [3,12]. (See "Gastrointestinal decontamination of the poisoned patient" and "Enhanced elimination of poisons".)
Charcoal should be withheld in patients who are sedated and potentially unable to protect their airway, unless endotracheal intubation is performed first. However, endotracheal intubation should not be performed solely for the purpose of giving activated charcoal.
Cardiac effects — In addition to hemodynamic effects (see 'Circulation' above), MDMA may produce cardiac ischemia. An electrocardiogram (ECG) should therefore be obtained in all patients with MDMA intoxication and cardiovascular symptoms. Chest pain associated with MDMA use should be evaluated and managed in a manner similar to that of cocaine-associated chest pain. Benzodiazepines (eg, lorazepam, 1 to 2 mg IV, repeated as needed) are an appropriate initial therapy for blood pressure control and agitation. Aspirin, nitroglycerin, and supplemental oxygen are all indicated. We recommend against the use of beta-blocking agents, including labetalol, unless other options are unavailable. (See 'Circulation' above.)
Psychomotor agitation — Psychomotor agitation should be treated with sedative medications. We prefer benzodiazepines as first-line agents, as they have an excellent safety profile and are readily available. Lorazepam (1 to 2 mg IV) has a rapid onset of sedative effects; repeat doses may be administered until agitation is controlled. Very high doses of benzodiazepines (ie, greater than 10 mg of lorazepam) may be required.
Butyrophenones (such as haloperidol and droperidol) interfere with heat dissipation, may prolong the QTc, and may reduce the seizure threshold. Given that hyperthermia and seizures are known consequences of MDMA toxicity, we suggest that butyrophenones not be used.
Minimizing stimuli, such as light and noise, is helpful. Physical restraint should be avoided, if possible, and should only be used until the patient can be chemically sedated. Antipsychotic agents are not indicated.
Hyperthermia — An accurate core body temperature should be obtained. Severe hyperthermia (temperature >41ºC; 107ºF) can be managed by immersion in an ice bath, if feasible, or by other means of active cooling until the core temperature is reduced to 100ºF. The temperature may continue to drop slightly after exiting an ice bath, but this after-drop is typically mild. Moderate hyperthermia should be treated with other cooling measures, including cooling blankets and the combination of cool water mist with fanning. (See "Severe nonexertional hyperthermia (classic heat stroke) in adults".)
If hyperthermia from serotonin syndrome is suspected, initial treatment with benzodiazepines and possibly cyproheptadine is appropriate [3,24]. If hyperthermia is refractory to these measures, intubation and paralysis should be performed. (See "Serotonin syndrome (serotonin toxicity)", section on 'Hyperthermia'.)
Hyponatremia — Asymptomatic and usually mild hyponatremia can be treated with fluid restriction alone, which usually leads to resolution of the hyponatremia within 12 to 24 hours. However, as mentioned above, MDMA use may be associated with the development of severe hyponatremia that can lead to neurologic symptoms (eg, confusion, seizures), cerebral edema, brain herniation, and death. The serum sodium is usually less than 120 meq/L (120 mmol/L).
Patients with marked neurologic symptoms should be treated initially with hypertonic saline (3 percent or 513 meq/L). One regimen that we have used was initially described in hyponatremic athletes participating in endurance events, such as marathon races, an acute form of hyponatremia similar to ecstasy intoxication. It consists of 100 mL of 3 percent saline given as an intravenous bolus, which should acutely raise the serum sodium concentration by 2 to 3 meq/L (mmol/L), thereby reducing the degree of cerebral edema. If neurologic symptoms persist or worsen, a 100 mL bolus of 3 percent saline can be repeated one or two more times at 10 minute intervals. (See "Exercise-associated hyponatremia", section on 'Use of hypertonic saline'.)
The serum sodium is monitored closely. Overly rapid correction in patients with marked hyponatremia for two days or more is associated with an increased risk of severe and often irreversible neurologic injury, called osmotic demyelination. However, patients with very acute hyponatremia, as occurs in ecstasy intoxication and exercise-associated hyponatremia, are at minimal risk for this complication. These issues are discussed in detail elsewhere. (See "Osmotic demyelination syndrome (ODS) and overly rapid correction of hyponatremia" and "Overview of the treatment of hyponatremia in adults".)
Seizures — Seizures, whether or not they are associated with hyponatremia, are treated with benzodiazepines and (if necessary) appropriate correction of the patient's serum sodium as described in the preceding section. The mechanism of MDMA-induced seizures makes phenytoin an illogical treatment choice, and we do not recommend its use. Seizures that occur in the setting of drug intoxication typically result from an altered balance of excitatory and inhibitory neurotransmitters. This mechanism is distinct from that of patients with a known seizure disorder, who generally have electrical instability in a discrete area of brain tissue amenable to treatment with sodium channel blocking agents, such as phenytoin.
Serotonin syndrome — Benzodiazepines, with or without cyproheptadine, remain the mainstay of treatment. Patients with significant hyperthermia as part of a severe serotonin syndrome require aggressive treatment. The management of serotonin syndrome is discussed elsewhere. (See "Serotonin syndrome (serotonin toxicity)".)
Disposition — Patients with severe toxicity, including cardiotoxicity, hypertensive emergency, severe neurologic symptoms, hyperthermia, serotonin syndrome, and hyponatremia/hypoosmolality should be managed in an intensive care setting. Patients with mild symptoms and no evidence of end-organ toxicity may be discharged after their symptoms resolve, usually within six to eight hours.
Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)
Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Treatment of acute poisoning caused by recreational drug or alcohol use".)
SUMMARY AND RECOMMENDATIONS
●Emergency treatment algorithm and epidemiology – MDMA (3,4-methylenedioxymethamphetamine) remains a popular drug of abuse, particularly among adolescents and young adults. A summary table to facilitate emergency management of clinically significant intoxication is provided (table 1).
●Onset and duration of toxic effects and pill contents – Peak effects of MDMA toxicity occur within two hours of ingestion and typically last four to six hours. Concentrations of MDMA contained in illicitly produced pills vary widely. Major toxicity and death may occur after ingestion of a single tablet. Tablets purported to contain MDMA may contain highly toxic MDMA analogs or completely different drugs altogether. (See 'Pharmacology and cellular toxicology' above and 'Kinetics' above.)
●Clinical presentation and possible complications – MDMA intoxication can cause a myriad of dangerous effects, including severe hypertension, hyperthermia, delirium, psychomotor agitation, and profound hyponatremia. Potential life-threatening complications include intracranial hemorrhage, myocardial infarction, aortic dissection, disseminated intravascular coagulation, rhabdomyolysis, seizure, and serotonin syndrome. (See 'Clinical features' above.)
●Differential diagnosis – The differential diagnosis for MDMA intoxication includes other sympathomimetic drugs of abuse (eg, cocaine, amphetamine, methamphetamine) and anticholinergic toxicity. Hypoglycemia, electrolyte disorders, intracranial hemorrhage, and infection should be considered. (See 'Differential diagnosis' above.)
Patients with hyperthermia and alterations in mental status who do not have a history strongly suggestive of MDMA or other drug intoxication should undergo lumbar puncture to rule out an infection of the central nervous system (CNS). (See 'Hyperthermia and related effects' above.)
●Laboratory testing – Routine laboratory evaluation of the poisoned patient includes (see 'Laboratory evaluation' above):
•Acetaminophen and salicylate blood concentrations
•Pregnancy test in women of childbearing age
When MDMA is suspected, additional testing should include the following:
•Basic serum electrolytes; if hyponatremia is present, a serum osmolality is recommended
•Creatine kinase and urine myoglobin
•Serum aminotransferase concentrations
•Coagulation studies (ie, aPTT, PT, INR, platelet count, d-dimer)
●Resuscitation and tracheal intubation – MDMA-associated hyponatremia frequently produces obtundation to a degree that necessitates endotracheal intubation. Standard induction or paralytic agents can be used to perform rapid sequence intubation (RSI). (See 'Initial resuscitation' above.)
●Treatment of hypertension and agitation – We recommend that severe hypertension and psychomotor agitation be treated with benzodiazepines (eg, lorazepam, 1 to 2 mg IV push; repeat until hypertension is controlled or the patient is sedated) (Grade 1B). Refractory hypertension may be treated with nitroprusside or phentolamine. (See 'Psychomotor agitation' above.)
We suggest butyrophenones (eg, haloperidol, droperidol) not be used to sedate patients with MDMA toxicity (Grade 2C). Butyrophenones interfere with heat dissipation, may prolong the QTc interval, and may reduce the seizure threshold. If possible, we prefer to avoid beta-blocking agents, including labetalol, in the treatment of acute sympathomimetic poisoning.
●Gastrointestinal decontamination – For a recent ingestion (ie, less than one hour) of MDMA, we suggest a single dose of activated charcoal (1 g/kg; maximum dose 50 g) be administered (Grade 2C). Charcoal should be withheld in patients who are sedated and potentially unable to protect their airway, unless endotracheal intubation is performed first. Intubation should not be performed solely for the purpose of giving charcoal. (See 'Gastrointestinal decontamination' above.)
●Treatment of hyponatremia – For patients with severe symptomatic hyponatremia (serum sodium usually less than 120 meq/L (mmol/L)), we recommend treatment with hypertonic saline (3 percent or 513 meq/L) (Grade 1C). This reduces the risk for life-threatening cerebral edema. We use the following regimen: 100 mL of 3 percent saline given as an intravenous (IV) bolus. This should acutely raise the serum sodium concentration by 2 to 3 meq/L (mmol/L). If neurologic symptoms persist or worsen, a 100 mL IV bolus of 3 percent saline can be repeated one or two more times at 10 minute intervals. (See 'Hyponatremia' above.)
Mild, asymptomatic hyponatremia can be treated with fluid restriction alone. This generally results in the resolution of hyponatremia within 12 to 24 hours.
●Treatment of other complications – Seizures, hyperthermia, and serotonin syndrome are treated in standard fashion. (See "Convulsive status epilepticus in adults: Classification, clinical features, and diagnosis" and "Severe nonexertional hyperthermia (classic heat stroke) in adults" and "Serotonin syndrome (serotonin toxicity)".)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Stephen J Traub, MD, former section editor of the toxicology program, for 20 years of dedicated service.
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