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Amphetamine Toxicity

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Last Update: May 6, 2024.

Continuing Education Activity

Amphetamine abuse remains prevalent in the United States (US), with significant implications for public health and individual well-being. The ramifications of amphetamine toxicity and overdose are profound, contributing to substantial morbidity and mortality rates. Notably, amphetamines' sympathomimetic properties precipitate adverse cardiovascular and neurological effects, with studies indicating their involvement in a significant proportion of drug-related deaths in the US. Symptoms of amphetamine toxicity span a spectrum, encompassing tachycardia, hypertension, impulsivity, aggression, serotonin syndrome, psychosis, and seizures, underscoring the complexity of its clinical manifestations. 

In this course, participants explore the multifaceted management of amphetamine toxicity. The dynamics of both acute and chronic amphetamine use and their profound impacts on cardiovascular, neurological, and psychiatric systems are discussed. Recognizing symptoms of amphetamine toxicity, such as tachycardia, hypertension, and serotonin syndrome, while recognizing the limitations of relying solely on drug metabolite testing for diagnosis, is also explored. Furthermore, collaboration and communication among interprofessional teams are  emphasized, as this enhances patient outcomes by leveraging the expertise of diverse healthcare professionals.

Objectives:

  • Differentiate between acute and chronic effects of amphetamine use to tailor appropriate management strategies.  
  • Interpret laboratory and radiologic findings to confirm amphetamine toxicity and rule out alternative diagnoses.
  • Screen patients for amphetamine use disorders and assess their risk of toxicity based on history and clinical presentation.
  • Communicate effectively with interdisciplinary teams to coordinate comprehensive care for patients with amphetamine toxicity.
Access free multiple choice questions on this topic.

Introduction

Amphetamine abuse is widespread and associated with a significant impact on cardiovascular and neurological systems in overdose. In many parts of the world, amphetamines have been an abused class of drugs since the 1930s. Methamphetamine (METH) and its derivative, 3,4-methylenedioxymethamphetamine (MDMA), are extensively abused drugs, and the acute effects of these drugs include increased alertness, hyperthermia, decreased appetite, and euphoria. However, long-term abuse can result in neurotoxicity and psychosis. Amphetamines increase the neurotransmission of dopamine (DA), serotonin (5-HT), and norepinephrine (NE) by entering neurons via the 5-HT and DA transporters and displacing storage vesicles. MDMA has a greater affinity for 5-HT transporters, causing an increased release of 5-HT. The clinical effects of amphetamine overdose are significant and usually observed in emergency departments.[1][2][3]

Etiology

Amphetamine use, both acute and chronic, may lead to amphetamine toxicity. Amphetamine use has increased steadily over time.[4] The reasons for the increased use of amphetamines are numerous, including a sustained desire for favorable drug effects like euphoria, mood elevation, and appetite suppression, the availability of amphetamine compounds as both legal and illegal substances, an increase in the production of amphetamines for sale in the illegal drug trade, and the affordability of illicit amphetamines as compared to other illicit drugs.[4] Recently, stress and anxiety related to the COVID-19 pandemic may have also contributed to increased amphetamine use.[5] Amphetamine dependence is not a prerequisite for toxicity, but those who become dependent on amphetamines may be at higher risk of experiencing it. Dependence is likely due to increased tolerance to amphetamine effects and the requirement of escalating doses to achieve the desired effect. 

Epidemiology

In 2021, it was estimated that 36 million people used amphetamines across the globe. The majority of amphetamine users (55%) are men. For people undergoing treatment for drug use disorders, amphetamines are the primary drug of abuse 18% of the time in the Americas and 42% of the time in Asia.[United Nations Office of Drugs and Crime World Drug Report, 2023] The 2023 "Monitoring the Future Survey" estimated that 2.1% of adolescents in the US used illicit amphetamines.[Monitoring the Future National Survey Results on Drug Use, 1975-2023] Additionally, an estimated 1.8 million Americans 12 years and older have a methamphetamine use disorder.[SAMHSA NSDUH, 2022]

Pathophysiology

Amphetamines are structural analogs of the neurotransmitter phenethylamine (see Image. Phenethylamine Chemical Structure and Image. Amphetamine Chemical Structure), which regulates monoamine neurotransmission through the modulation of the trace amine-associated receptor 1 (TAAR1) and inhibition of the vesicular monoamine transporter 2 (VMAT2). TAAR1 is expressed in multiple locations within the central nervous system (CNS), including the dorsal and ventral caudate nucleus, putamen, substantia nigra, nucleus accumbens, ventral tegmental area, locus ceruleus, amygdala, and raphe nucleus.[6] Many of these areas play important roles in the development of addiction. Thus, the use of amphetamines begets the desire to continue using amphetamines.

The effects of TAAR1 agonism may extend beyond the central nervous system. Downstream effects from receptor activation may lead to increased reactive oxygen species, mitochondrial dysfunction, and alterations in intracellular calcium. These metabolic abnormalities have been implicated in the accelerated development of cardiovascular disease.[7][8][9] Amphetamines also cause necrotizing vasculitis of small- and medium-sized blood vessels, which can yield a myriad of end-organ complications (strokes and neurodegenerative diseases, coronary artery disease, ischemic bowel disease). The underlying etiology is not well understood and may result from the amphetamines or potential adulterants or contaminants.[10][11][12][13][14]  

Toxicokinetics

Amphetamine has an oral bioavailability of about 75%. Peak plasma concentrations are found approximately 3 hours after ingestion. Peak cardiovascular effects occur approximately 1 hour after ingestion, while behavioral changes are seen around 2 hours after ingestion.[15] No ceiling effect has been noted.[16] However, these effects are relatively short-lived, owing to a rapid decline in monoamine release after peak concentrations are reached. Amphetamine is hepatically metabolized by multiple enzymes, including (cytochrome) CYP2D6, dopamine β-hydroxylase, and flavin-containing monooxygenase-3.[17] Only 30% to 40% of amphetamine is eliminated as an unchanged drug in the urine. An acidic urine pH traps amphetamine in the renal tubules and decreases its elimination half-life.[18] 

Methamphetamine can be ingested orally, insufflated nasally, smoked, or injected intravenously. Bioavailability is reliable (~70% or greater) with these ingestion routes. Peak serum concentrations of methamphetamine occur approximately 3 to 6 hours after oral ingestion. Nasal insufflation leads to a peak serum concentration in 5 to 10 minutes, and smoking leads to peak serum concentrations within 5 minutes. Methamphetamine is more lipophilic than amphetamine and is less prone to metabolism by monoamine oxidase. Methamphetamine is hepatically metabolized and renally eliminated, similarly to amphetamine. 

History and Physical

Amphetamines are used for fatigue, appetite suppression, and narcolepsy treatment. Patients experiencing amphetamine toxicity thus often present with anorexia, dehydration, weight loss, and insomnia. Patients may be highly agitated, even to the point of risking the safety of healthcare staff and themselves. Patients should be asked what drug(s) they used, the route of administration they utilized, and the duration of their drug use. Blood pressure, heart rate, and other vital signs should be taken immediately upon presentation. The physical examination should include assessments for hyperthermia, evidence of end-organ damage (eg, neurological deficits, respiratory compromise, or new cardiac murmurs), and skin ulcerations or abscesses. 

Evaluation

When patients appear intoxicated and have symptoms consistent with amphetamine toxicity, testing for metabolites of amphetamine can be useful to confirm a diagnosis of the condition. However, ingestion of some amphetamines, including 3,4-methylenedioxymethamphetamine, will not reliably result in a positive test for the presence of amphetamines.[19][20] Conversely, some non-amphetamine medications may cause false-positive results for the presence of amphetamines. These drugs include pseudoephedrine,[21] mebeverine,[22] metoprolol,[23] tetracaine,[24] dimethylamylamine,[25] aripiprazole,[26] and ranitidine.[27] Thus, clinicians should not rely on drug metabolite testing alone to make a diagnosis of amphetamine toxicity. Obtaining an accurate medication history for the patient may allow a diagnosis to be made independently of drug metabolite testing. Therefore, obtaining medication histories should always be a focus during the evaluation of patients who are intoxicated.

Additionally, laboratory and radiologic evaluation for patients with suspected amphetamine toxicity should focus on confirming that the toxic effects of amphetamines are present and ruling out other causes for them. Dehydration and hyponatremia may be confirmed with a basic metabolic panel. An electrocardiogram, chest x-ray, and troponin test are necessary to assess the presence of coronary ischemia, including myocardial infarction and aortic dissection. Computed tomography of the head is also useful to assess hemorrhagic stroke as a potential cause of neurologic deficits. Finally, obtaining serum creatine kinase and lactic acid levels may help identify muscle damage and tissue ischemia related to tonic-clonic seizures, myoclonus, or hyperthermia. 

Treatment / Management

Treating amphetamine toxicity is supportive. There are no specific antidotes for amphetamine or amphetamine-like compounds. Therefore, treatment should focus on symptom and complication management. Patients with agitation should be treated with parenteral benzodiazepines. Diazepam is an ideal choice if intravenous access is available; otherwise, intramuscular lorazepam or midazolam is appropriate. If the patient presents with hyperactive delirium, benzodiazepines should be avoided, and an intramuscular dose of ketamine at 4-5 mg/kg may be used to stabilize the patient's agitation. 

Patients who present with delirium may benefit from adjunctive treatment with a dopamine antagonist, like haloperidol. However, while the dopamine blockade can help treat the psychiatric and psychomotor disorders associated with amphetamine toxicity, these agents may cause harm. They can decrease the seizure threshold,[28] cause extrapyramidal side effects, increase heat production by altering thermoregulatory function,[29][30][31] and prolong the QTc interval. Thus, judicious and cautious use of these agents in the setting of amphetamine toxicity is required. 

Hypertension related to amphetamine toxicity may abate with agitation treatment. However, some patients may require antihypertensive treatment to combat hypertensive urgency or emergency. Peripheral vasodilators like nitroglycerin and nicardipine may be effective in lowering blood pressure. Beta-blockers should not be used as sole antihypertensive therapies as their use may lead to unopposed α-adrenergic tone and a worsened hypertensive state. Similarly to hypertension, hyperthermia may abate with the treatment of agitation. However, external cooling with ice baths, misting, or cooled IV fluids may also be required to achieve euthermia. External cooling therapies should be rapidly administered when patients present with temperatures exceeding 107 °F.  

Seizures should initially be treated with parenteral benzodiazepines. Barbiturates and propofol may be added for further seizure control. Phenytoin, fosphenytoin, and valproic acid should be avoided due to their ineffectiveness in aborting toxicologic seizures. There are no approved treatments for amphetamine use disorder. Naltrexone has been evaluated for this indication based on its ability to decrease the effects of the dopamine reward system. Some studies have shown promising results for naltrexone.[32][33] In contrast, others have shown a lack of appreciable effects on cravings or amphetamine use.[34][35][36] However, many of these studies were conducted on animals. There is an overall paucity of high-quality data from human subjects to base conclusions on naltrexone's efficacy. As a result, consultation with an addiction specialist, cognitive behavioral therapy, and group therapy remain the primary means to treat amphetamine use disorder.

Differential Diagnosis

To diagnose amphetamine toxicity, other toxicities need to be explored, including toxicities to cocaine, methylxanthine, phencyclidine, and other sympathomimetics. Neurocognitive disorders and stroke should also be ruled out. Schizophrenia, mania, alcohol withdrawal, and meningitis should also be considered.

Complications

Clinicians should screen patients experiencing amphetamine toxicity for complications related to the sympathetic surge that accompanies it. These complications include hemorrhagic strokes,[37][38][39] seizures,[40] hyperthermia,[41][42] serotonin syndrome, acute coronary syndrome,[43][44], cardiomyopathy,[45][46] cardiac valvulopathies,[47][48] aortic dissection,[49][50] rhabdomyolysis,[51] dehydration, acute kidney injury, arrhythmias, and hyponatremia.[52] Additionally, amphetamine toxicity may result in widespread vasospasm. These widespread vasospastic effects can cause ischemia anywhere in the body, including the bowel.[53][54][55][56] Lastly, amphetamine intoxication may be associated with psychosis, paranoid delusions, and hallucinations that resemble schizophrenia.[57][58][59]  

Patients who chronically use amphetamines have an increased risk of developing pulmonary hypertension,[60][61][62] heart failure, and embolic strokes. Additionally, patients who chronically use amphetamines often have poor nutritional status, [63][64] oral hygiene, and widespread skin lesions.[65][66] Frequently, skin lesions result from delusions parasitosis, or Ekbom syndrome, where patients pick at their skin to remove imaginary insects.[67] Chronic use of amphetamines can also cause choreoathetoid movements, which can persist from weeks to years after cessation of amphetamine use.[68][69]

Deterrence and Patient Education

When treating a patient with an amphetamine use disorder, it is important to first medically stabilize them and then discuss the complications associated with use and ascertain their readiness for help and treatment. If they desire treatment and sobriety, they should be connected to an outpatient clinic that can provide further management. 

Enhancing Healthcare Team Outcomes

Physicians, advanced practitioners, nurses, pharmacists, and other healthcare professionals play critical roles in managing amphetamine toxicity. They must accurately identify symptoms, assess severity, and differentiate toxicity from other conditions, utilizing comprehensive evaluations and medication histories. Effective communication and collaboration among team members facilitate coordinated care, ensuring patient safety and optimized outcomes. Clinicians must also apply evidence-based strategies in symptom management and complication prevention, utilizing supportive care approaches. Continuous evaluation and improvement of interventions enhance patient-centered care, promoting a holistic approach to addressing amphetamine abuse and associated toxicities.

Review Questions

Amphetamine Chemical Structure

Figure

Amphetamine Chemical Structure. The illustration describes the structure of the stimulant amphetamine. Public Domain via Wikimedia Commons

Structure of amphetamine

Figure

Structure of amphetamine. creative commons license

References

1.
Limanaqi F, Gambardella S, Biagioni F, Busceti CL, Fornai F. Epigenetic Effects Induced by Methamphetamine and Methamphetamine-Dependent Oxidative Stress. Oxid Med Cell Longev. 2018;2018:4982453. [PMC free article: PMC6081569] [PubMed: 30140365]
2.
Kronstrand R, Guerrieri D, Vikingsson S, Wohlfarth A, Gréen H. Fatal Poisonings Associated with New Psychoactive Substances. Handb Exp Pharmacol. 2018;252:495-541. [PubMed: 30105471]
3.
Simmler LD, Liechti ME. Pharmacology of MDMA- and Amphetamine-Like New Psychoactive Substances. Handb Exp Pharmacol. 2018;252:143-164. [PubMed: 29633178]
4.
Courtney KE, Ray LA. Methamphetamine: an update on epidemiology, pharmacology, clinical phenomenology, and treatment literature. Drug Alcohol Depend. 2014 Oct 01;143:11-21. [PMC free article: PMC4164186] [PubMed: 25176528]
5.
Mellos E, Paparrigopoulos T. Substance use during the COVID-19 pandemic: What is really happening? Psychiatriki. 2022 Mar 28;33(1):17-20. [PubMed: 35255473]
6.
Cisneros IE, Ghorpade A. Methamphetamine and HIV-1-induced neurotoxicity: role of trace amine associated receptor 1 cAMP signaling in astrocytes. Neuropharmacology. 2014 Oct;85:499-507. [PMC free article: PMC4315503] [PubMed: 24950453]
7.
Kevil CG, Goeders NE, Woolard MD, Bhuiyan MS, Dominic P, Kolluru GK, Arnold CL, Traylor JG, Orr AW. Methamphetamine Use and Cardiovascular Disease. Arterioscler Thromb Vasc Biol. 2019 Sep;39(9):1739-1746. [PMC free article: PMC6709697] [PubMed: 31433698]
8.
Tobolski J, Sawyer DB, Song SJ, Afari ME. Cardiovascular disease associated with methamphetamine use: a review. Heart Fail Rev. 2022 Nov;27(6):2059-2065. [PubMed: 35844009]
9.
Indave BI, Sordo L, Bravo MJ, Sarasa-Renedo A, Fernández-Balbuena S, De la Fuente L, Sonego M, Barrio G. Risk of stroke in prescription and other amphetamine-type stimulants use: A systematic review. Drug Alcohol Rev. 2018 Jan;37(1):56-69. [PubMed: 28485090]
10.
Citron BP, Halpern M, McCarron M, Lundberg GD, McCormick R, Pincus IJ, Tatter D, Haverback BJ. Necrotizing angiitis associated with drug abuse. N Engl J Med. 1970 Nov 05;283(19):1003-11. [PubMed: 4394271]
11.
Syed RH, Moore TL. Methylphenidate and dextroamphetamine-induced peripheral vasculopathy. J Clin Rheumatol. 2008 Feb;14(1):30-3. [PubMed: 18431096]
12.
Loewenhardt B, Bernhard M, Pierskalla A, Neumann-Haefelin T, Hofmann E. Neurointerventional treatment of amphetamine-induced acute occlusion of the middle cerebral artery by intracranial balloon angioplasty. Clin Neuroradiol. 2013 Jun;23(2):137-43. [PubMed: 22173373]
13.
Leithäuser B, Langheinrich AC, Rau WS, Tillmanns H, Matthias FR. A 22-year-old woman with lower limb arteriopathy. Buerger's disease, or methamphetamine- or cannabis-induced arteritis? Heart Vessels. 2005 Feb;20(1):39-43. [PubMed: 15700202]
14.
Bostwick DG. Amphetamine induced cerebral vasculitis. Hum Pathol. 1981 Nov;12(11):1031-3. [PubMed: 7319490]
15.
Angrist B, Corwin J, Bartlik B, Cooper T. Early pharmacokinetics and clinical effects of oral D-amphetamine in normal subjects. Biol Psychiatry. 1987 Nov;22(11):1357-68. [PubMed: 3663788]
16.
Heal DJ, Smith SL, Gosden J, Nutt DJ. Amphetamine, past and present--a pharmacological and clinical perspective. J Psychopharmacol. 2013 Jun;27(6):479-96. [PMC free article: PMC3666194] [PubMed: 23539642]
17.
Santagati NA, Ferrara G, Marrazzo A, Ronsisvalle G. Simultaneous determination of amphetamine and one of its metabolites by HPLC with electrochemical detection. J Pharm Biomed Anal. 2002 Sep 05;30(2):247-55. [PubMed: 12191709]
18.
Brams M, Mao AR, Doyle RL. Onset of efficacy of long-acting psychostimulants in pediatric attention-deficit/hyperactivity disorder. Postgrad Med. 2008 Sep;120(3):69-88. [PubMed: 18824827]
19.
Cody JT, Schwarzhoff R. Fluorescence polarization immunoassay detection of amphetamine, methamphetamine, and illicit amphetamine analogues. J Anal Toxicol. 1993 Jan-Feb;17(1):23-33. [PubMed: 8429622]
20.
Spiller HA, Ryan ML, Weston RG, Jansen J. Clinical experience with and analytical confirmation of "bath salts" and "legal highs" (synthetic cathinones) in the United States. Clin Toxicol (Phila). 2011 Jul;49(6):499-505. [PubMed: 21824061]
21.
DePriest AZ, Knight JL, Doering PL, Black DL. Pseudoephedrine and false-positive immunoassay urine drug tests for amphetamine. Pharmacotherapy. 2013 May;33(5):e88-9. [PubMed: 23065913]
22.
Bedussi F, Acerbis E, Noseda R, Demagistri D, Zamprogno E, Ceschi A. False-positive urine screen test for MDMA in a patient exposed to mebeverine. Br J Clin Pharmacol. 2021 May;87(5):2397-2398. [PubMed: 33200465]
23.
Leclercq M, Soichot M, Delhotal-Landes B, Bourgogne E, Gourlain H, Mégarbane B, Labat L. False positive amphetamines and 3,4-methylenedioxymethamphetamine immunoassays in the presence of metoprolol-two cases reported in clinical toxicology. J Anal Toxicol. 2020 Mar 07;44(2):200-205. [PubMed: 31384953]
24.
Wijngaard R, Parra-Robert M, Marés L, Escalante A, Salgado E, González-de-la-Presa B, To-Figueras J, Brunet M. Tetracaine from urethral ointment causes false positive amphetamine results by immunoassay. Clin Toxicol (Phila). 2021 Jun;59(6):500-505. [PubMed: 33112680]
25.
Vorce SP, Holler JM, Cawrse BM, Magluilo J. Dimethylamylamine: a drug causing positive immunoassay results for amphetamines. J Anal Toxicol. 2011 Apr;35(3):183-7. [PubMed: 21439156]
26.
Kaplan J, Shah P, Faley B, Siegel ME. Case Reports of Aripiprazole Causing False-Positive Urine Amphetamine Drug Screens in Children. Pediatrics. 2015 Dec;136(6):e1625-8. [PubMed: 26527556]
27.
Liu L, Wheeler SE, Rymer JA, Lower D, Zona J, Peck Palmer OM, Tamama K. Ranitidine interference with standard amphetamine immunoassay. Clin Chim Acta. 2015 Jan 01;438:307-8. [PubMed: 25242739]
28.
Pisani F, Oteri G, Costa C, Di Raimondo G, Di Perri R. Effects of psychotropic drugs on seizure threshold. Drug Saf. 2002;25(2):91-110. [PubMed: 11888352]
29.
Kreuzer P, Landgrebe M, Wittmann M, Schecklmann M, Poeppl TB, Hajak G, Langguth B. Hypothermia associated with antipsychotic drug use: a clinical case series and review of current literature. J Clin Pharmacol. 2012 Jul;52(7):1090-7. [PubMed: 21956608]
30.
Shiloh R, Schapir L, Bar-Ziv D, Stryjer R, Konas S, Louis R, Hermesh H, Munitz H, Weizman A, Valevski A. Association between corneal temperature and mental status of treatment-resistant schizophrenia inpatients. Eur Neuropsychopharmacol. 2009 Sep;19(9):654-8. [PubMed: 19493658]
31.
Evers SS, Calcagnoli F, van Dijk G, Scheurink AJ. Olanzapine causes hypothermia, inactivity, a deranged feeding pattern and weight gain in female Wistar rats. Pharmacol Biochem Behav. 2010 Nov;97(1):163-9. [PubMed: 20570692]
32.
Ray LA, Bujarski S, Courtney KE, Moallem NR, Lunny K, Roche D, Leventhal AM, Shoptaw S, Heinzerling K, London ED, Miotto K. The Effects of Naltrexone on Subjective Response to Methamphetamine in a Clinical Sample: a Double-Blind, Placebo-Controlled Laboratory Study. Neuropsychopharmacology. 2015 Sep;40(10):2347-56. [PMC free article: PMC4538349] [PubMed: 25801501]
33.
Moerke MJ, Banks ML, Cheng K, Rice KC, Negus SS. Maintenance on naltrexone+amphetamine decreases cocaine-vs.-food choice in male rhesus monkeys. Drug Alcohol Depend. 2017 Dec 01;181:85-93. [PMC free article: PMC5683900] [PubMed: 29040826]
34.
Sakloth F, Negus SS. Naltrexone maintenance fails to alter amphetamine effects on intracranial self-stimulation in rats. Exp Clin Psychopharmacol. 2018 Apr;26(2):195-204. [PMC free article: PMC5897164] [PubMed: 29528663]
35.
Guterstam J, Jayaram-Lindström N, Berrebi J, Petrovic P, Ingvar M, Fransson P, Franck J. Cue reactivity and opioid blockade in amphetamine dependence: A randomized, controlled fMRI study. Drug Alcohol Depend. 2018 Oct 01;191:91-97. [PubMed: 30096639]
36.
Stoops WW, Pike E, Hays LR, Glaser PE, Rush CR. Naltrexone and bupropion, alone or combined, do not alter the reinforcing effects of intranasal methamphetamine. Pharmacol Biochem Behav. 2015 Feb;129:45-50. [PMC free article: PMC4300270] [PubMed: 25459104]
37.
Winsløw F, Hansen NS, Jensen MB. Vertebral Artery Dissection Related to Amphetamine Abuse - A Case Report. J Cent Nerv Syst Dis. 2020;12:1179573520939340. [PMC free article: PMC7331755] [PubMed: 32655281]
38.
Wang AM, Suojanen JN, Colucci VM, Rumbaugh CL, Hollenberg NK. Cocaine- and methamphetamine-induced acute cerebral vasospasm: an angiographic study in rabbits. AJNR Am J Neuroradiol. 1990 Nov-Dec;11(6):1141-6. [PMC free article: PMC8332147] [PubMed: 2124040]
39.
Buxton N, McConachie NS. Amphetamine abuse and intracranial haemorrhage. J R Soc Med. 2000 Sep;93(9):472-7. [PMC free article: PMC1298104] [PubMed: 11089483]
40.
Goyal P, Sethi P, Sharma S. Prevalence of recreational substance use in patients presenting with seizures to a tertiary care hospital. Epilepsy Behav. 2021 Dec;125:108419. [PubMed: 34837845]
41.
Madea B, Ruppel E, Prangenberg J, Krämer M, Doberentz E. Expression of heat shock proteins 27, 60, and 70 in amphetamine and cocaine associated deaths. Forensic Sci Int. 2021 Dec;329:111088. [PubMed: 34773820]
42.
Green AR, Cross AJ, Goodwin GM. Review of the pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA or "Ecstasy"). Psychopharmacology (Berl). 1995 Jun;119(3):247-60. [PubMed: 7675958]
43.
O'Connor AD, Rusyniak DE, Bruno A. Cerebrovascular and cardiovascular complications of alcohol and sympathomimetic drug abuse. Med Clin North Am. 2005 Nov;89(6):1343-58. [PubMed: 16227066]
44.
Pozoga J, Snopek G, Dabrowski M. [Acute coronary syndrome after amphetamine use in a young male with myocardial bridging--a case report]. Kardiol Pol. 2005 Apr;62(4):381-2. [PubMed: 15928743]
45.
Kueh SA, Gabriel RS, Lund M, Sutton T, Bradley J, Kerr AJ, Looi JL. Clinical Characteristics and Outcomes of Patients with Amphetamine-Associated Cardiomyopathy in South Auckland, New Zealand. Heart Lung Circ. 2016 Nov;25(11):1087-1093. [PubMed: 27185546]
46.
Jacobs W. Fatal amphetamine-associated cardiotoxicity and its medicolegal implications. Am J Forensic Med Pathol. 2006 Jun;27(2):156-60. [PubMed: 16738435]
47.
Ayme-Dietrich E, Lawson R, Côté F, de Tapia C, Da Silva S, Ebel C, Hechler B, Gachet C, Guyonnet J, Rouillard H, Stoltz J, Quentin E, Banas S, Daubeuf F, Frossard N, Gasser B, Mazzucotelli JP, Hermine O, Maroteaux L, Monassier L. The role of 5-HT2B receptors in mitral valvulopathy: bone marrow mobilization of endothelial progenitors. Br J Pharmacol. 2017 Nov;174(22):4123-4139. [PMC free article: PMC5680644] [PubMed: 28806488]
48.
Naqvi TZ, Gross SB. Anorexigen-induced cardiac valvulopathy and female gender. Curr Womens Health Rep. 2003 Apr;3(2):116-25. [PubMed: 12628081]
49.
Westover AN, Nakonezny PA. Aortic dissection in young adults who abuse amphetamines. Am Heart J. 2010 Aug;160(2):315-21. [PMC free article: PMC2924822] [PubMed: 20691838]
50.
Swalwell CI, Davis GG. Methamphetamine as a risk factor for acute aortic dissection. J Forensic Sci. 1999 Jan;44(1):23-6. [PubMed: 9987866]
51.
Hu HY, Wei SY, Pan CH. Rhabdomyolysis observed at forensic autopsy: a series of 52 cases. Forensic Sci Med Pathol. 2018 Dec;14(4):424-431. [PubMed: 30056625]
52.
Farah R, Farah R. Ecstasy (3,4-methylenedioxymethamphetamine)-induced inappropriate antidiuretic hormone secretion. Pediatr Emerg Care. 2008 Sep;24(9):615-7. [PubMed: 18797371]
53.
Panikkath R, Panikkath D. Amphetamine-related ischemic colitis causing gastrointestinal bleeding. Proc (Bayl Univ Med Cent). 2016 Jul;29(3):325-6. [PMC free article: PMC4900786] [PubMed: 27365888]
54.
Green PA, Battersby C, Heath RM, McCrossan L. A fatal case of amphetamine induced ischaemic colitis. Ann R Coll Surg Engl. 2017 Sep;99(7):e200-e201. [PMC free article: PMC5697024] [PubMed: 28853604]
55.
Kurtz B, Alshoubi A, Nguyen K, Gehres E. Methamphetamine-Induced Bowel Ischemia in a 50-Year-Old Male. Case Rep Crit Care. 2022;2022:9690034. [PMC free article: PMC8988091] [PubMed: 35402052]
56.
Attaran H. Fatal Small Intestinal Ischemia Due to Methamphetamine Intoxication: Report of a Case With Autopsy Results. Acta Med Iran. 2017 May;55(5):344-347. [PubMed: 28724276]
57.
Medhus S, Rognli EB, Gossop M, Holm B, Mørland J, Bramness JG. Amphetamine-induced psychosis: Transition to schizophrenia and mortality in a small prospective sample. Am J Addict. 2015 Oct;24(7):586-9. [PubMed: 26332037]
58.
Ginovart N, Farde L, Halldin C, Swahn CG. Changes in striatal D2-receptor density following chronic treatment with amphetamine as assessed with PET in nonhuman primates. Synapse. 1999 Feb;31(2):154-62. [PubMed: 10024013]
59.
Boileau I, Dagher A, Leyton M, Gunn RN, Baker GB, Diksic M, Benkelfat C. Modeling sensitization to stimulants in humans: an [11C]raclopride/positron emission tomography study in healthy men. Arch Gen Psychiatry. 2006 Dec;63(12):1386-95. [PubMed: 17146013]
60.
Chen PI, Cao A, Miyagawa K, Tojais NF, Hennigs JK, Li CG, Sweeney NM, Inglis AS, Wang L, Li D, Ye M, Feldman BJ, Rabinovitch M. Amphetamines promote mitochondrial dysfunction and DNA damage in pulmonary hypertension. JCI Insight. 2017 Jan 26;2(2):e90427. [PMC free article: PMC5256132] [PubMed: 28138562]
61.
van Wolferen SA, Vonk Noordegraaf A, Boonstra A, Postmus PE. [Pulmonary arterial hypertension due to the use of amphetamines as drugs or doping]. Ned Tijdschr Geneeskd. 2005 Jun 04;149(23):1283-8. [PubMed: 15960135]
62.
Zamanian RT, Hedlin H, Greuenwald P, Wilson DM, Segal JI, Jorden M, Kudelko K, Liu J, Hsi A, Rupp A, Sweatt AJ, Tuder R, Berry GJ, Rabinovitch M, Doyle RL, de Jesus Perez V, Kawut SM. Features and Outcomes of Methamphetamine-associated Pulmonary Arterial Hypertension. Am J Respir Crit Care Med. 2018 Mar 15;197(6):788-800. [PMC free article: PMC5855067] [PubMed: 28934596]
63.
Seiden LS, Sabol KE, Ricaurte GA. Amphetamine: effects on catecholamine systems and behavior. Annu Rev Pharmacol Toxicol. 1993;33:639-77. [PubMed: 8494354]
64.
Ross LJ, Wilson M, Banks M, Rezannah F, Daglish M. Prevalence of malnutrition and nutritional risk factors in patients undergoing alcohol and drug treatment. Nutrition. 2012 Jul;28(7-8):738-43. [PubMed: 22356728]
65.
Laslett AM, Dietze P, Dwyer R. The oral health of street-recruited injecting drug users: prevalence and correlates of problems. Addiction. 2008 Nov;103(11):1821-5. [PubMed: 19032532]
66.
Smart RJ, Rosenberg M. Methamphetamine abuse: medical and dental considerations. J Mass Dent Soc. 2005 Summer;54(2):44-6, 48-9. [PubMed: 16149403]
67.
Yeh TC, Lin YC, Chen LF, Chiang CP, Mao WC, Chang HA, Kao YC, Tzeng NS. Aripiprazole treatment in a case of amphetamine-induced delusional infestation. Aust N Z J Psychiatry. 2014 Jul;48(7):681-2. [PubMed: 24563196]
68.
Rhee KJ, Albertson TE, Douglas JC. Choreoathetoid disorder associated with amphetamine-like drugs. Am J Emerg Med. 1988 Mar;6(2):131-3. [PubMed: 3355623]
69.
Lundh H, Tunving K. An extrapyramidal choreiform syndrome caused by amphetamine addiction. J Neurol Neurosurg Psychiatry. 1981 Aug;44(8):728-30. [PMC free article: PMC491095] [PubMed: 7299411]

Disclosure: Sarayu Vasan declares no relevant financial relationships with ineligible companies.

Disclosure: Brian Murray declares no relevant financial relationships with ineligible companies.

Disclosure: Garth Olango declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK470276PMID: 29262049

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