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Try out PMC Labs and tell us what you think. Learn More. They have become popular with participants in 'raves,' because they enhance energy, endurance, sociability and sexual arousal. This vogue among teenagers and young adults, together with the widespread belief that 'ecstasy' is a safe drug, has led to a thriving illicit traffic in it. But these drugs also have serious toxic effects, both acute and chronic, that resemble those previously seen with other amphetamines and are caused by an excess of the same sympathomimetic actions for which the drugs are valued by the users. Neurotoxicity to the serotonergic system in the brain can also cause permanent physical and psychiatric problems. A detailed review of the literature has revealed over 87 'ecstasy'-related fatalities, caused by hyperpyrexia, rhabdomyolysis, intravascular coagulopathy, hepatic necrosis, cardiac arrhythmias, cerebrovascular accidents, and drug-related accidents or suicide. The toxic or even fatal dose range overlaps the range of recreational dosage. The available evidence does not yet permit an accurate assessment of the size of the problem presented by the use of these drugs. The initial letters of the major portions of the latter name Methylene d ioxy-Meth a mphetamine give rise to the acronym MDMA, by which this substance is commonly designated in the clinical and research literature. A closely related compound, N-ethyl-3,4-methylene-dioxyamphetamine or MDEA, differs from MDMA only in having a 2-carbon ethyl group, rather than a 1-carbon methyl group, attached to the nitrogen atom of the amphetamine structure. In earlier years, the name was applied to 3,4-methylenedioxyamphetamine MDA. MDEA is also sometimes called ecstasy by its vendors and users, but is more often referred to as Eve. The 3 compounds are closely similar in their chemistry and in their biological effects, so that the description of MDMA in the rest of this review also applies in the main to MDEA, and to a considerable extent to MDA. Ecstasy differs from amphetamine and methamphetamine in one important respect. As shown in Fig. In this respect, it resembles the structure of the hallucinogenic material mescaline. As a result, the pharmacological effects of MDMA and MDEA are a blend of those of the amphetamines and mescaline, as will be described in later sections of this review. Arrows do not represent pathways of synthesis or metabolism; they merely indicate the closest resemblances of structure. Amphetamine was in fact marketed for weight-reduction purposes among others, in the s, though its sale was later sharply restricted because of its widespread abuse and the risk of dependence and other adverse effects. Like the amphetamines, MDMA and its related compounds are amines that can exist either as free bases or as salts of various acids. The free bases are volatile and, indeed, amphetamine itself was first marketed in this form in an inhaler, for use as a nasal decongestant. Theoretically, MDMA and MDEA could also be used in this fashion, but the methylenedioxy group raises the boiling point of the free base so high that it is impossible to use it by sniffing the vapour. As sold illicitly in Europe and North America, MDMA is typically prepared in very professional-looking tablets stamped with a wide variety of symbols according to the whim or imagination of the maker see illustration in Theune and colleagues 7. However, the actual composition of the tablets varies greatly, with respect to both the drug s contained in them and the amounts. The total amount consumed per occasion varies greatly among users. For this purpose, the most common dosage has been 1—2 tablets during the course of the party, 15 , 16 but occasional case reports have indicated doses as high as 10 tablets in combination with other drugs, 17 , 18 , 19 usually with toxic outcomes. In order to understand the highly varied effects of these drugs, both desired and undesired, on the user, it is helpful to review briefly the basic pharmacology of the ring-substituted amphetamines, including their pharmacokinetics and their mechanism of action in the brain and other organs. MDMA is readily absorbed from the intestinal tract and reaches its peak concentration in the plasma about 2 hours after oral administration. These concentrations are quite low, because the drug passes readily into the tissues, and much of it is bound to tissue constituents. It is helpful to remember these peak concentrations for comparison with the levels found in patients who have suffered the serious and sometimes fatal adverse effects described later in this review. The drug is broken down metabolically, mainly in the liver, where an enzyme designated CYP2D6 is chiefly responsible. Consequently, as the dose is increased and the higher-affinity enzymes are saturated, disproportionately large increases in blood and brain concentrations of the drug occur. Elimination of the drug from the body is moderately slow, the half-life for MDMA disappearance from the blood being of the order of 8 hours. Some of the metabolites of MDMA are still pharmacologically active, especially its first metabolite, MDA, so that the duration of action may be somewhat longer than the duration of MDMA itself in the body. There is now an abundance of evidence, both experimental and clinical, that MDMA and the other ring-substituted amphetamine derivatives act by increasing the net release of the monoamine neurotransmitters serotonin, noradrenaline and, to a smaller extent, dopamine from their respective axon terminals. There is a small amount of experimental evidence that the net release of acetylcholine may also be increased by MDMA, 33 but the importance of this effect in humans is unknown. It is clear, however, that the increase in the net release of serotonin and possibly dopamine is the major mechanism of action underlying the distinctive mental effects of MDMA, whereas the increased release of noradrenaline is mainly responsible for the physical effects that it shares with amphetamine. MDMA and its related compounds are generally produced as racemic mixtures, but the stereoisomers differ from each other in several important respects. The reported effects of MDMA vary according to the dose and the frequency and duration of use. In general, the effects desired by most users are those produced by low doses on single occasions. It is, therefore, convenient to describe the effects separately for acute single-occasion and chronic long-term use and, within each category, to describe separately the mental and the physical effects. A third category of effect, consisting of the serious or fatal toxicity seen at higher doses or in abnormally sensitive individuals, will be described separately. The desired effects for which MDMA is used are closely similar to those that account for the continuing popularity of the other amphetamines. Physically, it produces a marked increase in wakefulness, endurance and sense of energy, sexual arousal, and postponement of fatigue and sleepiness. However, it is not possible to say whether this is because of disappointment with the results, or because of difficulty obtaining the drug since its change in legal status. Like the amphetamines, MDMA also has adverse effects on many physical functions, even when taken in moderate doses for the recreational purposes described earlier. Stiffness and pain in the lower-back and limb muscles are very common complaints during the first 2—3 days after the use of MDMA. Headache, nausea, loss of appetite, blurred vision, dry mouth and insomnia are other commonly reported physical symptoms during the drug experience and immediately afterwards. Heart rate and blood pressure, which are usually elevated during the drug experience, tend to fluctuate more widely than normal during the following days. Undesired psychological acute effects commonly reported during the drug experience similarly represent an exaggeration of the effects for which the drug is taken. The increased arousal, if carried to excess, is converted into hyperactivity, flight of ideas with a resulting inability to focus one's thoughts in a sustained and useful manner and insomnia. Related complaints often include mild hallucinations, depersonalization a feeling of separation of the self from the body , anxiety, agitation, and bizarre or reckless behaviour. The day or 2 after drug use, the most common mental or mood complaints are difficulty concentrating, depression, anxiety and fatigue. Apart from the small number of people who have reported improvement or resolution of emotional or personality problems after the use of MDMA in psychotherapy, the long-term effects are virtually all adverse ones. They are all thought to arise from a neurotoxic action of the methylenedioxy derivatives of the amphetamines. The ability of MDMA to increase the concentration of serotonin in the synapse probably underlies its production of improved mood and of sensory alterations. However, at higher doses the massive release of serotonin not only gives rise to acute psychotic symptoms as described earlier but also causes chemical damage to the cells that released it. This damage has been clearly demonstrated in animal experiments with MDMA and related drugs. Although there are conflicting theories concerning the mechanism of this neurotoxicity, 4 , 27 , 63 it is clearly related to the excessive metabolic activity and neurotransmitter release in the serotonergic and, possibly, the dopaminergic neurons. In humans, there has been only one postmortem study of changes in the levels of serotonin and its main metabolite in the brain of a single long-term MDMA user. However, several types of experimental study in living humans have provided indirect evidence of serotonin neurotoxicity. Techniques such as positron emission tomography PET or single photon emission computed tomography SPECT are then used to detect the locations and amounts of the labelled compounds in the brain. Such studies permit either estimates or measurements of the numbers of functionally intact serotonin-releasing cells or serotonin-responsive cells in the living subject. By these means, it has been demonstrated that the brains of long-term MDMA users, when examined while free of the drug, have abnormally low levels of serotonin and its metabolites in the cerebrospinal fluid, 66 reduced numbers of serotonin transporter molecules, 67 , 68 , 69 increased numbers of glial cells, 70 and altered patterns of glucose metabolism and blood flow in certain parts of the brain. A major limitation of these studies is that, even if they demonstrate decreased numbers of serotonin cells and reduced serotonin system function in the brains of MDMA users, they cannot prove that the MDMA use caused the changes. The alterations in serotonin function might have been present before the drug use began, they might even have contributed to the start of drug use or they might be purely coincidental. It has been suggested that the demonstrated neurotoxic effects of MDMA on the serotonin system may be the possible cause of a variety of mental and behavioural problems that outlast the actual drug experience by months or years. These problems are quite varied in nature, but they all involve functions in which serotonin is known to play an important role. Among such persisting problems described in the literature are the following:. The same problems of interpretation arise in these cases as mentioned earlier in relation to studies of serotonin neurotoxicity in humans, namely, the difficulty of deciding whether the alterations found in patients with chronic use of MDMA were the cause of the drug use, the result of it or coincidental. Therefore, logic supports the view that these disturbances are indeed residual consequences of the drug use. As is the case for psychiatric problems, there are a number of physical problems that either appear after drug use is over, or that begin during the period of drug use but persist long afterwards. Among these are the following:. One case of parkinsonism and one of bilateral abducens paralysis have been attributed to damage to dopaminergic neurons. This section deals with very serious and potentially life-threatening physical problems that are clearly and directly attributable to the known pharmacological actions of the drug itself. There are 4 principal types of such serious toxicity: hepatic, cardiovascular, cerebral and hyperpyrexic. Each is described separately below, but these patterns of toxicity are not mutually exclusive, and in severe cases patients may have features of 2 or more types concurrently. A high proportion of the case reports of serious MDMA toxicity include the observation that the patients were jaundiced. Various explanations have been offered for this effect, including the possibility of an allergic drug reaction, a toxic contaminant in the individual batch of drug, or a secondary effect of hyperpyrexia, , which will be described later. However, the most probable explanation relates to the pathways of metabolism of the drug. A marked decrease in the level of free glutathione permits a series of biochemical changes massive influx of calcium, oxidative change in the cell-membrane lipids, and so on that result in cell death. The clinical picture in such cases is varied. On the whole, it is relatively mild, resembling a viral hepatitis, with jaundice, an enlarged tender liver, an increased bleeding tendency, raised liver enzyme levels in the blood and a biopsy picture of acute hepatitis that is not in any sense diagnostic of MDMA toxicity. Spontaneous recovery usually occurs over a period of a few weeks to many months, but in chronic users of MDMA there may be repeated attacks of hepatitis. The picture can be much more severe, however, progressing rapidly to a fulminating liver failure that proves fatal unless the patient is fortunate enough to receive a liver transplant. The largest series of ecstasy-related transplants reviewed so far is described by Brauer and colleagues, who found 9 cases in the literature plus one of their own; of these, 4 died after the transplant while 6 survived, having either fully or partially recovered. A newer and perhaps less drastic procedure is auxiliary liver transplantation, in which the recipient's own liver is left in place but a donor liver is inserted as well, in order to carry out the necessary liver functions while the recipient's own liver gradually recovers, at which time the auxiliary liver is removed. As noted earlier, MDMA and related drugs increase the net release not only of serotonin, but also of noradrenaline and dopamine. It is especially the noradrenaline that is responsible for most of the serious adverse effects on the cardiovascular system. These effects consist of 2 basic types: hypertension, with a consequent risk of ruptured blood vessels and internal hemorrhage, and tachycardia, with a consequently increased cardiac workload, and a resulting risk of heart failure. This type of hemorrhage affects the small vessels that are intrinsically weaker than the larger ones and does not require pre-existing damage to the vessel walls. Many of the fatal cases described later in this review had pulmonary edema, which is a sign of heart failure. Large amounts of sodium can be lost in sweat, and if the dancers drink large amounts of water in order to avoid overheating, the result is frequently hemodilution and resulting hyponatremia. An additional mechanism that can contribute to the same result is inappropriate secretion of the pituitary antidiuretic hormone, leading to retention of water by the kidneys, , but in most cases it is probably caused by excessive water intake following profuse sweating. This leads to passage of water from the blood into the tissues, including the brain. Many such cases have been reported. As noted earlier, the combination of the drug action, intense physical activity and a hot environment contribute to this increase. Even an increase of a few degrees in environmental temperature causes marked increases in body temperature and serotonin toxicity in the brains of rats treated with MDMA, but not in those treated with a physiological salt solution. The pattern of these changes closely resembles that seen in severe heatstroke. This protein is taken up by the kidney and excreted in the urine, but it is also toxic to the kidney itself. Renal failure is, therefore, an end result of the muscle damage and may be severe enough to require hemodialysis to prevent death from uremia. Because fibrinogen, platelets and other clotting factors are used up in the process, the remaining blood loses the ability to clot normally, so that hemorrhages can then occur. The treatment of the hyperpyrexic pattern of toxicity has been mainly symptomatic, an essential part being early recognition of the problem and rapid cooling of the body by ice-water sponging, intravenous infusion of chilled saline solution, gastric and bladder lavage with cooled fluids, and general supportive care. All of the severe forms of toxicity described earlier have been capable of causing death. Most of the cases of serious toxicity or fatality have involved blood levels ranging from 0. However, some have had levels as low as 0. This is an important point, because it demonstrates the degree to which the seriousness of the effects can be dependent on environmental factors other than the drug concentration. All the fatal cases that have been located through a literature search are summarized in Appendix 1, which includes additional reference material , , , , , , , , , , , , , , , available on the CMAJ Web site at www. It must be emphasized that what is described in the literature cannot be regarded as complete, because not every physician who sees such cases will publish case reports about them. It has been claimed that dependence is unlikely to become a serious problem, because the decrease in pleasurable or rewarding effects if the drug is used too frequently, and the increase in frequency of unpleasant effects, 41 , 44 would diminish the incentive to use the drug in a manner that could give rise to dependence. The same phenomenon occurs with the classical hallucinogens, which have not proven to give rise to dependence to nearly the same extent as alcohol, cannabis, benzodiazepines or opioids, for example. On the other hand, amphetamine and methamphetamine are at least as liable to produce dependence as cocaine. It was claimed that cocaine was not dependence producing when it began to reappear in the early s, and it took years of growing experience to rediscover what had been known about cocaine dependence some 50 years earlier. Kirsch 12 cites, for example, estimates of the number of doses produced by an illicit laboratory in the United States as growing from 10 a month in , to 30 a month in and a month in However, such figures cannot be regarded as accurate representations of the change in the extent of use in the population at large. Among occasional users, novelty seeking appears to be an important motivating force. From the foregoing review, one must conclude that the whole group of amphetamines and related drugs strongly resemble each other and cocaine, at least with respect to their toxic effects. The opioids have a clearly demonstrated dependence risk, but their intrinsic physical toxicity is considerably less dangerous than that of the amphetamine group. In contrast, many of the serious effects of the amphetamines are directly due to the action of the drug itself, as described earlier. The rates for deaths from accidents when driving, ecstasy, and heroin were as follows:. These figures indicate that the death rate from heroin is higher, but that the precision of the estimate is much lower for ecstasy, which probably reflects a more heterogeneous user population, with fewer ecstasy users being as risk seeking as some of the heroin users. This review of the literature indicates that ecstasy MDMA and related drugs are potentially dangerous, even in the doses typically used by participants at raves. Both the acute and the chronic effects can lead to serious and even fatal toxicity, the full extent of which cannot yet be estimated with accuracy. The variety of different adverse effects, including psychiatric, neurological, cardiovascular, hepatic, renal, thermoregulatory and even dental problems, indicates that patients with ecstasy-related difficulties may present in any part of the health care system and not only to emergency services. Because the main users are adolescents and young adults following the dictates of current drug fashion, physicians may need to be especially alert to such problems in an otherwise healthy population group. This article has been peer reviewed. Acknowledgements : I received an honorarium from the federal Department of Justice, Canada, for undertaking this review. I am indebted to M. Correspondence to: Dr. National Center for Biotechnology Information , U. Harold Kalant. Author information Copyright and License information Disclaimer. This article has been cited by other articles in PMC. Abtract 'Ecstasy' MDMA and related drugs are amphetamine derivatives that also have some of the pharmacological properties of mescaline. Open in a separate window. Routes of administration and dosage Like the amphetamines, MDMA and its related compounds are amines that can exist either as free bases or as salts of various acids. Pharmacology of MDMA and related drugs In order to understand the highly varied effects of these drugs, both desired and undesired, on the user, it is helpful to review briefly the basic pharmacology of the ring-substituted amphetamines, including their pharmacokinetics and their mechanism of action in the brain and other organs. Pharmacokinetics MDMA is readily absorbed from the intestinal tract and reaches its peak concentration in the plasma about 2 hours after oral administration. Pharmacodynamics There is now an abundance of evidence, both experimental and clinical, that MDMA and the other ring-substituted amphetamine derivatives act by increasing the net release of the monoamine neurotransmitters serotonin, noradrenaline and, to a smaller extent, dopamine from their respective axon terminals. Effects on the user The reported effects of MDMA vary according to the dose and the frequency and duration of use. Acute effects Desired effects The desired effects for which MDMA is used are closely similar to those that account for the continuing popularity of the other amphetamines. Undesired effects Like the amphetamines, MDMA also has adverse effects on many physical functions, even when taken in moderate doses for the recreational purposes described earlier. Long-term or residual effects Serotonin neurotoxicity Apart from the small number of people who have reported improvement or resolution of emotional or personality problems after the use of MDMA in psychotherapy, the long-term effects are virtually all adverse ones. Long-term psychiatric problems It has been suggested that the demonstrated neurotoxic effects of MDMA on the serotonin system may be the possible cause of a variety of mental and behavioural problems that outlast the actual drug experience by months or years. Residual physical problems As is the case for psychiatric problems, there are a number of physical problems that either appear after drug use is over, or that begin during the period of drug use but persist long afterwards. Major physical toxicity This section deals with very serious and potentially life-threatening physical problems that are clearly and directly attributable to the known pharmacological actions of the drug itself. Hepatic toxicity A high proportion of the case reports of serious MDMA toxicity include the observation that the patients were jaundiced. Cardiovascular toxicity As noted earlier, MDMA and related drugs increase the net release not only of serotonin, but also of noradrenaline and dopamine. Fatalities due to ecstasy All of the severe forms of toxicity described earlier have been capable of causing death. Comparison with other drugs From the foregoing review, one must conclude that the whole group of amphetamines and related drugs strongly resemble each other and cocaine, at least with respect to their toxic effects. Conclusions This review of the literature indicates that ecstasy MDMA and related drugs are potentially dangerous, even in the doses typically used by participants at raves. Footnotes This article has been peer reviewed. Competing interests : None declared. References 1. Int J Psychiatry Med ; Kalant OJ. The amphetamines — toxicity and addiction. 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Hepatology ; Dtsch Med Wochenschr ; Subarachnoidal haemorrhage associated with MDMA abuse. Arch Emerg Med ; Schweiz Rundsch Med Prax ; Retinal haemorrhage caused by 'ecstasy'. Br J Ophthalmol ; Manchanda S, Connolly MJ. Cerebral infarction in association with ecstasy abuse. Postgrad Med J ; Epileptische insulten, herseninfarct en rhabdomyolysis als complicaties van amfetamingebruik. Ned Tijdschr Geneesk ; Rothwell PM, Grant R. Cerebral venous sinus thrombosis induced by 'ecstasy'. Suarez RV, Riemersma R. Am J Forensic Med Pathol ; Satchell SC, Connaughton M. Inappropriate antidiuretic hormone secretion and extreme rises in serum creatinine kinase following MDMA ingestion. Br J Hosp Med ; Holden R, Jackson MA. Near-fatal hyponatraemic coma due to vasopressin over-secretion after 'ecstasy' 3,4-MDMA. Hyponatraemia and seizures after ecstasy use. Wilkins B. Cerebral oedema after MDMA 'ecstasy' and unrestricted water intake: hyponatraemia must be treated with low water input. 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A fatal case involving methylenedioxy-amphetamine. Clin Toxicol ; Death after ecstasy ingestion: neuropathological findings. American Psychiatric Association. Washington: The Association; Geneva: World Health Organization; Jansen KL. Ecstasy MDMA dependence. Maier's cocaine addiction Der Kokainismus. English translation. Musical preference as an indicator of adolescent drug use. Pedersen W, Skrondal A. Ecstasy and new patterns of drug use: a normal population study. MDMA 'ecstasy' consumption in the context of polydrug abuse: a report on patients. Internist ; Gore SM. Fatal uncertainty: death rate from use of ecstasy or heroin. Support Center Support Center. External link. Please review our privacy policy.

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