Ecstasy Ingestion Research Articles

Spontaneous pneumomediastinum and surgical emphysema presenting as rhinolalia following ecstasy ingestion: a case report

BackgroundWe present a unique case of rhinolalia as the first recognizable sign of spontaneous pneumomediastinum and surgical emphysema following drug use.Case presentationThis case presents a 17-year-old white male experiencing rhinolalia following ecstasy ingestion at a rave. Subsequent chest X-ray revealed extensive surgical emphysema, along with a continuous diaphragm sign indicative of pneumomediastinum. Computed tomography confirmed the diagnosis. The patient was managed conservatively with strict monitoring and 6 hourly electrocardiograms. Follow-up computed tomography on day 3 showed resolution of pneumomediastinum and surgical emphysema, and the patient was safely discharged. Notably, the patient experienced a temporary rhinolalia during the acute phase, which resolved spontaneously as his condition improved.ConclusionsThis case underscores the importance of considering spontaneous pneumomediastinum and surgical emphysema in the differential diagnosis of young individuals presenting with acute symptoms after drug use.

HAMMAN'S SYNDROME: A RARE CONSEQUENCE FOR A COMMON VICE

TOPIC: Disorders of the Mediastinum TYPE: Medical Student/Resident Case Reports INTRODUCTION: Roughly 42 million Americans have reported trying cocaine via myriad methods in their lifetime. Since the early 2000s, spontaneous pneumomediastinum as a result of intranasal cocaine use has been demonstrated though it remains a relatively rare occurrence. Though complications such as coronary vasospasm and thrombosis may prove a greater threat to life, it should remain a part of the clinician's differential when treating a patient with a history of cocaine abuse and chest pain. CASE PRESENTATION: A healthy 20-year-old male presented with chest pain, cough, and neck pain for 3 days. He was drinking with a friend and "snorted" cocaine a few times on the same night. A few hours into the evening, he experienced a sudden, sharp retrosternal chest pain, without radiation, and exacerbated by deep breathing. He denied trauma and denied vomiting, dry heaving, gagging, or other symptoms to cause concern for GI perforation as cause, despite drinking heavily that night.On evaluation, his oxygen saturation measured 98% on room air with normal pulse, blood pressure and temperature. Physical examination revealed extensive neck and chest wall subcutaneous emphysema. Electrocardiogram demonstrated normal sinus rhythm without arrhythmias or segmental changes. CT of the chest demonstrated large amounts of air in the superior mediastinum. Based on his history, severity of presentation, and laboratory investigations, there was no concern for mediastinitis or esophageal rupture. He did not require oxygen supplementation and his pain was well controlled, so he was discharged to his home. DISCUSSION: In 1939, Louis Virgil Hamman (1877–1946) described the co-occurrence of subcutaneous emphysema with spontaneous pneumomediastinum, thus coining the term Hamman's Syndrome for this particular malady. Subcutaneous emphysema occurs primarily within the head and neck due to anatomical proximity to the airway and pneumomediastinum as a result of cocaine insufflation is thought to be due to barotrauma, with rapid changes in intrathoracic and intra-alveolar pressures as the individual snorts and performs Valsalva maneuver. Though typically self-limited, complications of spontaneous pneumomediastinum to be aware of include airway compression, pneumopericardium, and mediastinitis. CONCLUSIONS: In a case of Hamman's Syndrome without a history of illicit drug use or trauma, it is prudent to investigate other secondary causes of spontaneous pneumomediastinum, such as esophageal or tracheobronchial rupture, that can prove fatal. Particularly in young males who abuse cocaine, the astute clinician must search for underlying causes of chest pain with recent drug use: coronary artery spasm or thrombosis, arrhythmia, pneumothorax, or pneumomediastinum. REFERENCE #1: Dadhwal R, Bulathsinghala C P, Choudhry I, et al. Cocaine-Induced Bronchial Laceration: A Rare Incidence. Cureus, 2021, 13(4): e14252. doi:10.7759/cureus.14252 REFERENCE #2: Jaensch, S.; Hwang, S.; Kuo, T. Spontaneous pneumomediastinum and subcutaneous emphysema following cocaine inhalation and ecstasy ingestion. Case Reports in Otolaryngology, 2019, Article ID 6972731: 1-4. https://doi.org/10.1155/2019/6972731 REFERENCE #3: Soares et al. Subcutaneous emphysema and pneumomediastinum following cocaine inhalation: a case report. Journal of Medical Case Reports, 2015, 9(195): 1-4. DOI 10.1186/s13256-015-0683-8 DISCLOSURES: No relevant relationships by Kendall Creed, source=Web Response No relevant relationships by Navkiran Randhawa, source=Web Response No relevant relationships by Sabrina Siddiqui, source=Web Response No relevant relationships by Victor Test, source=Web Response

WHIPPIT - WHIPPED THE LUNG

SESSION TITLE: Medical Student/Resident Disorders of the Pleura Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pneumothorax (PTX) can be a complication of invasive mechanical ventilation due to abrupt changes in pressure within the thoracic cavity. It can also occur due to sudden change in the intra-thoracic pressure as a complication of inhaled illicit substances such as cocaine and 3,4-Methylenedioxymethamphetamine (MDMA) (1,2). The recreational use of inhaled nitric oxide continues to rise, with prolonged inhalation leading to neurological complications (3). Here, we present a case of a PTX after inhalation of pressurized nitric oxide in a patient without any prior lung disease, a complication not previously reported. CASE PRESENTATION: A 25-year-old man with history of cannabis use disorder presented with sudden onset left sided chest pain and dyspnea that started after inhaling two canisters of Whippits (pressurized whipped cream chargers filled with nitric oxide). He was tachycardic and tachypneic upon presentation and was noted to have absent breath sounds over left hemi-thorax. Initial laboratory investigations including a complete blood count and comprehensive metabolic panel were unremarkable. Chest X-ray (CXR) revealed a large left PTX with complete collapse of the left lung. A chest tube was inserted on the left hemithorax with resolution of his symptoms and the PTX on imaging. A computed tomography of the chest showed no underlying lung disease. The patient was discharged with recommendations to abstain from inhaled nitric oxide use. DISCUSSION: PTX due to nitric oxide inhalation is uncommon, and to our knowledge no cases have been previously reported. However, PTX and pneumomediastinum from Valsalva maneuvers after use of inhaled drugs have been reported and have been associated with marijuana use (4,5,6). Although, there is no direct role of marijuana in the development of emphysema, high burden of inflammatory cells leading to lung injury and subsequent emphysema has been described (5). In our patient, who had no prior underlying lung disease, the development of PTX most likely resulted from sudden and rapid change in intra-alveolar pressure secondary to forced lung expansion from a Valsalva maneuver after inhalation of pressurized nitric oxide. CONCLUSIONS: Nitric oxide induced PTX has not been previously reported in the literature. In our patient, PTX in the absence of underlying primary lung disease can be explained by barotrauma from rapid inhalation of nitric oxide via Whippits. Further studies are warranted to evaluate the risk factors and incidence of PTX with pressurized nitric oxide inhalation. Reference #1: Ioannidis G, Lazaridis G, Baka S, et al. Barotrauma and pneumothorax. J Thorac Dis. 2015;7(Suppl 1):S38–S43. doi:10.3978/j.issn.2072-1439.2015.01.31 Reference #2: 2) Jaensch S, Hwang S, Shih-Wei-Kuo T. Spontaneous Pneumomediastinum and Subcutaneous Emphysema following Cocaine Inhalation and Ecstasy Ingestion. Case Reports in Otolaryngology. 2019; doi: 10.1155/2019/6972731 Reference #3: 3) Thompson AG, Leite MI, Lunn MP, Bennett DL. Whippits, nitrous oxide and the dangers of legal highs. Pract Neurol. 2015;15(3):207–209. doi:10.1136/practneurol-2014-001071 4) Hauben M, Hung EY. Pneumothorax as an adverse drug event: an exploratory aggregate analysis of the US FDA AERS database including a confounding by indication analysis inspired by Cornfield's condition. Int J Med Sci. 2013;10(8):965–973. Published 2013 Jun 13. doi:10.7150/ijms.5377 5) Mishra R, Patel R, Khaja M. Cannabis-induced bullous lung disease leading to pneumothorax: Case report and literature review. Medicine (Baltimore). 2017;96(19):e6917. doi:10.1097/MD.0000000000006917 6) Miller, W. Eugene, et al. “Pneumomediastinum Resulting from Performing Valsalva Maneuvers during Marihuana Smoking.” Chest, vol. 62, no. 2, 1972, pp. 233–234., doi:10.1378/chest.62.2.233. DISCLOSURES: No relevant relationships by Moeezullah Beg, source=Web Response No relevant relationships by Tasnim Islam, source=Web Response Consultant relationship with GSK Please note: $5001 - $20000 Added 04/23/2020 by Diego Maselli Caceres, source=Web Response, value=Consulting fee Consultant relationship with AstraZeneca Please note: $5001 - $20000 Added 04/23/2020 by Diego Maselli Caceres, source=Web Response, value=Consulting fee Consultant relationship with Sanofi/Regeneron Please note: $5001 - $20000 Added 04/23/2020 by Diego Maselli Caceres, source=Web Response, value=Consulting fee Speaker/Speaker's Bureau relationship with Sunovion Please note: $5001 - $20000 Added 04/23/2020 by Diego Maselli Caceres, source=Web Response, value=Honoraria Consultant relationship with Novartis Please note: $1001 - $5000 Added 04/23/2020 by Diego Maselli Caceres, source=Web Response, value=Consulting fee

Adolescent With Acute Liver Failure in the Setting of Ethanol, Cocaine, and Ecstasy Ingestion Treated With a Molecular Adsorbent Recirculating System

Recreational polypharmacy intoxication is a popular trend, particularly among adolescents and young adults. Acute liver failure is an uncommon complication of drug intoxication and has been described separately among patients intoxicated with ethanol, cocaine, and 3,4-methylenedioxy-methamphetamine (MDMA, ecstasy). Many patients with acute liver failure will die without liver transplant, and management of drug-induced acute liver failure is complicated by the fact that polysubstance abuse may be a contraindication for liver transplant, even among young patients.Here we report a case of acute liver failure in an adolescent male secondary to recreational intoxication with ethanol, cocaine, and ecstasy. This patient was not a candidate for liver transplantation. We describe successful treatment using a molecular adsorbent recirculating system (MARS®) or “liver dialysis” and review the literature pertaining to management options for this type of patient.

Pneumomediastinum as a complication of MDMA (3,4-methylenedioxymetamfetamine, Ecstasy) ingestion

MDMA (3,4-methylenedioxymethamfetamine, Ecstasy) is a widely used recreational drug. We present a case of pneumomediastinum as a complication of MDMA use in a 21-year-old man with no previous history of lung or gastrointestinal pathology. We have performed a literature review, and summarised the symptoms, signs, and prognosis for this under-recognised complication of a commonly used recreational drug. We recommend enquiring about illicit drug use in any patient presenting with spontaneous pneumomediastinum.

Survival following 'Green Rolex' ecstasy ingestion and severe serotonin syndrome

Summary‘Green Rolex’ is a form of ecstasy that has been associated with a number of deaths in the UK and elsewhere. We describe the case of an 18‐year‐old male who we believe is the only known survivor of severe serotoninergic syndrome associated with this drug. We describe our therapeutic approach with reference to current evidence.

A Rare Cause of Spontaneous Pneumomediastinum: Ecstasy Ingestion.

Ecstasy ingestion has life-threatening effects such as hyperpyrexia, rhabdomyolysis, disseminated intravascular coagulation, coma, and death. In the present report, we aimed to highlight ecstasy as a rare cause of spontaneous pneumomediastinum and its potential life-threatening effects. A 16-year-old female with dyspnea and chest pain presented to the emergency department. Chest computed tomography demonstrated pneumomediastinum at the level of the thoracic inlet and upper and posterior mediastinum. The patient was admitted to the thoracic surgery department with a preliminary diagnosis of spontaneous pneumomediastinum. She refused to answer any questions during the first visit, an a psychiatric consultation was requested. The most important finding of psychiatric consultation was ecstasy abuse, which could not be identified in the emergency department evaluation. Four days later, the symptoms resolved completely and control chest X-rays showed no complications; therefore, the patient was discharged. While investigating the etiology of spontaneous mediastinum, particularly in a young, healthy patient, ecstasy abuse should always be considered. Because the fatal complications that may develop due to ecstasy ingestion may be overlooked.

Cognitive disorders after sporadic ecstasy use? A case report

Memory problems and changes in hippocampal structures after chronic ecstasy use are well described in the literature. Cognitive problems after incidental ecstasy use are rare, and the few patients described in case reports returned to their normal cognitive level after a relative short period. FV is a 39-year-old man who used an ecstasy tablet in 2005. This resulted in severe confusion for a few days. The confusion was followed by persistent memory complaints and difficulties orientating in new surroundings. An extensive neuropsychological examination 7 years after the ecstasy use revealed a severe memory disorder. Furthermore, his performance on a virtual reality test of navigation showed serious problems navigating in new surroundings. In comparison with matched control subjects (Bayesian approach for single case studies) his scores were significantly impaired on several subtasks of the navigation test. On a magnetic resonance imaging (MRI) scan of the brain bilateral hippocampal atrophy and sclerosis were visible, comparable to previous MRI studies describing hippocampal damage following ecstasy ingestion. This case report describes persistent memory and navigation disorders after sporadic ecstasy use, supported by structural brain abnormalities seen on the MRI scan. These findings revive the debate on whether sporadic ecstasy use can cause persistent cognitive deficits.

Carvedilol inhibits the cardiostimulant and thermogenic effects of MDMA in humans: Lost in translation

We greatly appreciate the comments offered by Drs Rolle, Takematsu, and Hoffman and the opportunity to put our work into a wider perspective. We share the view that our work does not reflect the clinical situation but rather provides a proof of mechanism study, which aims to help to translate preclinical findings (Sprague et al., 2005) into the clinic. As we noted in the discussion of our work (Hysek et al., 2012b) the primary goal of the study was to investigate the role of adrenoceptors in the mechanism of action of MDMA in humans. Therefore, the study provided only indirect support for the use of carvedilol in the treatment of stimulant toxicity in which carvedilol would be administered following the ingestion of Ecstasy or other stimulants. Furthermore, we noted the limitation that the MDMA-induced increase in body temperature in our study was moderate and we do not know whether carvedilol would also be effective in cases of severe hyperthermia following ecstasy use.

Ecstacy-associated hyponatremia: why are women at risk?

Hyponatremia, serum sodium <135 mEq/L, is the most common electrolyte abnormality affecting ∼30% of hospitalized patients [1]. An infrequent yet serious complication of hyponatremia is hyponatremic encephalopathy. Hyponatremia can result in an influx of water to the intracellular space. This results in cellular swelling that can lead to cerebral edema and encephalopathy. Patients at highest risk of developing hyponatremic encephalopathy in the hospital setting are postoperative patients and patients with SIADH receiving hypotonic fluids [2]. Hyponatremic encephalopathy in the outpatient setting is usually seen as a complication due to medications such as thiazide diuretics or SSRIs, or can result from exerciseassociated hyponatremia or psychogenic polydypsia [3]. A significant risk factor for developing hyponatremic encephalopathy is female gender, with the majority of cases of death or permanent neurological injury from hyponatremic encephalopathy reported in females [4]. An increasingly common cause of hyponatremic encephalopathy in the outpatient setting is use of the recreational drug ecstasy (3,4-methylenedioxymethamphetamine [MDMA]) [5]. In this issue of NDT, van Dijken et al. [6] report on the high incidence of hyponatremia in females using ecstasy. Ecstasy is an illegal synthetic amphetamine that was initially developed as an appetite suppressant but never used for this purpose. It first emerged as a recreational drug in the 1980s popular with young adults at night club parties referred to as ‘rave parties’ [7]. A rave is typically a commercially arranged elaborate all-night dance party that combines electronic music played by disc jockeys with a laser light show. Rave parties are extremely popular in North America and Europe, with thousands of people in attendance at rave events. An annual New Year’s Eve rave party in Los Angeles is reported to have almost 50 000 attendants [8]. Ecstasy is frequently taken on such occasions for its mood-enhancement properties. Users experience feelings such as euphoria, increased empathy and sociability, happiness and a sense of well-being, and increased energy [9]. Ecstasy exerts its effect by the release of neuroactive compounds in the central nervous system, including serotonin, dopamine and norepinephrine [10]. With the rise in popularity of ecstasy, medical complications began to be reported including hyponatremia, non-traumatic rhabdomyolysis, seizures, acute kidney injury, hyperthermia, cardiac tachyarrhythmia and sudden death, to name a few [5, 11, 12]. Ecstasy is believed to be the third most commonly used illicit drug, following marijuana and amphetamines, and ahead of cocaine, with an estimated consumption of over 28 million tablets yearly [7]. Emergency medical services are frequently on site at large, commercially organized rave parties [8]. One of the most serious medical complications associated with ecstasy use is hyponatremic encephalopathy [11]. There are over 25 reports of ecstasy-associated hyponatremic encephalopathy in the literature, and over half of them are fatalities. Almost all cases are reported in young females between the ages of 15 and 30 with a serum sodium of ≤130 following the ingestion of just one dose of ecstasy [5]. Symptoms typically develop within 2–12 h of ecstasy ingestion. Presenting symptoms are headache, nausea and vomiting followed by altered mental status, coma, seizure, cardio respiratory arrest, brainstem herniation and death [5]. A common yet frequently unrecognized presenting feature in these patients is neurogenic pulmonary edema, also referred to as Ayus–Arieff syndrome (Figure 1). This complication was first reported in females with post-operative and exercise-associated hyponatremia [11, 13, 14]. This is a particularly dangerous complication as hypoxia impairs brain IN F O C U S

Extensive Subcutaneous Emphysema and Pneumomediastinum after Ecstasy Ingestion

Objective. To present a rare case of extensive subcutaneous emphysema and spontaneous pneumomediastinum following ingestion of Ecstasy in a young adult. We also review the relevant literature and discuss how this case supplements it. Case Report. We report a case of a 19-year-old man with a history of painless neck and chest swelling, and no chest pain or breathlessness, after consuming Ecstasy tablets. Radiological imaging showed evidence of pneumomediastinum and extensive subcutaneous emphysema. The patient remained well under observation and his symptoms improved with conservative management. Conclusions. Subcutaneous emphysema and pneumomediastinum after Ecstasy ingestion is uncommon. Cases are often referred to the otolaryngologist as they can present with neck and throat symptoms. Our case showed that the severity of symptoms may not correlate with severity of the anatomical abnormality and that pneumomediastinum should be suspected in Ecstasy users who present with neck swelling despite the absence of chest symptoms. Although all cases reported so far resolved with conservative management, it is important to perform simple investigations to exclude coexisting serious pathology.

Ecstasy‐induced acute coronary syndrome: Something to rave about

Ecstasy or 3,4-methylenedioxymethamphetamine is a commonly used illicit recreational drug, enjoying popularity for its stimulant effects. Although acute coronary syndrome is recognized after cocaine and methamphetamine use, association with Ecstasy use has rarely been reported. We report three cases of significantly delayed acute coronary syndrome and ST elevation myocardial infarction related to ingestion of Ecstasy.

ACUTE HIPPOCAMPAL SCLEROSIS FOLLOWING ECSTASY INGESTION

We report 2 patients presenting with brief tonic-clonic seizures following ecstasy (3,4-methylenedioxymethamphetamine [MDMA]) ingestion who initially showed hippocampal swelling and subsequently atrophy. ### Case reports. #### Case 1. A 25-year-old right-handed man presented following 2 generalized tonic-clonic seizures (GTCS). The first, lasting 30 seconds, occurred 5 hours after taking 2 ecstasy tablets and 8 units of alcohol. The following day he felt unwell and vomited several times but his partner did not report any other unusual behaviors until the afternoon when he had a further 2-minute GTCS, and presented to hospital. In the days prior to the ecstasy ingestion, he had been well. There was no past history or family history of seizures. There was a history of IV heroin and amphetamine use from age 17 until 22. More recently, he used ecstasy, approximately “half a tablet” every few months. Examination revealed the patient to be oriented, agitated, and febrile (38.5°C), but with no focal neurologic deficits and no neck stiffness. Investigations revealed renal impairment (serum creatinine 213 mmol/L; normal range 30-110 mmol/L), but otherwise normal electrolytes (serum sodium 139 mmol/L). There was leucocytosis (white cell count 19.0 × 106/L, lymphocytes 16.3 × 106/L; normal ranges 4-11 and 2-7.5 × 106/L). C-reactive protein was 9 mg/L (normal <8 mg/L). Cerebral CT was unremarkable. Chest x-ray, urine, and blood …

Neurotoxic Thioether Adducts of 3,4-Methylenedioxymethamphetamine Identified in Human Urine After Ecstasy Ingestion

3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy) is a widely misused synthetic amphetamine derivative and a serotonergic neurotoxicant in animal models and possibly humans. The underlying mechanism of neurotoxicity involves the formation of reactive oxygen species although their source remains unclear. It has been postulated that MDMA-induced neurotoxicity is mediated via the formation of bioreactive metabolites. In particular, the primary catechol metabolites, 3,4-dihydroxymethamphetamine (HHMA) and 3,4-dihydroxyamphetamine (HHA), subsequently cause the formation of glutathione and N-acetylcysteine conjugates, which retain the ability to redox cycle and are serotonergic neurotoxicants in rats. Although the presence of such metabolites has been recently demonstrated in rat brain microdialysate, their formation in humans has not been reported. The present study describes the detection of 5-(N-acetylcystein-S-yl)-3,4-dihydroxymethamphetamine (N-Ac-5-Cys-HHMA) and 5-(N-acetylcystein-S-yl)-3,4-dihydroxyamphetamine (N-Ac-5-Cys-HHA) in human urine of 15 recreational users of MDMA (1.5 mg/kg) in a controlled setting. The results reveal that in the first 4 h after MDMA ingestion approximately 0.002% of the administered dose was recovered as thioether adducts. Genetic polymorphisms in CYP2D6 and catechol-O-methyltransferase expression, the combination of which are major determinants of steady-state levels of HHMA and 4-hydroxy-3-methoxyamphetamine, probably explain the interindividual variability seen in the recovery of N-Ac-5-Cys-HHMA and N-Ac-5-Cys-HHA. In summary, the formation of neurotoxic thioether adducts of MDMA has been demonstrated for the first time in humans. The findings lend weight to the hypothesis that the bioactivation of MDMA to neurotoxic metabolites is a relevant pathway to neurotoxicity in humans.

Spontaneous Pneumomediastinum After Oral Ingestion of Ecstasy

We describe a 23 year old male who presented with sudden onset of facial swelling, nasal tone of voice and shortness of breath after taking eight tablets of ecstasy. He was found to have surgical emphysema and pneumomediastinum. Though spontaneous pneumomediastinum is well known in inhalation drug users who try to enhance alveolar resorbtion with repeated Valsalva manouvre, it is rather unusual to see it after oral ingestion of ecstasy. The probable causative event is the prolonged and excessive physical exertion involved in dancing at a “rave”. Acute physicians should be aware of the association and of its usually benign nature.

Severe aplastic anemia with hot pockets following daily Ecstasy ingestion

Severe aplastic anemia with hot pockets following daily Ecstasy ingestion

Severe Ecstasy poisoning in an 8-month-old infant

We report on an 8-month-old male infant who accidentally ingested an Ecstasy tablet (3,4-methylenedioxymetamphetamine, MDMA). Here we discuss, according to the available literature, the treatment, complications, and pharmacokinetics of MDMA intoxication in a young infant. Serum MDMA level 2 hours after ingestion was with 785 ng x mL(-1) above the dose considered lethal for adults (>500 ng x mL(-1)). After ingestion the patient showed life-threatening tachycardia of 210 beats min(-1), hyperthermia of 38.9 degrees C, seizures, and hypertension of 125/70 mmHg. Under supportive treatment (benzodiazepine, body cooling, rehydration therapy), 6 hours after admission, body temperature as well as the elevated blood pressure and heart beat had returned to normal values. Nine hours after ingestion the serum MDMA level was still 274 ng x mL(-1). The patient made a full clinical recovery and afterwards appeared to be a healthy boy. This case illustrates the need to consider the possibility of accidental Ecstasy ingestion in the differential diagnosis of a child suffering from convulsions with fever.

Does Hyperthyroidism Increase Risk of Death Due to the Ingestion of Ecstasy?

Ecstasy (3,4-methylenedioxymethamphetamine, MDMA) is a psychoactive amphetamine derivative widely used for recreational purposes. Deaths caused by acute drug intoxication with MDMA are rare but can often involve a severe hyperthermic episode. The factors underlying the increased risk of some ecstasy users to a fatal drug reaction are not known. We present a case report of a 24-year-old woman who developed fatal hyperthermia with multi-organ complications following MDMA use and was found at autopsy to have diffuse thyroid hyperplasia (Graves' disease). An antemortem blood MDMA concentration of 0.68 mg/L was measured in a sample obtained on admission to hospital. Although a cause and effect cannot be established, as the thyroid hormone is a major regulator of thermogenesis, we suggest that hyperthyroidism predisposed the subject to ecstasy-induced hyperthermia and that a pre-existing defect affecting temperature status could be one factor in explaining some ecstasy intoxication deaths.

Ecstasy tablets intoxication with lethal autcome

Ecstasy, 3,4-methylenedioxymethamphetamine (MDMA), is a synthetic compound increasingly popular as a recreational drug. Tablets known as ecstasy contain MDMA, but may also contain caffeine, ephedrine, paramethoxyamphetamine, 3,4-methylenedioxyamphetamine (MDA), amphetamine, methamphetamine, and ketamine. After absorption MDMA is metabolized to MDA, 4-hydroxy-3-metoxymetamphetamine (HMMA) and 4-hydroxy-3-metoxyamphetamine (HMA). After that HMMA and HMA are conjugated and excreted by urine. The aim of this report was to confirm by toxicological post mortem analyses of poisoned person organs that ecstasy had been the cause of his death. We reported the death of a 17-year-old boy after the ingestion of ecstasy. MDMA and metabolites were determined by multicolumn high performance liquid chromatography with UV spectral detection (HPLC-UV). Toxicological tests showed the presence of MDMA in all samples. When examining post mortem material (the organs), the highest concentrations were measured in the stomach (835,97 microg/g) and kidney (801,14 microg/g). The minimal concentration was in the liver (22,26 microg/g). The obtained results of MDMA and its metabolites concentrations showed abuse of a high dose of ecstasy.

Fatal hyponatremia in a young woman after ecstasy ingestion

A 20-year old, otherwise healthy, female college student presented in an unresponsive state with respiratory distress after ingesting ecstasy (3,4-methylenedioxymethamphetamine). She had initial plasma sodium concentration of 117 mmol/l. Physical examination, blood chemistry panel, urinary osmolality and electrolytes, arterial blood gas, chest X-ray, and CT scan of the brain. Hyponatremia associated with noncardiogenic pulmonary edema and cerebral edema. Administration of a total of 6.8 l of isotonic saline and 0.245 l of 3% hypertonic saline with sporadic administration of intravenous furosemide. The patient died approximately 12 h after admission.