Cocaine is a widely abused controlled substance. Cocaine use is associated with a myriad of side effects and a sequelae of consequences secondary to its harmful nature and potential adulterants, the most recently described and less known sequelae being leukoencephalopathy. In our case, we describe a 58-year-old male who presented to the ED with agitation and acute stroke-like symptoms with reported rapid onset. Cocaine induced toxic leukoencephalopathy is a diagnosis of exclusion, thus other etiologies of disease were ruled out in a full neurological and infectious workup; most importantly consisting of extensive brain imaging, alluding to the diagnosis of acute cocaine induced toxic leukoencephalopathy in an individual with a confirmed history of cocaine and cannabinoid abuse. Although there is no targeted therapy for the condition to our knowledge, we utilized a supportive approach to treatment in contrast to other reported treatment modalities which included the use of steroids, plasma exchange, and intravenous immunoglobulin. Furthermore, we describe the clinical evaluation and treatment throughout the patient\'s hospital course with his eventual marked improvement from initial presentation.

Gallstones, alcohol use, hypertriglyceridemia, and hypercalcemia have been considered the most common causes of acute pancreatitis; however, about 20% of the cases remain idiopathic since no definite cause can be established. It has been noticed that there is a small number of patients who have presented to the hospital with a diagnosis of acute pancreatitis who have concurrently been using cocaine yet have no recent alcohol use and no gallstones. The purpose of this series of case reports is to review the evidence behind the association between cocaine and pancreatitis. In most of the cases, the etiology of acute pancreatitis is usually straightforward. However, when faced with a patient who has acute pancreatitis but lacks the common causes such as alcoholism, gallstones, normal triglyceride levels, and no evidence of malignancy, it seems reasonable to consider drugs as a potential cause for pancreatitis.

We present a case here where a 57-year-old South Asian male with disturbed mental status developed multifocal leukoencephalopathy, which we believe was caused by cocaine usage. Cocaine was detected in the urine toxicological sample. Non-acute CT head, with a follow-up brain MRI demonstrating hyperintensity of the T2 FLAIR signal corresponding to diffusion restriction throughout the whole supratentorial white matter, involving semiovale and subcortical U fibres in the occipital lobes as well as posterior frontal and parietal centrum. It was less likely that the patient had posterior reversible encephalopathy syndrome (PRES), which can potentially manifest similarly in a clinical and imaging context because there was no abrupt rise of blood pressure at presentation or during the patient\'s stay. Extensive examinations were conducted to exclude additional factors that may contribute to the patient\'s appearance, including autoimmune, vasculitis, and infectious diseases. Levamisole, a significant chemical that is frequently used to increase the volume of cocaine samples and has been linked to neuronal damage, should be examined in individuals who use cocaine and exhibit these kinds of clinical symptoms. The patient was prescribed 250 mg of methylprednisolone twice daily for five days after it was determined that cocaine-induced neuronal toxicity was the cause of his symptoms. Although no improvement was seen right away, over the course of the next few days, he did exhibit a gradual, albeit slight, improvement in his mental status while residing in the nursing home. It is crucial to comprehend the possible connection between cocaine usage, a commonly abused drug, and people exhibiting similar clinical symptoms. To have a better understanding of the pathophysiology and possible treatment approach, more research is necessary as there is now no recommended therapy regimen.

Here, we report a case of body stuffing leading to severe cocaine toxicity. Medical management and supportive care are usually the best course of action in cases of body stuffing, as seen in our case. While surgery is rarely indicated, surgical consultation should occur early to ensure prompt intervention if obstruction or perforation occurs.

Cocaine is a highly addictive substance. Its poisoning can lead to potentially fatal multi-organ dysfunction. We report a case of cocaine overdose with severe multi-organ dysfunction. A healthy 51-year-old man was admitted to the emergency room due to behaviour changes and seizure after inhaling crack. Multiple dysfunctions were developed, with emphasis on liver and kidney dysfunction, due to their severity. The patient had marked hepatic cytolysis with a peak on the third day with alanine aminotransferase (ALT) and aspartate aminotransferase (AST): 7941 and 4453 IU/L, respectively with mild coagulopathy and hyperbilirubinemia. Underwent empirical treatment with acetylcysteine ​​with good clinical response. Also developed anuric AKIN3 acute kidney injury secondary to rhabdomyolysis, requiring treatment with intermittent haemodialysis. The approach to a case with severe multiorgan dysfunction is described, with special emphasis on the use of acetylcysteine. The good evolution of the patient can corroborate the use of this drug as a potential modifier of prognosis.

Takotsubo cardiomyopathy (TCM) is a well-recognized non-ischemic complication of physical and emotional stressors leading to heart dysfunction. Both thyroid storm and cocaine have been implicated with TCM to varying degrees. We present the case of a 26-year-old male with Graves\' disease and cocaine abuse who was hospitalized with thyroid storm resulting in takotsubo cardiomyopathy and cardiogenic shock. The patient had a long and complicated hospital course, requiring advanced therapies including extracorporeal membrane oxygenation and other medical and mechanical circulatory support therapies. With treatment for thyroid storm using antithyroid medications and steroids, the patient eventually had complete recovery of his left ventricular function and was ultimately weaned from pressors, inotropes and mechanical support.

As most cocaine users drink alcohol, it is interesting to understand how a non-lethal dose of alcohol affects the metabolism and toxicity of cocaine. In this study, we examined the correlation between dose-dependent toxicity and the metabolism/pharmacokinetic (PK) profile of cocaine with or without alcohol (ethanol, 1 g/kg) co-administration in rats. The cocaine toxicity in rats with or without alcohol co-administration is characterized by not only the commonly used LD50, but also the average times for the appearance of convulsion and death as well as total toxicity level (TTL) in the blood. All these data have consistently demonstrated that co-administration of alcohol increased cocaine toxicity, and that the alcohol-enhanced toxicity of cocaine is mainly attributed to the observed two additional metabolites (cocaethylene and norcocaethylene - products of chemical reactions of cocaine with alcohol catalyzed by metabolic enzymes carboxylesterase-1 and liver microsomal cytochrome P450 3A4) that are more toxic than cocaine itself. So, evaluation of the substance TTL should account for the blood levels of not only cocaine itself, but also its all toxic metabolites. In addition, for rats died of a lethal dose of cocaine (60 or 100 mg/kg) combined with 1 g/kg alcohol, we also determined the TTL at the time of death, demonstrating that death would occur once the TTL reached a threshold (~16 μM).

Posterior reversible encephalopathy syndrome (PRES) is a neurovascular sequence noted in patients with preeclampsia/eclampsia, solid-organ/bone marrow transplantation, and malignant hypertension. The mechanism in which PRES occurs has not yet been determined. It has been hypothesized that it may be related to endothelial cell dysfunction or injury leading to the compromise of the blood-brain barrier. The clinical presentations vary but are similar to symptoms of increased intracranial pressure, such as headache, visual changes, focal neurological deficits, seizures, and altered mental status. Although the pathology suggests reversibility, that is not always the case in which severe ischemic damage has occurred. We present a patient who came to the emergency room with a history of substance abuse and tested positive on a urinary toxicology screen for methamphetamine and cocaine. In the US, polysubstance use has been more prevalent in recent years. Furthermore, literature has highlighted the additive effects on one\'s blood pressure when such drugs are combined. Our patient presented with altered mental status, hypertension, and pinpoint pupils. Over the course of her stay, the patient\'s mentation slowly improved and was able to follow commands intermittently. We believe that this is the first documented case of polysubstance abuse in correlation to PRES. We hypothesize that the mechanism of PRES resulted from the multiplicative effect of several illicit drugs known to cause transient hypertensive episodes and their ability to disrupt the structural proteins imperative for the blood-brain barrier.

Symptomatic cocaine intoxication in the preoperative period is a potentially life-threatening condition, especially before emergent surgery. The anesthesiologist is faced with a dilemma where the patient is deemed unsafe for induction of general anesthesia but also in need of immediate surgical intervention. Cocaine is a local anesthetic and, as such, has been proposed to respond to lipid emulsion treatment as other local anesthetics would. We present a case supporting this statement and review the relevant published literature on the topic.

Cocaine toxicity has been a subject of study because cocaine is one of the most common and potent drugs of abuse. In the current study the effect of cocaine on human liver cancer cell line (HepG2) was assessed. Cocaine toxicity (IC50) on HepG2 cells was experimentally calculated using an XTT assay at 2.428 mM. The metabolic profile of HepG2 cells was further evaluated to investigate the cytotoxic activity of cocaine at 2 mM at three different time points. Cell medium and intracellular material samples were analyzed with a validated HILIC-MS/MS method for targeted metabolomics on an ACQUITY Amide column in gradient mode with detection on a triple quadrupole mass spectrometer in multiple reaction monitoring. About 106 hydrophilic metabolites from different metabolic pathways were monitored. Multivariate analysis clearly separated the studied groups (cocaine-treated and control samples) and revealed potential biomarkers in the extracellular and intracellular samples. A predominant effect of cocaine administration on alanine, aspartate, and glutamate metabolic pathway was observed. Moreover, taurine and hypotaurine metabolism were found to be affected in cocaine-treated cells. Targeted metabolomics managed to reveal metabolic changes upon cocaine administration, however deciphering the exact cocaine cytotoxic mechanism is still challenging.