An overview of non-cardiac cocaine toxicity

Glauser, Jonathan; Queen, John R.

doi:10.1016/j.jemermed.2006.05.044

Cited by 89 publications

(50 citation statements)

References 56 publications

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“…In the United States alone there are an estimated 1.5 million current cocaine users, with approximately 1700 people trying cocaine for the first time each day (Substance Abuse and Mental Health Services Administration, 2011). Although moderate doses of cocaine are often associated with "pleasurable" effects, large doses of cocaine can produce a variety of adverse effects including anxiety, convulsion, delirium, hypothermia, and chest pain, the latter of which results from cocaine-induced increases in mean arterial pressure (MAP) and heart rate (HR) (Olson et al, 1994;Glauser and Queen, 2007). These large-dose effects of cocaine account for the majority of all illicit drug-related R.K.S.…”

Section: Introductionmentioning

confidence: 99%

Repeated Administration of a Mutant Cocaine Esterase: Effects on Plasma Cocaine Levels, Cocaine-Induced Cardiovascular Activity, and Immune Responses in Rhesus Monkeys

Collins¹,

Brim²,

Noon³

et al. 2012

J Pharmacol Exp Ther

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Previous studies have demonstrated the capacity of a longacting mutant form of a naturally occurring bacterial double mutant cocaine esterase (DM CocE) to antagonize the reinforcing, discriminative, convulsant, and lethal effects of cocaine in rodents and reverse the increases in mean arterial pressure (MAP) and heart rate (HR) produced by cocaine in rhesus monkeys. This study was aimed at characterizing the immunologic responses to repeated dosing with DM CocE and determining whether the development of anti-CocE antibodies altered the capacity of DM CocE to reduce plasma cocaine levels and ameliorate the cardiovascular effects of cocaine in rhesus monkeys. Under control conditions, intravenous administration of cocaine (3 mg/kg) resulted in a rapid increase in the plasma concentration of cocaine (n ϭ 2) and long-lasting increases in MAP and HR (n ϭ 3). Administration of DM CocE (0.32 mg/kg i.v.) 10 min after cocaine resulted in a rapid hydrolysis of cocaine with plasma levels below detection limits within 5 to 8 min. Elevations in MAP and HR were significantly reduced within 25 and 50 min of DM CocE administration, respectively. Although slight (10-fold) increases in anti-CocE antibodies were observed after the fourth administration of DM CocE, these antibodies did not alter the capacity of DM CocE to reduce plasma cocaine levels or ameliorate cocaine's cardiovascular effects. Anti-CocE titers were transient and generally dissipated within 8 weeks. Together, these results suggest that highly efficient cocaine esterases, such as DM CocE, may provide a novel and effective therapeutic for the treatment of acute cocaine intoxication in humans.

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Section: Introductionmentioning

confidence: 99%

Repeated Administration of a Mutant Cocaine Esterase: Effects on Plasma Cocaine Levels, Cocaine-Induced Cardiovascular Activity, and Immune Responses in Rhesus Monkeys

Collins¹,

Brim²,

Noon³

et al. 2012

J Pharmacol Exp Ther

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“…The relationship with its plasma concentrations and its toxic effects has shown a wide variability between patients [1]. Cocaine is well-known for its cardiovascular complications such as stroke and cardiac arrest, and its respiratory problems [2]. Gastrointestinal complications are uncommon and little documented.…”

Section: Discussionmentioning

confidence: 99%

Cocaine-induced Fulminant Hepatitis

Roque¹,

Soy²,

Retto³

et al. 2017

J Gastrointest Dig Syst

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Cocaine abuse and intoxication is a global problem leading to many medical complications that can result in significant morbidity and mortality. We present the clinical case of a young man who presented with a fulminant hepatic failure, renal failure and a duodenal ulcer related to cocaine consumption. Keywords: Fulminant hepatitis; Cocaine; Clinical case Case PresentationA 28-year-old man was admitted to our hospital on November 14, 2016 because of psychomotor agitation with fear delusions after ingesting 0.5 g of cocaine. He had no medical history of interest. As a toxic consumption history, he referred being an excigarette smoker of a pack a day, referred an ex-consumption of 10-12 alcohol units per day, and an ex-consumption of cannabis. Cocaine consumption started at 16 years old but at that time it had become sporadic. On examination in the emergency department, the patient presented a Glasgow Coma Score (GCS) of 12 with bilateral mydriasis, skin and mucous dryness, tachycardia and self-limiting temperature peak of 39.5°C. First blood test analysis showed a 51% hematocrit (43-49), 219 K/mcl platelets (150-450), 13.98 K/mcl leukocytosis (4.4-11.3), a prothrombin time (PT) of 86% (65-100), a 2.67 mg/dl creatinine (0.7-1.2), a 63 mg/dl urea (16.6-48.5), a 0.42 mg/dl total bilirubin (0.1-1.2), a 93 U/L aspartate aminotransferase (AST) (0-40), a 28 U/L alanine transaminase (ALT) (0-41), a 23 U/L gamma-glutamyltransferase (GGT) (0-60), a 97 U/L alkaline phosphatase (ALP) (40-129), a 863 U/L creatine kinase (CK) (0-190) and a high anion gap metabolic acidosis: pH 7.18, 38 mmHg pCO 2 , 39 mmHg pO 2 and 14.2 mmol/L bicarbonate. Troponin curve realized at 3 hours was flat. Toxics in urine were tested, being only positive for cocaine. Ethyleneglycol and methanol serum levels were normal and hepatitis A, B and C viruses were negative. Blood test control at 3 hours showed increasing levels of CK to 5.529 U/L and at 6 hours CK levels had arisen to 16.242 U/L, creatinine levels to 3.31 mg/dl and PT had decreased to 52%. At 24 hours, CK levels were 49.162 U/L, creatinine levels had increased to 4.79 mg/dl, platelets had fallen to 39 K/mcl and International Normalized Ratio (INR) had increased to 5.54. Brain computerized tomography (CT) scan was normal. Initial supportive treatment (such as serum therapy and bicarbonate) was initiated in the emergency room.First diagnostic approach was an acute renal failure AKIN III probably due to microangiopathy and rhabdomyolysis because of cocaine consumption. In the following hours, the patient began with a decreased level of consciousness and oligoanuria. In blood test controls, platelet levels dropped to 18 K/mcl, INR increased to 5.54, total bilirubin increased to 2.03 mg/dl, AST increased to 3.610 U/L, ALT increased to 3.287 U/L, CK levels were about 33.327 U/L and creatinine levels were still increasing to 6.44 mg/dl. A fulminant hepatic failure was diagnosed in addition to an acute renal failure, since previous abdominal ultrasound found in his clinical history showed n...

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“…Cocaine is well-known for its cardiovascular complications such as stroke and cardiac arrest, and its respiratory problems [2]. Gastrointestinal complications are uncommon and little documented.…”

Section: Discussionmentioning

confidence: 99%

Cocaine-induced Fulminant Hepatitis

Roque¹

2017

GHOA

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Gastroenterol Hepatol Open Access 2017, 7(2): 00234 presented a Glasgow Coma Score (GCS) of 12 with bilateral mydriasis, skin and mucous dryness, tachycardia and selflimiting temperature peak of 39.5ºC. First blood test analysis showed a 51% hematocrit [43][44][45][46][47][48][49] and a high anion gap metabolic acidosis: pH 7.18, 38 mmHg pCO2, 39 mmHg pO2 and 14.2 mmol/L bicarbonate. Troponin curve realized at 3 hours was flat. Toxics in urine were tested, being only positive for cocaine. Ethyleneglycol and methanol serum levels were normal and hepatitis A, B and C viruses were negative.Blood test control at 3 hours showed increasing levels of CK to 5.529 U/L and at 6 hours CK levels had arisen to 16.242 U/L, creatinine levels to 3.31 mg/dL and PT had decreased to 52%. At 24 hours, CK levels were 49.162 U/L, creatinine levels had increased to 4.79 mg/dL, platelets had fallen to 39 K/mcL and International Normalized Ratio (INR) had increased to 5.54. Brain computerized tomography (CT) scan was normal. Initial supportive treatment (such as serum therapy and bicarbonate) was initiated in the emergency room.First diagnostic approach was an acute renal failure AKIN III probably due to microangiopathy and rhabdomyolysis because of cocaine consumption. In the following hours, the patient began with a decreased level of consciousness and oligoanuria. In blood test controls, platelet levels dropped to 18 K/mcL, INR increased to 5.54, total bilirubin increased to 2.03 mg/dL, AST increased to 3.610 U/L, ALT increased to 3.287 U/L, CK levels were about 33.327 U/L and creatinine levels were still increasing to 6.44 mg/ dL. A fulminant hepatic failure was diagnosed in addition to an acute renal failure, since previous abdominal ultrasound found in his clinical history showed no abnormalities.Liver transplant was rejected by our transplant referent center because of active cocaine consumption. The patient was then admitted to Intensive Care Unit (ICU) and progressively developed a complete anuria with top creatinine levels of 10.1 mg/dL accompanied by anasarca. Regarding the hepatic failure, the patient presented jaundice, a top of grade II hepatic encephalopathy, an episode of severe hypoglycemia and, analytically, the lower PT was 8%, top bilirubin total level was 16.95 mg/dL, AST top level of 5.788 U/L, ALT top level of 5.875 U/L and the lower platelet level was 18 K/mcL. The patient started renal replacement therapy with continuous venovenous hemodiafiltration that was changed to standard hemodyalisis when clinical status allowed it, besides vitamin K and plasma transfusions when needed. Low oxygen therapy was also required due to pleural effusion caused by accumulated hypervolemia. The patient was hemodynamically stable and conscious at all times without presenting signs of hepatic insufficiency (except for a short period of encephalopathy grade II presented at the first day). Furthermore, an ultrasound guided evacuator paracentesis was required because of the development of tension ascites that conditioned respiratory ...

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An overview of non-cardiac cocaine toxicity

Cited by 89 publications

References 56 publications

Repeated Administration of a Mutant Cocaine Esterase: Effects on Plasma Cocaine Levels, Cocaine-Induced Cardiovascular Activity, and Immune Responses in Rhesus Monkeys

Repeated Administration of a Mutant Cocaine Esterase: Effects on Plasma Cocaine Levels, Cocaine-Induced Cardiovascular Activity, and Immune Responses in Rhesus Monkeys

Cocaine-induced Fulminant Hepatitis

Cocaine-induced Fulminant Hepatitis

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