Cocaine-induced platelet defects.

Jennings, Lisa K.; White, Marijane; Sauer, Curtis M.; Mauer, Alvin M.; Robertson, James T.

doi:10.1161/01.str.24.9.1352

Cited by 43 publications

(17 citation statements)

References 31 publications

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“…Our results confirmed and extended previous observations that chronic cocaine use is associated with platelet activation which is a prominent finding after recent consumption. Two reports showed cocaine-associated inhibition of platelet function assessed by light transmission platelet aggregation studies [18,19]. The apparent discrepancy with our findings may be explained by partial platelet activation in vivo which may cause a decrease in platelet response in vitro.…”

Section: Discussioncontrasting

confidence: 99%

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Platelet activation in chronic cocaine users: Effect of short term abstinence

Pereira¹,

Sáez²,

Pallavicini³

et al. 2011

Platelets

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Cocaine abuse increases the risk of cardiac and cerebrovascular events, such as myocardial infarction and ischemic stroke. The underlying mechanisms leading to these complications are not fully understood although intravascular thrombus formation has been observed. The aim of this study was to investigate the existence of platelet activation and the effect of short-term abstinence in chronic cocaine consumers. We studied 23 cocaine dependent individuals (aged 20-54 years) who met DSM-IV criteria for cocaine dependence and 20 controls. Samples were obtained at baseline, within 72 h of last drug exposure and after 4 weeks of controlled abstinence. Monocyte-platelet aggregates (MPA) were measured by flow cytometry. Plasma levels of soluble CD40L (sCD40L), Neutrophil-Activating Peptide-2 (NAP-2) and regulated on activation normal T cells expressed and secreted (RANTES) were determined by ELISA. Levels of MPA, sCD40L, NAP-2 and RANTES were significantly higher (all p < 0.05) in cocaine addicts compared to controls at baseline. All the parameters returned to values similar to the control group after 4-weeks' abstinence. Levels of sCD40L and RANTES were associated with an index of intensity of drug consumption (p< 0.02). Our results demonstrate that cocaine use induces platelet activation which is a prominent finding after recent consumption. The persistence over time of this condition may contribute not only to acute thrombotic complications but also to the development of early-onset atherosclerotic process observed in cocaine abusers.

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Section: Discussioncontrasting

confidence: 99%

“…In chronic users Rinder et al found increased expression of surface p-selectin on circulating platelets [17]. However, some studies have shown that cocaine may decrease platelet function under certain conditions [18,19].…”

Section: Introductionmentioning

confidence: 99%

Platelet activation in chronic cocaine users: Effect of short term abstinence

Pereira¹,

Sáez²,

Pallavicini³

et al. 2011

Platelets

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“…49 We found no direct evidence of peripheral platelet destruction or immune phenomena in our patient's peripheral blood smear or laboratory testing. Systemically, cocaine is shown to augment platelet aggregation 50,51 ; however, high-local concentrations may inhibit clot formation and lead to bleeding. 51 Neither, however, would explain the thrombocytopenia.…”

Section: Cocaine's Effect On Other Organsmentioning

confidence: 99%

“…Systemically, cocaine is shown to augment platelet aggregation 50,51 ; however, high-local concentrations may inhibit clot formation and lead to bleeding. 51 Neither, however, would explain the thrombocytopenia. Our patient's prothrombin and partial thromboplastin times were increased, but his fibrinogen level dropped to only 180 mg/dL at its lowest.…”

Section: Cocaine's Effect On Other Organsmentioning

confidence: 99%

Cocaine-Induced Agitated Delirium

Plush

Shakespeare

Jacobs

et al. 2013

J Intensive Care Med

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Cocaine use continues to be a major public health problem in the United States. Although many of the initial signs and symptoms of cocaine intoxication result from increased stimulation of the sympathetic nervous system, this condition can present as a spectrum of acuity from hypertension and tachycardia to multiorgan system failure. Classic features of acute intoxication include tachycardia, arterial vasoconstriction, enhanced thrombus formation, mydriasis, psychomotor agitation, and altered level of consciousness. At the extreme end of this toxidrome is a rare condition known as cocaine-induced agitated delirium. This syndrome is characterized by severe cardiopulmonary dysfunction, hyperthermia, and acute neurologic changes frequently leading to death. We report a case of cocaine-induced agitated delirium in a man who presented to our institution in a paradoxical form of circulatory shock. Rapid evaluation, recognition, and proper management enabled our patient not only to survive but also to leave the hospital without neurologic sequelae.

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“…Jennings and colleagues postulated that cocaine may inhibit platelet function, particularly when high local concentrations are achieved. 12 Thus studies directly exposing isolated platelets to cocaine in vitro, 12 28 or challenging isolated platelets in vitro after previous in vivo drug exposure, 29 are best suited to explain such local haemorrhagic events.…”

Section: Haemorrhagic Versus Thrombotic Effectsmentioning

confidence: 99%

Echocardiographic features of cardiac involvement in Fabry's disease

Nakayama¹,

Tsumura²,

Yoshimaru³

2000

Heart

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Objective-To determine whether there is evidence of platelet activation following in vivo cocaine administration in humans, as cocaine abuse is associated with myocardial infarction and stroke, and platelet activation leading to thrombosis is a possible mechanism. Setting-University hospital. Design and subjects-Following a randomised, double blind crossover design, 14 healthy volunteers were studied twice, receiving cocaine (2 mg/kg intranasally) once and placebo once. Flow cytometric analysis of P-selectin expression (an granule membrane protein found on the surface of activated platelets), quantification of the platelet specific proteins platelet factor 4 and thromboglobulin, and measurement of platelet containing microaggregate and platelet microparticle (fragment) formation were used to assess platelet activation. Circulating von Willebrand factor antigen (vWF) was measured to evaluate a possible role of endothelial stimulation concurrent with platelet activation. Results-There was an increase in both platelet factor 4 (mean (SD), 16 (7) to 39 (22) IU/ml, p = 0.04) and thromboglobulin (70 (20) to 98 (26) IU/ml, p < 0.01) at 120 minutes following cocaine administration. Platelet containing microaggregate formation was increased at 40 minutes (from 47 (3.2)% to 54 (2.0)%, p < 0.001) and 80 minutes (55 (2.5)%, p = 0.04). Bleeding time decreased following cocaine from 10 (1) to 9 (1) minutes (p = 0.07). No changes in any of the measured variables were noted following placebo administration. Conclusions-Cocaine exposure causes platelet activation, granule release, and platelet containing microaggregate formation. These data support the view that cocaine, even at the relatively low doses commonly self administered by occasional abusers, may promote thrombosis and predispose healthy individuals to ischaemic events. Platelet inhibitors should be considered early in any patient with suspected cocaine related ischaemia. (Heart 2000;83:688-695)

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Cocaine-induced platelet defects.

Cited by 43 publications

References 31 publications

Platelet activation in chronic cocaine users: Effect of short term abstinence

Platelet activation in chronic cocaine users: Effect of short term abstinence

Cocaine-Induced Agitated Delirium

Echocardiographic features of cardiac involvement in Fabry's disease

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