Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cocaine is the second most used illicit drug; cocaine induces platelet activation and formation of thrombus. Thrombotic effects of cocaine can lead to vascular injuries, cerebrovascular accident and myocardial infarct. Less common, cocaine use disorder leads to thrombi formation in both ventricles and renal artery infarct as seen in our patient.
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PMID:Acute renal infarction, transient ischemic attack, and biventricular thrombi secondary to substance use disorder: A case report. 3111 Jul 4

Cocaine-regulated and amphetamine-regulated transcript (CART) is a neuropeptide with reported neuroprotective effects in ischemic cerebral injury. However, its mechanism has not yet been elucidated. Herein, we investigated the role and mechanism of CART in synaptic plasticity in neurons after ischemic cerebral stroke. We found that the survival rate of the oxygen-glucose deprivation (OGD) neurons was increased after CART treatment. Moreover, CART treatment significantly attenuated ischemia-induced neuronal synaptic damage and increased synaptophysin expression. In addition, the number of presynaptic vesicles was increased and the postsynaptic density (PSD) was thickened after CART treatment. Mechanistically, CART treatment enhanced the expression of Arc mRNA in a cAMP response element binding protein (CREB) dependent manner in OGD neurons, and blockade of CREB by KG-501 eliminated the protective effect of CART. Collectively, CART protected the synaptic structure in neurons after ischemic cerebral injury by increasing the Arc expression via upregulating p-CREB.
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PMID:Cocaine- and amphetamine-regulated transcript protects synaptic structures in neurons after ischemic cerebral injury. 3200

Cocaine is a highly addictive recreational drug that is a well-known cause of a variety of disease processes such as stroke, myocardial infarction, and even sudden cardiac death. In current literature, venous thrombosis secondary to cocaine abuse remains under-examined, while the harmful effects of the drug within the arterial vasculature are well-studied and understood. Our case presents a patient who was found to have a large pulmonary embolism and pulmonary infarction after several days of cocaine abuse. This report serves to raise awareness of a potentially life-threatening effect of this drug and to encourage prompt diagnosis and treatment of cocaine-induced pulmonary embolism.
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PMID:Cocaine: A Provoking Risk Factor in Venous Thromboembolism. 3202 39

Cocaine is a vasoactive substance, and its consumption has increased throughout the world. There are many neurological complications caused by chronic cocaine use, which include headache, aneurysmal formation, ischemic stroke, hemorrhagic stroke (subdural and subarachnoid hemorrhage), seizures, etc. Headache is one of the most common symptoms that appear after cocaine use. It may occur due to dopaminergic and serotoninergic system impairment. Cocaine causes vasoconstriction by stimulation of the sympathetic nervous system and decreases the reuptake of epinephrine, norepinephrine, serotonin, and dopamine. Reversible cerebral vasoconstriction syndrome (RCVS) is well accepted with cocaine use, which occurs most commonly in middle-aged adults and females. The relation between cocaine consumption and time of occurrence of headache has been described according to which some people suffer from headaches immediately after the cocaine use, some within 40 to 90 minutes of a cocaine binge, and some even after the cocaine abstinence for long period. The diagnosis of a cocaine-induced headache depends on history, physical examination, and cerebrovascular imaging findings. And its management is done according to cause that is responsible for headache.
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PMID:Cocaine-Induced Headache: A Review of Pathogenesis, Presentation, Diagnosis, and Management. 3300 42


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