Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cocaine abuse and its association with vascular disease has become common in the medical literature. A variety of vascular problems have been described including neurovascular complications, cardiovascular complications, aortic dissection, venous thrombosis, mesenteric artery thrombosis, and renal infarction. The pathogenesis of these vascular complications has largely been related to increased adrenergic activity leading to vasospasm. Interaction of cocaine with the vascular endothelium resulting in thrombosis or vasculitis has also been suggested. We report a case of diffuse aneurysmal change of the aorta associated with an atypical inflammatory component consistent with possible cocaine induced vasculitis.
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PMID:Accelerated atherosclerosis, aneurysmal disease, and aortitis: possible pathogenetic association with cocaine abuse. 152 57

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

We describe a 36-year-old white man with an aggressive, midline intranasal and naso and oropharyngeal destructive process temporally associated with heavy (3 g/week) abuse of nasal cocaine. Necrosis and atrophy of the inferior and middle nasal turbinates bilaterally, prominent naso and oropharyngeal ulcers, and nasal septal perforation were observed clinically. Biopsies of a necrotic posterior oropharyngeal ulcer revealed focal areas of chronic inflammation and necrosis, but there was no evidence of vasculitis or granuloma formation. Serum was negative for antineutrophil cytoplasmic antibody. The oropharyngeal ulcer improved with abstinence from cocaine. Nasal septal perforation is a well recognized complication of nasal cocaine insufflation. Our case illustrates that a more aggressive midline intranasal and intrapharyngeal destructive process mimicking limited Wegener's granulomatosis and midline reticulosis can be associated with nasal cocaine abuse.
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PMID:Nasal cocaine abuse causing an aggressive midline intranasal and pharyngeal destructive process mimicking midline reticulosis and limited Wegener's granulomatosis. 238 8

Four young individuals with histories of heavy cocaine abuse occurring several hours to days before the development of acute symptoms of severe headaches, disorientation, and subsequent stupor were shown to harbor subcortical cerebral hemorrhages. Thorough workup of these patients revealed no underlying pathology (i.e., arteriovenous malformations) or other possible causes such as hemorrhage into a tumor. It is well known that heroin, ephedrine, and methamphetamine use may result in cerebral vasculitis, but only one case study in the literature has reported on cerebral vasculitis with ischemic stroke secondary to cocaine abuse. The possibility of heavy cocaine use should be considered, along with the previously mentioned drugs, when a young, previously healthy person presents with a deep cerebral hemorrhage.
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PMID:Subcortical cerebral hemorrhages associated with cocaine abuse: CT and MR findings. 291 Sep 22

A case of cerebral vasculitis in a previously healthy 22-year-old man with a history of cocaine abuse is described. Cerebral angiograms showed evidence of vasculitis. A search for possible causes other than cocaine produced no results. We now include cocaine with methamphetamines, heroin, and ephedrine as illicit drugs that can cause cerebral vasculitis.
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PMID:Cerebral vasculitis associated with cocaine abuse. 365 26

Cocaine abuse has been associated with various cerebrovascular complications, including vasculitis. We describe a patient who presented with neurologic defects associated with cocaine abuse. Although angiography raised the suggestion of vasculitis, biopsy revealed a lack of inflammatory changes, and other aspects of the clinical course also militated against inflammatory vasculitis. This case was reminiscent of recently described patients initially suspected of having primary central nervous system (CNS) vasculitis but subsequently considered to have "benign angiopathy." We suggest that benign angiopathy of the CNS can occur as a result of cocaine abuse.
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PMID:Central nervous system angiopathy associated with cocaine abuse. 779 Nov 83

Argentina is facing an increase in cocaine use by adolescents and young adults from every socioeconomic background. It is calculated that up to 10% of all cocaine passing through this country is locally sold and consumed. Nevertheless, local information describing common cocaine-related neurological events is scarce. From August 1988 to March 1993, 13 patients were evaluated with neurological disease associated with cocaine abuse. Among these 13 patients (Table 1), the mean age was 29; 70% were men. Patients most commonly used the nasal route (snorting). Concomitant abuse of other intoxicants, especially alcohol, was frequent (85%). The major neurological complications included one or more seizures (n = 7), ischemic stroke (n = 2) (Fig. 1-2), hemorrhagic stroke (n = 2) associated with arteriovenous malformation (Fig. 3a-b), memory disturbances (n = 1) and paroxysmal dystonia (n = 1). Psychiatric complaints were present in all patients. Mortality was not observed. There was no correlation between the appearance of complications and the amount of cocaine used, or prior experience with this drug. Only one of the 7 patients with seizures had a previous history of seizures. All had generalized tonic-clonic seizures, and one had concomitant absence episodes. Cocaine modulates central neurotransmitters and has direct cerebrovascular effects. The neurological complications appear to be related to cocaine hyperadrenergic effects, striatal dopaminergic receptor hypersensitivity and perhaps vasculitis. Structural changes in the brain of long-term cocaine abusers could explain the persistence of neurologic symptoms after drug withdrawl.
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PMID:[Neurologic complications by cocaine abuse]. 799 Jun 84

A variety of central nervous system pathology has been associated with cocaine abuse, including cerebral vasculitis. We report a case of a 25-year-old woman who died of hypoxic encephalopathy following cardiac arrest due to cocaine abuse. Autopsy revealed a distinctive cerebral vasculitis with features characteristic of hypersensitivity drug included vasculitis. The significance of cerebral vasculitis associated with cocaine is reviewed.
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PMID:Cerebral vasculitis associated with cocaine abuse. 851 25

In humans, chronic cocaine abuse is associated with changes in the central nervous system (CNS). Neuropathological changes include cerebrovascular events, EEG abnormalities, vasculitis, seizures, and decrements in neurobehavioral performance. The acute administration of cocaine is associated with acute psychotic episodes and paranoid states while withdrawal from the drug is often associated with depressed mood. The mechanistic basis of these behavioral states is not known. Given the structural and functional changes associated with cocaine use, we propose that the chronic heavy use of cocaine may result in a neuropsychiatric syndrome which might be associated with neuropsychological changes that are not obvious during routine clinical evaluation of drug-using individuals. This disconnection syndrome, because of its sublety, might have deleterious effects on both acute and long-term therapeutic interventions with these subjects. An approach which deals with cocaine abuse as a neuropsychiatric disorder might be more beneficial to the long-term goal of treating these patients. This approach entails a neurobehavioral evaluation which will be comprised of a thorough neurological and psychiatric examination, neuropsychological testing, and imaging studies. The results of this evaluation would provide a more rational basis for cognitive and/or pharmacological therapies.
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PMID:Chronic cocaine use as a neuropsychiatric syndrome: a model for debate. 882 75

Cocaine has wide-ranging effects on the immune and neuroendocrine systems (Fiala et al., 1996) resembling an inflammatory "stress" response with upregulation of pro-inflammatory cytokines and stimulation of the HPA axis (Gan et al., 1997). Cocaine abuse has also been associated with vascular pathology, including vasculitis, vasospasm and hemorrhage. These effects suggest that cocaine could perturb the function of endothelial cells, including the blood-brain barrier, and influence the progression to AIDS in HIV-infected individuals (Shapshak et al., 1997; Goodkin et al., 1997). In order to understand clinical consequences of cocaine abuse, it is important to gain insight into molecular and cellular basis of cocaine's effects on immune and endothelial cells. Cocaine's in vitro effects on (a) permeability, (b) immune cell migration, (c) adhesion molecules, and (d) cytokine expression were investigated in a blood-brain barrier model constructed with brain microvascular endothelial cells and fetal astrocytes with the following results: (a) cocaine and tumor necrosis factor-alpha (TNF-alpha) increased the model's permeability to inulin similarly in a dose-responsive fashion; (b) cocaine (10(-4) to 10(-8_ M) enhanced monocyte migration across the barrier with the maximum increase, approximately 100%, by 10(-5) M cocaine; (c) cocaine treatment also increased the expression of endothelial adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecules-1 (VCAM-1) and platelet/endothelial cell adhesion molecule-1 (PECAM-1); (d) although the cocaine in vitro effects on cytokine production by mononuclear cells have been difficult to assess due to a heterogeneity in the degree of responsiveness between individuals, the data suggest that mononuclear cells from cocaine addicts are sensitized to in vitro cocaine challenge with hypersecretion of inflammatory cytokines. Cocaine's in vivo manifestations are compatible with these in vitro effects: (A) chronic cocaine treatment of rats significantly increased rolling white blood cell flux, leukocyte-endothelium adhesion, and ICAM-1 expression in the mesentery (House et al., 1996); (B) cocaine injection to cocaine-dependent subjects tipped the balance of cytokine secretion by mononuclear cells to Th1-type (Gan et al., 1997), and (C) cocaine injection stimulated the hypothalamic-pituitary axis (HPA) to increase both anti- and pro-inflammatory hormonal secretion. Collectively, these results suggest that the immune effects of cocaine on endothelial, immune and neuroendocrine cells impair the function of the blood-brain, barrier, increase cell emigration from the blood vessels, in particular into the brain, and may cause vasculitis. These effects could also increase importation of HIV-1 into the brain.
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PMID:Cocaine enhances monocyte migration across the blood-brain barrier. Cocaine's connection to AIDS dementia and vasculitis? 966 72


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