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)

Stroke is a frequently reported, though uncommon, complication of drug abuse, primarily cocaine. The pathogenesis is uncertain, although such cerebrovascular events may result from sympathetically mediated vasoconstriction of cerebral vessels. Amphetamine, another sympathomimetic amine that is commonly abused, may also cause strokes by producing cerebral vasospasm and/or vasculitis. Amphetamine and its derivatives are frequent adulterants of illegally obtained cocaine and may also be used concurrently; the effect(s) of this combination of drugs upon the cerebral vasculature is not known. Our aim was to develop an animal model that would enable us to study the ability of these drugs to produce acute cerebral vasospasm and to observe the response to IV administration of amphetamine and cocaine, either alone or together. Magnified basilar artery arteriograms were obtained in 12 New Zealand white rabbits before and after IV administration of cocaine, methamphetamine, or both, at various dosages. Low doses produced mild vasodilatation. At higher doses, the animals who received cocaine and methamphetamine alone showed little or no basilar artery spasm, but coadministration produced definite basilar artery vasospasm, reflecting a synergistic vasoconstrictive effect. If a similar response exists in the human cerebral vasculature, then this could help explain the cause of strokes associated with drug abuse.
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PMID:Cocaine- and methamphetamine-induced acute cerebral vasospasm: an angiographic study in rabbits. 212 40

Heroin, cocaine, amphetamines, sympathomimetic drugs can cause cerebral angiopathy. We report 2 patients with cerebrovascular disorders after ingestion of a nasal vasoconstrictor containing phenylpropanolamine (P.P.A.). The first patient had two acute repetitive attacks of severe headache and vomiting, occurring after a daily treatment with 180 mg of P.P.A. during 6 weeks. The second patient had an intracerebral hemorrhage, occurring some hours after taking for the first time 120 mg of P.P.A. In both cases, cerebral angiography, performed in the next week, demonstrated segmental narrowing and dilatations of medium-size intracranial arteries. None of the usual causes of cerebral vasculitis were present. The outcome was favorable and follow-up angiograms showed the disappearance of the beading pattern. P.P.A. is widely used over the counter in diet pills and stimulants. Cerebral vascular complications have been rarely reported, always hemorrhagic and often associated with cerebral vasculitis. They are unrelated to duration or dosage of treatment. The mechanism is unclear but could result from several factors: chronic or paroxystic high blood pressure, immuno-allergic vasculitis, arterial spasm, direct "toxic" effect of the P.P.A. on the arterial wall may be increased by other drugs and caffeine.
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PMID:[Benign cerebral angiopathies and phenylpropanolamine]. 304 37

We reviewed our experience with 72 patients, aged 15 to 45 years, who were hospitalized for nontraumatic intracerebral hemorrhages (ICHs) between 1978 and 1985. Evaluation included arteriography in 61 patients. Computed tomography demonstrated 41 lobar, 11 putaminal, four thalamic, four pontine, four intraventricular, two caudate, two midbrain, two cerebellar, one globus pallidum, and one corpus callosum hemorrhage. Forty-three patients, with either progressive neurologic deterioration, arteriovenous malformations (AVMs), or saccular aneurysms underwent surgery. The overall in-hospital survival, including those patients treated medically, was 87.5%. A presumed cause for the ICH was found in 55 (76.4%) patients. The main causes were ruptured arteriovenous malformations (21), hypertension (11), ruptured saccular aneurysms (seven), and sympathomimetic drug abuse (five). Surgical explorations demonstrated a necrotizing angiitis in one patient and arteriovenous malformations in two patients who had negative arteriograms. Young patients with nontraumatic ICHs represent a heterogeneous group. A cause can be established in most patients. Arteriovenous malformations account for less than one third of the hemorrhages in young adults, and other causes should be sought.
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PMID:Nontraumatic intracerebral hemorrhage in young adults. 357 58

After smoking "crack," the free-base form of cocaine, a 27-year-old man suffered an infarction of most of the territory of the right middle cerebral artery. Concomitant drug use seemed to have been limited to ethanol and ibuprofen. Search for other possible causes was negative. Angiography revealed narrowing of the supraclinoid portion of the right internal carotid artery (ICA) and cutoff of at least two distal branches. There was no beading or irregularity to suggest vasculitis. Crack may have induced vasospasm in the ICA through recognized sympathomimetic actions of cocaine.
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PMID:Cerebral infarction in a user of free-base cocaine ("crack"). 378 75

A case of intracerebral hemorrhage and characteristic angiographic changes associated with methamphetamine is reported. A 23-year-old woman suddenly complained of headache, nausea, vomiting and gait disturbance several minutes after intravenous injection of 30 mg of methamphetamine. She was admitted with consciousness disturbance, aphasia and right hemiparesis 26 hours after the onset. CT scan revealed subcortical hemorrhage in the left fronto-parietal region. Left carotid angiogram showed irregular segmental arterial narrowing, "beading" of the anterior and middle cerebral arteries. Emergency craniotomy was performed and a left fronto-parietal hematoma was removed totally. Histologically, the surgical specimen showed many vessels in which included thrombi with perivascular hemorrhage. Post-operative course was uneventful. Repeat carotid angiogram 4 months after the operation revealed normal anterior and middle cerebral arteries. We discussed about associations between the abuse of methamphetamine and the occurrence of intracranial hemorrhage and characteristic angiographic changes. As far as we know, there were 23 reports in an extensive review of the literature on intracranial hemorrhage associated with methamphetamine abuse. In the present case "beading" of the intracranial vessels may be related to angiitis induced by methamphetamine. Both the presence of arterial inflammation and increased blood pressure caused by sympathomimetic action of methamphetamine are probably the important factors in the occurrence of intracranial hemorrhage associated with methamphetamine.
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PMID:[Intracerebral hemorrhage and characteristic angiographic changes associated with methamphetamine--a case report]. 379 Mar 61

Intracerebral haemorrhage accounts for 15% of strokes. Its mechanisms include hypertension, cerebral amyloid angiopathy, rupture of vascular malformations, bleeding into primary or metastatic brain tumours, coagulopathies (due to the use of anticoagulants and thrombolytic agents), sympathomimetic drug effect (amphetamines, phenylpropanolamine, and cocaine), and vasculitis. The clinical presentation reflects both the general effects of increased intracranial pressure, and the neurological deficits that result from the specific location of the haemorrhage. Its diagnosis is based on computerized tomography, which identifies haemorrhage as a high-attenuation mass within the brain substance, and magnetic resonance imaging, which in addition estimates the age of the haemorrhage by identifying sequential patterns of transformation of the haemoglobin molecule within the haematoma. The mortality in intracerebral haemorrhage is dependent on the size and location of the haematoma. A reliable clinical parameter for the prediction of outcome is the Glasgow Coma Scale score at presentation. The management of intracerebral haemorrhage involves: (a) the prevention and treatment of increased intracranial pressure; and (b) the choice between surgical and nonsurgical treatment, a clinical decision that is still controversial as a result of the paucity of controlled clinical data comparing both treatment modalities.
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PMID:Intracerebral haemorrhage. 749 20

We present the case of a 33-year-old white male truck driver with a ten-year history of 3.5-g/wk "crank" and "peanut butter methamphetamine" inhalation (methamphetamine and propylhexedrine, respectively). This patient developed marked pulmonary hypertension as a probable consequence of abuse of these drugs. Proposed mechanisms of disease invoke toxic endothelial injury, hypoxic insult, direct spasm, vasculitis, and dysregulation of mediators of vascular tone. The possible role of genetics is discussed in reference to variability of human response to sympathomimetic challenge.
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PMID:Pulmonary hypertension associated with long-term inhalation of "crank" methamphetamine. 810 99

Amphetamine use in certain parts of the United States has risen dramatically. Methamphetamine, the most-common illicitly abused type of amphetamine, can be inhaled, injected intravenously, or smoked. It is a potent sympathomimetic that may lead to vascular events including myocardial infarction and stroke. Because of the demographics of drug use, these potentially devastating events usually occur in relatively young patients. The pathophysiology of stroke related to amphetamine use is multifactorial. Elevation in blood pressure, vasculitis, or other vascular toxicity are postulated as major mechanisms. Four cases of stroke associated with the use of methamphetamine, all occurring in patients ranging in age from 29-45 years, are described. Methamphetamine use appears to be a risk factor for the development of stroke. The rise in methamphetamine use will undoubtedly result in increased Emergency Department admissions with clinical presentations very similar to those of cocaine intoxication.
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PMID:Methamphetamine-related stroke: four cases. 1033 41

Cocaine, derived from the leaves of the shrub Erythroxylon coca, which grows on the slopes of the Andes, remains one of the most widely abused illicit drugs (Johnson et al., 1993). Its abuse appears to be increasing and as a result, so is its trafficking across borders, with ever-increasing sophistication of concealment (Rouse, 1992). Over the past few years, cases of cocaine intoxication have been reported, resulting from ruptured packets of cocaine that have been swallowed, or inserted into the vagina or rectum by couriers (drug smugglers), so called 'body packers' or 'mules' (Westli and Mittleman, 1981; Ricaurte and Langston, 1995). Cocaine is a powerful sympathomimetic and central nervous system stimulant, an overdose of which causes primarily cardiac, neurological and psychiatric effects (Ricaurte and Langston, 1995). Acute toxicity is dose-related and is characterized in the first place by its sympathomimetic effects, which include tachycardia, hypertension and hyperthermia arrythmias, followed by seizures. Brainstem depression and cardio-respiratory collapse, stroke, coma, intracranial vasculitis, myocardial infarction and sudden death have all been reported in cocaine abuse (Ricaurte and Langston, 1995). We present a fatal case with neurological and psychiatric symptoms, but without the usual cardiac and systemic signs.
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PMID:Body packer: cocaine intoxication, causing death, masked by concomitant administration of major tranquilizers. 1105 42

Alcohol abuse has been linked to intracranial hemorrhage, both intracerebral and subarachnoid. Some studies have found a dose-response relationship, so that increasing levels of abuse are associated with greater risk of hemorrhage. However, alcohol abuse has not been clearly linked to cerebral infarction, and some studies find that mild-to-moderate drinking appears to be associated with a decreased risk of cerebral infarction. Intravenous administration of drugs of abuse predisposes to endocarditis, which may lead to embolic stroke. Associations have been reported between various sympathomimetic drugs and cerebral infarction. A possible mechanism for cerebral infarction is focal arterial vasoconstriction and occasionally cerebral vasculitis. Associations have also been reported between various sympathomimetic drugs and intracranial hemorrhage. A likely mechanism for intracranial hemorrhage is acute arterial hypertension. With the exception of endocarditis, management of stroke related to drug abuse is largely supportive, with emphasis on supportive care to prevent stroke complications, physical and occupational therapy, and aggressive addiction rehabilitation.
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PMID:Cerebrovascular complications of alcohol and sympathomimetic drug abuse. 1250 9


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