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)

Rendu-Osler disease is a familial disorder transmitted as an autosomal dominant trait of high penetrance. It is characterized by telengiectasias of the skin, mucous membranes and viscera, associated with recurrent bleedings. Neurological complications (brain abcesses and hemorrhagic manifestations) occur in 10% of the patients. Neurological symptoms are often associated with arteriovenous fistula of the lung (50%). Ischaemic strokes occuring in such patients with an hemorrhagic disease while unfrequent, have been described. The pathophysiology of stroke in that case remains unclear. Polycythemia causing hyperviscosity, air embolism following hemoptysis, paradoxical embolism through right-to-left shunt have been proposed. We report a new case of ischaemic strokes occuring in a caucasian forty-year-old woman, with Rendu-Osler disease (familial history, epistaxis, telengiectasias) and with an arteriovenous malformation of the right lung. She presented two strokes and one transient ischaemic attack. Her pulmonary malformation was occluded by embolization. The role of arteriovenous malformation in the pathophysiology of strokes is discussed.
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PMID:[Ischemic cerebrovascular complications in Rendu-Osler disease: a case]. 876 58

Childhood ischemic stroke, including arterial ischemic stroke (AIS) and sinovenous thrombosis (SVT), is relatively rare in children but can result in devastating morbidity and mortality. An understanding of the etiology of childhood stroke is important because strategies for primary and secondary prevention can be devised. Prothrombotic disorders may contribute to the etiology of childhood stroke, and include deficiencies of antithrombin, protein C, protein S, plasminogen, and presence of Factor V Leiden, Prothrombin gene G20210A, dysfibrinogenemia, antiphospholipid antibodies, hyperhomocysteinemia, and elevated lipoprotein (a). The overall incidence of prothrombotic disorders in childhood AIS is estimated to be 20% to 50% in most studies and, in childhood SVT, to be 33% to 99%. In addition, hyperlipidemia, polycythemia, iron deficiency anemia, and platelet disorders may result in a prothrombotic state associated with ischemic stroke. The etiologic contribution of these prothrombotic disorders to initial and recurrent stroke has not been clearly defined; however, additional risk factors are usually present in affected children. Given the prevalence of prothrombotic disorders in childhood stroke, and their likely causative role, children with stroke should be screened for prothrombotic disorders. Future prospective and multicenter studies will elucidate the contribution of specific prothrombotic disorders to initial and recurrent stroke, and optimal therapy.
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PMID:Prothrombotic disorders and ischemic stroke in children. 1120 19

Hypertension, hypercholesterolemia, and coronary artery disease are among the risk factors of cerebrovascular accidents. After age, hypertension is the most powerful stroke risk factor. Abnormalities of serum lipids are regarded as risk factors for cerebrovascular accidents. A significant reduction in stroke risk among persons treated with cholesterol-reducing medicines known as statins are reported. Stroke risk nearly doubles in those with antecedent coronary artery disease. Moreover, polycythemia and high hematocrit levels are considered to be potential stroke risk factors. Minor thalassemia is associated with decreased prevalence of arterial hypertension and myocardial infarction (the second effect observed only in males.) Total cholesterol and LDL levels are lower in minor thalassemics, as is the blood viscosity. Therefore, it could be hypothesized that minor thalassemia could afford some protection against cerebrovascular accidents.
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PMID:Minor thalassemia as a protective factor against cerebrovascular accidents. 1220 71

The oxygen-dependent, renal cytokine eythropoietin (Epo) is well known to increase red cell production. Binding of Epo to the Epo receptor (EpoR) represses apoptosis of erythroid progenitor cells, thereby allowing their final maturation. We and others showed that Epo and its receptor are expressed in many other tissues, including brain, spinal cord, retina and testis. The presence of a blood barrier suggests that Epo plays a local role in these organs. Indeed, therapeutically applied or hypoxically induced Epo has been shown to reduce the infarct volume in various stroke animal models, to prevent retinal degeneration, and to ameliorate spinal cord injury. In a study conducted by Ehrenreich and colleagues, stroke patients treated with Epo showed reduced infarct volume, fast neurological recovery and improved clinical outcome. In analogy to its function on erythroid progenitor cells, this neuroprotective effect of Epo might be explained by repression of programmed cell death. Apart from neuroprotection, there is an assumption that Epo present in breast milk has the potential to protect against mother-to-infant transmission of HIV. When using Epo at high doses for longer time periods; however, care has to be taken to control the resulting chronic polycythemia that most probably caused enlarged cerebral infarct volumes in a transgenic mouse model that due to Epo-overexpression reached hematocrit levels of about 0.8. Overall, these data strongly support the notion that Epo will soon find new applications in the clinic.
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PMID:Non-erythroid functions of erythropoietin. 1471 31

We report a rare case of recurrent brain abscess associated with congenital pulmonary arteriovenous fistula. A 52-year-old man was admitted to our hospital in October, 1999 because of a sudden stroke-like onset of right hemiparesis, right hemiparesthesia, dysarthria and sensory aphasia. He had a history of previous brain abscess in the right cerebellar hemisphere. It had been removed in 1991. CT scan at the time of the current admission disclosed a low-density area in the left parietal region. The mass was ring-enhanced after injection of contrast medium. On MRI the mass lesion was depicted as low-intensity on T1-weighted image and high-intensity on T2-weighted image. The mass was ring-enhanced after administration of Gd-DTPA. In spite of conservative treatment the size of the abscess increased considerably with marked surrounding edema. The brain abscess was successfully treated with aspiration and drainage, and the residual mass was resected. The patient also had a history of arteriovenous fistula in the lower lobe of his right lung. This had been excised in 1965. However, he had no signs, symptoms or family histories of hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease). Contrast enhanced CT scan of the chest showed nodular lesions connected to vascular shadows in the right lower lung field. Pulmonary angiograms also revealed multiple arteriovenous fistulas in the lower lobe of the right lung. He was not dyspneic or cyanotic, but his hypoxia, polycythemia, and recurrent brain abscess were thought to be caused by pulmonary arteriovenous fistula. The fistulas were embolized with coils via a percutaneous catheter. Pulmonary arteriovenous fistula should be treated aggressively either by surgery and/or by coil embolization in order to prevent the complication of brain abscess.
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PMID:[Recurrent brain abscess associated with congenital pulmonary arteriovenous fistula: a case report]. 1497 25

This study questioned the effect of living and training at moderate altitude on cardiac morphological and functional adaptations and tested the incidences of potential specific adaptations compared with aerobic sea level training on maximal left ventricular performance. Sea level-native rats were randomly assigned to N (living in normoxia), NT (living and training 5 days/wk for 5 wk in normoxia), CH (living in hypoxia, 2,800 m), and CHT (living and training 5 days/wk for 5 wk in hypoxia, 2,800 m) groups. Cardiac adaptations were evaluated throughout the study period by Doppler echocardiography. Maximal stroke volume (LV(SVmax)) was measured during volume overloading before and after the study period. Finally, at the end of the study period, passive pressure-volume relationships on isolated heart and cardiac weighing were obtained. Altitude training resulted in a specific left ventricular (LV) remodeling compared with NT, characterized by an increase in wall thicknesses without any alteration in internal dimensions. These morphological adaptations associated with hypoxia-induced alterations in pulmonary outflow and preload conditions led to a decrease in LV filling and subsequently no improvement in LV performance during resting physiological conditions in CHT compared with NT. Such a lack of improvement was confirmed during volume overloading that simulated maximal effort (LV(SVmax) pretest: NT = 0.58 +/- 0.05, CHT = 0.57 +/- 0.08 ml; posttest: NT = 0.72 +/- 0.06, CHT = 0.58 +/- 0.07 ml; NT vs. CHT in posttest session, P < 0.05). Maximal aerobic velocities increased to the same extent in NT and CHT rats despite marked polycythemia in the latter. The lack of LV(SVmax) improvement resulting from altitude training-induced cardiac morphological and functional adaptations could be responsible for this phenomenon.
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PMID:Cardiac remodeling and functional adaptations consecutive to altitude training in rats: implications for sea level aerobic performance. 1528 45

Apart from its hematopoietic function, erythropoietin (Epo) exerts neuroprotective activity upon reduced oxygenation or ischemia of brain, retina, and spinal cord. To examine whether Epo has an impact on the retrograde degeneration of retinal ganglion cells (RGCs) following optic nerve transection in vivo, we made use of our transgenic mouse line tg21 that constitutively expresses human Epo preferentially in neuronal cells without inducing polycythemia. We show that the tg21 retina expresses human Epo and that RGCs in this mouse line carry the Epo receptor. Upon axotomy, the RGCs of Epo transgenic tg21 mice were protected against degeneration, as compared with wild-type control animals. Western blot analysis revealed decreased phosphorylation levels of STAT-5 and reduced expression of Bcl-XL in RGCs of axotomized tg21 animals, suggesting that the corresponding pathways are not crucial for Epo's neuroprotective activity. Increased phosphorylation levels of ERK-1/-2 and Akt, as well as decreased caspase-3 activity, however, were observed in injured tg21 retinae. Injection of selective inhibitors of ERK-1/-2 (PD98059) or Akt (Wortmannin) pathways into the vitreous space revealed that transgenic Epo protected the RGCs by a pathway involving ERK-1/-2 but not Akt. In view that axotomy-induced degeneration of RGC occurs slowly, and considering the earlier data on the safety and efficacy of Epo in human stroke patients, we predict the clinical implementation of recombinant human Epo not only in patients with acute ischemic stroke, but also with more delayed degenerative neurological diseases.
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PMID:Erythropoietin protects from axotomy-induced degeneration of retinal ganglion cells by activating ERK-1/-2. 1555 72

Complications of chronic hypoxia, including erythrocytosis, hyperviscosity, abnormalities of hemostasis, cerebral abscesses, stroke, and endocarditis, are among the most common consequences of cyanotic heart disease in adults. The compensatory erythrocytosis of cyanotic heart disease can become pathologic by causing an increase in blood viscosity, thereby decreasing perfusion and resulting in decreased total oxygen delivery and increased risk of venoocclusive/hyperviscosity syndrome. Treatment of hyperviscosity secondary to erythrocytosis in cyanotic heart disease is controversial. Data is limited but suggest that phlebotomy has the potential to increase exercise capacity, reduce the symptoms of hyperviscosity, and reduce the potential risk of vasoocclusive disease in selected patients with polycythemia secondary to cyanotic heart disease. Unfortunately, repeated phlebotomy can quickly lead to iron deficiency, resulting in microcytic erythrocytes that induce higher viscosity than normocytic erythrocytes, which may increase the risk for venoocclusive events. There are limited data on the use of hydroxyurea to suppress erythrocytosis in this patient population. The authors conclude that until newer approaches to decreasing hematocrit without inducing iron deficiency are shown to be safe and efficacious, phlebotomy should only be used for the acute resolution of hyperviscosity symptoms. In addition, the use of hydroxyurea should be limited to patients with recurrent symptoms.
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PMID:Blood is thicker than water: the management of hyperviscosity in adults with cyanotic heart disease. 1717 81

Placental chorioangiomas are benign vascular tumors. Large chorioangiomas cause several obstetric complications, including premature labor, placental abruption, polyhydramnios, fetal hydrops, fetal growth restriction, fetal hepatosplenomegaly, cardiomegaly, congestive heart failure, and fetal death. The neonatal complications are hydrops fetalis, microangiopathic hemolytic anemia, and thrombocytopenia. The cause of perinatal cerebral arterial infarction remains unclear in the majority of cases. Investigators have reported a number of obstetric and neonatal complications in the setting of perinatal stroke, including birth asphyxia, preeclampsia, chorioamnionitis, cardiac anomalies, polycythemia, systemic infection, and genetic thrombophilias. We present a rare case of perinatal cerebral infarction associated with placental chorioangioma.
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PMID:Perinatal cerebral arterial infarction associated with a placental chorioangioma. 1852 77

The association between testosterone-replacement therapy and cardiovascular risk remains unclear with most reports suggesting a neutral or possibly beneficial effect of the hormone in men and women. However, several cardiovascular complications including hypertension, cardiomyopathy, stroke, pulmonary embolism, fatal and nonfatal arrhythmias, and myocardial infarction have been reported with supraphysiologic doses of anabolic steroids. We report a case of an acute ST-segment elevation myocardial infarction in a patient with traditional cardiac risk factors using supraphysiologic doses of supplemental, intramuscular testosterone. In addition, this patient also had polycythemia, likely secondary to high-dose testosterone. The patient underwent successful percutaneous intervention of the right coronary artery. Phlebotomy was used to treat the polycythemia acutely. We suggest that the chronic and recent "stacked" use of intramuscular testosterone as well as the resultant polycythemia and likely increased plasma viscosity may have been contributing factors to this cardiovascular event, in addition to traditional coronary risk factors. Physicians and patients should be aware of the clinical consequences of anabolic steroid abuse.
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PMID:Anabolic steroids, acute myocardial infarction and polycythemia: a case report and review of the literature. 1933 62


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