Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032463 (polycythemia vera)
 3,374 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although polycythemia vera is one of the reported causes for cerebral infarction, isolated cerebellar infarction, a rare disorder, was never reported in combination with polycythemia vera. This is a report of a 72-year-old woman in whom isolated cerebellar infarction was the presenting manifestation of polycythemia vera. The patient was treated with recurrent phlebotomies until the hematocrit decreased to < 45%. This treatment was followed by marked neurological improvement. A better awareness of the possibility of cerebellar infarction in polycythemia vera may disclose additional cases.
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PMID:Isolated cerebellar infarction as a presenting symptom of polycythemia vera. 129 11

An abnormal hemoglobin was suspected in a 70-year-old Japanese male with cerebral infarction and erythremia with high performance liquid chromatography assay of Hb A1c. The hemoglobin variant migrated to the anode more rapidly than Hb A. Structure determination studies, including amino acid analysis of the abnormal peptide and DNA sequencing of a partially cloned alpha-globin gene, demonstrated that it is a new hemoglobin variant which has been named Hb Kanagawa [alpha 40(C5)Lys----Met]. This variant showed an increased oxygen affinity, decreased heme-heme interaction, and a lowered 2,3-diphosphoglycerate effect relative to normal.
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PMID:Hb Kanagawa [alpha 40(C5)Lys----Met]: a new alpha chain variant with an increased oxygen affinity. 163 55

The cause of stroke in a young adult can usually be ascertained with proper workup. One of the most common causes is atherosclerotic cerebrovascular disease, and cigarette smoking is an important risk factor in young adults. Several types of nonatherosclerotic cerebral vasculopathy can also result in premature cerebral infarction; these include cervicocephalic arterial dissection, nonpenetrating traumatic arterial disease, moyamoya disease, fibromuscular dysplasia, vasculitis, and migraine. Cardiac embolism may play a more important role than was previously thought, and hematologic disorders (eg, sickle cell disease, polycythemia rubra vera, coagulation problems) are known to predispose patients to stroke. A careful history of risk factors and a thorough neurologic and cardiovascular examination followed by adequate testing, including angiography, are essential to diagnosis.
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PMID:Diagnosis of stroke in young adults. 356 68

A 36-year-old man presented with sudden onset of hemorrhagic cerebral infarction in association with polycythemia vera. On admission this patient manifested semicomatous state and left hemiplegia which were gradually progressed. X ray CT demonstrated a severe hemorrhagic infarction in right MCA territory accompanying marked shift of midline structures. Cerebral angiograms represented occlusion of right MCA showing floating emboli in the internal carotid. Hematocrit value was found to be high as 61.2 per cent. Elevated ICP levels were noted by means of epidural pressure monitoring. Deterioration of patient status was considered to be based on impairment of cerebral circulation due to hemostasis by elevated blood viscosity. In addition to administration of mannitol solution, intermittent exsanguinations, 1000 ml in total amount, were performed and hematocrit levels were corrected by hemodilution. Consciousness level was remarkably improved in accordance with reduction of ICP, which well corresponded to values of hematocrit. Level of ICP and tissue perfusion are convinced to be strongly affected by hemorheological factor in the state of raised ICP.
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PMID:[Hemodilutional therapy in raised intracranial pressure; observations in a case of cerebral infarction associated with polycythemia vera]. 370 72

Hyperviscosity of the blood is a known cause of ischemic cerebral infarction. A case of polycythemia vera complicated by a watershed infarction is presented.
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PMID:Watershed infarction in a case of polycythemia vera. 376 64

The observation of apparent dural sinus opacification in a polycythemic patient with cerebral infarction prompted a review of 300 computed tomographic scans for the significance of dense dural sinuses. Fifteen patients including 11 neonates, were identified; each of them had dense dural sinuses and elevated hematocrit or red blood cell indices or both. With only one exception, computed tomography also showed various low attenuation parenchymal abnormalities. A typical cerebral infarction pattern was seen in six and parenchymal hemorrhage in one. Nonthrombotic dural sinus opacification is a sign of increased blood viscosity in patients with congenital heart disease, hemoconcentration states, polycythemia of the newborn, and polycythemia rubra vera. These patients are at high risk for hypoxemic cerebral insult, which can be detected by cranial computed tomography.
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PMID:Radiodense dural sinuses: new CT sign in patients at risk for hypoxemic insult. 679 79

Two patients with cyanotic congenital heart disease (CHD) and erythremia were seen for abrupt onset of focal neurologic deficits and/or seizure without signs of infection or increased intracranial pressure. Clinical features and initial computed tomography (CT) in both cases suggested stroke. Subsequent CT scans demonstrated cerebral abscess, proved at operation. Review of records of patients with CHD at the University of Rochester (NY) Medical Center from 1965 to 1981 disclosed 12 cases with brain abscess but only two cases with aseptic cerebral infarction. All but one patient with abscess were cyanotic. One third of patients with abscess had a clinical picture suggesting stroke. Clinical or radiologic features of half the cases indicated that cerebral infarction may have led to abscess formation. Diagnosis of brain abscess and immediate antibiotic therapy should be strongly considered in patients with cyanotic CHD who suffer a suspected cerebral infarction.
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PMID:Cyanotic congenital heart disease with suspected stroke. Should all patients receive antibiotics? 683 Apr 69

Fernando and Chir 1st reported an association between chorea and oral contraceptives (OCs) in 1966. Differential diagnosis of chorea, in addition to Sydenham chorea, include Wilson disease; encephalitis; Huntington chorea; drug intoxication; benign familial chorea; pregnancy; systemic lupus erythematosus; Henoch-Schonlein purpura; polycythemia vera; hypocalcemia; hyperthyroidism; carbon monoxide poisoning; cerebral infarction, and; intracranial tumor. Chorea can also occur as an untoward side-effect of OC therapy, as shown by the case report of a 20-year old white woman. Chorea associated with OC therapy occur unilateraly but has also been bilateral in 37% of reported cases. 8 of 24 reported cases (33%) had a prior history of rheumatic fever - mean age of patient was 22 years (range, 16 to 40 years). The time between initiation of OC therapy and appearance of choreiform movements can vary from 6 days to 9 months, with a mean of 3 months. Time between discontinuation of OC therapy and cessation of symptoms vary from 3 days to 3 months, with a mean of 5 weeks. Speculations by various authors on the pathogenesis of chorea are described.
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PMID:Chorea associated with oral contraceptive therapy. 739 41

The clinical course of 16 patients with polycythemia vera (PV), treated in the period 1982 to 1993, was shown. Splenomegaly occurred in three fourths of these patients (75%), and hypertension was a major symptom. Thrombosis such as myocardial infarction and cerebral infarction was noted. Eight patients was treated with myelosuppressive agents and the 8 other patients were treated with phlebotomy. A 70-year-old male who was treated with mitobronitol (DBM) developed acute myeloblastic leukemia (AML) 11 years later. He was treated with multi-combination chemotherapy (BHAC-DMP), and entered complete remission, followed by early relapse. He became refractory to chemotherapy and died of acute pneumonia 6 months later. Median survival of 16 cases of PV was more than 10 years, and long-term treatment and care are necessary.
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PMID:[A clinical study of sixteen polycythemia vera cases--acute myeloblastic leukemia in patients with polycythemia vera]. 799 24

Polycythemia vera (PV) can produce cerebral infarction. The mechanisms proposed by most authors are hyperviscosity-related diminished cerebral blood flow and platelet function abnormalities. We present a 36-year-old woman whose initial clinical manifestation of PV consisted of cerebral ischemia due to a carotid thrombus, as well as occlusion of the middle cerebral artery and cortical branches of the anterior cerebral artery demonstrated by angiography. To our knowledge, this is the first published case of cerebral infarction in PV caused by a thrombus of an extracranial artery. Therefore, PV can produce ischemic stroke due to thrombosis not only in small distal arteries or arterioles but also in the carotid artery or main branches. Treatment of intraluminal thrombus in non-arteriosclerotic carotid artery is discussed. Myeloproliferative disorders, including PV, must be suspected in all stroke patients with an elevated platelet count, even in those who have potential causes of reactive thrombocytosis.
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PMID:[Carotid thrombus and cerebral infarction as the initial clinical manifestation of polycythemia vera]. 1589 49


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