Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 39-year-old Japanese female who had been followed as chronic myelogenous leukemia (CML) since 1984 was admitted to our hospital because of dizziness. On admission, platelet count markedly increased (245 X 10(4)/microliters) in spite of daily administration of busulfan 2 mg. She was diagnosed as accelerated phase CML with thrombocytosis. So we tried to use interferon alpha (IFN-alpha) finally given in a dose of 9 X 10(6) U daily by subcutaneous injection. After that, platelet count decreased to 70 X 10(4)/microliters and megakaryocyte count in bone marrow decreased from 887.5/microliters to 395.7/microliters. But we had to stop IFN-alpha because of severe side effects.
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PMID:[Thrombocytosis in chronic myelogenous leukemia (CML) controlled by interferon alpha (IFN-alpha)]. 276 64

A clinicopathological study was performed on 46 patients with chronic myeloproliferative diseases (CMPD) showing a thrombocythemia in excess of 1,000 x 10(9)/liter. When applying rigid diagnostic criteria only 23 patients were compatible with the initially suspected diagnosis of primary thrombocythemia (PTH). Comparison of PTH with the other entities of CMPD (CGL, 10, AMM, 6, and polycythemia, 7 cases) revealed a sustained elevation of the platelet count observable over a period of 2 to 8 years, no marked leukocytosis or abnormalities of the differential blood count, and a normal score of the leukocyte alkaline phosphatase. Episodes of hemorrhage and thrombosis as well as neurological symptoms (paresthesias, dizziness, headache), were encountered frequently as clinical manifestations in PTH. Survival time in PTH was significantly longer than in CGL with accompanying thrombocythemia. In a consecutively biopsied population of patients with CMPD, incidence of PTH was about 8%. In PTH the characteristic histopathology of the bone marrow consisted of an isolated (monolinear) proliferation of the megakaryocytes (density 127 +/- 47/mm2) without gross abnormalities of this cell lineage or a conspicuous increase in neutrophilic granulo- or erythrocytopoiesis. These lesions are significantly different from the morphological findings in the other CMPD with extreme thrombocytosis.
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PMID:Chronic myeloproliferative diseases with an elevated platelet count (in excess of 1,000,000/microliter): a clinicopathological study on 46 patients with special emphasis on primary (essential) thrombocythemia. 350 37

At presentation the history of an 87-year-old woman included progressive memory loss, repeated transient ischaemic attack, increasing fatigue, dizziness, palpitations and frequent falls. Investigations revealed erythrocytosis, leukocytosis, thrombocytosis, normal arterial oxygen concentration and an increased red cell volume. Polycythaemia vera was diagnosed and was successfully managed by phlebotomy with half a unit twice a week and rechecks of her haematocrit, initially; she reported marked improvement after 2 weeks of treatment. The alternative treatments for polycythaemia vera are discussed; in addition to venesection, conventional treatments include bone-marrow depressive agents such as phosphorus-32 and chemotherapy with agents such as hydroxyurea. More recent developments include isovolumic erythrocytophoresis, alpha-interferon and ticlopidine. All of the treatments are associated with complications, or other disadvantages, thrombotic complications in the case of phlebotomy, malignancies in the case of most myelosuppressive treatments, and problems of compliance in others. The optimal treatment for polycythaemia vera is a judicious combination of the alternatives, depending on the phase of the disease, the age of the patient, and other prognostic factors.
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PMID:Primary polycythaemia vera in the elderly. 802 Jun 39

Familial chronic myeloproliferative syndrome (CMS) was observed in five members from two different generations of the same kindred. Diagnosis included agnogenic myeloid metaplasia (case 1), polycythemia vera (case 2), and essential thrombocythemia (cases 3-5). Cases 1-3 were siblings, case 5 was the daughter of case 1, and case 4 was the cousin of cases 1, 3. Age at diagnosis ranged from 28 to 75 years, cases 1 and 3 were male, and the others were female. The diagnosis was made after an episode of cerebral thrombosis in one patient, during a study for headache and dizziness in another, and fortuitously in the three remainders. All patients had splenomegaly and varying degrees of thrombocytosis. The cytogenetic exam was normal in all four cases. A woman patient was treated with interferon during a pregnancy. Fetal growth was retarded, and the newborn showed bone and genital malformations. No environmental leukemogen factor was found. This familial case strengthens Dameshek's theory of a common pathogenesis of CMS and suggests a genetic and hereditary etiology.
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PMID:Familial myeloproliferative syndrome. 819 53

Neurological symptoms of transient unsteadiness, dysarthria, dysphasia, dysbasia, transient monoor hemiparesis, hemiparesis, scintillating scotomas, amaurosis fugax, vertigo, dizziness, migraine accompaniments, syncope and seizures were the presenting manifestations of thrombocythemia in various myeloproliferative disorders. Erythromelalgia preceded or followed the neurologic ischemic attacks. The neurologic and ocular attacks usually had a sudden onset, lasted for a few seconds to several minutes and occurred independently or sequentially rather than simultaneously. This clinical syndrome is caused by platelet-mediated ischemic and thrombotic processes in the end-arterial microvasculature and reflects the existence of a platelet dependent and aspirin responsive arterial thrombophilia in thrombocythemia as novel disease entity, which confirms and elucidates Mitchell's hypothesis.
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PMID:Atypical transient ischemic attacks in thrombocythemia of various myeloproliferative disorders. 895 74

Bleeding and thrombosis are major causes of morbidity and mortality in patients with chronic myeloproliferative disorders. We retrospectively evaluated 101 consecutive patients affected by primary thrombocytosis (46 male, 55 female, aged 18-84 years; mean +/- SD 61 +/- 15) followed for a period ranging from 6 months up to 10 years (median 5 years) at our hematological unit. At the time of diagnosis 48 patients were asymptomatic; 26 had clinical evidence of atherothrombosis (cerebral ischemic attacks, ischemic heart disease, peripheral occlusive arterial disease), ten had venous thrombosis, four experienced major hemorrhages, 23 presented microvascular ischemic manifestations namely erythromelalgia, paresthesias, acrocyanosis and dizziness. At presentation 51.2% of the patients had elevated serum lactic dehydrogenase, 34.5% hyperuricemia, and 23.4% serum creatinine > 1.2 mg/dL. Color Doppler ultrasound provided evidence of vascular stenosis or medium-intimal hyperplasia of epiaortic vessels in 48.9% of patients studied, and similar alterations of lower limb arteries in 23.8% of cases. Therapy modality included an antiplatelet agent (picotamide 300 mg/bid); a cytoreductive agent (busulphan, hydroxyurea, pipobroman or melphalan) was used when platelet count was > 800000/microL. Symptoms due to microvascular ischemia promptly regressed after picotamide and cytoreductive therapy. During follow-up. nine patients suffered from atherothrombotic events (transient ischemic attacks, ischemic stroke, unstable angina pectoris) and five developed deep vein thrombosis or superficial thrombophlebitis. Five patients experienced major hemorrhages (two melena, two hematuria, one perioperative bleeding); the two gastrointestinal hemorrhages occurred in patients self-medicated with non steroidal anti-inflammatory drugs, and the two episodes of hematuria occurred on oral anticoagulant therapy and aspirin respectively. No major bleeding occurred in patients on continuative therapy with picotamide, even in the presence of upper digestive tract disorders. Seven patients died: mortality resulted from one sudden coronary death, three solid neoplasia, one blast crisis, one anile, and one massive hemorrhage due to abdominal aortic prosthesis tearing. Our study suggests that a long-term antithrombotic prophylaxis with picotamide may be of benefit in patients affected by primary thrombocytosis; a controlled clinical trial is warranted to assess whether picotamide can ameliorate the natural history of the disease.
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PMID:Thrombotic and hemorrhagic complications in chronic myeloproliferative disorders. 895 59

We present an 86-years-old woman's case with paralysis in her left hand of abrupt apparition, accompanied by arterial hypertension and dizziness. The investigation revealed erythrocytosis, leukocytosis, thrombocytosis, with normal arterial O2 saturation (O2 SAT), increased of his red cell volume and blood viscosity. The polycythaemia vera (PV) was diagnose and the paralysis disappeared, when 24 hours before a phlebotomy was practiced, and the function was recovered by the hand. We analysed the presents diagnostics criteria of the disease defined by Polycythaemia Vera Study Group (PVSG). The different treatments for PV are discussed; in addition to venesection, conventional treatment include chemotherapy with hydroxyurea and pipobroman, as well as the erythropheresis, -interferon and aspirin. All of the treatments are associated with complications; thrombotic in the case of phlebotomy; malignancies and gastrointestinal bleeding in the case of myelosuppressive treatments and aspirin. We think the optimal treatment for PV is a judicious combination of the available alternatives, depending on the phase of the disease, and the age of the patient.
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PMID:[Primary polycythaemia vera in the elderly]. 958 Jan 77

A 15-year-old African-American female presented with prolonged menstrual bleeding accompanied by a 1-week history of weakness, fatigue, dizziness, and bifrontal headaches. Her previous period was 5 weeks earlier, lasted 3 weeks, with heavy passage of clots. Family history is significant for bleeding disorders. Her platelet count was in the 60,000-80,000 range, platelet aggregometry was low, and antiplatelet antibodies positive; she received platelet transfusion that increased and stabilized her platelet count. She was diagnosed with reactive thrombocytosis due to severe iron deficiency anemia. She was placed on ethynil estradiol plus norethindrone therapy until her platelet count rose to 2,275,000.
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PMID:Severe Menorrhagia. 1036

Imatinib mesylate targets the adenosine triphosphate (ATP)-binding sites of the protein tyrosine kinase domains associated with Bcr-abl, the platelet-derived growth factor (PDGF) and c-kit. In idiopathic myelofibrosis (IMF) PDGF is considered to be one of the growth factors responsible for the development of bone marrow fibrosis. Recently, it has been shown that imatinib has antifibrogenic effect on bone marrow fibrosis in chronic myelogenous leukemia. Treatment with imatinib alone in IMF has been associated with significant side effects. In this study, the safety and efficacy of imatinib therapy in IMF, either administered as a single agent or in combination with hydroxyurea (HU) and/or alpha-interferon (IFN-alpha) are evaluated. Eleven patients (median age, 63 years; range, 33-82 years) with IMF (n = 8) or postpolycythemic myelofibrosis (PPMF) (n = 3) were studied All patients had been treated with HU (n = 9) and/or IFN (n = 7) before study entry. In all but one patient, treatment with these agents was discontinued when imatinib therapy was instituted. One patient continued IFN when treatment with imatinib was started. Imatinib was given at a dose of 400 mg/day. Nine patients were in an advanced disease phase. The patients have been followed for a median period of 2 months (range, 0.5-12 months). Treatment with imatinib has been stopped in six patients (55%), because of overt side effects (n = 4), recurrence of transitory dizziness and visual defects owing to a rising platelet count (n = 1), or the occurrence of an acute subdural hemorrhage that was evacuated without neurological deficits (n = 1). In nine patients imatinib treatment was followed by a rise in leukocyte and platelet counts that required combination with HU or IFN. The combined treatment modalities were followed by a rapid decrease in cell counts and were well tolerated apart from IFN side effects. A beneficial effect of imatinib was documented in three patients. It is concluded that leukocytosis and thrombocytosis are seen in most patients with myelofibrosis during treatment with imatinib. Combination therapy with HU or IFN seems safe and well tolerated and followed by a decrease in disease activity. A subgroup of patients in an early disease phase might benefit from imatinib therapy alone.
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PMID:Imatinib mesylate in idiopathic and postpolycythemic myelofibrosis. 1463 3

Essential thrombocythemia (ET) is a clonal myeloproliferative disorder characterized by sustained thrombocytosis, isolated hyperplasia of megakaryocytic lineage, and association with thrombotic or bleeding episodes. It is extremely rare in childhood and frequently presents without evident clinical signs. We describe a 3-year-old girl with severe headache and dizziness suffering from ET, who was treated with Interferon-alpha-2a (IFN) based on the potent effect of this agent to inhibit myeloid colonies induced by phytohemagglutinin A stimulated leukocyte conditioned medium (PHA-LCM). Bone-marrow-derived mononuclear cells of this patient did not exhibit spontaneous colony formation but responded to recombinant human (rh) erythropoietin (EPO), rh granulocyte-colony stimulating factor (G-CSF), granulocyte-macrophage (GM)-CSF, and stem-cell factor in addition to PHA-LCM. After 65 months of in vivo IFN treatment, the patient experienced a sustained partial remission with platelet counts varying between 400 and 600 x 10(3)/microl.
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PMID:Long-lasting partial remission by Interferon-alpha treatment in a child with essential thrombocythemia. 1642 12


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