Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurologic and visual symptoms frequently occurred in 56 reported patients with essential thrombocythemia (ET). They may either precede or follow the well-known microcirculatory complications of ET of acroparesthesias, erythromelalgia, and acrocyanosis or ischemia of one or more toes. In comparison with transient ischemic attacks in patients with vascular risk factors, the usual neurologic presentation of ET consists of brief attacks of sudden cerebral or visual dysfunction, which can be either well localized or diffuse and entirely nonspecific. A dull and throbby headache usually lasting for several hours frequently accompanies the neurologic symptoms. Visual symptoms are less frequent and include transient monocular blindness and global symptoms such as scintillating scotomas and attacks of blurred vision. Neurologic and visual symptoms may leave minor sequelae but are generally nondisabling. The striking similarity to migraine, together with the absence of vascular risk factors and the striking efficacy of aspirin treatment supports the hypothesis that the ischemic neurologic and visual symptoms in ET are caused by shear rate-induced intravascular activation and aggregation of platelets with subsequent transient sludging or occlusion of the cerebral arterial microvasculature. Available data show that both the erythromelalgic distress and the ischemic neurologic attacks in ET are completely abolished by control of platelet function with low dose aspirin alone or reduction of platelet counts to normal as well as by the combination of platelet reducing therapy and low-dose aspirin. Early recognition and appropriate treatment of neurologic symptoms in patients with ET is therefore of great clinical relevance.
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PMID:Neurologic and visual symptoms in essential thrombocythemia: efficacy of low-dose aspirin. 926 53

Thrombotic events are frequent in polycythemia vera (PV) and in essential thrombocythemia (ET). The frequency of thrombotic complications at presentation of PV and ET is nearly 50%. The spectrum of thrombotic complications is broad: thrombosis of arteries, veins and microvessels have been reported. Venous thrombosis can involve all territories but PV and TE are the commonest underlying etiology for Budd-Chiari Syndrome and splanchnic veins thrombosis. Endogenous erythroid-colony formation may be seen in up to 78% of patients thought to have Budd Chiari Syndrome and in 48% of splanchnic veins thrombosis. Major arterial thrombotic complications occur in 20%, especially in the extremities and in cerebral circulation. Microcirculatory disturbances are common in ET, occurring in 29% at presentation and 27% during follow up. In the extremities, erythromelalgia, a characteristic syndrome of red and congested extremities with raised temperature and painful burning sensations, is noticed in 30 to 50% of TE. Other microcirculatory manifestations like acrocyanosis, blue toes, digital gangrene can occur. All of these manifestations are highly sensitive to aspirin. Cerebral microcirculatory symptoms occur in about one-third of patients: migraine, transient visual symptoms like scotomata, blurred vision are characterized by a sudden onset, a short duration and a sequential course. Three kinds of leg ulcers have been described: leg ulceration as a consequence of microcirculatory thrombosis, exceptionally, pyoderma gangrenosum, and leg ulcers attributed to side effects of hydroxyurea. Microcirculatory leg ulcers are the most common: they are painful, inflammatory and sometimes, necrotic. They heal with treatment of SMP. Hydroxyurea-induced leg ulcers are painful, fibrous and multiple in 60%. Cessation of hydroxyurea typically leads to wound healing. The Polycythemia Vera Study Group (PVSG) established diagnostic criteria for PV and TE. Because SMP can have incompletely expressed disease, other authors have proposed determination of serum erythropoietin, examination of bone marrow histology, and spontaneous endogenous colony assays for diagnosis of PV or TE. The individual thrombotic risk depends on elevated hematocrit for PV, age (> 60) and prior thrombosis for PV and TE. Congenital and acquired (antiphospholipid syndrome) thrombotic states probably increase the risk of thrombosis.
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PMID:[When should a myeloproliferative syndrome be suggested in vascular medicine?]. 1592 69