Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Packed red cell volume (VPRC) and total blood volume chiefly affect oxygen transport to tissues and produce the syndrome of polycythemic hyperviscosity. Several studies have demonstrated that a raised VPRC increases the blood viscosity and, under a measured pressure, decreases the flow rate in a capillary tube. Reduced flow results in a less effective tissue perfusion. The oxygen transport at different values of VPRC is shown by an inverted arc-like curve: at normal VPRC levels the oxygen transport is optimal. Hypervolemia affects oxygen transport to tissues: at the same VPRC values, hypervolemic patients have a better oxygen transport. In polycythemia vera (PV), hypervolemia may partially reduce the damage due to the increased blood viscosity. However, in some local areas where fixed vessel diameter (from arteriosclerosis) limits the increased blood flow, hyperviscosity may result in a local tissue ischemia. A relative iron deficiency with associated microcytosis due to venesection frequently occurs in PV. It is also associated with a delayed red blood cell filtration which may contribute to hyperviscosity. When thrombocytosis is present, the risk of thrombotic complications is furthermore increased. We report symptoms and signs at the onset in a series of 80 patients affected by PV. All patients have a minimum follow-up of 4 years. We also report the course of the illness, the treatment effectiveness (venesection, dibromomannitol) on clinical symptoms, the survival curve with analysis of prognostic factors at the onset and the causes of death.
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PMID:[Polycythemic hyperviscosity syndromes]. 667 89

Essential thrombocythemia is a clonal myeloproliferative disorder, characterized predominantly by a markedly elevated platelet count without known cause. We report a case that was recognized during investigation of a transient ischemic attack, and review the neurologic findings in 33 patients with unequivocal essential thrombocythemia under prospective study by the Polycythemia Vera Study Group. Twenty-one patients had neurologic manifestations at some point during their course, including headache (13 patients), paresthesiae (10), posterior cerebral circulatory ischemia (9), anterior cerebral circulatory ischemia (6), visual disturbances (6) and epileptic seizures (2). All patients with neurologic symptoms responded satisfactorily to treatment, although continuous or repeated treatment was often required. Therapeutic recommendations include plateletpheresis for major thrombo-hemorrhagic phenomena, or megakaryocyte suppression with radioactive phosphorus, alkylating agents (such as melphalan), or hydroxyurea; minor symptoms may respond to platelet antiaggregating agents.
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PMID:Neurologic manifestations of essential thrombocythemia. 668 92

Platelet aggregation and circulating platelet aggregates (CPAs) were evaluated in 18 patients with myeloproliferative disorders, both with and without thrombocytosis. No specific patterns of platelet aggregation were detected, but 11 of 18 patients demonstrated abnormal aggregation to epinephrine, nine of 18 had abnormal aggregation to adenosine diphosphate, and seven of 18 had abnormal aggregation to collagen. There was no definitive correlation of bleeding episodes with abnormal aggregation. However, significant bleeding was observed in a patient with a platelet count of 1,500,000/cu mm and abnormal aggregation. The aggregation defects persisted despite lowering of platelet count. Evidence of increased circulating platelet aggregates and normal platelet aggregation was seen in two patients, one of whom had transient cerebral ischemic attacks relieved by antiplatelet therapy, with return of the CPA index to normal. In two patients with digital ischemia, claudication, and angiographic evidence of peripheral vascular disease, no laboratory evidence of increased circulating platelet aggregates was observed, but one patient had regression of symptoms with antiplatelet therapy.
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PMID:Abnormal platelet function in myeloproliferative disorders. 689 52

Four drugs that inhibit platelet function have been evaluated for their antithrombotic effects in humans. These are aspirin, dipyridamole, hydroxychloroquine and sulphinpyrazone. Aspirin has been shown to reduce the number of transient ischemic attacks (TIA), stroke and death in patients with multiple TIA. The reduction in TIA was greatest in males who were normotensive and when there was an angiographically demonstrated lesion in the carotid artery that accounted for the symptoms. Aspirin reduced venous thrombosis and non-fatal and fatal pulmonary embolism in patients after surgery for fractured hip and after elective hip replacement. There is evidence that the prophylactic effect of aspirin may be greater in male patients. Aspirin reduced the frequency of arteriovenous shunt thrombosis. Aspirin abolished symptoms in patients with peripheral ischemia associated with thrombocytosis and spontaneous platelet aggregation. There is no conclusive evidence at the present time that aspirin is effective in patients with coronary artery artery disease. Dipyridamole in combination with oral anticoagulants is effective in reducing the frequency of systemic embolism in patients with prosthetic heart valve replacement but is ineffective in patients with transient cerebral ischemic attacks or for the prevention of venous thromboembolism. Hydroxychloroquine was effective in reducing postoperative venous thrombosis in patients undergoing general abdominothoracic surgery but the evidence that it was effective in patients undergoing orthopaedic surgery is inconclusive. Sulphinpyrazone may be effective in reducing the frequency of sudden cardiac deaths in patients in the first year after myocardial infarction when it is started within 25 to 35 days after the infarction. Sulphinpyrazone reduced the incidence of arteriovenous shunt thrombosis in patients undergoing chronic hemodialysis and in combination with anticoagulants, it reduced the frequency of recurrent venous thrombosis. There have been no large scale trials of platelet suppressant drugs in clinical cancer and successful treatment of thromboembolic disorders cannot be used to predict success in the treatment of malignant disease.
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PMID:Antithrombotic effects of drugs which suppress platelet function: their potential in prevention growth of tumour cells. 705 Oct 35

Fifty consecutive patients with thrombocythemia (35 men and 15 women) were diagnosed as primary thrombocythemia (PT) in 30 and thrombocythemia associated with polycythemia vera (PV) in 20. The symptoms were platelet-mediated erythromelalgia in 16 PT and 15 PV, coronary artery disease in 3 PT and 2 PV, atypical cerebral ischemic attacks in 8 PT and 3 PV, paradoxical thrombosis and bleeding in 3 PT and 2 PV and hemorrhages alone in 6 PT and 2 PV patients. Erythromelalgia was localized in the forefoot sole and toes in 28, the fingertips in 9, the handpalm in 2. Untreated erythromelalgia progressed to acrocyanosis or peripheral ischemia with necrosis in a toe or fingertip in 14 cases. Painful red, warm and indurated erythromelalgic hot spots in the skin of the upper legs were misdiagnosed as superficial thrombophelebitis in 5 PT and 2 PV patients. Erythromelalgia in thrombocythemia already occurred at slightly increased platelet counts above 400 x 10(9)/l. The curative effect of aspirin on erythromelalgia in thrombocythemia was consistently accompanied by a significant increase of platelet counts. Erythromelalgia and bleeding paradoxically occurred in 5 patients at platelet counts between 1000 and 2000 x 10(9)/l. In this situation aspirin prevents erythromelalgic and microcirculatory circulation disturbances, but further increases the risk of serious bleeding complications. Presenting hemorrhagic manifestations in thrombocythemia were observed at platelet counts in excess of 1000 x 10(9)/l in 9 PT and 4 PV patients as severe epistaxis in 5, atypical ecchymoses in 3, gastrointestinal bleeding in 2 and secondary bleeding in 3. The concept of platelet-mediated erythromelalgia, thrombosis and hemorrhages in thrombocythemia is discussed.
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PMID:Erythromelalgic, thrombotic and hemorrhagic manifestations in 50 cases of thrombocythemia. 895 72

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

The vascular complications in patients with polycythemia vera are microvascular circulatory disturbances typical of thrombocythemia including erythromelalgia, peripheral ischemia, atypical cerebral ischemic attacks, and major arterial and venous thrombotic events. These are positively related to hematocrits due to the increased red cell mass and its concomitant increased whole blood viscosity. Phlebotomy does not prevent the aspirin-responsive microcirculatory circulation disturbances in polycythemia vera because thrombocythemia (platelet count > 400 x 10(9)/L) persists. The risk of major vascular ischemic episodes in poorly controlled polycythemia vera at hematocrits between 0.45 and 0.50 is rather high. The risk of vascular complications in polycythemia vera is best controlled by maintaining the hematocrit at less than 0.45 and the platelet count below 400 x 10(9)/L. The microvascular syndrome associated with thrombocythemia in early stage polycythemia vera in remission by phlebotomy is easily and best controlled by low-dose aspirin (50 to 100 mg) or by selective reduction of platelet count to normal with low-dose myelosuppressive agents. The potential leukemogenic myelosuppressive agents busulfan and hydroxyurea and the nonleukemogenic cytosine interferon-alpha have proven to be effective in the control of the proliferative phase of polycythemia vera. However, data on the natural history of polycythemia vera and the best treatment modality of the various stages of myeloproliferative disease are still lacking.
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PMID:Erythromelalgia and vascular complications in polycythemia vera. 938 3

Vascular tone control is essential in blood pressure regulation, shock, ischemia-reperfusion, inflammation, vessel injury/repair, wound healing, temperature regulation, digestion, exercise physiology, and metabolism. Here we show that a well-known growth factor, FGF2, long thought to be involved in many developmental and homeostatic processes, including growth of the tissue layers of vessel walls, functions in vascular tone control. Fgf2 knockout mice are morphologically normal and display decreased vascular smooth muscle contractility, low blood pressure and thrombocytosis. Following intra-arterial mechanical injury, FGF2-deficient vessels undergo a normal hyperplastic response. These results force us to reconsider the function of FGF2 in vascular development and homeostasis in terms of vascular tone control.
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PMID:Fibroblast growth factor 2 control of vascular tone. 946 Nov 94

Postsplenectomy thrombocytosis is a well recognised complication about which there is little published information. Therefore, postoperative complications of this effect have not been emphasised. An experience with a case of superior mesenteric artery thrombosis and small intestinal ischemia following splenectomy is reported. We reviewed the literature, but we wasn't able to find any case, whereas the association between splenectomy and mesenteric or portal vein thrombosis is well known. Pathogenesis of postsplenectomy thrombocytosis is poorly understood. Theories to explain it include removal of the splenic sequestration effect or removal of a regulatory humoral factor produced by the spleen. Both mechanisms could be operative at the same time, explaining the observation that some patients develop thrombocytosis related complications soon after surgery, while others after a longer time. The literature on the thromboembolic risk of postsplenectomy thrombocytosis is inconclusive and no studies have established whether patients with thrombocytosis following splenectomy should be treated with anticoagulants or antiplatelet medications in order to prevent thrombotic complications. Certainly, a recommendation for the routine use of these drugs cannot be made on the basis of one observation, but the need for controlled studies must be stressed.
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PMID:[Massive thrombosis of the superior mesenteric artery following splenectomy. A coincidence?]. 1047 65

We present five patients with serious ischemia of the fingers caused by intra-arterial injection injury, trauma, rheumatoid arthritis, chronic myeloid leukemia with thrombocytosis and thoracic-outlet syndrome. The treatment consisted of thrombectomy and intra-arterial lysis if possible and intra-arterial infusion of 80 microg PGE1/24 h in combination with 25,000 U of heparin/24 h for 6-10 days. PGE1 and heparin were administered through a 3-F catheter introduced surgically into a forearm artery. In three cases a complete remission was possible, in the other two cases the therapy led to significant improvement. No side effects or complications were noticed.
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PMID:[Experience with the therapy of acute finger ischemia by high-dose intra-arterial infusion of PGE1 through a surgically introduced catheter]. 1055 Mar 45


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