Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low molecular weight heparins are well established in the prophylaxis of deep vein thrombosis in patients with general surgery, in high risk patients undergoing elective hip surgery or emergency surgery and also in patients with an enhanced risk of thrombosis who are treated in medical wards. There are, however, many possibilities for improving prophylaxis and treatment with LMWH. The mechanisms by which low molecular weight heparins and also unfractionated heparin inhibit thrombus formation are not fully understood. The inhibition of thrombin formation and local effects at the endothelial level may be more important than antithrombin-III mediated effects on factor IIa and on factor Xa. For most low molecular weight heparins the most effective dose regimens to be used in patients at high risk have not yet been established. Low molecular weight heparins may be more effective in the treatment of deep venous thrombosis than unfractionated heparin. In the therapeutic studies published so far the major intention was to show that low molecular weight heparins can prevent the progression of deep venous thrombosis and pulmonary embolism to the same extent as unfractionated heparin. Extended treatment regimens, however, may lead to a relevant thrombus reduction. Outpatient treatment for a longer period of time with results not far from those obtained with thrombolysis seem possible especially in elderly patients. Low molecular weight heparins in their present form or modified low molecular weight heparins may be useful for long-term treatment of patients with atherosclerosis with the aim of regression of atherosclerotic lesions. New forms of application, e.g. inhalation, may render long-term treatment more feasible.
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PMID:Low molecular weight heparins--state-of-the-art and unsolved issues. 818 Mar 24

Nineteen patients (age 60 +/- 14) with amaurosis fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of amaurosis fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent amaurosis fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acid-vitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for > or = 1 year on therapy, without adverse treatment side effects. When amaurosis fugax occurs without carotid artery atherosclerosis or other known causes, thrombophilia or hypofibrinolysis, or both are nearly universal, safely treatable, reversible pathoetiologies.
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PMID:Amaurosis fugax caused by heritable thrombophilia-hypofibrinolysis in cases without carotid atherosclerosis: thromboprophylaxis prevents subsequent transient monocular partial blindness. 1745 20