Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.69 (APC)
 16,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The identification of constitutional and/or acquired risk factor is of major importance in the treatment of thromboembolic disease in young people; it contributes to evaluate the risk of recurrence and to define the period of oral prophylactic anticoagulant treatment. Several congenital or acquired abnormalities of haemostasis are actually defined. In this paper, we report the case of a 34-year-old man who developed a deep venous thrombosis, five months before the diagnosis of megaloblastic anemia, probably due to pernicious anemia. The thrombosis was partially explained by the acquired hyperhomocysteinemia induced by vitamin B12 deficiency. Moreover, activated protein C resistance due to factor V Leiden, was revealed in our patient. This latter improved under anticoagulant treatment combined with vitamin B12. Combination in one individual, of different risk factors predisposing to inherited and/or acquired thrombophilia, results in increased risk for thrombo-embolic disease, suggesting synergic interaction between these factors.
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PMID:[Association of tow thrombotic risk factors: factor V Leiden and hyperhomocysteinemia. A case report]. 1670 35

We report three male patients of younger age group presented with acute vein thrombosis of different sites, right lower limb, cortical venous sinuses thrombosis with cerebral vascular accident and third case is mesenteric vein thrombosis. All patients were Vegetarian, had low level of cobalamin with marked hyper homocysteinemia with normal serum and red cell folic acid. The low Cobalamin level was not suspected secondary to pernicious anemia, based on the fact that there was no evidence of atrophic gastritis and an absence of antiparietal cell antibodies. There were no evident of immobilization, recent surgery, malignancy, antiphospholipid antibody, myeloproliferative disorder, and hormone replacement therapy. No deficiencies in protein C, protein S, or antithrombin III, normal factor V Leiden, no prothrombin gene mutation 20210A and no clone for paroxysmal nocturnal hemoglobin-urea were detected, no cause was found for the thrombosis apart from their secondary hyperhomocysteinemia.
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PMID:Three different presentation of same pathophysiology. 2332 77