Cases reported "Hyperhomocysteinemia"

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1/27. Hyperhomocysteinaemia and upper extremity deep venous thrombosis: a case report.

    A case is presented of a 24 yr old military aircrew applicant who developed a right axillary subclavian deep venous thrombosis following physical exertion. Investigations revealed damage to the right axillary subclavian venous system and limitation to flow. Coagulation studies also showed an elevated plasma homocysteine level. hyperhomocysteinemia has recently been recognized as a risk factor for venous thromboembolic disease. Damage caused by the thrombosis, the hyperhomocysteinemia and environmental factors encountered in flight, may predispose him to recurrent episodes of thrombosis. This complex case involves aspects of hematology and the nature of coagulation which are only just being elucidated and as yet are poorly understood, and highlights some serious aeromedical implications for pilots afflicted with these conditions.
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ranking = 1
keywords = venous thrombosis, deep
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2/27. hyperhomocysteinemia as a cause of superior vena cava syndrome.

    A case is presented in which superior vena cava (SVC) syndrome was caused by a stenosis of the SVC due to thrombosis. hyperhomocysteinemia was diagnosed as a possible underlying mechanism. The role of hyperhomocysteinemia as a risk factor for the development of recurrent venous thrombosis, its diagnosis, and treatment are discussed.
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ranking = 0.19928718689126
keywords = venous thrombosis
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3/27. Familial thrombophilia associated with homozygosity for the cystathionine beta-synthase 833T-->C mutation.

    Severe hyperhomocysteinemia due to cystathionine beta-synthase (CBS) deficiency is a strong risk factor for premature cardiovascular disease. Among untreated patients, approximately 50% have suffered a thromboembolic event by 30 years of age. We report on 3 sisters with severe hyperhomocysteinemia due to homozygosity for the CBS 833T-->C mutation. These patients, who displayed no other known thrombophilic predisposition, had suffered single or multiple venous thrombosis before CBS deficiency was diagnosed relatively late in life. In this family, homozygosity for the 833T-->C mutation was associated with a mild phenotype with respect to other sequelae of CBS deficiency. Consequently, our results indicate that most cases with this genotype may remain undiagnosed. Investigated family members heterozygous for the 833T-->C mutation displayed normal total homocysteine in plasma (tHcy) levels, even when they were homozygous for the methylenetetrahydrofolate reductase 677C-->T polymorphism. The prevalence of homozygosity for the 833T-->C mutation has previously been estimated at no less than 1:20 500 in our population. Because a reduction of the severely elevated levels of tHcy in CBS deficiency reduces cardiovascular risk and because homozygosity for the 833T-->C mutation is more prevalent than previously thought, our results emphasize the importance of measuring tHcy routinely in thrombophilia screening.
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ranking = 0.19928718689126
keywords = venous thrombosis
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4/27. Acute renal vein thrombosis, oral contraceptive use, and hyperhomocysteinemia.

    Oral contraceptive use and hyperhomocysteinemia are considered to be relatively weak risk factors for venous thromboembolism. We report a case of acute renal vein thrombosis, a rare and aggressive form of thromboembolism, that occurred in a 21-year-old woman taking oral contraceptives, who was subsequently found to have marked hyperhomocysteinemia. This case suggests that the oral contraceptive and hyperhomocysteinemia may interact in a synergistic manner in the pathogenesis of thrombosis. In oral contraceptive users who develop venous thrombosis in the absence of other risk factors, clinicians should consider investigations for an underlying prothrombotic biochemical disorder.
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ranking = 0.57740448994164
keywords = venous thrombosis, vein thrombosis, vein
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5/27. Extensive deep vein thrombosis in a young woman. Case report.

    We report a case of a young lady with an extensive deep vein thrombosis (DVT) diagnosed by CT scan and duplex ultrasound examination. Contributory factors were relative immobilisation, oral contraception and hyperhomocysteinemia after methionine loading. No other thrombophilic factors could be found. The three main causes of hyperhomocysteinemia are genetic defects, nutritional deficiencies and insufficient elimination. In our case a genetic defect for one of the key enzymes of homocysteine metabolism, may be the underlying cause. Besides stopping oral contraceptive drugs, anticoagulation and supplementation with pyridoxine and folate was started. family screening was carried out and revealed other members with hyperhomocysteinemia. Whether therapy with pyridoxine and folate can substantially reduce the recurrence of venous thromboembolic disease remains to be established.
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ranking = 4.9623765364512
keywords = deep vein thrombosis, deep vein, vein thrombosis, vein, deep
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6/27. menorrhagia and adenomyosis in a patient with hyperhomocysteinemia, recurrent pelvic vein thromboses and extensive uterine collateral circulation treatment by supracervical hysterectomy.

    A 37-year-old patient had recurring thromboses, occlusion of the left femoral vein with hereditary hyperhomocysteinemia, hypermenorrhea and anaemia. Conservative therapy with endometrium ablation and gestagene failed. A supracervical hysterectomy was done to preserve the presacral and left lateral, dorsal and caudal collaterals beside the uterus, and prevent a postoperative congestion, especially of the left leg.
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ranking = 0.011493176318603
keywords = vein
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7/27. Extensive cerebral venous thrombosis associated with moderate hyperhomocyst(e)inemia and successfully treated with thrombolysis.

    Cerebral venous thrombosis (CVT) is a relatively rare condition caused by multiple etiologies, usually secondary to hypercoagulable states. The optimal treatment is controversial, especially in the presence of hemorrhagic infarcts. We describe an unusual patient with extensive CVT associated with moderate hyperhomocyst(e)inemia who was aggressively treated with chemical and mechanical thrombolysis with an excellent outcome.
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ranking = 0.9964359344563
keywords = venous thrombosis
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8/27. Cutaneous necrosis revealing the coexistence of an antiphospholipid syndrome with acquired protein s deficiency, factor v Leiden and hyperhomocysteinemia.

    We report an exceptional case of cutaneous necrosis due to the coexistence of 4 thrombophilic factors, inherited and acquired. We would like to draw attention to these unrecognized associations. CASE REPORT: A 72-year-old woman was admitted with a 5 month history of necrotic nonhealing, painful ulcer of both legs and recently a purple toe. She had a history of 3 deep venous thromboses of the leg complicated by pulmonary embolism. A skin biopsy of the ulcer and purple toe showed only thrombosis in the dermal vessel. Laboratory findings showed a circulating lupus anticoagulant, positive anticardiolipin antibodies, antinuclear antibodies (1/320 dilution) and an anti Sm. Moreover, activated protein c resistance associated with factor v Leiden mutation and hyperhomocysteinemia was found; protein S was transiently low. With iloprost, oral anticoagulant, vitamin B12 and folic acid, the evolution was good, with healing of ulcer. COMMENTS: cutaneous necrosis can reveal hypercoagulable states, sometimes complex. We find 4 thrombophilic factors in our case, i.e. antiphospholipid antibodies, factor v Leiden, protein s deficiency and hyperhomocysteinemia. This is exceptional but highlights the role of several constitutional and acquired thrombophilic factors in the genesis of thrombosis. Extended protein C pathway disturbances could explain the mechanism that leads to cutaneous necrosis, in this patient, with an antiphospholipid syndrome. This case shows that it is necessary in some circumstances to make a complete hemostatic laboratory search to detect several thrombophilic factors. If they are present they can justify an oral anticoagulant treatment and a familial screening.
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ranking = 0.00071281310874004
keywords = deep
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9/27. Recurrent leg ulcers in a young man with hyperhomocysteinemia, factor v Leiden and impaired fibrinolysis.

    We present a young male patient referred to our hospital with leg ulcers on both legs that were more than 3 years refractory to standard treatment with compression therapy. By thrombophilia screening factor v Leiden mutation, hyperhomocysteinemia and evidence for impaired fibrinolysis were found. Treatment with folic acid in combination with long-term oral anticoagulant therapy was added to non-elastic compression therapy. The leg ulcers showed slow improvement and complete healing within 3 years. During a 6-year follow-up period neither new thrombo-embolic events occurred nor recurrence of ulcerations. This case suggests a potential synergistic pathogenic role of factor v Leiden, hyperhomocysteinemia and impaired fibrinolysis in the development of postthrombotic syndrome and his sequelae. We postulate that increased formation of thrombi in the microcirculation of the skin in combination with ambulatory venous hypertension due to recurrent deep venous thrombosis might explain our observation.
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ranking = 0.2
keywords = venous thrombosis, deep
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10/27. Cerebral vein thrombosis and mild hyperhomocysteinemia: three new cases.

    Mild hyperhomocysteinemia is an established risk factor for deep vein thrombosis. We report three patients with cerebral vein thrombosis (CVT) in which the only risk factor we were able to identify was increased blood homocysteine levels and the C677T polymorphism in both alleles of the methylene tetrahydrofolate reductase MTHFR gene. We suggest that hyperhomocysteinemia should also be a risk factor for CVT. Since this condition can be effectively and safely corrected by drugs, we suggest that homocysteine levels should be routinely determined in patients with idiopatic CVT, and even mildly increased levels corrected pharmacologically, in the hope of reducing the risks associated with this condition.
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ranking = 1.3705926103406
keywords = deep vein thrombosis, deep vein, vein thrombosis, vein, deep
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