Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate the effects of recombinant human erythropoietin (rh-EPO) in patients with cancer-related anaemia. Thirty-six ambulatory patients who had malignant neoplasms and haemoglobin (Hb) values of < 11 g/dl (Pretoria is 1,310 m above sea level) entered the study. Patients with renal insufficiency or anaemia caused by bleeding or haemolysis, and patients with iron deficiency or megaloblastic anaemia, were not entered in the study. 22 IU/kg rh-EPO was given subcutaneously 3 times/week. The dose was escalated if Hb values did not rise after 4 weeks. All 36 patients were evaluable for toxicity. Side effects ascribed to rh-EPO were pain or discomfort at the site of injection (12 patients), heart palpitations (3 patients), skin rash (2 patients) and hypertension, deep vein thrombosis, and myalgia in 1 patient each. Thirty of the 36 patients who entered the study were evaluable for response. There were 16 females and 14 males among the evaluable patients. Median age was 64.5 years. Response, defined as an increase of Hb of at least 2 g/dl or to 12.5 g/dl, for at least 1 month, was documented in 12 patients. This was accompanied by an improvement in performance status and occurred within 1 month in 5 of the 12 patients who responded. rh-EPO has a limited but measurable therapeutic value for patients with cancer-associated anaemia.
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PMID:Recombinant human erythropoietin in the treatment of cancer-related anaemia. 797 Apr 93

We describe a 30-year-old male who presented with acute onset of breathlessness, tachycardia, and palpitations associated with distension of jugular vein and clear lungs on physical examination. The chest X-ray was normal and ECG was showing S1Q3T3 and right ventricular strain pattern. His 2-D echocardiography was showing dilated right atrium, right ventricular dilatation and moderate pulmonary arterial hypertension. He was found to have thrombosis involving left side of deep venous system with normal superficial venous system (Doppler proved). All routine blood investigations for etiology of recurrent DVT were normal except serum homocyteine level, which was significantly raised. Megaloblastic anemia on peripheral smear and hyperhomocysteinemia prompted us to search for its cause, which was subsequently found to be vitamin B12 deficiency. Such an association of megaloblastic anemia due to vitamin B12 deficiency leading to hyperhomocysteinemia and subsequent thrombosis in left venous system presenting as acute pulmonary embolism has not been described earlier in the medical literature.
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PMID:Hyperhomocysteinemia masquerading as pulmonary embolism. 1471 Sep 83

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

Vitamin B12 deficiency may be induced by long-term use of metformin, which may in turn lead to hyperhomocysteinemia. Thus, hyperhomocysteinemia may increase the risk of vascular thrombosis in diabetic patients, when metformin is used and a homozygous methylenetetrahydrofolate reductase (MTHFR) C677T mutation is present. We report a 65-year-old Taiwanese diabetic woman who was treated with metformin for 6 years and who had suffered from swelling of the left lower extremity for 3 months. Ascending venography confirmed the diagnosis of proximal deep vein thrombosis, while hyperhomocysteinemia, megaloblastic anemia caused by vitamin B12 deficiency, and a homozygous C677T mutation of the MTHFR gene were also found. She had no identifiable venous thrombotic risk factors other than hyperhomocysteinemia, which seemed to be caused by both MTHFR C677T homozygous mutation and vitamin B12 deficiency. With the substitution of insulin injection for metformin, short-term supplement of vitamin B12, and anticoagulant therapy for the deep vein thrombosis, her anemia and hyperhomocysteinemia recovered rapidly. The deep vein thrombosis also responded well. Our findings highly suggested the role of metformin in causing vitamin B12 deficiency, which may serve as an additional risk factor for venous thrombosis in diabetic patients. Our report also highlights the need to check vitamin B12 levels during metformin treatment.
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PMID:Hyperhomocysteinemia, deep vein thrombosis and vitamin B12 deficiency in a metformin-treated diabetic patient. 1858 23