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

Heparin remains the most effective antithrombotic drug. It acts by combining with plasma antithrombin, thereby accelerating the neurtalisation of thrombin and other acitvated coagulation factors. Full-dose intravenous heparin is indicated in all cases of pulmonary embolism and established deep venous thrombosis, unless there exist compelling contraindications. Continuous intravenous infusion of heparin appears to be safer than intermittent injection. Low-dose subcutaneous heparin is effective in preventing the initial occurrence of thigh vein thrombi and in reducing the incidence of fatal pulmonary embolism in general surgical patients over the age of 40. The efficacy of low-dose heparin in preventing pulmonary emboli following hip surgery has not been established. The incidence of severe heparin-induced thrombocytopenia appears to be rising. Platelet counts should be performed in all patients receiving heparin by any mode of administration.
 ...
PMID:Heparin Therapy: regimens and management. 31 90

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
 ...
PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

Nadroparin calcium is a low molecular weight heparin with a mean molecular weight of 4.5 kD. Compared with unfractionated heparin, nadroparin calcium has a greater ratio of anti-factor Xa/anti-factor IIa activity. Nadroparin calcium has a longer half-life and greater bioavailability than unfractionated heparin and can be administered by subcutaneous injection once daily for prophylaxis and twice daily for treatment. In clinical trials, nadroparin calcium has been shown to be at least as effective as unfractionated heparin in preventing deep venous thrombosis (DVT) after various surgical procedures including major orthopaedic and abdominal surgery, and in maintaining the patency of the extracorporeal circulation in adults and children undergoing haemodialysis. Nadroparin calcium is well tolerated, the most common adverse event associated with its use being the development of minor haematoma at the operative incision site. In postmarketing surveillance data to date, the incidence of major haemorrhage related to nadroparin calcium use has been very low (< 1%). Nadroparin calcium has also been associated with a very low incidence of thrombocytopenia (< 0.001%). Thus, nadroparin calcium is an effective alternative to unfractionated heparin in the prophylaxis or treatment of thromboembolic venous events, with the advantages of more convenient administration and a lower incidence of thrombocytopenia.
 ...
PMID:Nadroparin calcium. A review of its pharmacology and clinical applications in the prevention and treatment of thromboembolic disorders. 128 May 70

Low molecular weight heparins are increasingly prescribed in France. Prepared from standard heparin by depolymerisation, they show a markedly decreased anti IIa activity and a anti Xa/anti IIa ratio ranging from 2 to 4. Their mode of action in the coagulation system is still not well known and it is difficult to explain the mechanism of their antithrombotic effect, demonstrated in vivo. They seem to inhibit the first traces of thrombin and then counteract the priming and amplification of coagulation. Their fibrinolytic activity is also a disputed question, but seems to be lower than that of standard heparin. The pharmacological studies show a venous as well as arterial antithrombotic activity of a low molecular weight heparin on several animal models, a lower but not negligible bleeding risk as compared to unfractionated heparin. Furthermore heparin fragments have a weak interaction with platelets, which allow to foresee a greater efficacy of LMWH than standard heparin in arterial thrombosis. Some very rare cases of thrombocytopenia in patients treated with LMW heparins have been recently reported. The compared pharmacokinetics of heparins gave proof of a renal elimination of low molecular weight heparin and a bio availability of about 90% after subcutaneous injection. Many clinical studies allowed to define indications of heparin fragments in prophylactic treatment after surgery as well as in medical patients and in curative treatment in case of deep vein thrombosis. However, others studies must be carried out to define the real efficacy of such a treatment during pulmonary embolism, disseminated intravascular coagulation and myocardial infraction, or during thrombotic complications after vascular surgery.
 ...
PMID:[The new heparins]. 131 47

Heparin-associated thrombocytopenia (HAT) type II, a severe side effect of heparin therapy, is thought to be induced by an immunological mechanism. By crossreactivity studies we have demonstrated that sera of patients with HAT type II activate platelets in vitro not only after the addition of heparin but also after addition of a chemically polysulphated chondroitin-like substance, Arteparon, used for treatment of degenerative joint disease. In addition here, we describe a patient who developed deep venous thrombosis and pulmonary embolism following administration of Arteparon and typical HAT type II with thrombocytopenia, 36 h after the first administration of heparin. This patient had never received heparin, but had repeatedly been treated with Arteparon for degenerative joint disease. We conclude that this patient had been presensitized by Arteparon, as indicated by his clinical course. In vitro studies again confirm crossreactivity between heparin and Arteparon.
 ...
PMID:Heparin-associated thrombocytopenia in a patient treated with polysulphated chondroitin sulphate: evidence for immunological crossreactivity between heparin and polysulphated glycosaminoglycan. 138 26

An unusually prolonged case of heparin-induced severe thrombocytopenia and decompensated disseminated intravascular coagulation (DIC) is described. The patient, treated with heparin at a dosage of 25,000 units/day for 3 days and 12,500 units/day for an additional 4 days because of a clinically suspected deep venous thrombosis, developed (4 days after the discontinuation of heparin) a clinical and laboratory picture of severe DIC, manifested by subcutaneous hematomas and ecchymoses. Platelet count was 24 x 10(9)/l, fibrinogen level 89 mg/dl and fibrin-degradation products between 3,200 to 6,400 ng/ml. A thorough laboratory and instrumental evaluation failed to demonstrate any underlying disorder. No heparin-dependent aggregating factor was detected in the serum of the patient. The patient recovered spontaneously. Whereas fibrinogen and fibrin-degradation products reverted to normality within four weeks, platelet count normalization was delayed until the sixth week after heparin discontinuation.
 ...
PMID:An unusually prolonged case of heparin-induced thrombocytopenia and disseminated intravascular coagulation. 139 4

Antiphospholipid syndrome (APS) is an entity characterized by recurrent thrombotic events and may occur spontaneously or in the context of systemic lupus erythematosus (SLE). We describe an English Canadian family in whom the propositus, a woman with Graves' disease and SLE, was found to have a lupus anticoagulant and anticardiolipin antibody (aCL). A brother with deep vein thrombosis, pulmonary emboli, bilateral adrenal hemorrhage and thrombocytopenia, circulating anticoagulant and aCL had a positive antinuclear antibody and Coombs' test, but no other features of SLE. Fourteen members of 3 generations of this family underwent clinical assessments, serological testing and HLA typing. The propositus' mother had a family history of autoimmune thyroid disease and the father had aCL, but was asymptomatic. The thyroid disease and the SLE were associated with HLA-B8, DR3 haplotype. The aCL and the anticoagulant were associated with HLA-B60, DR4 haplotype. Both these haplotypes were present in the propositus. Among the other 4 carriers of the haplotype B60, DR4, 3 demonstrated significant titers of aCL. Our findings support the reported association between APS and the HLA haplotype DR4 in patients of English descent with SLE.
 ...
PMID:A family study of the antiphospholipid syndrome associated with other autoimmune diseases. 143 7

The frequency of thromboembolic complications in burn patients has been estimated to range from 0.4% to 7%. The clinical significance of these events is often debated and has prompted some centers to adopt the routine prophylactic use of low dose heparin prophylaxis. A 10 year review of 2,103 burn patients treated at this institution was undertaken. Twenty-five (1.2%) patients, with a mean age of 40.0 years and an average burn size of 49.3% total body surface area (TBSA), were identified as having significant pulmonary thromboembolism (PTE). In only 3 (0.14%) patients was the thromboembolism considered to be a cause of death. Nineteen (0.9%) patients, with an average age of 36.7 years and a mean burn size of 48.3% TBSA, developed clinically evident deep venous thrombosis (DVT); however, in only 1 (0.05%) patient did the disease progress to fatal PTE. A review of the literature reveals a 0.6% to 5% incidence of complications related to low dose heparin therapy which includes bleeding, thrombocytopenia, and arterial thrombosis. We feel that the infrequency of clinically significant PTE and DVT in burn patients and the comparable or greater rate of complications associated with heparin prophylaxis mitigate against the routine use of low dose heparin therapy except in patients at high risk for these events.
 ...
PMID:Thromboembolic complications in thermally injured patients. 145 88

We describe a case of thrombocytopenia and deep venous thrombosis in a boy who received heparin to maintain patency of a central venous catheter. Measurement of the release of serotonin labeled with carbon 14 confirmed the presence of heparin-induced thrombocytopenia. Children receiving heparin therapy should be monitored for the possibility of heparin-induced thrombocytopenia.
 ...
PMID:Heparin-induced thrombocytopenia in a child. 846 23

A previously healthy 16-year-old girl complaining of fever, hemosputum, chest pain and dyspnea was hospitalized. On admission, physical examination revealed mental confusion, holosystolic heart murmur, and swelling of the left foot. Laboratory investigations showed anemia, leukocytosis, thrombocytopenia, activation of inflammatory reactions, prolongation of PT and APTT, and hypoxia. Antinuclear antibody test was negative. There were no other findings suggestive of collagen diseases such as SLE. Chest X-ray showed consolidation in the left lower lung field and pleural effusion. Echocardiography disclosed a mass lesion in the left atrium in contact with the mitral valve, and mitral regurgitation. No findings indicative of an infectious etiology were present. The patient rapidly improved with high dose corticosteroid and anticoagulant therapy. A venogram of the lower extremity disclosed deep venous thrombosis. A lung ventilation-perfusion scan revealed multiple pulmonary thromboemboli. Elevation of anticardiolipin antibody was noted. Based on these findings, the diagnosis of primary antiphospholipid syndrome was made. Further administration of steroid and anticoagulant resulted in decrease of the titer of anticardiolipin antibody. This is the second report of primary antiphospholipid syndrome in Japan. The clinical significance of this disease is also discussed.
 ...
PMID:[A case of primary antiphospholipid syndrome with fever, pulmonary thromboembolism and endocardial lesion]. 162 84


1 2 3 4 5 6 7 8 9 10 Next >>