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)

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.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

Inflammation often is considered a contributing factor to both thrombosis and disseminated intravascular coagulation. The molecular mechanisms that dictate which of these clinical manifestations will result from the inflammatory stimulus remain obscure. Bacterial infection and certain tumors are common initiators of the disseminated intravascular coagulant response. Complement activation resulting from bacterial infection shares with selected tumors the capacity to generate or release membrane particles that lack functional adhesion receptors and hence could circulate to amplify a disseminated intravascular coagulant response. We developed a model of venous thrombosis that resulted in localized thrombus formation without disseminated intravascular coagulation. The model involves infusion of tumor necrosis factor, blockade of protein C and a partial decrease in venous flow caused by ligation of the superficial femoral vein without obstruction of the deep formal vein. Infusion of phospholipid vesicles into this model resulted in amplification of a localized thrombotic response into a consumptive response. Seven different groups of animals were studied. The first three groups established the conditions necessary to produce deep vein thrombosis. The second four groups established the conditions necessary to produce disseminated intravascular coagulation. The infusion of phospholipid vesicles plus tumor necrosis factor and anti-protein C antibody resulted in consumption of fibrinogen, the production of thrombin/antithrombin complexes, a fall in platelet count, and venous thrombosis. Without ligation and catheterization phospholipid vesicles failed to produce the consumptive response. We conclude, therefore, that phospholipid vesicles can amplify a local thrombotic response into a consumptive response, and that vesiculation accompanying inflammation is one means by which localized coagulant activity may be amplified to produce disseminated intravascular coagulation.
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PMID:Infusion of phospholipid vesicles amplifies the local thrombotic response to TNF and anti-protein C into a consumptive response. 874 82

We here describe a case of multiple pyomyositis in a 62-year-old man who had systemic chemotherapy for recurrent lung cancer. His initial symptoms consisted of fever and general fatigue, followed by progressive pain and swelling in his extremities, which mimicked deep venous thrombosis along with bacterial infection. He was admitted to the hospital for intravenous administration of antibiotics. MRI appeared very useful to find the intramuscular fluid collections with circumferential inflammatory changes, which confirmed diagnosis of the multiple pyomyositis. Surgical drainage as well as intravenous administration of antibiotics worked very well and improved clinical symptoms in a few weeks after the treatments. He could resume normal activities with minimum functional impairments in the extremities. Pyomyositis should be kept in mind as one of the adverse effects after chemotherapy for malignant tumors.
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PMID:[A case of multiple pyomyositis after chemotherapy for lung cancer]. 1677 Jan 9

Neuroleptic malignant syndrome (NMS) is a physiologic phenomenon that has been associated with the use of both first- and second-generation antipsychotics resultant to their ability to block dopamine blockade in the basal ganglia and hypothalamic regions of the brain. The typical reaction involves the presentation of muscle rigidity, changes in mental status, temperature elevation, labile blood pressure, and elevations in creatinine kinase and white blood cell counts. The reaction is most often reported early in the course of therapy but is well documented to have the potential to occur at any point in time. Untreated NMS can be fatal, often from secondary causes such as deep venous thrombosis and pulmonary embolism. Treatment involves immediate discontinuation of the offending agent, supportive therapy of clinical symptoms, and may include the use of the skeletal muscle relaxant, dantrolene sodium, or the dopaminergic agents bromocriptine or amantadine. In this case, we present a patient who developed symptoms of NMS during the cross-taper and conversion from quetiapine to clozapine. The patient was treated for NMS; however, his clinical diagnosis was never able to be definitively determined as he was initially evaluated for septicemia and later treated for suspected bacterial infection with antibiotics, and clozapine-associated side effects cannot be ruled-out as a contributing source to the clinical presentation. The estimated Naranjo Scale score for this case report is 3.
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PMID:Suspected neuroleptic malignant syndrome during quetiapine-clozapine cross-titration. 2150 95

Thrombophlebitis of the portal venous system (PVS) with superimposed bacterial infection (septic pylephlebitis) is an extremely rare complication of Crohn's disease (CD), and therefore diagnosis of septic pylephlebitis is difficult without high clinical suspicion. A 16-year old male patient who was diagnosed with CD 3 months earlier was admitted with recurrent fever and abdominal pain. CD activity had been well controlled with conventional medical treatment during a follow-up period. Abdominal contrast-enhanced computed tomography showed massive thrombosis in the PVS without evidence of intra-abdominal infection, and blood cultures were positive for Streptococcus viridians. There was no evidence of deep vein thrombosis or pulmonary thromboembolism, and all laboratory tests for thrombophilia were normal. Based on these findings, the patient was diagnosed with septic pylephlebitis complicated with CD, and was successfully treated with intravenous antibiotic therapy combined with anticoagulation. This case suggests that early comprehensive evaluation is crucial for immediate diagnosis and proper treatment of septic pylephlebitis in patients with CD who present with fever and abdominal pain of unknown origin, even with stable disease activity and absence of other intra-abdominal infections.
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PMID:Septic pylephlebitis as a rare complication of Crohn's disease. 2362 37

Neutrophils, early mediators of the innate immune defense, are recruited to developing thrombi in different types of thrombosis. They amplify intravascular coagulation by stimulating the tissue factor-dependent extrinsic pathway via inactivation of endogenous anticoagulants, enhancing factor XII activation or decreasing plasmin generation. Neutrophil-dependent prothrombotic mechanisms are supported by the externalization of decondensed nucleosomes and granule proteins that together form neutrophil extracellular traps. These traps, either in intact or fragmented form, are causally involved in various forms of experimental thrombosis as first indicated by their role in the enhancement of both microvascular thrombosis during bacterial infection and carotid artery thrombosis. Neutrophil extracellular traps can be induced by interactions of neutrophils with activated platelets; vice versa, these traps enhance adhesion of platelets via von Willebrand factor. Neutrophil-induced microvascular thrombus formation can restrict the dissemination and survival of blood-borne bacteria and thereby sustain intravascular immunity. Dysregulation of this innate immune pathway may support sepsis-associated coagulopathies. Notably, neutrophils and extracellular nucleosomes, together with platelets, critically promote fibrin formation during flow restriction-induced deep vein thrombosis. Neutrophil extracellular traps/extracellular nucleosomes are increased in thrombi and in the blood of patients with different vaso-occlusive pathologies and could be therapeutically targeted for the prevention of thrombosis. Thus, during infections and in response to blood vessel damage, neutrophils and externalized nucleosomes are major promoters of intravascular blood coagulation and thrombosis.
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PMID:Propagation of thrombosis by neutrophils and extracellular nucleosome networks. 2792 71