Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.5 (thrombin)
 33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We had a sixty-five year old male patient who suddenly complained of dyspnea and fever with pulmonary tuberculosis, severe respiratory failure, disseminated intravascular coagulation (DIC) and intractable bilateral pneumothoraces. From the first hospital day severe hypoxemia which did not respond to conventional oxygen therapy developed with a diffuse ill-defined reticulo-nodular shadow in the plain chest x-ray film. On the 2nd hospital day mechanical ventilation with 2cmH2O PEEP was introduced. Antituberculous agents as well as corticosteroids were started suspecting acute interstitial pneumonia with pulmonary tuberculosis and adult respiratory distress syndrome (ARDS). Medication was followed by the treatment of Gabexate mesilate and heparin against DIC on laboratory data. Though clinical findings and pulmonary infiltrate on chest x-ray film transiently improved, right pneumothorax occurred suddenly on the 6th day followed with left pneumothorax on the 36th day. Tube drainage of both pleural spaces and repeated instillation of thrombin-rich oxycel cotton via bronchofiberscope failed to stop air leakage. He ultimately expired on 49th hospital day. At postmortem lung had multiple bilateral bulla several of which ruptured to the pleural site and caseating necrotic area containing bacilli positively stained with Ziehl-Nielsen stain in the bilateral upper lobe. No typical caseating necrotic lesion, however, was found in the other lung tissue. Therefore, it seemed to show a chronic phase of diffuse alveolar damage (DAD).
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PMID:[A case of pulmonary tuberculosis associated with severe respiratory failure, DIC and intractable bilateral pneumothoraces]. 148 64

We present a 65-year-old female with myelodysplastic syndrome (MDS) who has attended our O.P.D. since 1983. In early December, 1990, dyspnea on effort developed which then progressed to dyspnea at rest at the end of December. She was admitted on January 8 with orthopnea. Chest X-ray films revealed loss of vascular shadows of the right lung. Blood gas analysis showed hypoxemia and hypocapnemia. Abnormalities in the coagulation-fibrinolytic system (increased TAT (thrombin-anti-thrombin III complex) and alpha 2-PIC (plasmin inhibitor complex)), possibly due to MDS, were detected. The diagnosis of pulmonary thromboembolism was made by pulmonary perfusion scintigram and pulmonary arteriography. After commencement of anticoagulation therapy on January 15, the subjective symptoms, blood gas analysis, pulmonary scintigram, and disorders of the coagulation-fibrinolytic system improved. The patient was discharged on March 5, 1991. The present case of myelodysplastic syndrome was associated with abnormalities of the coagulation-fibrinolytic system and was complicated by pulmonary thromboembolism.
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PMID:[Pulmonary thromboembolism associated with myelodysplastic syndrome]. 156 27

A 55-yr-old male with carcinoma of bladder received transurethral coagulation (TUC) under epidural anesthesia. A few min after the operation, he went into anaphylactic shock during irrigation of urinary bladder with thrombin solution. The symptoms were epigastralgia, circulatory collapse, skin rashes over the whole body and dyspnea. Oxygen inhalation and iv administration of epinephrine and steroid were performed, and his general condition improved within several hours. On the 2nd day after recovery from the anaphylactic shock, the patient received prick test on several agents which he had been given during operation. Prick test and RAST (radioallergosorbent test) on thrombin were positive. Based on our experience, thrombin may act to produce anaphylactic reaction. Although anaphylactic shock following topical thrombin is rare, we feel that thrombin should not be used without prick test.
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PMID:[Anaphylactic shock following topical use of thrombin for irrigation of urinary bladder]. 223 33

The Gaboon viper has acquired an impressive reputation which is at least partly unfounded. This handsome animal with such striking features is undoubtedly docile which accounts for the very low incidence of bite amongst humans. There are only six detailed clinical reports on the effect of bite and these are summarized in the review. The viper does indeed produce prodigious amounts of venom, but the toxicity, weight for weight, is rather low compared to other poisonous snakes. Venom extractions have been carried out on four snakes over a 13-year-period and the effects of this venom have been studied in a variety of experimental animals. Systemic envenomation is characterized by immediate abrupt hypotension, subsequent cardiac damage and dyspnoea. The individual venom components responsible for these effects have not been isolated but it seems likely that the two enzymes which have been studied extensively (phospholipase A2 and the thrombin-like enzyme, gabonase) do not contribute significantly to lethality. We propose three principal activities which give rise to the major signs of systemic envenomation. Haemorrhagin; causing widespread damage to microvasculature which leads to the pulmonary oedema and hence dyspnoea, and locally causes blistering. Cardiotoxin; a long-acting material causing cardiac muscle damage, arrhythmia and ultimately cardiac failure. Peripheral vasodilator; a short acting effect, operating either locally via bradykinin formation and/or unknown peptides or centrally on the vasomotor centre.
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PMID:The Gaboon viper (Bitis gabonica): its biology, venom components and toxinology. 639 43

A 33 year old woman presented with dyspnea and dizziness. These symptoms had recurred several times during the months preceding. At initial investigation we palpated a tumor in the upper abdomen corresponding to the sonographic finding of a 10 X 10 cm sized cystic tumor in the liver. Because of reduction of fibrinogen, prolonged thrombin time and thrombocytopenia a malignant disease involving the liver and producing pulmonary embolism and disseminated intravascular coagulation was suspected. However, during routine echocardiography a right atrial mass prolapsing in the right ventricle was detected. After normalization of fibrinogen and thrombin-time following a low dose heparin therapy a myxoma sized 6 X 5 cm was removed from the right atrium. The patient did not recover and died 20 days following surgery. At autopsy the liver tumor proved to be a benign cholangioendothelial cyst.
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PMID:[Recurring pulmonary artery embolisms and disseminated intravascular coagulation in right atrial myxoma]. 672 75

Deep-vein thrombosis (DVT) and pulmonary embolism are among the most common complications of heparin-induced thrombocytopenia (HIT), an antibody-mediated adverse effect of heparin that leads paradoxically to in vivo activation of platelets and the coagulation system. Inappropriate treatment of HIT-associated DVT with warfarin can cause the DVT to progress to limb gangrene: this results from impaired ability of the protein C natural anticoagulant pathway to down-regulate thrombin generation, thus leading to microvascular thrombosis and tissue necrosis. Appreciation of the importance of coagulation system activation in HIT provides a rationale for treatments that reduce thrombin generation, either via inhibiting factor Xa (danaparoid) or via inhibiting thrombin directly (lepirudin). Clinicians should know how to distinguish HIT from other thrombocytopenic disorders: for example, thrombocytopenia associated with pulmonary embolism can mimic HIT (pseudo-HIT), and acute dyspnea that can mimic acute pulmonary embolism can result from acute in vivo platelet activation in a patient with HIT antibodies who receives heparin bolus therapy (pseudo-pulmonary embolism).
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PMID:Venous thromboembolism in heparin-induced thrombocytopenia. 1091 44

Coumarin poisoning in dogs is not unusual and is in most cases caused by warfarin, a coumarin derivative which is used as a rodenticide. Competitive inhibition of vitamin K with an incomplete synthesis of the coagulation factors II, VII, IX and X can lead to a significant bleeding tendency. We observed a 3-year old male West Highland White Terrier with a reduced general condition and dyspnoea together with a massive haemothorax. Administration of vitamin K1 (3 mg/kg) led to a rapid improvement of the condition. Coagulation analysis revealed a prolonged activated recalcification time (ARCT), prothrombin time (PT) and aPTT with uncharacteristic thrombin time (TT); factor II, VII and X activities were reduced while factor V activity was normal, all of which are characteristic for coumarin poisoning. HPLC did not reveal the presence of warfarin but of phenoprocoumon, a drug used for thromboembolic prophylaxis in humans. This observation has not been described for dogs to date.
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PMID:[Case report. Phenprocoumon (Marcumar, Falithrom) as an unusual reason for coumarin poisoning in a dog]. 1259 69

A 57-year-old woman was admitted to our hospital because of severe dyspnea due to pulmonary hemorrhage and rapidly progressive renal failure. The patient was positive for perinuclear pattern anti-neutrophil cytoplasmic antibody (p-ANCA) and was manifested with gastrointestinal bleeding and brain hemorrhage. Thus, she was diagnosed as having microscopic polyangiitis (MPA). Laboratory examination demonstrated severe thrombocytopenia, increased prothrombin time and a high concentration of fibrin degradation products. In addition, the elevated plasma levels of D-dimer, thrombin-antithrombin complex and plasmin-plasmin inhibitor complex led us to make a diagnosis of disseminated intravascular coagulation (DIC). Complication of DIC was considered to have caused further deterioration in bleeding tendency due to MPA in the present case. The patient was treated with plasma exchange, hemodialysis, administration of corticosteroid including pulse therapy and cyclophosphamide. Continuous infusion of gabexate mesilate proved effective for improvement of systemic bleeding tendency. However, she finally died of severe infectious diseases. In conclusion, it is suggested that ANCA-associated vasculitis could be accompanied by DIC and gabexate mesilate may be a useful therapeutic agent for these disorders.
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PMID:Microscopic polyangiitis associated with marked systemic bleeding tendency caused by disseminated intravascular coagulation. 1451 75

Acute bilateral renal cortical necrosis is a very rare cause of acute renal failure. We report here for the first time a case related to antiphospholipid syndrome, paraneoplastic of a lung neoplasia. A 46-year-old male smoker without medical history was admitted for acute dyspnea and anuria. Biological examination showed acute renal failure associated with hyperkalemia, high serum lactate dehydrogenase level, and prolonged activated thrombin time (ratio 1.29). Chest radiograph showed a right laterotracheal round lesion. A percutaneous left renal biopsy showed cortical necrosis, and renal arteriography confirmed bilateral cortical necrosis. Blood examination showed antiphospholipid antibodies type anticardiolipin. Chest computed tomographic scan confirmed the presence of a lung tumor. Two years after tumor surgery, the patient was still anuric and on long-term hemodialysis therapy, but antiphospholipid antibody results were negative. This case describes the first association of antiphospholipid syndrome to epidermoid lung cancer, shown by cortical bilateral necrosis. It also emphasizes the utility of renal biopsy in case of an unusual acute renal failure.
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PMID:Renal cortical necrosis related to paraneoplastic antiphospholipid syndrome. 1673 3

Bronchoscopic lung-volume reduction for hyperinflated air-trapping disease is currently being investigated. A 41-year-old woman with pulmonary lymphangioleiomyomatosis presented with exertional dyspnea. A chest computed tomographic scan showed hyperinflation with diffuse cystic lesions throughout both lung fields. To reduce lung volume, transbronchial autologous blood was followed by thrombin solution, which was infused into cystic areas under fluoroscopic guidance. A post-treatment computed tomographic scan showed volume reduction corresponding to decreased total lung capacity by 240 mL on body plethysmography. Dyspnea was significantly improved. Bronchoscopic treatment by blood infusion is less invasive and appears clinically valuable, potentially providing therapeutic benefit in hyperinflated lung diseases such as lymphangioleiomyomatosis.
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PMID:Bronchoscopic blood injection reducing lung volume in lymphangioleiomyomatosis. 1932 67


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