Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We encountered a 63-year-old man whose dry cough due to interstitial pneumonia had been successfully with an anti-thrombin drug, argatroban, which was given to treat exacerbated Buerger's disease. We therefore prospectively evaluated fibrinogen, fibrin-degradating product D-dimer, thrombin anti-thrombin III complex, and plasmin anti-plasmin complex in patients with interstitisal lung diseases. In a preliminary study, we found that some patients actually had elevated levels of these markers. These findings suggested that increased coagulability was involved in the pathophysiology of interstitial pneumonia. In this study, we measured the levels of serum-soluble thrombomodulin as a marker of endothelial cell damages that lead to hemostasis. We found that serum levels of thrombomodulin were high in about 35% of patients with sarcoidosis, interstitial pneumonia associated with collagen diseases, or idiopathic interstitial pneumonia. Furthermore, these levels decreased as the patients' conditions improved. Although further evaluation is needed, these results suggest that endothelial cell damage and hemostasis are involved in the pathophysiology of interstitial pneumonia.
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PMID:[Evaluation of serum thrombomodulin in patients with interstitial pneumonia]. 784 12

A 56-year-old man was transferred to our department from the department of oral surgery, with a high fever and a cough. He had inhaled a fibrinolysin-deoxyribonuclease mixture (Elase) to treat inflammation in the oral cavity after resection of an oral tumor. A chest X-ray film showed diffuse patchy shadows in both lung fields. Bronchoalveolar lavage fluid had an abnormally high number of lymphocytes and transbronchial lung biopsy revealed interstitial infiltration by lymphocytes and histiocytes, with granulomatous lesions. The patient was treated with steroids, and his clinical condition improved markedly. He accidentally inhaled the drug again, and the coughing and fever began again. The drug lymphocyte stimulation test was positive only for the fibrinolysin-deoxyribonuclease mixture. Based on these findings, we diagnosed pneumonitis induced by this fibrinolysin-deoxyribonuclease mixture. To our knowledge, this is the first reported case of pneumonitis caused by this fibrinolysin-doxyribonuclease mixture.
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PMID:[Pneumonitis in a patient who inhaled a fibrinolysin-deoxyribonuclease mixture]. 858 26

A 16-year-old girl arrived intubated to the emergency department. She had shortness of breath and cough for 2 days with leg pain. On arrival, she was hemodynamically stable with an unremarkable physical exam. Electrocardiogram revealed a prolonged QT interval; laboratory work-up was normal except for an elevated dimerized plasmin fragment D. Acute pulmonary embolism was confirmed by a chest computed tomography scan. A lower extremity duplex scan was negative and echocardiogram revealed a patent foramen ovale with bidirectional shunting. An inferior vena cava filter was placed to prevent acute recurrence and unfractionated heparin was initiated. The next day she was noted to have right hemiparesis. Stroke was confirmed by magnetic resonance imaging. The patient underwent mechanical clot retrieval and was discharged on anticoagulation therapy to a brain rehabilitation unit.
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PMID:A case of pulmonary embolism and stroke in a 16-year-old girl. 2261 72

In this rostrum we aim to increase awareness of anaphylaxis in infancy in order to improve clinical diagnosis, management, and prevention of recurrences. Anaphylaxis is increasingly reported in this age group. Foods are the most common triggers. Presentation typically involves the skin (generalized urticaria), the respiratory tract (cough, wheeze, stridor, and dyspnea), and/or the gastrointestinal tract (persistent vomiting). Tryptase levels are seldom increased because of infant anaphylaxis, although baseline tryptase levels can be increased in the first few months of life, reflecting mast cell burden in the developing immune system. The differential diagnosis of infant anaphylaxis includes consideration of age-unique entities, such as food protein-induced enterocolitis syndrome with acute presentation. Epinephrine (adrenaline) treatment is underused in health care and community settings. No epinephrine autoinjectors contain an optimal dose for infants weighing 10 kg or less. After treatment of an anaphylactic episode, follow-up with a physician, preferably an allergy/immunology specialist, is important for confirmation of anaphylaxis triggers and prevention of recurrences through avoidance of confirmed specific triggers. Natural desensitization to milk and egg can occur. Future research should include validation of the clinical criteria for anaphylaxis diagnosis in infants, prospective longitudinal monitoring of baseline serum tryptase levels in healthy and atopic infants during the first year of life, studies of infant comorbidities and cofactors that increase the risk of severe anaphylaxis, development of autoinjectors containing a 0.1-mg epinephrine dose suitable for infants, and inclusion of infants in prospective studies of immune modulation to prevent anaphylaxis recurrences.
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PMID:Anaphylaxis: Unique aspects of clinical diagnosis and management in infants (birth to age 2 years). 2544 36

Amniotic fluid embolism (AFE) is one of the catastrophic complications of pregnancy in which amniotic fluid, fetal cells, hair, or other debris enters into the maternal pulmonary circulation, causing cardiovascular collapse. Etiology largely remains unknown, but may occur in healthy women during labour, during cesarean section, after abnormal vaginal delivery, or during the second trimester of pregnancy. It may also occur up to 48 hours post-delivery. It can also occur during abortion, after abdominal trauma, and during amnio-infusion. The pathophysiology of AFE is not completely understood. Possible historical cause is that any breach of the barrier between maternal blood and amniotic fluid forces the entry of amniotic fluid into the systemic circulation and results in a physical obstruction of the pulmonary circulation. The presenting signs and symptoms of AFE involve many organ systems. Clinical signs and symptoms are acute dyspnea, cough, hypotension, cyanosis, fetal bradycardia, encephalopathy, acute pulmonary hypertension, coagulopathy etc. Besides basic investigations lung scan, serum tryptase levels, serum levels of C3 and C4 complements, zinc coproporphyrin, serum sialyl Tn etc are helpful in establishing the diagnosis. Treatment is mainly supportive, but exchange transfusion, extracorporeal membrane oxygenation, and uterine artery embolization have been tried from time to time. The maternal prognosis after amniotic fluid embolism is very poor though infant survival rate is around 70%.
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PMID:Amniotic fluid embolism. 2727 41