Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We treated 80 patients with sudden hearing loss and 70 patients with chronic decreasing cochlear function to date with intravenous infusion of a glycoprotein analogous to recombinant tissue-type plasminogen activator (rt-PA): 3 mg dissolved in 250 mg of physiological saline given every 12 hours intravenously. Specifically excluded were patients with known abnormal coagulation. We treated no patient for longer than 20 days. Before therapy, 6 months therapy began, and at the end of treatment, all patients underwent the following instrumental examinations: prothrombin and fibrinogen level measurements, liminal tonal audiometry, tympanometry, and assessment of otoacoustic emissions and otoacoustic products of distortion. Daily during the treatment, we monitored the patients by liminal tonal audiometry and assessment of otoacoustic emissions with linear click emission and otoacoustic products of distortion. We discharged patients when their audibility threshold stabilized. No patient experienced side effects due to the treatment, and functional results were excellent in all (even more so if compared with the protocols of therapy previously used for these kinds of diseases). The tissue plasminogen activator was used with remarkable success for the treatment of sudden hearing loss; this study shows remarkable success with a very low dose of rt-PA as compared to the standard dosage used for treatment of myocardial infarction.
Int Tinnitus J 2005
PMID:The use of recombinant tissue-type plasminogen activator for the treatment of sudden and chronic hearing loss. 1663 20

A 61-year-old man, with a history of right clavicular fracture 35 years prior, visited our hospital due to the sudden onset of vertigo and tinnitus following weakness and numbness in his left arm and leg. He also had a 6-month history of right arm pain with overuse. Brain MRI showed acute brain infarcts in the right posterior cerebral artery territory. Intravenous alteplase was administered 188 minutes after onset. Although heparin infusion was commenced on day 2, he had vertigo again on day 9, and MRI showed a recurrent brain infarct in the right posterior inferior cerebellar artery territory. Ultrasound examination revealed occlusion of his right subclavian artery beneath the old right clavicular fracture as well as mobile thrombus in the proximal portion of the right subclavian artery. We speculated that a pseudarthrosis at the site of the old right clavicular fracture had repetitively pressed the right subclavian artery. Subsequently, we considered thrombi, which had developed in the proximal portion of the right subclavian artery, migrated into the right vertebral artery, causing recurrent emboli in the vertebrobasilar artery territory.
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PMID:[Vertebrobasilar territory embolisms due to the ununited fracture of the right clavicle from 35 years ago]. 3027 Mar 40