Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040425 (tonsillitis)
 1,594 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present the case of a 38-year-old man who developed acute myopericarditis, mimicking acute myocardial infarction, as manifested by electrocardiographic, echocardiographic alterations and elevated cardiac enzymes complicating Lancefield group A beta-hemolytic streptococcal tonsillitis. After receiving oral penicillin, the clinical recovery was complete. Fever, tachycardia and chest discomfort resolved within a few days. Furthermore, enzyme levels and C-reactive protein returned to normal within eight days.
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PMID:Acute nonrheumatic myopericarditis associated with group A hemolytic streptococcal tonsillitis in a male ICU-nurse. 1039 54

The developments and trends of hemostatic and antithrombotic drugs in Japan were investigated chronologically for the last 50 years after the 2nd World War. 1. Hemostatic drugs are classified into three groups ; capillary stabilizers, blood coagulants and antifibrinolytics. l) As to capillary stabilizers, flavonoid (rutin, 1949), adrenochrome derivative (carbazochrome, 1954) and conjugated estrogen (Premarin, 1964) were introduced therapeutically. Especially, the soluble types of adrenochrome compounds (Adona 1956, S-Adchnon, 1962) were devised and used widely in Japan. 2) Drugs concerning blood coagulation, thrombin, introduced in 1953, and hemocoagulase, a snake venom introduced in 1966, were used clinically. V.K. groups producing various coagulation factors were introduced as V.K1 (Phytonadione, 1962) and V.K2 (rnenatetrenone,1972), and they were admitted in "The Japanese Pharmacopoeia"editions 8 and 14, respectively). 3) Regarding antifibrinolytic drugs, Japanese researchers have made remarkable contributions. e-Aminocapronic acid (Ipsilon, 1962) and tranexamic acid (Transamin, 1965) were developed and used for various abnormal bleedings or hemorrhage associated with plasmin over-activation. tranexamic acid also proved to suppress inflammations of the throat such as tonsillitis, pharyngitis or laryngitis. 2. Antithrombotic drugs are also divided into three groups; anticoagulants, antiplatelet drugs and fibrinolytics.1) The anticoagulants used therapeutically by injection are heparins (Na-salt, 1951; Ca-salt, 1962) and low-molecular-weight heparins such as dalteparin (1992), parnaparin (1994) and reviparin (1999). The low molecule compounds are superior to the original heparins in reducing the risk of bleeding. As oral anticoagulants, coumarin derivatives, dicumarol (1950), ethylbiscoumacetate (1954), phenylindandione (1956) and warfarin (1962) are known. Warfarin potassium is the main drug for oral therapy of thromboembolism lately. Gabexate mesilate (1989) and nafamostat mesilate (1989) were developed in Japan and used for DIC and acute pancreatitis to inhibit protease enzymes. Argatroban is a unique antithrombin product developed by Japanese researchers in 1990, and is used for vascular or cerebral thrombosis. After noticing in 1968 that aspirin inhibits platelet aggregation and prevents myocardial infraction, projects for developing antiplatelet drugs were initiated worldwide. Ticlopidine, originally developed in France, was introduced in 1981 and prevailed widely in Japan for reducing the risk of thrombotic stroke. Aspirin itself was recognized by the FDA (USA) as an antithrombotic drug in 1988, and was also approved by Japanese authorities in 2000. PGE1 clathrate compounds have also been developed as antiplatelet drugs; alprostadil alfadex for injection (1979), and limaprost alfadex for oral use (1988). The PGI2 product, beraprost sodium, for oral use followed them in 1992. Other antiplatelet drugs with unique mechanisms explored in Japan: Ozagrel (1988), which inhibits TXA2 synthetase, cilostazol (1988), which inhibits cAMP phosphodiesterase, and sarpogrelate (1993), which blocks 5HT in platelets, are the notable drugs in this field. Ethyl icosapentate, from fish oil, is available for antiplatelet therapy. Concerning the fibrinolytic system, plasminogen activators are useful for thromboembolism. The streptokinase from bacterial origin developed in the USA and Europe was not introduced, and urokinase (1965) was the first plasminogen activator developed in Japan. Then tissue plasminogen activators (t-PA) tisokinase (cell culture, 1991), alteplase (genetical recombination, 1991), nateplase (genetical recombination, 1996), monteplase (1998) and pamiteplase (1998) were developed and approved for acute myocardial infarction. Nasaruplase (prourokinase, cell culture,1991) was also approved for the same indication. While the development of the hemostatic drugs ceased in the 1960s, avid project studies for antithrombotic drugs including fibrinolytics began in the 1980s and are progressing now towards new molecular targets. This may be due to the increasing tendency of cardiovascular thromboembolic diathesis in Japan. (The figures in parentheses are the years approved by the Japanese Ministry of Health, Labor and Welfare.)
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PMID:[A 50-year history of new drugs in Japan-the development and trends of hemostatics and antithrombotic drugs]. 1457 69

In the period of 30 years, i.e. from 1973 to 2002, we noticed in Croatia 6 sudden and unexpected cardiac deaths in male athletes during or after training. Two were soccer players, 2 athletic runners, one was a rugby player and one was a basketball player. All of them were without cardiovascular symptoms. At the forensic autopsy, the first athlete, aged 29, had chronic myocarditis and thickened left ventricular wall of 15 mm. The second, aged 21, had an acute myocardial infarction of the posterior wall with normal coronaries and thickened left ventricular wall of 15 mm. The third aged 17, had hypoplastic right coronary artery and narrowed ascending aorta, suppurant tonsillitis and subacute myocarditis. Two athletes, aged 29 and 15, had hypertrophic cardiomyopathy and normal coronaries, and one dilated aorta. The sixth, aged 24, had arrhythmogenic cardiomyopathy of the right ventricle. All the 6 athletes died suddenly, obviously because of malignant ventricular arrhythmias. In Croatia the death rate among athletes reached 0.15/100 000, in others who practice exercise reached 0.74/100,000 and the difference is highly significant (c2=14.487, Poisson rates=3.81, P=0.00014) and in physicians-specialists reached 33.6/100,000. Preventive medical examinations are essential, especially in athletes before physical exercise, as are other investigations in every case suspicious of heart disease, including electrocardiogram (ECG), stress ECG, echocardiography and stress-echocardiography and other findings if indicated. Physical exercise is contraindicated in acute respiratory infection: in 2 of those cases had been a cause of death as a trigger.
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PMID:Sudden cardiac death due to physical exercise in male competitive athletes. A report of six cases. 1644 87