Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ARDS occurs in patients with no underlying pulmonary diseases, induced by stresses, such as lung injury, acute pancreatitis or infections. It is an acute respiratory disorder which manifests as acute dyspnea, hypoxemia and lowered pulmonary compliance. Greene et al, used balloon pulmonary angiogram (BOPA) as diagnostic tool to morphologically observe the pulmonary disorder. To study the dynamic pulmonary circulation and morphology of the peripheral pulmonary artery of ARDS, we performed this method for acute cardiac failure and ARDS patients. Pulmonary hemodynamic changes in ARDS revealed mild pulmonary hypertension and increased PVR, while C.I. and PCWP remained within a normal range. The findings of BOPA in ARDS showed that the frequency of PAFD correlated with the the presence of an elevated PVR and DIC, and pulmonary vasoconstriction was detected by measurement of PA diameter (B/A2).
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PMID:[ARDS: circulatory factors and their evaluation]. 203 88

Experimental studies of acute inflammation of the tracheobronchial lumen of rats suggest that protease inhibitor increases in tracheobronchial secretions in order to control inflammation. Recent studies have shown that the polyvalent protease inhibitor, Miraclid, derived from human urine, is useful for treating DIC and acute pancreatitis. In view of this information, local administration of Miraclid was expected to diminish acute inflammation of the respiratory tract by creating a favorable balance in the protease-antiprotease system. Before the chemotherapeutic use of locally administered Miraclid, the inhibitory activity of Miraclid on various proteases was first estimated in vitro. Administration of Miraclid by means of ultrasonic nebulization was then investigated in rats. The results can be summarized as follows. 1. During ultrasonic nebulization, the inhibitory activity of Miraclid on protease was decreased by means of mechanical stimulation in comparison to the activity before nebulization. 2. Compared to administration of physiological saline into the tracheobronchial lumen, administration of Miraclid by means of ultrasonic nebulization decreased the fibrinolytic activity in tracheobronchial secretions.
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PMID:Effect of ultrasonic nebulization of Miraclid on the proteolytic activity in tracheobronchial secretions of rats. 260 43

Factor VIII-related antigen (VIIIR:Ag) was consistently higher than factor-VIII procoagulant activity (VIII:C) in 57 patients with clinical conditions characterized by acute-phase reactions. Two different methods for measuring VIII:C (one- and two-stage assays) and VIIIR:Ag (electroimmunodiffusion and immunoradiometric assay) gave concordant results in the majority of cases. In 43% of plasma samples, crossed immunoelectrophoresis in agarose gel was characterized by the appearance of an additional, fast-moving precipitin peak which was immunologically identical with the major, slower-moving VIIIR:Ag peak. The fast-moving peak was detected in all the patients with clinical conditions typically associated with increased plasma proteolysis (DIC, acute pancreatitis, during thrombolytic therapy). It was present in a smaller proportion of cases with liver and renal failure and malignancies and in the post-operative period. The additional VIIIR:Ag peak is thought to be the result of in vivo factor VIII/von Willebrand factor fragmentation by proteolytic enzymes.
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PMID:Alterations of factor VIII von Willebrand factor in clinical conditions associated with an increase in its plasma concentration. 679 81

The autopsy of a 10-month-old infant girl who died suddenly after a 2-day illness revealed acute pancreatitis and DIC. While the definitive etiology remains unknown, retention of pancreatic juice accompanying proliferation of papillary epithelium within the pancreatic duct adjacent to the ampulla Vater was suggested. Acute interstitial pancreatitis was assumed to have resulted from suppurative inflammation of the pancreatic duct. DIC was probably caused by the release of pancreatic enzymes.
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PMID:Sudden death due to infantile pancreatitis. 713 2

A pregnant woman with severe preeclampsia developed HELLP syndrome and acute pancreatitis. She underwent an emergency caesarean section. In this patient, attention had to be paid to complicating cranial hemorrhage, rupture of liver subcapsular hematoma, acute renal failure, DIC, hypovolemic shock and sepsis. Therefore, we used a calcium blocker, diuretics and a protease inhibitor and examined the liver and pancreas by abdominal X ray-CT.
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PMID:[HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome and acute pancreatitis complicated with severe preeclampsia]. 909 10

The etiology of acute pancreatitis is based on several causes, among which idiopathic nature (< 30%) is second to biliary stone disease (60-70%). It is still under debate whether alcohol as the main cause of chronic pancreatitic disease can cause acute pancreatitis. Based on Opie's "obstruction theory" of 1901 and experimental data, it is now widely accepted that the gallstone passage into or through the terminal biliopancreatic ductal system triggers acute (necrotizing) pancreatitis by causing pancreatic ductal obstruction. However, the sequential intracellular mechanisms in the pathogenesis of acute pancreatitis remain unclear. A co-localization hypothesis has been proposed to explain the premature intracellular activation of trypsinogen to trypsin: due to a yet unknown defect in the intracellular protein transport and sorting system within the acinar cell, lysosomal hydrolases (i.e. cathepsin B) and secretory proteins (i.e. trypsinogen) co-localize in a fragile postgolgi vacuole where activation can occur. In addition, alterations of exo- and endocytosis at the apical pole exist (i.e. secretion block). The pathophysiological events are characterized by local and systemic hypovolemia and (micro)circulatory failure aggravating necrosis, followed by ARDS, renal failure and several other severe complications (i.e. sepsis and DIC). The systemic overflow of proteolytic enzymes (i.e. PLA-2) and kinins plays a major role as mediating factor in severe cases, resulting in multiorgan failure.
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PMID:[Etiology, pathogenesis and pathophysiology of acute pancreatitis]. 928 10

Acute pancreatitis is discussed from the point of view her complications. The survey of local, organ and system complication is demonstrated, and the Atlanta classification is recalled. The complications are demonstrated at the mild acute pancreatitis and also at the severe acute pancreatitis. The complications are demonstrated on the own group of patients (period 1995-1997). Severe respiratory failure came later, but the letality was high. The renale or hepatorenale failure came formerly and equally as DIC were combined with practically absolutely letality.
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PMID:[Complications in acute pancreatitis]. 1008 59

The HELLP syndrome (HS) belongs to the list of obstetric complications believed to be associated with coagulation disorders. It was formerly thought that chronic intravascular clotting (DIC) in the placental vessels was the main cause. A hypercoagulable state has been reported in cases of severe HS associated with microvascular abnormalities that may involve cerebral, placental, hepatic and renal vessels. A case of acute pancreatitis and DVT of inferior cava in a pregnant woman, presenting with HS at 29 weeks, who was found to have a R506Q mutation, is reported. Preeclampsia-associated pancreatitis and DVT have rarely been reported. It is hypothesized that APC-R and Factor V Leiden mutation may prove to be new and more important markers capable of predicting a more significant maternal morbidity associated with HS. Thrombosis prophylaxis may be considered during pregnancy in order to reduce hazardous multiorgan failure (MOF) in women who are heterozygous for Factor V Leiden mutation.
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PMID:Acute pancreatitis and deep vein thrombosis associated with HELLP syndrome. 1023 Feb 42

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