Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Determination of the complement titer in the serum and plasm of 120 patients with chronic liver diseases showed that in eight (7%) patients with cirrhosis of the liver, chronic active or chronic inactive hepatitis complement in the serum was less than half in the plasma. The dissociation of complement serum and plasma was due to cold activation of the classical pathway of complement in vitro since serum drawn from these patients at 37 degrees C lost hemolytic activity in 4 hours when transferred to a cold environment. Neither HB antigen nor cryoglobulin participated in this phenomenon. The activation of complement in the cold could be prevented by increasing the ionic strength, or by adding vitamin E or, to a lesser extent its vehicle HCO-60, while heparin, Trasylol, soybean trypsin inhibitor, or hirudin had no effect. Trans-AMCHA prevented activation in one case. It is speculated that a factor appearing as a result of blood clotting is able to activate the classical pathway of complement in the cold; it is probably not related to Hageman factor (factor XII), factor VII, thrombin, kallikrein.
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PMID:Cold activation of complement i. presence of coagulation-related activator. 5 81

Plasma prekallikrein (kallikreinogen) and kallikrein inhibitor, assayed with the kaolin activable esterase method, have been evaluated in 20 patients with hepatic cirrhosis, in 12 cases with jaundice from acute viral hepatitis, and in 9 normal. A significant reduction of the plasma prekallikrein in cirrhosis has been found. A lowering of plasma prekallikrein has also been observed in viral hepatitis; in this condition, however, the modifications were less important than those obtained in cirrhosis. In three cases of hepatitis, the behaviour of the plasma prekallikrein and kallikrein inhibitor have been controlled during the period of the disease and compared with the behaviour of some conventional parameters, such as serum transaminases and bilirubin. An important increase of the prekallikrein level has been observed during the improvement of hepatitis. These data confirm the implication of the prekallikrein-kallikrein system in severe liver diseases, and indirectly points out the role of the liver in maintaining the physiological balance of the kallikrein system.
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PMID:Prekallikein and kallikrein inhibitor in liver cirrhosis and hepatitis. 108 79

Activity of kallikrein, content of prekallikrein, antitryptic and BAEE-esterase activities as well as content of alpha 1-antitrypsin and heparin were studied in blood serum of patients with the B type of serum hepatitis (SH) of various severity. Presence of kallikrein in the active form, increase in content of prekallikrein, distinct increase in BAEE-esterase and antitryptic activities as well as in content of alpha 1-antitrypsin and heparin were observed in blood serum of the patients with middle and severe forms of the impairment. Severe form of the hepatitis complicated with the acute liver encephalopathy was characterized by the radically new state exhibiting further increase in activity of free kallikrein, decrease in content of prekallikrein as well as in BAEE-esterase activity as compared with middle and severe forms of SH not complicated with the acute liver encephalopathy. Immunochemical analyses showed distinct decrease in the content of alpha 1-antitrypsin in blood serum of the patients with SH impaired also by acute liver encephalopathy. Besides, high level of the antitryptic activity was observed in severe forms of the hepatitis both with the encephalopathy and without of its. Further increase in the activity of free heparin was found in all the three forms of SH. Elevation of the antithrombin III inhibitory activity in presence of heparin was apparently responsible for an increase in the antitryptic activity under conditions of severe forms of SH when content of alpha 1-antitrypsin decreased. Activation of the kinin system and decrease in the alpha 1-antitrypsin synthesis, caused by destructive processes in liver tissue, are considered as factors deteriorating the disease development.
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PMID:[Kallikrein and prekallikrein content and antitryptic activity in the blood serum in serum hepatitis of varying degrees of severity]. 697 40

We have previously reported that the endocytosis of rat plasma kallikrein (RPK) by hepatocytes is a calcium-independent and beta-galactoside-dependent mechanism. We now report the clearance of RPK by the liver of four groups of rats: normal, inflamed (48 h ex-turpentine) and two groups chronically treated with CCl4 (52 mg/kg per week, intragastrically, for 9-12 weeks). Each liver was isolated, exsanguinated and perfused at 37 degrees C with 30 mL of BSA-Krebs-Henseleit-bicarbonate medium containing 10 nmol/L RPK. Although all rats received the same mild CCl4 treatment, the liver histology showed that they evolved either to severe hepatitis (serum alanine aminotransferase [ALT] 4852 +/- 885 U/L, parenchymatous necrosis in the perivenous region) or to compensated cirrhosis (serum ALT 209 +/- 42 U/L, vigorous fibrous encircling regeneration nodules); neither jaundice nor ascites was noted. The results show that serum albumin was not altered among the groups and that: the acute-phase response by itself (inflamed group) increased RPK clearance rate (3.01 +/- 0.59 mL/min) as compared with the normal group (1.85 +/- 0.14 mL/min); the CCl4 treatment, although induced an acute-phase response, decreased (P < 0.01) RPK clearance rates (0.80 +/- 0.11 mL/min hepatitis group and 0.98 +/- 0.10 mL/min cirrhosis group). These findings suggest that the hepatic clearance rate of plasma kallikrein is an early indicator of liver injury.
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PMID:Plasma kallikrein clearance by the liver of chronic carbon tetrachloride-treated rats. 778 62

Evaluation of kallikrein-kinin circulatory system was performed via kallikrein, prekallikrein, a1-inhibitor proteinase, a2-macroglobulin, kininase-II and proteolytic activity in 60 patients with chronic persisting hepatitis and incalculous cholecystitis. Two types of kallikrein-kinin system reaction were revealed: hyperkininogenesis in 85% and hypokininogenesis in 15% of all the patients. The problem of fasting diabetics influence on kininogenesis was investigated as well.
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PMID:[Evaluation of the kallikrein-kinin system in patients with chronic impairments of the hepatobiliary system as affected by fasting-diet therapy]. 950 69