Cl esterase inhibitor

History. This includes the severity grading of the clinical reaction, the time of administration and onset of symptoms, the concomitant use of other drugs, foods or compounds (latex), previous history of drug allergy, atopy in the personal or family history, other underlying conditions such as mastocytosis or Cl esterase inhibitor deficiency. The actual preparation in its galenic identity should be stored or at least listed. 

The alternative pathway may become activated by lipopolysaccharides, endotoxin (sepsis), virus, fungi, immunoglobulin A-antigen (IgA-Ag) immunocom-plexes, and foreign material. These activate C3, after which the common pathway of complement activation takes place (Fig. 4). There are also a number of inhibitors that regulate and control complement activation. The most important are the Cl-esterase inhibitor (Cl-Inh) and the membrane attack complex inhibitor factor (MACIF CD59). In sepsis a relative deficiency of Cl-Inh has been reported. Administration of Cl-Inh to patients with septic shock attenuates complement acti-... 

Fig. 4. The classical and alternative pathway cascade of complement activation. activation Cl-inh., Cl-esterase inhibitor MACIF, membrane attack complex inhibiting factor (—CD59).

H6. Hack, C. E., Ogilvie, A. C., Eisele, B., Jansen, P. M Wagstaff, J., and Thijs, L. G Initial studies on the administration of Cl-esterase inhibitor to patients with septic shock or with a vascular leak syndrome induced by interleukin-2 therapy. Prog. Clin. Biol. Res. 388, 335-357 (1994). 

Razis PA, Coulson IH, Gould TR, Findley IL. Acquired Cl esterase inhibitor deficiency. Anaesthesia 1986 41(8) 838-40. 

Hereditary angioedema, which is characterized by episodic bouts of swelling of submucosal and subcutaneous tissue, is due to a hereditary abnormality of Cl esterase inhibitor, either a deficiency of the normal enzyme or more rarely the presence of an abnormal enzyme. If Cl esterase inhibitor deficiency can be demonstrated, infusion of concentrated Cl esterase inhibitor is effective in treating the attack. In three studies, no adverse effects were recorded (1-3). 

Allergic reactions to Cl esterase inhibitor concentrate have been observed, including possible exacerbation of... 

The use of Cl esterase inhibitor concentrate has been associated with transmission of hepatitis C, but this can be prevented by heat treatment (5). 

Visentin DE, Yang WH, Karsh J. Cl-esterase inhibitor transfusions in patients with hereditary angioedema. Ann Allergy Asthma Immunol 1998 80(6) 457-61. 

Nomura S, Hashimoto J, Osawa G. Can Cl esterase inhibitor concentrate be a cause of the exacerbation of hereditary angioneurotic oedema Vox Sang 1995 69(1) 85. 

A 64-year-old man with no history of allergy had progressive fatigue, loss of appetite, and facial edema after 6 months of interferon alfa-2b treatment for chronic hepatitis C (319). Angioedema was diagnosed and it resolved after withdrawal of interferon alfa and a short course of prednisolone. Serum immunoglobuhn E and plasma bradykinin concentrations were raised, but the Cl esterase inhibitor and serum complement concentrations were normal. 

Non-IgE-mediated anaphylactic reactions to polyacrylonitrile membranes have been reported (2,3). The effects are enhacing in those using ACE inhibitors (4,5), perhaps because of an effect of bradykinin (6), which is released by the membranes (2,8,9) and whose metabolism is inhibited by ACE inhibitors. The effects also occur to a lesser extent in those taking angiotensin receptor antagonists (7) and in those with Cl esterase inhibitor deficiency (10). Treating the membranes with polyethyleneimine prevents bradykinin release (11). 

Ebo DG, Stevens WJ, Bosmans JL. An adverse reaction to angiotensin-converting enzyme inhibitors in a patient with neglected Cl esterase inhibitor deficiency. J Allergy Clin Immunol 1997 99 425-6. 

Reversible peripheral edema has been reported in five women taking the proton pump inhibitors omeprazole, lansoprazole, or pantoprazole for 7-15 days for peptic disorders in recommended standard doses (29). Edema disappeared within 2-3 days of withdrawal and reappeared in all five patients after re-exposure. High-dose intravenous infusions of omeprazole and pantoprazole (8 mg/hour) caused peripheral edema in three of six young female volunteers and two of six female volunteers respectively. The edema disappeared within 24 hours of stopping the infusion. Similar high doses of omeprazole did not produce edema in male volunteers. Subsequent studies performed on 10 female volunteers to elucidate the cause of the edema did not show any changes in concentrations of serum hormones or Cl esterase inhibitor. 

Pharmacological inhibition of the key enzymes responsible for the consecutive activation of cascade of reactions, including aprotinin, tranexamic acid, aminocapron acid, Cl-esterase inhibitor, antioxidants, and free radical scavengers are also under evaluation to improve hemocompatibility. Research into the modification of surfaces with integrin (receptors that link cellular components to extracellular matrix proteins) fragments, such as peptides with RGD amino acid sequence, has been conducted to increase hemocompatibility and biocompatibility. Further research into the improvement of device... 

Cerexin, Cinobac, Cinobact, Cinobactin, Gugecin, Nossacin, Noxigram, Uronorm cl-esterase inhibitor cyproheptadine ciprofloxacin ciprofloxacin ciprofloxacin Lipanor, Modalim Ciflox, Ciloxan Ophthalmic, Cimogal, Ciplox, Cipro, Ciprobay Uro, Cipromycin, Ciproxin, Italnik, Kenzoflex,... 

The principle of assaying inhibitors by synthetic substrate methodology is simple. In the presence of an excess of the enzyme under study, the enzymatic activity remaining after reaction with the inhibitor is inversely related to the concentration of the inhibitor. Because reliable and easy to perform techniques with natural substrates have not been available, synthetic substrate assays for inhibitors have gained wide acceptance and commercial kits for some are available. Some of the inhibitors which are of interest are antithrombin III, a -antiplasmin, a -antitrypsin. Cl esterase inhibitor, and... 

Pharming Cl esterase inhibitor, fibrinogen, collagen I II, Lactoferrin, Factor VII, Factor IX 56-58... 

It increases the concentration of Cl esterase inhibitor in patients with hereditary angioedema. This leads to an increased level of the C4 component of complement, which may be deficient in these patients, thus decreasing the number and severity of attacks of this disorder. 

Angioedema is caused by hereditary impairment of Cl -esterase inhibitor or acquired development of antibodies against it. The I7a-alkylated androgens, such as stanozolol and danazol, stimulate hepatic synthesis of the esterase inhibitor and thereby decrease the frequency of acute attacks. In women, virilization is a potential side effect. In children, virilization and premature epiphyseal... 

Mart N, Luu RA, Fernandez RC. Bordetella pertussis binds hiunan Cl esterase inhibitor during the virulent phase, to evade complement-mediated killing. J Infect Dis 2007 195 585-588. 

XII Hageman factor The first factor in the intrinsic pathway. A/, 74000 (bovine), 76000 (human). Single chain glycoprotein. Activated by plasmin, kallikrein and XII,. Inhibited by antithrombin III (inhibition accelerated by heparin). Cl esterase inhibitor and lima bean trypsin inhibitor. Activation of XII initiated by contact with abnormal surfaces. 

Upper and lower endoscopy, laparoscopic surgery, associated biopsies, and treatment with glucocorticoids and antibiotics had been unsuccessful. Complement and Cl esterase inhibitor corwentrations were normal After withdrawal of lisinopril, her symptoms resolved. 

Craig TJ, Wasserman RL, Levy RJ, Bewtra AK, Schneider L, Packer F, Yang WH, Keinecke HO, Kiessling PC. Prospective study of rapid relief provided by Cl esterase inhibitor in emergency treatment of acute laryngeal attacks in hereditary angioedema. J Clin Immunol 2010 30(6) 823-9. 

Dorresteijn MJ, Visser T, Cox LA, Bouw MP, Pillay J, Koenderman AH, Strengers PF, Leenen LP, van der Hoeven JG, Koenderman L, Pickkers P. Cl-esterase inhibitor attenuates the inflammatory response during human endotoxemia. Crit Care Med 2010 38(11) 2139-45. 

Catecholamine, binding sites, 336 Catechol-O-methyltransferase, 554-561 affinity labeling, 559-561 assay and isolation, 559 Cathepsin B, 206 Cathepsin G, 201, 206 Cellobiose, 365 Cephalosporin, 531 Cl esterase, inhibitors 115,116,120 Chitobiose, 365, 366 Chitotriose, 365, 366 Chlorambuoyl groups, 627 Cliloramphenicol, 90, 336, 630, 634, 635 analogs, 702-707... 

Despite cases of transmission of hepatitis C associated with intravenous immunoglobulin in the 1990s, no cases of transmission of hepatitis, HIV, or Creutzfeldt-Jakob disease have since been reported with immunoglobulins [6 J. Before 1996, PCCs (prothrombin complex concentrates) were associated with minimal risk of transmission of infective agents [7 ]. There are no documented cases of viral transmission in patients with von Willebrand disease or hemophilia A treated with Haemate P/Humate P in over 25 years of clinical experience in Europe and more than 17 years in the USA [ ]. In the IMPACT-1 and IMPACT-2 trial in 124 patients there were no cases of HIV, hepatitis, or human B19 virus conversion. Furthermore, no cases of viral transmission have been reported during 30 years of post-marketing surveillance of Cl-esterase inhibitor concentrate [9, 10 ]. 

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