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13. Long-Term Outcomes with Subcutaneous C1-Inhibitor Replacement Therapy for Prevention of Hereditary Angioedema Attacks

Author

Zuraw, B, Katelaris, C, Sussman, G, Keith, PK, Yang, W, Hebert, J, Hanzlikova, J, Staubach-Renz, P, Martinez-Saguer, I, Magerl, M, Aygoren-Pursun, E, Farkas, H, Reshef, A, Kivity, S, Neri, S, Crisan, I, Caballero, T, Baeza, ML, Hernandez, MD, Li, H, Lumry, W, Bernstein, JA, Hussain, I, Anderson, J, Schwartz, LB, Jacobs, J, Manning, M, Levy, D, Riedl, M, Christiansen, S, Zuraw, BL, Cicardi, M, Craig, T, Longhurst, H, Grattan, C, Bork, K, Kreuz, W, Jacobs, I, Pragst, I, Herget, S, Dalton, S, Clement, C, Mycroft, S, Pawaskar, D, Zhang, Y, Machnig, T, Waldhauser, H, Feuersenger, H, Lawo, JP, Lang, D, Hoernlein, S, Mildenberger, M, Foeller, K, Ellis, F, Wood, D, Walsh, M, Qu, QL, Mueller-Stark, K, Feussner, A, Kalina, U, Ma, X, Rigsby, S, Scheffler, E, Fischer, JF, Kolb, C, Katelaris, CH, Frankum, B, Keat, K, Philip, B, Lee, JA, Urriola, N, Lee, MW, Sussman, GL, Levi, G, Gould, W, Ferrie, P, Rosenberg, E, Waserman, S, O'Quinn, J, Gagnon, R, Vachova, M, Stauerbach-Renz, P, Weber, A, Zimmer, S, Gilfert, T, Lang, B, Escuriola-Ettingshausen, C, Maurer, M, Metz, M, Schoepke, N, Altrichter, S, Hawro, T, Schwabe, D, Graff, J, Behrens, F, Kohm, M, Andarawewa, S, Temesszentandrasi, G, Kohalmi, VK, Kidon, M, Kadar, L, Benor, S, Bonanni, E, Wu, M, Zanichelli, A, Mansi, M, Rizzotto, A, Giardino, F, Fidone, F, Varga, M, Iftene, M, Badiu-Tisa, ID, Cabanas, R, Pedrosa, M, Rivero-Paparoni, D, Gomez-Traseira, C, Alvez, A, Phillips, E, Prieto, A, Zubeldia, J, Ibanez, E, Almero, R, Buckland, M, Grigoriadou, S, Manson, A, Yeatman, N, Laffan, J, Nasr, I, Ghurye, R, Rehman, T, Schaeffer, C, Ghaffari, G, Kelbel, T, Reddy, V, Buyantseva, L, Mende, C, Jose, J, Novchicht, T, Li, HH, Scarupa, M, Economides, A, White, M, Kaliner, M, Ward, C, Shaikh, S, Johnson, T, Kosh, L, Dauphin, P, Baker, J, Persons, S, Newman, A, Noonan, MJ, Lumry, WR, Poarch, KP, Tucker, J, Aguilar, D, Noth, D, Bernstein, J, Bernstein, D, Evans, S, Crawford, M, McGuckin, SD, McCollum, JR, Bradley, B, Wagner, C, Cartwright, A, Bonner, J, Soong, W, Sikora, M, Lemke, M, Luthin, P, Youngblood, B, DeBerry, E, Gilbert, E, Zhao, W, Ward, B, Alvarez, A, Kumar, S, Akl, E, Curl, J, Silva, K, Mostofi, T, Schultz, N, Manning, ME, Davis, A, Nelson, J, Levy, DS, Christiansen, SC, and COMPACT Investigators

Subjects
Hereditary angioedema, HAEGARDA, Long-term, Prophylaxis, Subcutaneous, Safety, C1-esterase inhibitor
Abstract

BACKGROUND: For the prevention of attacks of hereditary angioedema (HAE), the efficacy and safety of subcutaneous human C1-esterase inhibitor (C1-INH [SC]; HAEGARDA, CSL Behring) was established in the 16-week Clinical Study for Optimal Management of Preventing Angioedema with Low-Volume Subcutaneous C1-Inhibitor Replacement Therapy (COMPACT). OBJECTIVE: To assess the long-term safety, occurrence of angioedema attacks, and use of rescue medication with C1-INH(SC). METHODS: Open-label, randomized, parallel-arm extension of COMPACT across 11 countries. Patients with frequent angioedema attacks, either study treatment-naive or who had completed COMPACT, were randomly assigned (1:1) to 40 IU/ kg or 60 IU/kg C1-INH(SC) twice per week, with conditional uptitration to optimize prophylaxis (ClinicalTrials.gov registration no. NCT02316353). RESULTS: A total of 126 patients with a monthly attack rate of 4.3 in 3 months before entry in COMPACT were enrolled and treated for a mean of 1.5 years; 44 patients (34.9%) had more than 2 years of exposure. Mean steady-state C1-INH functional activity increased to 66.6% with 60 IU/kg. Incidence of adverse events was low and similar in both dose groups (11.3 and 8.5 events per patient-year for 40 IU/kg and 60 IU/kg, respectively). For 40 IU/kg and 60 IU/kg, median annualized attack rates were 1.3 and 1.0, respectively, and median rescue medication use was 0.2 and 0.0 times per year, respectively. Of 23 patients receiving 60 IU/kg for more than 2 years, 19 (83%) were attack-free during months 25 to 30 of treatment. CONCLUSIONS: In patients with frequent HAE attacks, long-term replacement therapy with C1-INH(SC) is safe and exhibits a substantial and sustained prophylactic effect, with the vast majority of patients becoming free from debilitating disease symptoms. (C) 2019 The Authors. Published by Elsevier Inc. on behalf of the American Academy of Allergy, Asthma & Immunology.

Published
2019

16. P150 ORAL PROPHYLAXIS WITH BCX7353 REDUCES HAE ATTACK RATES AND IS WELL-TOLERATED: APEX-2 STUDY RESULTS

Author

Zuraw, B., primary, Lumry, W., additional, Banerji, A., additional, Aygoren-Pursun, E., additional, Bernstein, J., additional, Johnston, D., additional, Christiansen, S., additional, Riedl, M., additional, Cicardi, M., additional, Maurer, M., additional, Cornpropst, M., additional, Dobo, S., additional, Iocca, H., additional, Nagy, E., additional, Murray, S., additional, Collis, P., additional, and Sheridan, W., additional

Published
2019
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17. P154 SAFETY AND TOLERABILITY OF ONCE-DAILY ORAL KALLIKREIN INHIBITOR BCX7353 IN PHASE 3 APEX-2 HAE STUDY

Author

Riedl, M., primary, Lumry, W., additional, Banerji, A., additional, Aygoren-Pursun, E., additional, Bernstein, J., additional, Maurer, M., additional, Cicardi, M., additional, Christiansen, S., additional, Zuraw, B., additional, Dobo, S., additional, Cornpropst, M., additional, Iocca, H., additional, Nagy, E., additional, Murray, S., additional, Collis, P., additional, Sheridan, W., additional, and Johnston, D., additional

Published
2019
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25. The international WAO/EAACI guideline for the management of hereditary angioedema-The 2017 revision and update

Author

Maurer, M., primary, Magerl, M., additional, Ansotegui, I., additional, Aygören-Pürsün, E., additional, Betschel, S., additional, Bork, K., additional, Bowen, T., additional, Balle Boysen, H., additional, Farkas, H., additional, Grumach, A. S., additional, Hide, M., additional, Katelaris, C., additional, Lockey, R., additional, Longhurst, H., additional, Lumry, W. R., additional, Martinez-Saguer, I., additional, Moldovan, D., additional, Nast, A., additional, Pawankar, R., additional, Potter, P., additional, Riedl, M., additional, Ritchie, B., additional, Rosenwasser, L., additional, Sánchez-Borges, M., additional, Zhi, Y., additional, Zuraw, B., additional, and Craig, T., additional

Published
2018
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26. International consensus on the diagnosis and management of pediatric patients with hereditary angioedema with C1 inhibitor deficiency

Author

Farkas, H, Martinez Saguer, I, Bork, K, Bowen, T, Craig, T, Frank, M, Germenis, Ae, Grumach, As, Luczay, A, Varga, L, Zanichelli, A, Aberer, W, Andrejevic, S, Aygoeren Pürsün, E, Banerji, A, Bara, Na, Bas, M, Bernstein, J, Betschel, S, Björkander, J, Boccon Gibod, I, Bouillet, L, Bova, M, Boysen, Hh, Branco Ferreira, M, Bygum, A, Caballero, T, Cancian, M, Castaldo, A, Christiansen, S, Cicardi, M, Drouet, C, Fabiani, J, Gompels, M, Gonzalez Quevedo MT, Gooi, J, Gower, R, Gökmen, Nm, Grivcheva Panovska, V, Guilarte, M, Gülbahar, O, Hack, E, Hakl, R, Harmat, G, Mjeseňák, M, Jolles, S, Kaplan, A, Katelaris, C, Kosnik, M, Kőhalmi, Kv, Leibovich, I, Levi, M, Li, H, Longhurst, Hj, Lumry, W, Magerl, M, Malbran, A, Martin, L, Maurer, M, Mihály, E, Moldovan, D, Murdjeva, M, Nagy, Ib, Nielsen, Ew, Nieto, S, Nordenfelt, P, Obtulowitzc, K, Pedrosa, M, Porębski, G, Prior, N, Reshef, A, Riedl, Ma, Rosenkranz, B, Schmid Grendelmeier, P, Péter, S, Speletas, M, Staevska, M, Stobiecki, M, Triggiani, Massimo, Veszeli, N, Wuillemin, W, Xiang, Zy, Yamamoto, B, and Zuraw, B.

Subjects
Male, Abdominal pain, Pediatrics, diagnosis, Comorbidity, Disease, Severity of Illness Index, Ecallantide, 0302 clinical medicine, Risk Factors, Diagnosis, Immunology and Allergy, heterocyclic compounds, 030212 general & internal medicine, Hereditary angioedema, Pediatric, Hereditary Angioedema Types I and II, Age Factors, Disease Management, Combined Modality Therapy, Immunodeficiencies, Management, Female, Original Article, Symptom Assessment, medicine.symptom, management, Algorithms, medicine.drug, medicine.medical_specialty, C1 inhibitor deficiency, Immunology, 03 medical and health sciences, Meta-Analysis as Topic, medicine, Humans, Mucous Membrane, Adult patients, business.industry, Original Articles, bacterial infections and mycoses, medicine.disease, hereditary angioedema, respiratory tract diseases, Clinical trial, pediatric, 030228 respiratory system, Differential diagnosis, business, Biomarkers
Abstract

BACKGROUND: The consensus documents published to date on hereditary angioedema with C1 inhibitor deficiency (C1-INH-HAE) have focused on adult patients. Many of the previous recommendations have not been adapted to pediatric patients. We intended to produce consensus recommendations for the diagnosis and management of pediatric patients with C1-INH-HAE.METHODS: During an expert panel meeting that took place during the 9th C1 Inhibitor Deficiency Workshop in Budapest, 2015 (www.haenet.hu), pediatric data were presented and discussed and a consensus was developed by voting.RESULTS: The symptoms of C1-INH-HAE often present in childhood. Differential diagnosis can be difficult as abdominal pain is common in pediatric C1-INH-HAE, but also commonly occurs in the general pediatric population. The early onset of symptoms may predict a more severe subsequent course of the disease. Before the age of 1 year, C1-INH levels may be lower than in adults; therefore, it is advisable to confirm the diagnosis after the age of one year. All neonates/infants with an affected C1-INH-HAE family member should be screened for C1-INH deficiency. Pediatric patients should always carry a C1-INH-HAE information card and medicine for emergency use. The regulatory approval status of the drugs for prophylaxis and for acute treatment is different in each country. Plasma-derived C1-INH, recombinant C1-INH, and ecallantide are the only agents licensed for the acute treatment of pediatric patients. Clinical trials are underway with additional drugs. It is recommended to follow up patients in an HAE comprehensive care center.CONCLUSIONS: The pediatric-focused international consensus for the diagnosis and management of C1-INH-HAE patients was created.

Published
2016
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33. Evidence-based recommendations for the therapeutic management of angioedema owing to hereditary C1 inhibitor deficiency: consensus report of an International Working Group

Author

Cicardi, M, Bork, K, Caballero, T, Craig, T, Hh, L, Longhurst, H, Reshef, A, Zuraw, B, Aberer, W, Aygören Pürsün, E, Banerji, A, Bjorkander, J, Boccon Gibod, I, Bouillet, L, Grenoble, F, Bova, M, Bowen, T, Calgary, C, Branco, F, Bygum, A, Cancian, M, Castel Branco, M, de Carolis, C, Mihály, E, Fabiani, J, Farkas, H, Gompels, M, Gower, R, Groffik, A, Grumach, A, Guillarte, M, Hack, E, Hernandez, L, Kaplan, A, Lara, A, Leibovich, I, Li, H, Lock, B, Lumry, W, Malbran, A, Martinez Saguer, I, Matta, C, Maurer, M, Moldovan, D, Montinaro, V, Nieto, S, Nordenfelt, P, Obtulovicz, K, Perricone, R, Prior, N, Riedl, M, Rodrigues do, V, Savoca, C, Spaeth, P, Staubach Renz, P, Stobiecki, M, Triggiani, M, Vacchini, R, Varga, L, Zanichelli, A, Zarchi, K, Zeerleder, S, and Zingale, L

Subjects
C1 inhibitor, Immunology, Angioedemas, Hereditary, Angioedemas, Complement C1 Inactivator Proteins, bradykinin receptor antagonist, Bradykinin, hereditary angioedema, Settore MED/16 - Reumatologia, kallikrein inhibitor, Hereditary, consensus document, Bradykinin Receptor Antagonists, Complement C1 Inhibitor Protein, Humans, Kallikreins, Peptides, Immunology and Allergy
Abstract

Angioedema owing to hereditary deficiency of C1 inhibitor (HAE) is a rare, life-threatening, disabling disease. In the last 2 years, the results of well-designed and controlled trials with existing and new therapies for this condition have been published, and new treatments reached the market. Current guidelines for the treatment for HAE were released before the new trials and before the new treatments became available and were essentially based on observational studies and expert opinion. To provide evidence-based HAE treatment guidelines supported by the new studies, a conference was held in Gargnano del Garda, Italy, from September 26 to 29, 2010. The meeting hosted 58 experienced HAE expert physicians, representatives of pharmaceutical companies and representatives of HAE patients' associations. Here, we report the topics discussed during the meeting and evidence-based consensus about management approaches for HAE in adult/adolescent patients.

Published
2012

36. The Effect of Location on the Value of Ornamental Trees Using the Example of a Green Space in Lublin

Author

Czernyszewicz Eugenia, Szymańska Małgorzata, Żuraw Beata, and Leziak Katarzyna

Subjects
value of trees, ornamental trees, location, valuation, q51, q56, q26, q19, o18, o13, d71, Real estate business, HD1361-1395.5
Abstract

This paper examines and identifies, using a specific example, how the location of trees influences their value. For the valuation of trees outside a forest area, appraisers often employ methods recommended for estimating forest stands, which significantly reduces the value of trees and valued properties. The tree-valuation method developed by SZCZEPANOWSKA et al. (2010) was used in our study. First, we compiled an inventory of trees located on plots intended for expropriation. The study covered all specimens with trunk circumferences of over 25 centimetres, which amounted to a total of 76 trees. We considered the value of the trees in the conditions of the actual location, which means that our calculations included house gardens in the city and the values of the same trees in hypothetical growth conditions: tree stands in rural and urban areas, green spaces in urban and rural areas, housing estates, roads and streets (both urban and rural), and historic areas, health resorts and health-resort protection zones.

Published
2019
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46. Requirement of phosphatidylinositol 3-kinase activity for bradykinin stimulation of NF-kappaB activation in cultured human epithelial cells.

Author

Pan, Z K, Christiansen, S C, Ptasznik, A, and Zuraw, B L

Abstract

The signaling mechanisms utilized by bradykinin (BK) to activate the transcription factor nuclear factor kappaB (NF-kappaB) are poorly defined. We previously demonstrated that BK-stimulated NF-kappaB activation requires the small GTPase RhoA. We present evidence that BK-induced NF-kappaB activation both activates and requires phosphatidylinositol 3-kinase (PI 3-kinase) in A549 human epithelial cells. Pre-treatment with the PI 3-kinase-specific inhibitors, wortmannin, and LY294002 effectively blocked BK-induced PI 3-kinase activity. Wortmannin and LY294002 also abolished BK-induced NF-kappaB activation, as did transient transfection with a dominant negative mutant of the p85 subunit. BK-stimulated PI 3-kinase activity and NF-kappaB activation were sensitive to pertussis but not cholera toxin, suggesting that the B2 BK receptors transducing the response were coupled to Galphai or Galphao heterotrimeric G proteins. Tumor necrosis factor alpha (TNFalpha) also stimulated increased PI 3-kinase activity, however TNFalpha-stimulated NF-kappaB activation was not affected by the PI 3-kinase inhibitors or the p85 dominant negative mutant. These findings provide evidence that BK-induced NF-kappaB activation utilizes a signaling pathway that requires activity of both RhoA and PI 3-kinase and is distinct from the signaling pathway utilized by TNFalpha. Furthermore, we show that the p85 regulatory subunit is required for activation of PI 3-kinase activity by this G protein-coupled receptor.

Published
1999

47. Detection of in vitro and in vivo cleavage of high molecular weight kininogen in human plasma by immunoblotting with monoclonal antibodies

Author

Berrettini, M, Lammle, B, White, T, Heeb, MJ, Schwarz, HP, Zuraw, B, Curd, J, and Griffin, JH

Abstract

Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system. After elution from SDS polyacrylamide gels, each of the two bands showed coagulant activity. Six murine monoclonal antibodies (Mabs) against HMWK were produced and purified. In immunoblotting studies, three Mabs bound to the isolated alkylated heavy chain and one to the alkylated light chain of HMWK, whereas the remaining two bound only to the single-chain or unreduced two-chain molecule. None of the Mabs inhibited the clotting activity of HMWK or its binding to kaolin. Two of the Mabs, one directed against the light chain and one against the heavy chain, were used as specific probes to study HMWK in plasma samples using an immunoblotting technique. The anti-light chain Mab identified two distinct bands (approximately 120,000 and approximately 105,000 mol wt) in normal human plasma, but not in plasma from patients with hereditary HMWK deficiency. The anti-heavy chain Mab detected two additional bands (approximately 60,000 and approximately 54,000 mol wt) corresponding to low-mol-wt kininogen (LMWK) in normal plasma. A sensitive and specific quantitative immunoblotting assay of HMWK antigen in plasma was developed. Moreover, the immunoblotting technique with the anti-light chain Mab was used to detect the cleavage of HMWK in plasma samples after in vitro or in vivo activation of the contact system. The anti- light chain Mab demonstrated in vivo activation and cleavage of HMWK during an angioedema attack in a patient with hereditary angioedema and C1-inhibitor deficiency.

Published
1986
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48. Stimulation of primary in vitro IgE antibody responses in culture of human peripheral mononuclear cells.

Author

Nonaka, M, Zuraw, B L, O'Hair, C H, and Katz, D H

Abstract

Experiments are presented herein that demonstrate the capacity to stimulate human peripheral mononuclear cells to synthesize and secrete significant quantities of IgE molecules in vitro by exposure to appropriate concentrations of 2,4-dinitrophenyl (DNP)-protein conjugates, pokeweed mitogen (PWM), or a combination of DNP-proteins and PWM. Cultures stimulated in this fashion synthesize increased quantities of both total IgE and DNP-specific IgE antibody molecules. This in vitro human IgE antibody system should provide a useful tool for further exploration of regulatory control of IgE responses in both normal humans and those manifesting various forms of IgE-mediated allergic disorders.

Published
1981
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50. Corticosteroid-induced gene expression in allergen-challenged asthmatic subjects taking inhaled budesonide.

Author

Kelly, M. M., King, E. M., Rider, C. F., Gwozd, C., Holden, Neil S., Eddleston, J., Zuraw, B., Leigh, R., O'Byrne, P. M., Newton, R., Kelly, M. M., King, E. M., Rider, C. F., Gwozd, C., Holden, Neil S., Eddleston, J., Zuraw, B., Leigh, R., O'Byrne, P. M., and Newton, R.

Abstract

BACKGROUND AND PURPOSE Inhaled corticosteroids (ICS) are the cornerstone of asthma pharmacotherapy and, acting via the glucocorticoid receptor (GR), reduce inflammatory gene expression. While this is often attributed to a direct inhibitory effect of the GR on inflammatory gene transcription, corticosteroids also induce the expression of anti-inflammatory genes in vitro. As there are no data to support this effect in asthmatic subjects taking ICS, we have assessed whether ICS induce anti-inflammatory gene expression in subjects with atopic asthma. EXPERIMENTAL APPROACH Bronchial biopsies from allergen-challenged atopic asthmatic subjects taking inhaled budesonide or placebo were subjected to gene expression analysis using real-time reverse transcriptase-PCR for the corticosteroid-inducible genes (official gene symbols with aliases in parentheses): TSC22D3 [glucocorticoid-induced leucine zipper (GILZ)], dual-specificity phosphatase-1 (MAPK phosphatase-1), both anti-inflammatory effectors, and FKBP5 [FK506-binding protein 51 (FKBP51)], a regulator of GR function. Cultured pulmonary epithelial and smooth muscle cells were also treated with corticosteroids before gene expression analysis. KEY RESULTS Compared with placebo, GILZ and FKBP51 mRNA expression was significantly elevated in budesonide-treated subjects. Budesonide also increased GILZ expression in human epithelial and smooth muscle cells in culture. Immunostaining of bronchial biopsies revealed GILZ expression in the airways epithelium and smooth muscle of asthmatic subjects. CONCLUSIONS AND IMPLICATIONS Expression of the corticosteroid-induced genes, GILZ and FKBP51, is up-regulated in the airways of allergen-challenged asthmatic subjects taking inhaled budesonide. Consequently, the biological effects of corticosteroid-induced genes should be considered when assessing the actions of ICS. Treatment modalities that increase or decrease GR-dependent transcription may correspondingly affect corticosteroid efficacy.

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