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1. The factor VIII treatment history of non-severe hemophilia A

Author

Abdi, A., Kloosterman, F.R., Eckhardt, C.L. (Corien), Male, C. (Christoph), Castaman, G. (Giancarlo), Fischer, K, Beckers, E.A.M. (Erik), Kruip, M.J.H.A. (Marieke), Peerlinck, K., Mancuso, M.E., Santoro, C., Hay, C.R.M. (Charles R.), Platokouki, H. (Helena), Bom, J.G., Gouw, S.C. (S.), Fijnvandraat, K., Hart, D.P. (Daniel), Abdi, A., Kloosterman, F.R., Eckhardt, C.L. (Corien), Male, C. (Christoph), Castaman, G. (Giancarlo), Fischer, K, Beckers, E.A.M. (Erik), Kruip, M.J.H.A. (Marieke), Peerlinck, K., Mancuso, M.E., Santoro, C., Hay, C.R.M. (Charles R.), Platokouki, H. (Helena), Bom, J.G., Gouw, S.C. (S.), Fijnvandraat, K., and Hart, D.P. (Daniel)

Abstract

Background: In patients with non-severe hemophilia A, we lack detailed knowledge on the timing of treatment with factor VIII (FVIII) concentrates. This knowledge could provide information about the expected treatment timing in patients with severe hemophilia A treated with non-replacement therapies. Objective: To assess the FVIII treatment history in patients with non-severe hemophilia A. Methods: Patients with non-severe hemophilia (baseline FVIII activity [FVIII:C] 2-40 IU/dL) were included from the INSIGHT study. The primary outcome was median age at first FVIII exposure (ED1). In a subgroup of patients for whom more detailed information was available, we analyzed the secondary outcomes: median age at first 20 EDs, annualized bleeding rate for all bleeds (ABR), joint bleeds (AJBR), and major spontaneous bleeds (ASmBR). Results: In the total cohort (n = 1013), median baseline FVIII activity was 8 IU/dL (interquartile range [IQR] 4-15) and the median age at ED1 was 3.7 years (IQR 1.4-7.7). Median age at ED1 rose from 2.5 years (IQR 1.2-5.7) in patients with FVIII:C 2-5 IU/dL to 9.7 years (IQR 4.8-16.0) in patients with FVIII:C 25-40 IU/dL. In the subgroup (n = 104), median age at ED1, ED5, ED10, and ED20 was 4.0 years (IQR 1.4-7.6), 5.6 years (IQR 2.9-9.3), 7.5 years (IQR 4.4-11.3), and 10.2 years (IQR 6.5-14.2), respectively. Median ABR, AJBR, and ASmBR were 1.1 (IQR 0.5-2.6), 0.3 (IQR 0.1-0.7), and 0 (IQR 0-0), respectively. Conclusion: This study demonstrates that in non-severe hemophilia A, the age at first FVIII exposure increases with baseline FVIII:C and that major spontaneous bleeds rarely occur.

Published
2020
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2. The factor VIII treatment history of non-severe hemophilia A

Author

Abdi, A, Kloosterman, FR, Eckhardt, CL, Male, C, Castaman, G, Fischer, K, Beckers, EAM, Kruip, Marieke, Peerlinck, K, Mancuso, ME, Santoro, C, Hay, CRM, Platokouki, H, Bom, Josine, Gouw, SC, Fijnvandraat, K, Hart, DP, Abdi, A, Kloosterman, FR, Eckhardt, CL, Male, C, Castaman, G, Fischer, K, Beckers, EAM, Kruip, Marieke, Peerlinck, K, Mancuso, ME, Santoro, C, Hay, CRM, Platokouki, H, Bom, Josine, Gouw, SC, Fijnvandraat, K, and Hart, DP

Published
2020

3. Desmopressin in moderate hemophilia a patients: A treatment worth considering

Author

Loomans, J.I. (Janneke I.), Kruip, M.J.H.A. (Marieke), Carcao, M. (M.), Jackson, S. (Shannon), Velzen, A.S. (Alice) van, Peters, M.A.D. (Marjolein), Santagostino, E. (Elena), Platokouki, H. (Helen), Beckers, E.A.M. (Erik), Voorberg, J. (Jan), Bom, J.G. (Anske) van der, Fijnvandraat, K., Loomans, J.I. (Janneke I.), Kruip, M.J.H.A. (Marieke), Carcao, M. (M.), Jackson, S. (Shannon), Velzen, A.S. (Alice) van, Peters, M.A.D. (Marjolein), Santagostino, E. (Elena), Platokouki, H. (Helen), Beckers, E.A.M. (Erik), Voorberg, J. (Jan), Bom, J.G. (Anske) van der, and Fijnvandraat, K.

Abstract

Desmopressin increases endogenous factor VIII levels in hemophilia A. Large inter-individual variation in the response to desmopressin is observed. Patients with a lower baseline factor VIII activity tend to show a reduced response, therefore, desmopressin is less frequently used in moderate hemophilia A patients (baseline factor VIII activity 1-5 international units/deciliter), even though factor VIII levels may rise substantially in some of them. We aim to describe the response to desmopressin in moderate hemophilia A patients and to identify predictors. We selected data on 169 patients with moderate hemophilia from the multicenter Response to DDAVP In non-severe hemophilia A patients: in Search for dEterminants (RISE) cohort study. Adequate response to desmopressin was defined as a peak factor VIII level ≥ 30, and excellent response as ≥ 50 international units/deciliter after desmopressin administration. We used univariate and multiple linear regression techniques to analyze predictors of the peak factor VIII level. Response was considered adequate in 68 patients (40%), of whom 25 showed excellent response (15%). Intravenous administration, age, pre-desmopressin factor VIII activity and von Willebrand factor antigen, peak von Willebrand factor activity and desmopressin-induced rise in von Willebrand factor antigen were significant predictors of peak factor VIII level and explained 65% of the inter-individual variation. In 40% of moderate hemophilia A patients, desmopressin response was adequate, thus it is important not to withhold this group of patients from desmopressin responsiveness. Among the six predictors that we identified for desmopressin-induced factor VIII rise, factor VIII activity and desmopressin-induced rise in von Willebrand factor antigen had the strongest effect.

Published
2018
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6. Vaccinations are not associated with inhibitor development in boys with severe haemophilia A

Author

Poli Van Creveldkliniek Medisch, Child Health, Circulatory Health, Datamanagement 1, Platokouki, H., Fischer, K., Gouw, S. C., Rafowicz, A., Carcao, M., Kenet, G., Liesner, R., Kurnik, K., Rivard, G. E., van den Berg, H. M., Poli Van Creveldkliniek Medisch, Child Health, Circulatory Health, Datamanagement 1, Platokouki, H., Fischer, K., Gouw, S. C., Rafowicz, A., Carcao, M., Kenet, G., Liesner, R., Kurnik, K., Rivard, G. E., and van den Berg, H. M.

Published
2018

7. Desmopressin in moderate hemophilia A patients: a treatment worth considering

Author

Loomans, JI, Kruip, Marieke, Carcao, M, Jackson, S, van Velzen, AS, Peters, M, Santagostino, E, Platokouki, H, Beckers, E, Voorberg, J, van der Bom, JG, Fijnvandraat, K, Loomans, JI, Kruip, Marieke, Carcao, M, Jackson, S, van Velzen, AS, Peters, M, Santagostino, E, Platokouki, H, Beckers, E, Voorberg, J, van der Bom, JG, and Fijnvandraat, K

Published
2018

11. Continuous infusion of recombinant factor VIII formulated with sucrose in surgery: non-interventional, observational study in patients with severe haemophilia A

Author

Poli Van Creveldkliniek Medisch, Circulatory Health, Meijer, K, Rauchensteiner, S, Santagostino, E, Platokouki, H, Schutgens, R E G, Brunn, M, Tueckmantel, C, Valeri, F, Schinco, P C, Poli Van Creveldkliniek Medisch, Circulatory Health, Meijer, K, Rauchensteiner, S, Santagostino, E, Platokouki, H, Schutgens, R E G, Brunn, M, Tueckmantel, C, Valeri, F, and Schinco, P C

Published
2015

12. MYH9-Related Disease: A Novel Prognostic Model to Predict the Clinical Evolution of the Disease Based on Genotype-Phenotype Correlations

Author

Pecci, A, Klersy, C, Gresele, P, Lee, Kj, De Rocco, D, Bozzi, V, Russo, G, Heller, Pg, Loffredo, G, Ballmaier, M, Fabris, F, Beggiato, E, Kahr, Wh, Pujol Moix, N, Platokouki, H, Van Geet, C, Noris, P, Yerram, P, Hermans, C, Gerber, B, Economou, M, De Groot, M, Zieger, B, De Candia, Erica, Fraticelli, V, Kersseboom, R, Piccoli, Gb, Zimmermann, S, Fierro, T, Glembotsky, Ac, Vianello, F, Zaninetti, C, Nicchia, E, Güthner, C, Baronci, C, Seri, M, Knight, Pj, Balduini, Cl, Savoia, A., De Candia, Erica (ORCID:0000-0003-0942-2819), Pecci, A, Klersy, C, Gresele, P, Lee, Kj, De Rocco, D, Bozzi, V, Russo, G, Heller, Pg, Loffredo, G, Ballmaier, M, Fabris, F, Beggiato, E, Kahr, Wh, Pujol Moix, N, Platokouki, H, Van Geet, C, Noris, P, Yerram, P, Hermans, C, Gerber, B, Economou, M, De Groot, M, Zieger, B, De Candia, Erica, Fraticelli, V, Kersseboom, R, Piccoli, Gb, Zimmermann, S, Fierro, T, Glembotsky, Ac, Vianello, F, Zaninetti, C, Nicchia, E, Güthner, C, Baronci, C, Seri, M, Knight, Pj, Balduini, Cl, Savoia, A., and De Candia, Erica (ORCID:0000-0003-0942-2819)

Abstract

MYH9-related disease (MYH9-RD) is a rare autosomal-dominant disorder caused by mutations in the gene for nonmuscle myosin heavy chain IIA (NMMHC-IIA). MYH9-RD is characterized by a considerable variability in clinical evolution: patients present at birth with only thrombocytopenia, but some of them subsequently develop sensorineural deafness, cataract, and/or nephropathy often leading to end-stage renal disease (ESRD). We searched for genotype-phenotype correlations in the largest series of consecutive MYH9-RD patients collected so far (255 cases from 121 families). Association of genotypes with noncongenital features was assessed by a generalized linear regression model. The analysis defined disease evolution associated to seven different MYH9 genotypes that are responsible for 85% of MYH9-RD cases. Mutations hitting residue R702 demonstrated a complete penetrance for early-onset ESRD and deafness. The p.D1424H substitution associated with high risk of developing all the noncongenital manifestations of disease. Mutations hitting a distinct hydrophobic seam in the NMMHC-IIA head domain or substitutions at R1165 associated with high risk of deafness but low risk of nephropathy or cataract. Patients with p.E1841K, p.D1424N, and C-terminal deletions had low risk of noncongenital defects. These findings are essential to patients' clinical management and genetic counseling and are discussed in view of molecular pathogenesis of MYH9-RD.

Published
2014

13. MYH9-Related Disease: A Novel Prognostic Model to Predict the Clinical Evolution of the Disease Based on Genotype-Phenotype Correlations

Author

Pecci, A, Klersy, C, Gresele, P, Lee, Kjd, De Rocco, D, Bozzi, V, Russo, G, Heller, Pg, Loffredo, G, Ballmaier, M, Fabris, F, Beggiato, E, Kahr, Wha, Pujol Moix, N, Platokouki, H, Van Geet, C, Noris, P, Yerram, P, Hermans, C, Gerber, B, Economou, M, De Groot, M, Zieger, B, De Candia, Erica, Fraticelli, V, Kersseboom, R, Piccoli, Gb, Zimmermann, S, Fierro, T, Glembotsky, Ac, Vianello, F, Zaninetti, C, Nicchia, E, Güthner, C, Baronci, C, Seri, M, Knight, Pj, Balduini, Cl, Savoia, A., De Candia, Erica (ORCID:0000-0003-0942-2819), Pecci, A, Klersy, C, Gresele, P, Lee, Kjd, De Rocco, D, Bozzi, V, Russo, G, Heller, Pg, Loffredo, G, Ballmaier, M, Fabris, F, Beggiato, E, Kahr, Wha, Pujol Moix, N, Platokouki, H, Van Geet, C, Noris, P, Yerram, P, Hermans, C, Gerber, B, Economou, M, De Groot, M, Zieger, B, De Candia, Erica, Fraticelli, V, Kersseboom, R, Piccoli, Gb, Zimmermann, S, Fierro, T, Glembotsky, Ac, Vianello, F, Zaninetti, C, Nicchia, E, Güthner, C, Baronci, C, Seri, M, Knight, Pj, Balduini, Cl, Savoia, A., and De Candia, Erica (ORCID:0000-0003-0942-2819)

Abstract

MYH9-related disease (MYH9-RD) is a rare autosomal-dominant disorder caused by mutations in the gene for nonmuscle myosin heavy chain IIA (NMMHC-IIA). MYH9-RD is characterized by a considerable variability in clinical evolution: patients present at birth with only thrombocytopenia, but some of them subsequently develop sensorineural deafness, cataract, and/or nephropathy often leading to end-stage renal disease (ESRD). We searched for genotype-phenotype correlations in the largest series of consecutive MYH9-RD patients collected so far (255 cases from 121 families). Association of genotypes with noncongenital features was assessed by a generalized linear regression model. The analysis defined disease evolution associated to seven different MYH9 genotypes that are responsible for 85% of MYH9-RD cases. Mutations hitting residue R702 demonstrated a complete penetrance for early-onset ESRD and deafness. The p.D1424H substitution associated with high risk of developing all the noncongenital manifestations of disease. Mutations hitting a distinct hydrophobic seam in the NMMHC-IIA head domain or substitutions at R1165 associated with high risk of deafness but low risk of nephropathy or cataract. Patients with p.E1841K, p.D1424N, and C-terminal deletions had low risk of noncongenital defects. These findings are essential to patients' clinical management and genetic counseling and are discussed in view of molecular pathogenesis of MYH9-RD.

Published
2014

14. Factor VIII gene (F8) mutation and risk of inhibitor development in nonsevere hemophilia A.

Author

Eckhardt, C.L., Velzen, A.S. van, Peters, M., Astermark, J., Brons, P.P., Castaman, G., Cnossen, M.H., Dors, N., Escuriola-Ettingshausen, C., Hamulyak, K., Hart, D.P., Hay, C.R., Haya, S., Heerde, W.L. van, Hermans, C., Holmstrom, M., Jimenez-Yuste, V., Keenan, R.D., Klamroth, R., Laros-van Gorkom, B.A.P., Leebeek, F.W., Liesner, R., Makipernaa, A., Male, C., Mauser-Bunschoten, E., Mazzucconi, M.G., McRae, S., Meijer, K., Mitchell, M., Morfini, M., Nijziel, M., Oldenburg, J., Peerlinck, K., Petrini, P., Platokouki, H., Reitter-Pfoertner, S.E., Santagostino, E., Schinco, P., Smiers, F.J., Siegmund, B., Tagliaferri, A., Yee, T.T., Kamphuisen, P.W., Bom, J.G. Van Der, Fijnvandraat, K., Eckhardt, C.L., Velzen, A.S. van, Peters, M., Astermark, J., Brons, P.P., Castaman, G., Cnossen, M.H., Dors, N., Escuriola-Ettingshausen, C., Hamulyak, K., Hart, D.P., Hay, C.R., Haya, S., Heerde, W.L. van, Hermans, C., Holmstrom, M., Jimenez-Yuste, V., Keenan, R.D., Klamroth, R., Laros-van Gorkom, B.A.P., Leebeek, F.W., Liesner, R., Makipernaa, A., Male, C., Mauser-Bunschoten, E., Mazzucconi, M.G., McRae, S., Meijer, K., Mitchell, M., Morfini, M., Nijziel, M., Oldenburg, J., Peerlinck, K., Petrini, P., Platokouki, H., Reitter-Pfoertner, S.E., Santagostino, E., Schinco, P., Smiers, F.J., Siegmund, B., Tagliaferri, A., Yee, T.T., Kamphuisen, P.W., Bom, J.G. Van Der, and Fijnvandraat, K.

Abstract

Item does not contain fulltext, Neutralizing antibodies (inhibitors) toward factor VIII form a severe complication in nonsevere hemophilia A, profoundly aggravating the bleeding pattern. Identification of high-risk patients is hampered by lack of data that take exposure days to therapeutic factor VIII concentrates into account. In the INSIGHT study, we analyzed the association between F8 mutation and inhibitor development in patients with nonsevere hemophilia A (factor VIII 2-40 IU/dL). This analysis included 1112 nonsevere hemophilia A patients from 14 centers in Europe and Australia that had genotyped at least 70% of their patients. Inhibitor risk was calculated as Kaplan-Meier incidence with cumulative number of exposure days as the time variable. During 44 800 exposure days (median, 24 exposure days per patient; interquartile range [IQR], 7-90), 59 of the 1112 patients developed an inhibitor; cumulative incidence of 5.3% (95% confidence interval [CI], 4.0-6.6) after a median of 28 exposure days (IQR, 12-71). The inhibitor risk at 50 exposure days was 6.7% (95% CI, 4.5-8.9) and at 100 exposure days the risk further increased to 13.3% (95% CI, 9.6-17.0). Among a total of 214 different F8 missense mutations 19 were associated with inhibitor development. These results emphasize the importance of F8 genotyping in nonsevere hemophilia A.

Published
2013

15. Factor VIII gene (F8) mutation and risk of inhibitor development in nonsevere hemophilia A.

Author

Eckhardt, C.L., Velzen, A.S. van, Peters, M., Astermark, J., Brons, P.P., Castaman, G., Cnossen, M.H., Dors, N., Escuriola-Ettingshausen, C., Hamulyak, K., Hart, D.P., Hay, C.R., Haya, S., Heerde, W.L. van, Hermans, C., Holmstrom, M., Jimenez-Yuste, V., Keenan, R.D., Klamroth, R., Laros-van Gorkom, B.A.P., Leebeek, F.W., Liesner, R., Makipernaa, A., Male, C., Mauser-Bunschoten, E., Mazzucconi, M.G., McRae, S., Meijer, K., Mitchell, M., Morfini, M., Nijziel, M., Oldenburg, J., Peerlinck, K., Petrini, P., Platokouki, H., Reitter-Pfoertner, S.E., Santagostino, E., Schinco, P., Smiers, F.J., Siegmund, B., Tagliaferri, A., Yee, T.T., Kamphuisen, P.W., Bom, J.G. Van Der, Fijnvandraat, K., Eckhardt, C.L., Velzen, A.S. van, Peters, M., Astermark, J., Brons, P.P., Castaman, G., Cnossen, M.H., Dors, N., Escuriola-Ettingshausen, C., Hamulyak, K., Hart, D.P., Hay, C.R., Haya, S., Heerde, W.L. van, Hermans, C., Holmstrom, M., Jimenez-Yuste, V., Keenan, R.D., Klamroth, R., Laros-van Gorkom, B.A.P., Leebeek, F.W., Liesner, R., Makipernaa, A., Male, C., Mauser-Bunschoten, E., Mazzucconi, M.G., McRae, S., Meijer, K., Mitchell, M., Morfini, M., Nijziel, M., Oldenburg, J., Peerlinck, K., Petrini, P., Platokouki, H., Reitter-Pfoertner, S.E., Santagostino, E., Schinco, P., Smiers, F.J., Siegmund, B., Tagliaferri, A., Yee, T.T., Kamphuisen, P.W., Bom, J.G. Van Der, and Fijnvandraat, K.

Abstract

Item does not contain fulltext, Neutralizing antibodies (inhibitors) toward factor VIII form a severe complication in nonsevere hemophilia A, profoundly aggravating the bleeding pattern. Identification of high-risk patients is hampered by lack of data that take exposure days to therapeutic factor VIII concentrates into account. In the INSIGHT study, we analyzed the association between F8 mutation and inhibitor development in patients with nonsevere hemophilia A (factor VIII 2-40 IU/dL). This analysis included 1112 nonsevere hemophilia A patients from 14 centers in Europe and Australia that had genotyped at least 70% of their patients. Inhibitor risk was calculated as Kaplan-Meier incidence with cumulative number of exposure days as the time variable. During 44 800 exposure days (median, 24 exposure days per patient; interquartile range [IQR], 7-90), 59 of the 1112 patients developed an inhibitor; cumulative incidence of 5.3% (95% confidence interval [CI], 4.0-6.6) after a median of 28 exposure days (IQR, 12-71). The inhibitor risk at 50 exposure days was 6.7% (95% CI, 4.5-8.9) and at 100 exposure days the risk further increased to 13.3% (95% CI, 9.6-17.0). Among a total of 214 different F8 missense mutations 19 were associated with inhibitor development. These results emphasize the importance of F8 genotyping in nonsevere hemophilia A.

Published
2013

16. Factor VIII gene (F8) mutation and risk of inhibitor development in nonsevere hemophilia A.

Author

Eckhardt, C.L., Velzen, A.S. van, Peters, M., Astermark, J., Brons, P.P., Castaman, G., Cnossen, M.H., Dors, N., Escuriola-Ettingshausen, C., Hamulyak, K., Hart, D.P., Hay, C.R., Haya, S., Heerde, W.L. van, Hermans, C., Holmstrom, M., Jimenez-Yuste, V., Keenan, R.D., Klamroth, R., Laros-van Gorkom, B.A.P., Leebeek, F.W., Liesner, R., Makipernaa, A., Male, C., Mauser-Bunschoten, E., Mazzucconi, M.G., McRae, S., Meijer, K., Mitchell, M., Morfini, M., Nijziel, M., Oldenburg, J., Peerlinck, K., Petrini, P., Platokouki, H., Reitter-Pfoertner, S.E., Santagostino, E., Schinco, P., Smiers, F.J., Siegmund, B., Tagliaferri, A., Yee, T.T., Kamphuisen, P.W., Bom, J.G. Van Der, Fijnvandraat, K., Eckhardt, C.L., Velzen, A.S. van, Peters, M., Astermark, J., Brons, P.P., Castaman, G., Cnossen, M.H., Dors, N., Escuriola-Ettingshausen, C., Hamulyak, K., Hart, D.P., Hay, C.R., Haya, S., Heerde, W.L. van, Hermans, C., Holmstrom, M., Jimenez-Yuste, V., Keenan, R.D., Klamroth, R., Laros-van Gorkom, B.A.P., Leebeek, F.W., Liesner, R., Makipernaa, A., Male, C., Mauser-Bunschoten, E., Mazzucconi, M.G., McRae, S., Meijer, K., Mitchell, M., Morfini, M., Nijziel, M., Oldenburg, J., Peerlinck, K., Petrini, P., Platokouki, H., Reitter-Pfoertner, S.E., Santagostino, E., Schinco, P., Smiers, F.J., Siegmund, B., Tagliaferri, A., Yee, T.T., Kamphuisen, P.W., Bom, J.G. Van Der, and Fijnvandraat, K.

Abstract

Item does not contain fulltext, Neutralizing antibodies (inhibitors) toward factor VIII form a severe complication in nonsevere hemophilia A, profoundly aggravating the bleeding pattern. Identification of high-risk patients is hampered by lack of data that take exposure days to therapeutic factor VIII concentrates into account. In the INSIGHT study, we analyzed the association between F8 mutation and inhibitor development in patients with nonsevere hemophilia A (factor VIII 2-40 IU/dL). This analysis included 1112 nonsevere hemophilia A patients from 14 centers in Europe and Australia that had genotyped at least 70% of their patients. Inhibitor risk was calculated as Kaplan-Meier incidence with cumulative number of exposure days as the time variable. During 44 800 exposure days (median, 24 exposure days per patient; interquartile range [IQR], 7-90), 59 of the 1112 patients developed an inhibitor; cumulative incidence of 5.3% (95% confidence interval [CI], 4.0-6.6) after a median of 28 exposure days (IQR, 12-71). The inhibitor risk at 50 exposure days was 6.7% (95% CI, 4.5-8.9) and at 100 exposure days the risk further increased to 13.3% (95% CI, 9.6-17.0). Among a total of 214 different F8 missense mutations 19 were associated with inhibitor development. These results emphasize the importance of F8 genotyping in nonsevere hemophilia A.

Published
2013

17. Factor VIII gene (F8) mutation and risk of inhibitor development in nonsevere hemophilia A

Author

Eckhardt, CL, van Velzen, AS, Peters, M, Astermark, J, Brons, PP, Castaman, G, Cnossen, Marjon, Dors, N, Escuriola-Ettingshausen, C, Hamulyak, K, Hart, DP, Hay, CRM, Haya, S, van Heerde, WL, Hermans, C, Holmstrom, M, Jimenez-Yuste, V, Keenan, RD, Klamroth, R, Laros-Van Gorkom, BAP, Leebeek, Frank, Liesner, R, Makipernaa, A, Male, C, Mauser-Bunschoten, E, Mazzucconi, MG, Mcrae, S, Meyer, K, Mitchell, M, Morfini, M, Nijziel, M, Oldenburg, J, Peerlinck, K, Petrini, P, Platokouki, H, Reitter-Pfoertner, SE, Santagostino, E, Schinco, P, Smiers, FJ, Siegmund, B, Tagliaferri, A, Yee, TT, Kamphuisen, PW, van der Bom, JG (Anske), Fijnvandraat, K, Eckhardt, CL, van Velzen, AS, Peters, M, Astermark, J, Brons, PP, Castaman, G, Cnossen, Marjon, Dors, N, Escuriola-Ettingshausen, C, Hamulyak, K, Hart, DP, Hay, CRM, Haya, S, van Heerde, WL, Hermans, C, Holmstrom, M, Jimenez-Yuste, V, Keenan, RD, Klamroth, R, Laros-Van Gorkom, BAP, Leebeek, Frank, Liesner, R, Makipernaa, A, Male, C, Mauser-Bunschoten, E, Mazzucconi, MG, Mcrae, S, Meyer, K, Mitchell, M, Morfini, M, Nijziel, M, Oldenburg, J, Peerlinck, K, Petrini, P, Platokouki, H, Reitter-Pfoertner, SE, Santagostino, E, Schinco, P, Smiers, FJ, Siegmund, B, Tagliaferri, A, Yee, TT, Kamphuisen, PW, van der Bom, JG (Anske), and Fijnvandraat, K

Published
2013

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