17 results on '"Kotalova R"'
Search Results
2. 791 Outcome of Czech Infants with Biliary Atresia After 10 Years Period (1998-2009)
- Author
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Kotalova, R, primary, Blahova, K, additional, Rygl, M, additional, Snajdauf, J, additional, and Keil, R, additional
- Published
- 2010
- Full Text
- View/download PDF
3. Czech national survey to identify hospitalized children at risk of malnutrition
- Author
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Pozler, O., Barnetová, D., Bronský, J., Frühauf, P., Jimramovský, F., Karásková, E., Kotalová, R., Lokaj, P., Nevoral, J., Sýkora, J., Šípková, E., Šuláková, A., and Czech NutriAction working group
- Published
- 2013
- Full Text
- View/download PDF
4. Association of IL23R p.381Gln and ATG16L1 p.197Ala with Crohn disease in the Czech population.
- Author
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Dusatkova P, Hradsky O, Lenicek M, Bronsky J, Nevoral J, Kotalova R, Bajerova K, Vitek L, Lukas M, Cinek O, Dusatkova, Petra, Hradsky, Ondrej, Lenicek, Martin, Bronsky, Jiri, Nevoral, Jiri, Kotalova, Radana, Bajerova, Katerina, Vitek, Libor, Lukas, Milan, and Cinek, Ondrej
- Published
- 2009
- Full Text
- View/download PDF
5. 35th Annual Meeting of the European Association for the Study of Diabetes : Brussels, Belgium, 28 September-2 October 1999
- Author
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Ad Darts Memo, Morris For The Collaboration, Juhl, C., Porksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th, Muller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Bjorn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H-M, Oksanen, L., Tuomainen, T-P, Kontula, K., Salonen, J. T., Dekker, J. M., Boks, P., Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., Macalpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M. Jr, Kozakova, H., Kaas, A., Kofronova, O., Tlaskalova-Hogenova, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sorensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Hasko, G., Szabo, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H-H, Genediab, Study Group, Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabak, A. Gy, Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Canton, A., Burgos, R., Hernandez, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simo, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., Mcdermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y-S, Sternesjo, J., Sandler, S., Chen, M-C, Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Breant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. I., Hamilton-Wessler, M., Markussen, J., Bergman, R. N., Melki, V., Hanaire-Broutin, H., Bessieres-Lacombe, S., Gedec, Study Group, Tauber, J-P, Home, P. D., Lindholm, A., Riis, A., European Insulin Aspart Study Group, Rosenstock, J., Schwartz, S., Clark, C., Edwards, M., Donley, D., Us Dm, Study Group Of Insulin Glargine In Type, Swift, P., Mortensen, H. B., Lynggaard, H., Hougaard, P., Hvidore Study group on Childhood Diabetes, Cull, C. A., Neil, H. A. W., Frighi, V., Manley, S. E., Holman, R. R., Turner, R. C., Ukpds, Group, Steiner, G., Dais, Project Group, Davis, W. A., Weeraratna, T., Bruce, D. G., Davis, T. M. E., Verges, B., Duvillard, L., Pont, F., Florentin, E., Gambert, Ph, Benko, B., Ljubic, S., Turk, Z., Granic, M., Marz, W., Wollschlager, H., Klein, G., Neiss, A., Wehling, M., Huxtable, S. J., Saker, P. J., Walker, M., Frayling, T. M., Levy, J. C., O Rahilly, S., Hattersley, A. T., Mccarthy, M. I., Orecchio, A., Giacchini, A., Dominici, R., Canettieri, G., Trinti, B., Zani, M., Andreoli, M., Sciacchitano, S., Silva, A. M., Whitecross, K., Pasco, J., Kotowicz, M., Nicholson, G., Zimmet, P., Boyko, E. J., Collier, G. R., Frittitta, L., Pizzuti, A., Argiolas, A., Graci, S., Goldfine, I. D., Bozzali, M., Ercolino, T., Costanzo, B., Iacoviello, L., Tassi, V., Trischitta, V., Wauters, M., Rankinen, T., Mertens, I., Chagnon, M., Bouchard, C., Gaal, L., Sivenius, K., Valve, R., Hakkarainen, V., Niskanen, L., Laakso, M., Uusitupa, M., Beridze, N., Japaridze, M., Kurashvili, R., Dundua, M., Kebuladze, G., Kazakhashvili, N., Offley-Shore, B., Thomas, B., Ghebremeskel, K., Crawford, M., Lowy, C., Eriksson, Ulf J., Martin Siman, C., Wisse, Bert, Gittenberger-De Groot, Adriana C., Wentzel, P., Eriksson, U. J., Wender-Ozegowska, E., Drews, K., Biczysko, R., Bronisz, A., Rosc, D., Graczykowska-Koczorowska, A., Kotschy, M., Sokup, A., Kohnert, K. D., Besch, W., Strese, J., Frick, U., Zander, E., Kemer, W., Skrha, J., Kvasnicka, J., Kalvodova, B., Hilgertova, J., Schatteman, K., Goossens, F., Scharpe, S., Leeuw, I., Hendriks, D., Legakis, I. N., Panayiotou, D., Mountokalakis, Th D., Enderle, M. D., Beckmann, P., Balletshofer, B., Rittig, K., Maerker, E., Volk, A., Meisner, C., Jacob, S., Matthaei, S., Haring, H. U., Rett, K., Ueda, K., Nakagawa, T., Shimajiri, Y., Kokawa, M., Matsumoto, E., Sasaki, H., Sanke, T., Nanjo, K., Mckinnon, Caroline M., Macfarlane, Wendy M., Docherty, Kevin, Furukawa, N., Shirotani, T., Kishikawa, H., Kaneko, K., Araki, E., Shichiri, M., Prentki, M., Roduit, R., Susini, S., Buteau, J., Ejrnas, A. M., Andersen, N. Aa, Osterhoff, M., Mohlig, M., Ortmann, J., Bikashaghi, F., Mayer, C., Bikashagi, F., Ackermans, M. T., Pereira Arias, A. M., Bisschop, P. H. L. T., Endert, E., Sauerwein, H. P., Romijn, J. A., Gastaldelli, A., Baldi, S., Pettiti, M., Natali, A., Frascerra, S., Camastra, S., Toschi, E., Ferrannini, E., Stingl, H., Krssak, M., Bischof, M. G., Krebs, M., Furnsinn, C., Nowotny, P., Waldhausl, W., Roden, M., Neeft, M., Meijer, A. J., Bavenholm, P., Pigon, J., Efendic, S., Kastenbauer, T., Sauseng, S., Sokol, G., Auinger, M., Irsigler, K., Abbott, C. A., Carrington, A. L., Faragher, B., Kulkarni, J., Ross, E. R. E., Boulton, A. J. M., Armstrong, D. G., Hadi, S., Nguyen, H. C., Harkless, L. B., Jirkovska, A., Kasalicky, P., Hosova, J., Skibova, J., Uccioli, L., Caselli, A., Giacomozzi, C., Macellari, V., Giurato, L., Lardieri, L., Menzinger, G., Pham, H. T., Rosenblum, B. I., Lyons, T. E., Giurini, J. M., Smakowski, P., Chrzan, J. S., Habershaw, G. M., Veves, A., Foster, A. M., Bates, M., Doxford, M., Edmonds, M. E., Kecha, O., Winkler, R., Martens, H., Collette, J., Lefebvre, P. J., Greiner, D., Geenen, V., Atlan-Gepner, C., Naspetti, M., Valero, R., Barad, M., Lepault, F., Vialettes, B., Naquet, P., Galan, B., Netea, M. G., Hancu, N., Smits, P., Meer, J. W. M., Osterbye, T., Jorgensen, K. H., Tranum-Jensen, J., Fredman, P., Hoy, M., Bokvist, K., Olsen, H. L., Horn, T., Gromada, J., Laub, R., Lohmann, T., Hahn, H. J., Adler, T., Emmrich, F., Rabuazzo, A. M., Lupi, R., Dotta, F., Patane, G., Marselli, L., Realacci, M., Piro, S., Del Guerra, S., Santangelo, C., Navalesi, R., Purrello, F., Marchetti, P., Vos, P., Visser, L., Haan, B. J., Klok, P., Schilfgaarde, R., Poppema, S., Juang, J-H, Kuo, C-H, Hsu, B. R-S, Nacher, V., Perez, M., Biarnes, M., Raurell, M., Soler, J., Montanya, E., Ritzel, R., Maubach, J., Busing, M., Becker, T., Klempnauer, J., Hucking, K., Schmiegel, W. H., Nauck, M. A., Boucek, P., Saudek, F., Adamec, M., Kozitarova, R., Jedinakova, T., Vlasakova, Z., Bartos, V., Maffi, P., Bertuzzi, F., Aldrighetti, L., Taglietti, M. V., Castelnuovo, A., Pozza, G., Di Carlo, V., Secchi, A., Renier, G., Mamputu, J-C, Gillespie, J. S., Mcmaster, D., Mercer, C., Trimble, E. R., Lecomte, M., Vericel, E., Paget, C., Ruggiero, D., Lagarde, M., Wiernsperger, N., Pricci, F., Leto, G., Amadio, L., Cordone, S., Iacobini, C., Catalano, S., Violi, F., Rotella, C. M., Pugliese, G., Zicari, A., Gradini, R., Sale, P., Pala, L., Cresci, B., Giannini, S., Manuelli, C., Dahlfors, G., Arnqvist, H. J., Gonelle-Gispert, C., Halnan, P. A., Sadoul, K., Wolter, S., Lang, J., Niwa, T., Yu, W., Hidaka, H., Senda, T., Niki, I., Fukasawa, T., Renstrom, E., Barg, S., Seward, E., Rorsman, P., Rutter, G. A., Molinete, M., Lilla, V., Ravazzola, M., Halban, P. A., Efanov, A. M., Bertorello, A. M., Zaitsev, S. V., Zwiller, J., Berggren, P-O, Msengul, A., Salman, F., Sargrn, M., Ozer, E., Karsidaǧ, K., Salman, S., Gedik, S., Satman, I., Dinccaǧ, N., Yilmaz, M. T., Lloyd, A., Hopkinson, P. K., Testa, M. A., Blonde, L., Turner, R. R., Hayes, J., Simonson, D. C., Ven, N. C. W., Lubach, C. H. C., Snoek, F. J., Mollema, E. D., Ploeg, H. M., Danne, T., Hoey, H., Mcgee, H., Fitzgerald, H., Lernmark, B., Thernlund, G., Fredin, K., Hagglof, B., Lugari, R., Anna, C., Ugolotti, D., Dei Cas, A., Barilli, A. L., Sard, L., Marani, B., Iotti, M., Zandomeneghi, R., Gnudi, A., Kjems, L. L., Volund, Aa, Toft-Nielsen, M., Damholt, M. B., Hilsted, L., Hughes, T. E., Krarup, T., Holst, J. J., Young, A., Gottlieb, A., Fineman, M., Kolterman, O., Cancelas, J., Garcia-Martinez, J. A., Villanueva-Penacarrillo, M. L., Valverde, I., Malaisse, W. J., Filipsson, K., Ahren, B., Balkan, B., Kwasnik, L., Battle, B., Li, X., Egan, J. M., Clocquet, A. R., Elahi, D., Petrella, E., Pricket, K., Petersen, K. F., Sullivan, J. T., Amatruda, J. M., Livingston, J. N., Shulman, G. I., Freyse, E-J, Knospe, S., Glund, K., Demuth, H-U, Walker, D., Malik, R. A., Reljanovic, M., Barada, A., Milicevic, Z., Tack, Cees J., Croatian Study Group for Diabetic Amyotrophy, Goldstein, David S., Huysen, C., Stevens, M. J., Cao, X., Sundkvist, G., Dahlin, L-B, Eriksson, K-F, Rosen, I., Lattimer, S. A., Sima, A. A. F., Sullivan, K., Shaw, J. E., Courten, M. P., Zimmet, P. Z., Gourdy, P., Ruidavets, J. B., Arveiler, D., Amouyel, Ph, Bingham, A., Tauber, J. P., Lam, K. S. L., Wat, N. M. S., Lam, T. H., Janus, E. D., Pablos, P., Rodriguez, F., Martinez, J., Sanchez, V., Santana, C., Garcia, I., Macias, A., Levin, K., Hother-Nielsen, O., Henriksen, J. E., Beck-Nielsen, H., Brechtel, K., Machann, J., Koch, M., Nielsen, M., Loblein, K., Becker, R., Denignger, M., Renn, W., Machicao, F., Claussen, C. D., Schick, F., Diraison, F., Moulin, P., Beylot, M., Thams, P., Capito, K., Eliasson, Lena, Barg, Sebastian, Gopel, Sven, Kanno, Takahiro, Renstrom, Erik, Meda, P., Charollais, A., Gjnovci, A., Calabrese, A., Wonkam, A., Caton, D., Wisznievski, L., Serre, V., Cogne, F., Bauquis, J., Bosco, D., Huarte, J., Herrera, P., Gotfredsen, C. F., Vessby, B., Kanwu, Study Group, Manuel Y Keenoy, B., Engelen, W., Vertommen, J., Schrans, S., Louheranta, A., Lindstrom, J., Tuomilehto, J., Finnish Diabetes Prevention Study Group, Segal, K. R., Heymsfield, S., Hauptman, J., Boldrin, M., Lucas, C., Pandolfi, A., Cetrullo, D., Polishchuck, R., Alberta, M., Pellegrini, G., Calafiore, A., Vitacolonna, E., Capani, F., Consoli, A., Halleux, C. M., Gillot, E. F., Brichard, S. M., Planken, M., Corthouts, B., Peiffer, F., Scholten, D., Walke, M., Assert, R., Pirags, V., Pedula, K. L., Hillier, T. A., Brown, J. B., Eurodiab, Prospective Complications Study Group, Santini, S. A., Marra, G., Cotroneo, P., Manto, A., Di Leo, M. A. S., Di Gregorio, S., Tordi, A., Pitocco, D., Ruotolo, V., Ghirlanda, G., Temelkova-Kurktschiev, T., Schaper, F., Koehler, C., Henkel, E., Hanefeld, M., Mancini, L., Citterio, F., Cotroneo, A., Ceroone, S., Castagneto, M., Rajbhandari, S. M., Dent, M. T., Plater, M. E., Harris, N. D., Tesfaye, S., Ward, J. D., Dupuy, O., Mayaudon, H., Lecoules, S., Bauduceau, B., Palou, M., Farret, O., Molinie, C., Antonelli-Incalzi, R., Fuso, L., Giordano, A., Calcagni, M. L., Todaro, L., Basso, S., Tramaglino, L. M., Troncone, L., Pistelli, R., Guillot, R., Bringuier, A., Porokhov, B., Guillausseau, P. J., Feldmann, G., Zivanic, S., Cizmic, M., Dragojevic, R., Vanovic, M., Borghouts, L. B., Kranenburg, G. P. J., Schaart, G., Keizer, H. A., Niess, A. M., Dickuth, H. H., Lutz, O., Barbe, P., Calazel-Fournier, C., Hernandez, G., Saint-Martin, F., Galitzky, J., Goncalves, A. A., Da Silva, E. C., Brito, I. J. L., Da Silva, C. A., Lawrence, N. J., Kousta, E., Mulnier, H., Penny, A., Millauer, B., Johnston, D. G., Robinson, S., Perriello, G., Pimenta, W., Pampanelli, S., Lucidi, P., Lepore, M., Porcellati, F., Cordoni, M. C., Feo, P., Bolli, G. B., Sjostrand, M., Holmang, A., Lonnroth, P., Hauer, B., Grauer, P., Artzner, S., Lang, R., Stumvoll, M., Monti, L. D., Piatti, P. M., Gemone, F., Valsecchi, G., Magni, M., Barbieri, E., Setola, E., Sandoli, E. P., Galli-Kienle, M., Pontiroli, A. E., Nichols, Gregory A., Brown, Jonathan B., Salzsieder, E., Boltz, H., Ramirez, J. C., Rutscher, A., Fischer, U., Koenig, Ch, Friske, M., Schramm, W., Landgraf, R., Bachmann, W., Bangemann, M., Groeneveld, G., Edvell, Anders, Lindstrom, Per, Tsiotra, P., Koukourava, A., Raptis, S. A., Tsigos, C., Boutou, E., Triandaffilopoulou, A., Egido, E. M., Rodriguez-Gallardo, J., Gutierrez, E., Garcia, P., Silvestre, R. A., Marco, J., Khan, Akhtar, Ling, Zong-Chao, Ahren, Bo, Efendic, Suad, Bunting, C., Du, X., Zhi Sui, G., Rosen, P., Koschinsky, T., Kearney, T. M., Sharp, P. S., Lapolla, A., Fedele, D., Martano, L., Garbeglio, M., Seraglia, R., Favretto, D., Traldi, P., Meerwaldt, R., Smit, A. J., Links, Th P., V Roon, A. M., Graaf, R., Gans, R. O. B., Deyneli, O., Ersoz, H. O., Gogas, D., Fak, A. S., Akalin, S., Veglio, M., Sivieri, R., Chinaglia, A., Scaglione, L., Neuropathy Study Group of the Italian Society of the Study of Diabetes, Le, T., Wong, N., Detrano, R., Charles, M. A., Colhoun, H. M., Francis, D. P., Rubens, M., Underwood, S. R., Fuller, J. H., Knudsen, E., Sato, A., Nielsen, F. S., Bonora, E., Kiechl, S., Willeit, J., Oberhollenzer, F., Egger, G., Bonadonna, R., Muggeo, M., Festa, A., D Agostino, R. Jr, Howard, G., Mykkanen, L., Tracy, R. P., Haffner, S. M., Poulsen, P., Vach, K., European Group for the Study of Insulin Resistance (EGIR), Ijzerman, R. G., Bakker, S. J. L., Truster, J., Crowther, N. J., Cameron, N., Gray, I. P., Chaillous, L., Carel, J. C., Thivolet, C., Boitard, C., Charbonnel, B., Sai, P., Study Group, D. I. O. R., Decochez, K., Keymeulen, B., Somers, G., Dorchy, H., Rottiers, R., Winnock, F., Ver Elst, K., Weets, I., Pipeleers, D., Gorus, F., Seebaum, S., Schumm-Draeger, P-M, Petzoldt, R., Federlin, K., Bonnevie-Nielsen, V., Martensen, P. M., Justesen, J., Worsaa, A., Karlsson, Maria, Sederholm, Sofia, Ludvigsson, Johnny, Belicar, P., Dale, C., Vague, Ph, Alessis, C., Lassmann-Vague, V., Bode, B. W., Gross, T. M., Ghegan, M., Steed, R. D., Davidson, P. C., Ordonez, A., Rubio, J. L., Sulleiro, J. M., Buendia, J. P., Zamora, J., Castillo, M., Schaupp, L., Ellmerer, M., Brunner, G. A., Sendlhofer, G., Schlack, Ch, Skrabal, F., Wach, P., Pieber, T. R., Heinemann, L., Kramer, U., Klotzer, H. M., Hermann, M., Non-Invasive Task Force, Cosgrove, K. E., Chapman, J. C., Shepherd, R. M., Mcintyre, S., Butler, P. C., Dunne, M. J., Brekardin, E., Dorschner, H., Schwanstecher, C., Schwanstecher, M., Uhde, I., Emmanouilidou, E., Teschemacher, A. G., Pouli, A. E., Gylfe, E., Tengholm, A., Hellman, B., Perfetti, R., Aggarwal, S., Muller, Gunter, Welte, Stefan, Wied, Susanne, Valverde, A. M., Mur, C., Kahn, C. R., Benito, M., Rondinone, C. M., Peterson, T., Laviola, L., Belsanti, G., Logoluso, F., Napoli, R., Davalli, A. M., Weir, G. C., Giorgino, R., Giorgino, F., Flesch, S., Hompesch, B., Rave, K., Susanto, F., Kuhn-Velten, W. N., Heise, T., Rendell, M., Dole, J., Rosiglitazone Study Group, Esper, R. J., Stein, E., Lemme, L., Cerivastatin/Bezafibrate Latin America Study Group, Rubinstein, A., Maritz, F. J., Soule, S., Market, A., Chajek-Shaul, T., Maislos, M., Tal, S., Stolero, D., Hidm, Investigators, Josefsen, K., Beckmann, H., Petersen, C., Ekman, R., Efanova, I., Zaitsev, S., Berggren, P. O., Birkenbach, M., Holl, R. 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D., Reggio, H., Peraldi-Roux, S., Henningsson, R., Salehi, A., Lundquist, I., Stickings, P., Mistry, S., Ratcliff, H., Morris, S. M. Jr, Cunningham, J. M., Ekelund, M., Ermakova, N. V., Paulssen, R. H., Florholmen, J., Carmellini, M., Mosca, F., Longo, D., Squatrito, S., Clement, L., Magnan, C., Vincent, M., Penicaud, L., Assimacopoulos-Jeannet, F., Vigneri, R., Rolfsen, S. E. D., Gregersen, S., Hermansen, K., Blondeau, B., Rojas, I., Novials, A., Femandez-Usac, E., Cristobal, P., Higham, C. E., Lawrie, L., Sherman, K. I. J., Birch, N., Tito, P., Robinson, C. V., Koning, E. J. P., Verbeek, J. S., Esapa, C., Laube, B., Powell, D. S., Maksoud, H., Charge, S. B. P., Matthews, D. R., Stratton, I. M., Karlsson, S., Myrsen-Axcrona, U., Ostlund, B., Sundler, F., Bertrand, G., Puech, R., Bockaert, J., Persson-Sjogren, S., Taljedal, I-B, Mooney, M. H., O Harte, F. P. M., Simonsson, E., Abdel-Halim, Samy M., Yanagida, K., Arima, T., Yada, T., Egea, J. 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S., Murphy, L., Rodger, N. W., Ross, S. A., Ryan, E., Yale, J-F, Wolever, T. M. S., Haller, T., Elias, I., Segal, P., Standi, E., Rybka, J., Sencer, E., Schlcnzka, A., Vakkilainen, J., Tsaglis, H., Ioannidis, I., Giakoumaki, A., Amantou, A., Komitopoulos, N., Georgiou, S., Varsamis, E., Katsilambros, N., El Gayar, M., Shereba, N., Botros, R., Fikry, R., Jackson, D., Balme, M., Silva-Nunes, J., Alves, J., Bogalho, P., Gardete-Correia, L., Nunes-Correa, J., Kot Atkova, A., Nemcova, D., Vrbikova, J., Zamrazil, V., Meyer, L., Delbachian, I., Lehert, P., Cugnardey, N., Drouin, P., Guerci, B., Wagner, O. F., Jones, N. P., Vallance, S. E., Thompson, K. A., Miller, A. K., Inglis, A. M. L., Patterson, S., Jorkasky, D., Freed, M. I., Mathisen, A. L., Schneider, R., Rubin, C., Houser, V., Beebe, K. L., Kortboyer, J. M., Eckland, D. J. 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6. Down-regulation of OATP1B proteins correlates with hyperbilirubinemia in advanced cholestasis
- Author
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Eva Sticova, Lodererova, A., Steeg, E., Frankova, S., Kollar, M., Lanska, V., Kotalova, R., Dedic, T., Schinkel, A. H., and Jirsa, M.
- Subjects
Cholestasis ,MSB - Microbiology and Systems Biology ,Life ,Biomedical Innovation ,Bilirubin ,ELSS - Earth, Life and Social Sciences ,Biology ,Immunohistochemistry ,Liver disease ,Healthy Living ,Organic anion transporter - Abstract
Aim: Organic anion-transporting polypeptides OATP1B1 and OATP1B3 are sinusoidal membrane transporters mediating liver uptake of a wide range of substrates including conjugated and unconjugated bilirubin, xenobiotics and drugs. Absence of OATP1Bs in the liver causes Rotor syndrome. Our aim was to correlate OATP1B expression with hyperbilirubinemia in common liver diseases. Methods: Immunoreactivity of five antibodies against human OATP1Bs was tested on frozen and formalin-fixed paraffin-embedded liver tissue of mouse strains transgenic for SLCO1B1 or SLCO1B3 and on human specimens. The proportion of hepatocytes expressing OATP1Bs was then assessed immunohistologically in formalin-fixed paraffin-embedded liver samples obtained from patients with hepatocellular and primary biliary liver diseases. UGT1A1 promoter TATA-box and SLCO1B1 rs4149056 genotyping was performed to rule out individuals predisposed to hyperbilirubinemia. Results: The most specific detection of OATP1B3 was achieved with the H-52 (sc-98981) antibody. OATP1B1 was specifically recognized with the ESL (ab15441) anti-OATP1B1 antibody, but only in frozen sections. The MDQ (ab15442) anti-OATP1B1 antibody cross-reacted with both OATP1B proteins in liver tissue of the transgenic mouse strains. Expression of the OATP1B proteins was decreased in advanced liver diseases and inversely correlated with serum bilirubin levels. The reduction was more pronounced in advanced primary biliary diseases (1.9±1.1 vs. 2.7±0.6; P=0.009). Conclusions: Down-regulation of OATP1B proteins may contribute to pathogenesis of jaundice accompanying advanced cholestatic liver diseases.
7. OUTCOME OF CZECH INFANTS WITH BILIARY ATRESIA AFTER 10 YEARS PERIOD 19982009
- Author
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Kotalova, R., Blahova, K., Rygl, M., Snajdauf, J., and Keil, R.
- Published
- 2010
8. Constitutively active Lyn kinase causes a cutaneous small vessel vasculitis and liver fibrosis syndrome.
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de Jesus AA, Chen G, Yang D, Brdicka T, Ruth NM, Bennin D, Cebecauerova D, Malcova H, Freeman H, Martin N, Svojgr K, Passo MH, Bhuyan F, Alehashemi S, Rastegar AT, Uss K, Kardava L, Marrero B, Duric I, Omoyinmi E, Peldova P, Lee CR, Kleiner DE, Hadigan CM, Hewitt SM, Pittaluga S, Carmona-Rivera C, Calvo KR, Shah N, Balascakova M, Fink DL, Kotalova R, Parackova Z, Peterkova L, Kuzilkova D, Campr V, Sramkova L, Biancotto A, Brooks SR, Manes C, Meffre E, Harper RL, Kuehn H, Kaplan MJ, Brogan P, Rosenzweig SD, Merchant M, Deng Z, Huttenlocher A, Moir SL, Kuhns DB, Boehm M, Skvarova Kramarzova K, and Goldbach-Mansky R
- Subjects
- Humans, Dasatinib, Inflammation metabolism, Neutrophils metabolism, Phosphorylation, Endothelial Cells metabolism, src-Family Kinases genetics, src-Family Kinases metabolism, Vasculitis genetics
- Abstract
Neutrophilic inflammation is a hallmark of many monogenic autoinflammatory diseases; pathomechanisms that regulate extravasation of damaging immune cells into surrounding tissues are poorly understood. Here we identified three unrelated boys with perinatal-onset of neutrophilic cutaneous small vessel vasculitis and systemic inflammation. Two patients developed liver fibrosis in their first year of life. Next-generation sequencing identified two de novo truncating variants in the Src-family tyrosine kinase, LYN, p.Y508*, p.Q507* and a de novo missense variant, p.Y508F, that result in constitutive activation of Lyn kinase. Functional studies revealed increased expression of ICAM-1 on induced patient-derived endothelial cells (iECs) and of β2-integrins on patient neutrophils that increase neutrophil adhesion and vascular transendothelial migration (TEM). Treatment with TNF inhibition improved systemic inflammation; and liver fibrosis resolved on treatment with the Src kinase inhibitor dasatinib. Our findings reveal a critical role for Lyn kinase in modulating inflammatory signals, regulating microvascular permeability and neutrophil recruitment, and in promoting hepatic fibrosis., (© 2023. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)
- Published
- 2023
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9. Conjugated Hyperbilirubinemia in Infants: Is There Still a Role for ERCP?
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Stovicek J, Hlava S, Keil R, Drabek J, Lochmannova J, Koptová P, Wasserbauer M, Frybova B, Snajdauf J, Kotalova R, and Rygl M
- Subjects
- Cholangiopancreatography, Endoscopic Retrograde adverse effects, Humans, Hyperbilirubinemia, Infant, Choledocholithiasis diagnostic imaging, Choledocholithiasis surgery, Cholestasis etiology, Pancreatitis
- Abstract
Over a twenty-year period, we performed 255 ERCP procedures in infants aged up to 1 year. ERCP was indicated in cholestatic infants with suspicion of biliary obstruction. The most common diagnosis was biliary atresia (48%), choledochal cysts (13%), and choledocholithiasis (4%). The procedure complication rate was 13.7%. Hyperamylasemia occurred in 12.9%. More severe complications were rare-0.8% of ERCP procedure. There were no cases of postprocedural pancreatitis or death. Our study has proved that ERCP is a safe and reliable method in this age group. Its high specificity and negative predictive value for extrahepatic biliary atresia can prevent unnecessary surgeries in patients with normal bile ducts or endoscopically treatable pathologies., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2021 Jan Stovicek et al.)
- Published
- 2021
- Full Text
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10. ABCB4 disease mimicking morbus Wilson: A potential diagnostic pitfall.
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Sticova E, Neroldova M, Kotalova R, Subhanova I, and Jirsa M
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- Child, Diagnosis, Differential, Humans, Male, ATP Binding Cassette Transporter, Subfamily B deficiency, Cholestasis, Intrahepatic diagnosis, Hepatolenticular Degeneration diagnosis
- Abstract
Introduction: Progressive familial intrahepatic cholestasis type 3 (PFIC3) is a rare autosomal recessive cholestatic liver disorder caused by genetic deficiency of ATP-binding cassette subfamily B member 4 (ABCB4), a hepatocanalicular floppase translocating phospholipids from the inner to the outer leaflet of the canalicular membrane lipid bilayer. PFIC3 is characterised by production of hydrophilic bile with lithogenic properties which is harmful to the hepatobiliary epithelia. Chronic cholestasis in some patients may be accompanied by excessive accumulation of copper in the liver and by increased urinary copper excretion, the findings mimicking Wilson disease (WD)., Methods and Results: We report an 11 y/o male patient with growth retardation, mild craniofacial dysmorphic features and chronic liver disease, initially diagnosed and treated as WD. Whereas genetic testing for WD was negative, further molecular and histopathological analysis revealed two novel mutations (c.833+1G>T and c.1798T>A) in ABCB4 and complete absence of the ABCB4/MDR3 protein in the liver, determining PFIC3 as the correct diagnosis., Conclusion: PFIC3 and WD display pleomorphic and sometimes overlapping clinical and laboratory features, which may pose a differential diagnostic problem. Since the patient management in WD and PFIC3 differs significantly, an early and accurate diagnosis is crucial for optimising of therapeutic approach and prevention of possible complications.
- Published
- 2020
- Full Text
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11. Choledochal Cyst with 17q12 Chromosomal Duplication.
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Kotalova R, Dusatkova P, Drabova J, Elblova L, Dedic T, Cinek O, Lebl J, and Pruhova S
- Subjects
- Anastomosis, Roux-en-Y, Chromosomes, Human, Pair 17 genetics, Humans, Infant, Newborn, Jejunum surgery, Liver surgery, Liver Cirrhosis pathology, Male, Choledochal Cyst genetics, Chromosome Duplication, Gene Dosage, Hepatocyte Nuclear Factor 1-beta genetics
- Abstract
The 17q12 chromosomal region carries the HNF1B gene, mutations of which cause various conditions. When searching for HNF1B/17q12 rearrangements among children with biliary atresia and/or choledochal cysts, we identified a male proband carrying a 17q12 duplication spanning 1698 kb that included 24 genes from TBC1D3C to HNF1B. The boy presented with cholestatic jaundice at the age of 2 weeks due to a choledochal cyst sized 15 ×12 mm (type Ia according to the Todani classification). He underwent a shunt surgery consisting of a hepaticojejunostomy using Roux-en-Y loop at the age of 2 months, which led to a permanent relief of cholestasis. Perioperative liver histology revealed significant hepatic fibrosis and bile ductular proliferation. At 17 years, he has a mildly enlarged liver with decreased elasticity, an upper-normal-sized spleen, normal biochemistry values, and no renal or hepatic cysts. We report the first hepatobiliary phenotype in a patient with an HNF1B overdosage., (© 2017 John Wiley & Sons Ltd/University College London.)
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- 2018
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12. Down-regulation of OATP1B proteins correlates with hyperbilirubinemia in advanced cholestasis.
- Author
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Sticova E, Lodererova A, van de Steeg E, Frankova S, Kollar M, Lanska V, Kotalova R, Dedic T, Schinkel AH, and Jirsa M
- Subjects
- Animals, Bilirubin blood, Biomarkers blood, Cholestasis diagnosis, Cholestasis genetics, Down-Regulation, Fixatives, Formaldehyde, Frozen Sections, Hepatocytes pathology, Humans, Hyperbilirubinemia diagnosis, Hyperbilirubinemia genetics, Immunohistochemistry, Liver pathology, Liver-Specific Organic Anion Transporter 1, Mice, Transgenic, Organic Anion Transporters genetics, Organic Anion Transporters, Sodium-Independent genetics, Paraffin Embedding, Retrospective Studies, Solute Carrier Organic Anion Transporter Family Member 1B3, Tissue Fixation methods, Cholestasis metabolism, Hepatocytes metabolism, Hyperbilirubinemia metabolism, Liver metabolism, Organic Anion Transporters metabolism, Organic Anion Transporters, Sodium-Independent metabolism
- Abstract
Aim: Organic anion-transporting polypeptides OATP1B1 and OATP1B3 are sinusoidal membrane transporters mediating liver uptake of a wide range of substrates including conjugated and unconjugated bilirubin, xenobiotics and drugs. Absence of OATP1Bs in the liver causes Rotor syndrome. Our aim was to correlate OATP1B expression with hyperbilirubinemia in common liver diseases., Methods: Immunoreactivity of five antibodies against human OATP1Bs was tested on frozen and formalin-fixed paraffin-embedded liver tissue of mouse strains transgenic for SLCO1B1 or SLCO1B3 and on human specimens. The proportion of hepatocytes expressing OATP1Bs was then assessed immunohistologically in formalin-fixed paraffin-embedded liver samples obtained from patients with hepatocellular and primary biliary liver diseases. UGT1A1 promoter TATA-box and SLCO1B1 rs4149056 genotyping was performed to rule out individuals predisposed to hyperbilirubinemia., Results: The most specific detection of OATP1B3 was achieved with the H-52 (sc-98981) antibody. OATP1B1 was specifically recognized with the ESL (ab15441) anti-OATP1B1 antibody, but only in frozen sections. The MDQ (ab15442) anti-OATP1B1 antibody cross-reacted with both OATP1B proteins in liver tissue of the transgenic mouse strains. Expression of the OATP1B proteins was decreased in advanced liver diseases and inversely correlated with serum bilirubin levels. The reduction was more pronounced in advanced primary biliary diseases (1.9±1.1 vs. 2.7±0.6; P=0.009)., Conclusions: Down-regulation of OATP1B proteins may contribute to pathogenesis of jaundice accompanying advanced cholestatic liver diseases.
- Published
- 2015
13. Hepatic phenotypes of HNF1B gene mutations: a case of neonatal cholestasis requiring portoenterostomy and literature review.
- Author
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Kotalova R, Dusatkova P, Cinek O, Dusatkova L, Dedic T, Seeman T, Lebl J, and Pruhova S
- Subjects
- Biliary Atresia complications, Biliary Atresia diagnosis, Birth Weight, Central Nervous System Diseases complications, Central Nervous System Diseases diagnosis, Cholangiopancreatography, Magnetic Resonance, Cholestasis diagnosis, Cholestasis genetics, DNA Mutational Analysis, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 diagnosis, Female, Genetic Predisposition to Disease, Humans, Infant, Infant, Newborn, Infant, Small for Gestational Age, Kidney Diseases, Cystic complications, Kidney Diseases, Cystic diagnosis, Phenotype, Treatment Outcome, Biliary Atresia genetics, Central Nervous System Diseases genetics, Cholestasis surgery, Dental Enamel abnormalities, Diabetes Mellitus, Type 2 genetics, Hepatocyte Nuclear Factor 1-beta genetics, Kidney Diseases, Cystic genetics, Mutation, Portoenterostomy, Hepatic
- Abstract
Hepatocyte nuclear factor 1-β (HNF1B) defects cause renal cysts and diabetes syndrome (RCAD), or HNF1B-maturity-onset diabetes of the young. However, the hepatic phenotype of HNF1B variants is not well studied. We present a female neonate born small for her gestational age [birth weight 2360 g; -2.02 standard deviations (SD) and birth length 45 cm; -2.40 SD at the 38(th) gestational week]. She developed neonatal cholestasis due to biliary atresia and required surgical intervention (portoenterostomy) when 32-d old. Following the operation, icterus resolved, but laboratory signs of liver dysfunction persisted. She had hyperechogenic kidneys prenatally with bilateral renal cysts and pancreatic hypoplasia postnatally that led to the diagnosis of an HNF1B deletion. This represents the most severe hepatic phenotype of an HNF1B variant recognized thus far. A review of 12 published cases with hepatic phenotypes of HNF1B defects allowed us to distinguish three severity levels, ranging from neonatal cholestasis through adult-onset cholestasis to non-cholestatic liver impairment, all of these are associated with congenital renal cysts and mostly with diabetes later in life. We conclude that to detect HNF1B variants, neonates with cholestasis should be checked for the presence of renal cysts, with special focus on those who are born small for their gestational age. Additionally, patients with diabetes and renal cysts at any age who develop cholestasis and/or exocrine pancreatic insufficiency should be tested for HNF1B variants as the true etiological factor of all disease components. Further observations are needed to confirm the potential reversibility of cholestasis in infancy in HNF1B mutation/deletion carriers.
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- 2015
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14. Disease activity is an important factor for indeterminate interferon-γ release assay results in children with inflammatory bowel disease.
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Hradsky O, Ohem J, Zarubova K, Mitrova K, Durilova M, Kotalova R, Nevoral J, Zemanova I, Dryak P, and Bronsky J
- Subjects
- Adolescent, Adrenal Cortex Hormones adverse effects, Adrenal Cortex Hormones therapeutic use, Body Weight, Child, Colitis, Ulcerative complications, Colitis, Ulcerative pathology, Crohn Disease complications, Crohn Disease pathology, Female, Humans, Inflammatory Bowel Diseases pathology, Latent Tuberculosis complications, Latent Tuberculosis metabolism, Male, Platelet Count, Risk Factors, Serum Albumin metabolism, Inflammatory Bowel Diseases complications, Interferon-gamma metabolism, Interferon-gamma Release Tests, Latent Tuberculosis diagnosis, Tuberculin Test
- Abstract
Background: Interferon-γ release assay (IGRA) is widely used for screening of latent tuberculosis (TB) before and during biological therapy (BT). An indeterminate result of IGRA represents a limitation in the management of inflammatory bowel disease (IBD). Data on factors influencing IGRA results are scarce in children. The aim of the study was to identify factors influencing IGRA results in children with IBD., Methods: Seventy-two children with IBD (59 Crohn disease, 11 ulcerative colitis, 2 IBD-unclassified) indicated for BT were tested for TB infection (history, TB skin test, chest radiograph, IGRA; QuantiFERON-TB Gold in tube [QFT]) and consecutively retested using QFT in 1-year intervals., Results: We recorded 165 results of QFT (3% positive, 87% negative, and 10% indeterminate results). During follow-up we identified 4 conversions of negative QFT to positivity (3%) and 4 reversions (4%). Patients with indeterminate results of QFT had significantly lower actual weight-for-height z score (P = 0.022), higher platelet count (P = 0.00017), and lower levels of serum albumin (P = 0.015) compared with patients with positive or negative QFT. Indeterminate QFT was associated with corticosteroid treatment, BT, and disease activity, but not with treatment by immunomodulators. In a subanalysis of patients with Crohn disease alone, Pediatric Crohn's Disease Activity Index was identified as single independent risk factor for indeterminate results (P = 0.00037)., Conclusions: Although corticosteroid treatment is traditionally considered to be the main risk factor for indeterminate results of IGRA, the disease activity of IBD has even more profound effects on the results.
- Published
- 2014
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15. Fecal calprotectin levels in children is more tightly associated with histological than with macroscopic endoscopy findings.
- Author
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Hradsky O, Ohem J, Mitrova K, Durilova M, Kotalova R, Nevoral J, Kolho KL, and Bronsky J
- Subjects
- Adolescent, Age Factors, Area Under Curve, Biomarkers analysis, Case-Control Studies, Child, Child, Preschool, Feasibility Studies, Female, Humans, Inflammatory Bowel Diseases blood, Inflammatory Bowel Diseases immunology, Inflammatory Bowel Diseases pathology, Male, Predictive Value of Tests, ROC Curve, Up-Regulation, Colon chemistry, Colon immunology, Colon pathology, Colonoscopy, Feces chemistry, Ileum chemistry, Ileum immunology, Ileum pathology, Inflammation Mediators analysis, Inflammatory Bowel Diseases diagnosis, Leukocyte L1 Antigen Complex analysis, Point-of-Care Systems
- Abstract
Background: Children with suspected bowel inflammation require an invasive endoscopic procedure, which is usually performed under general anesthesia. To improve the selection of candidates for endoscopy, fecal calprotectin level has been proposed as a noninvasive marker of intestinal inflammation. In the future, home testing is a likely option. Thus, the aim of this study was to affirm the association between bedside-measured fecal calprotectin concentration and histological and endoscopic findings in a panel of patients with suspected chronic bowel inflammation., Methods: Stool samples and microscopic and macroscopic findings from 41 patients, who underwent ileocolonoscopy for suspicion of bowel inflammation, were consecutively obtained between April 2009 and December 2010. Stool samples were analyzed using the bedside fecal calprotectin enzyme-linked immunosorbent assay (Quantum Blue; Bühlmann, Laboratories AG, Switzerland)., Results: Fecal calprotectin levels were elevated in 18 children with bowel inflammation on endoscopy (median at the upper limit of undiluted samples, 300 μg/g) compared with 23 children without bowel inflammation (median, 105 μg/g; p < 0.00097). Similarly, the fecal calprotectin level was elevated in 25 children with positive histological findings as assessed by a pathologist (median, 300 μg/g) compared with 16 children without histological inflammation (median, 73 μg/g; p < 0.000014). Based on the optimal area under the curve, we calculated the cutoff fecal calprotectin level for bowel inflammation on endoscopy as 167 μg/g (area under the curve, 0.86; 95% confidence interval (CI), 0.81 - 0.92) and on histological examination as 280 μg/g (area under the curve, 0.78; 95% CI, 0.70 - 0.86). Fecal calprotectin level was more sensitive than endoscopy for diagnosis of microscopic bowel inflammation (p = 0.000014)., Conclusions: Our results clearly show that even the bedside test for fecal calprotectin level, using the optimal cut-off value, is feasible enough in determining candidates for an endoscopic procedure in order to confirm bowel inflammation and is more tightly associated with histological findings than with endoscopic findings. Thus, the calprotectin level reflects histological activity, even in cases with normal endoscopic findings. The bedside test described herein is a sufficient screening method for this purpose.
- Published
- 2014
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- View/download PDF
16. Symptom positivity is essential for omitting biopsy in children with suspected celiac disease according to the new ESPGHAN guidelines.
- Author
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Nevoral J, Kotalova R, Hradsky O, Valtrova V, Zarubova K, Lastovicka J, Neubertova E, Trnkova M, and Bronsky J
- Abstract
The aim of this study was to assess the accuracy of serological tests in combination with clinical symptoms for diagnosing celiac disease (CD) according to the new proposed European Society for Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) criteria. We retrospectively assessed children and adolescents aged 16 months -19 years who were examined for suspicion of CD (n = 345). Evaluation of clinical symptoms and the presence of tissue transglutaminase (anti-TG-IgA) and endomysial antibodies (EMA-IgA) as well as intestinal biopsies was performed in all patients. Human leukocyte antigens (HLAs) were not included. Among 345 biopsied children, 213 (62 %) children had anti-TG titers >10 times the upper limit of normal (ULN) and positive EMA antibodies. Ninety-nine (29 %) children also had symptoms suggestive of CD in addition to EMA positivity and elevated titers of anti-TG >10 times the ULN. In patients who were asymptomatic, but positive for EMA, and had anti-TG antibodies >10 times the ULN, the specificity of tests for Marsh 2-3 was only 85 %, while in symptomatic patients with the same antibodies levels, the specificity was 99 %. Conclusion: Our results reveal that intestinal biopsies could be omitted in 28 % of patients when the new ESPGHAN guidelines are applied. Due to high accuracy of serological tests in combination with clinical symptoms for diagnosis of CD, the new guideline seems to be applicable even without the use of HLA testing.
- Published
- 2013
- Full Text
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17. Incidence of Crohn disease in the Czech Republic in the years 1990 to 2001 and assessment of pediatric population with inflammatory bowel disease.
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Pozler O, Maly J, Bonova O, Dedek P, Frühauf P, Havlickova A, Janatova T, Jimramovsky F, Klimova L, Klusacek D, Kocourkova D, Kolek A, Kotalova R, Marx D, Nevoral J, Petro R, Petru O, Plasilova I, Seidl Z, Sekyrova I, Semendak N, Schreierova I, Stanek J, Sykora J, Sulakova A, Toukalkova L, Travnickova R, Volf V, Zahradnicek L, and Zenisková I
- Subjects
- Adolescent, Age Factors, Child, Child, Preschool, Colitis drug therapy, Colitis epidemiology, Colitis, Ulcerative complications, Colitis, Ulcerative drug therapy, Colitis, Ulcerative epidemiology, Crohn Disease complications, Crohn Disease drug therapy, Crohn Disease epidemiology, Czech Republic epidemiology, Disease Progression, Drug Therapy, Combination, Female, Growth Disorders etiology, Humans, Incidence, Infant, Inflammatory Bowel Diseases complications, Male, Prospective Studies, Retrospective Studies, Adrenal Cortex Hormones therapeutic use, Aminosalicylic Acids therapeutic use, Azathioprine therapeutic use, Inflammatory Bowel Diseases drug therapy, Inflammatory Bowel Diseases epidemiology
- Abstract
Background: The aim of this study was to assess the pediatric population that suffered from inflammatory bowel disease (IBD) in the Czech Republic and to determine the incidence of Crohn disease (CD) in children up to 15 years age between 1990 and 2001., Methods: Diagnostic criteria for CD, ulcerative colitis (UC), and indeterminate colitis (IC) were defined. Medical records provided a source of basic information about the children. A standardized protocol was filled out and sent to the coordinator of the study. All protocols were checked to see whether the data corresponded to the defined criteria and then were processed further. The study was retrospective in character for the years 1990 to 1999 and prospective for the years 2000 and 2001., Results: Diagnostic criteria were met in 470 patients with IBD; 201 of them turned 18 years old during the study period. CD was diagnosed in 223 patients. The incidence of CD in children up to 15 years of age increased from 0.25/100,000 in 1990 to 1.25/100,000 in 2001. Eighty-two percent of children with CD were treated with aminosalicylates in combination with corticosteroids; 29% of patients received azathioprine. Severe growth retardation was recorded in 6.4% of adolescents with CD at the age of 18. UC was diagnosed in 202 patients. Therapy with aminosalicylates only was sufficient for control of the disease in 23% patients; 68% children were treated with corticosteroids, 15 of them (23% of the whole group) received additional azathioprine. Criteria for IC were met in 9.8% of all patients with IBD., Conclusion: This study confirmed an increase in incidence of CD in children younger than 15 years in the Czech Republic.
- Published
- 2006
- Full Text
- View/download PDF
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