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4. Healthy First-Degree Relatives of Patients with Type 1 Diabetes Exhibit Significant Differences in Basal Gene Expression Pattern of Immunocompetent Cells Compared to Controls: Expression Pattern as Predeterminant of Autoimmune Diabetes

Author

Stechova, K., Kolar, M., Blatny, R., Halbhuber, Z., Vcelakova, J., Hubackova, M., Petruzelkova, L., Sumnik, Z., Obermannova, B., Pithova, P., Stavikova, V., Krivjanska, M., Neuwirth, A., Kolouskova, S., and Filipp, D.

Published
2012
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5. Effect of hydrolyzed infant formula vs conventional formula on risk of type 1 diabetes the TRIGR randomized clinical trial

Author

Knip M., Akerblom H. K., Altaji E., Becker D., Bruining J., Castano L., Danne T., De Beaufort C., Dosch H. -M., Dupre J., Fraser W. D., Howard N., Ilonen J., Konrad D., Kordonouri O., Krischer J. P., Lawson M. L., Ludvigsson J., Madacsy L., Mahon J. L., Ormisson A., Palmer J. P., Pozzilli P., Savilahti E., Serrano-Rios M., Songini M., Taback S., Vaarala O., White N. H., Virtanen S. M., Wasikowa R., Mandrup-Poulsen T., Arjas E., Lernmark A., Laara E., Schmidt B., Hyytinen M., Koski K., Koski M., Merentie K., Pajakkala E., Reunanen A., Salonen M., Terhonen T., Virkkunen S., Cuthbertson D., Gainer B., Hadley D., Malloy J., Nallamshetty L., Shanker L., Bradley B., Lough G., Fraser W., Sermer M., Taback S. P., Franciscus M., Nucci A., Palmer J., Alahuhta K., Barlund S., Korhonen T., Kovanen L., Lehtonen E., Niinisto S., Pekkala M., Sorkio S., Toivanen L., Vahatalo L., Uusitalo U., Ohman T., Bongiorno R., Catteau J., Fraser G., Lloyd M., Crock P., Giles M., Siech K., See D. W., Brown C., Craig M., Johnston A., Bere L. J., Clarson C. L., Jenner M., McManus R., Renato N., Lovell M., Higo D., Kent N., Kwan J., Marshall C., Metzger D., Chanoine J. -P., Stewart L., Thompson D., Edwards A., Lange I., Mercer J., Pacaud D., Josephine H., Schwarz W., Stephure D. K., Boer J., Chatur T., Chick C., Couch B., Demianczuk N., Girgis R., Marks S., Ryan E., Thompson M., Dean H. J., Grant L., Hamelin K., LaForte J., Murphy L., Catte D., Schneider C., Sellers E. A. C., Woo V., Boland A., Clark H. D., Cooper T., Gruslin A., Karovitch A., Keely E., Malcolm J. C., Sauro V., Tawagi G. F., Andrighetti S., Arnold G., Barrett J., Blumer I., Daneman D., Donat D., Ehrlich R., Feig D., Gottesman I., Gysler M., Karkanis S., Kenshole A., Knight B., Lackie E., Lewis V., Martin M. J., Maxwell C., Oliver G., Panchum P., Shilletto N., Simone A., Skidmore M., Turrini T., Wong S., Allen C., Belanger L., Bouchard I., Ferland S., Frenette L., Garrido-Russo M., Leblanc M., Imbeault J., Morin V., Olivier G., Weisnagell J., Costain G., Dornan J., Heath K., MacSween M. -C., McGibbon A., Ramsay C., Sanderson F., Sanderson S., Benabdesselam L., Gonthier M., Huot C., Thibeault M., Laforte D., Legault L., Perron P., Armson A., Canning P., Cummings E. A., Ivanko V., McLeod L., Mokashi A., Scott K., Bridger T., Crane J., Crummell C., Curtis J. C., Dawson C., Joyce C., Newhook L. A., Newman S., Druken E., Begum-Hasan J., Breen A., Houlden R., Woods M., Carrson G., Kelly S., Martel M. J., Penner M., Sankaran K., Hardy-Brown K., King N., White R. A., Park M., Popkin J., Robson L., Coles K., Al Taji E., Cerna M., Cerny M., Francova H., Hainerova I., Kothankova H., Koukalova R., Krakorova V., Mendlova P., Sitova R., Stechova K., Vavrinec J., Vosahlo J., Zlatohlavkova B., Brazdova L., Faksova P., Gregorova D., Kantor L., Malkova K., Venhacova J., Venhacova P., Cipra A., Skvor J., Budejovice C., Tomsikova Z., Botkova-Krauseova H., Mockova A., Paterova P., Gogelova P., Kandrnalova J., Einberg U., Jakovlev U., Posiadlo S., Rannaste E., Raukas R., Riikjarv M. -A., Valla K., Astover V., Kirss A., Retpap J., Taht E., Tillmann V., Vahtra S., Heikkila M., Hirvasniemi M., Luopajarvi K., Johansson S., Kleemola P., Laukkanen E., Parkkola A., Pigg H. -M., Puttonen H., Renlund M., Salonen K., Suomalainen H., Tenkula T., Teramo K., Jarvenpaa A. -L., Hamalainen A. -M., Jussila R., Kiiveri S., Haavisto H., Holopainen S., Kupiainen H., Leeve T., Lumme K., Nironen T., Tenhola S., Tiilikainen T., Keinonen H., Lautala P., Salonen P., Vesanto M., Aspholm A. S., Asunta P., Ikavalko H., Jason E., Jaminki S., Kekki P., Koskinen M., Lehtimaki S., Lahde J., Makela M., Peltoniemi S., Poutiainen L., Ranta K., Salonsaari T., Sarviharju-Tujula S. -L., Selvenius J., Siljander H., Haanpaa P. -L., Holm C., Juutilainen A., Jarvelainen V., Kangaskolkka-Keskilohko A. -M., Laino E., Marjamaki L., Suominen E., Ylitalo S., Hokkanen M., Lounamaa R., Matikainen M., Nuuja A., Paalanen I., Puupponen A. R., Salo-Edwards H., Alanne S., Kultti T., Linjama H., Muhonen K., Vaaraniemi M., Talvitie T., Backman M., Hanhijarvi R., Koivula P., Lindstrom K., Martikainen A., Nurmi P., Bjork A., Huopio H., Komulainen J., Lehtomaki S., Muikku E., Pesola J., Sankilampi U., Arkkola T., Hekkala A., Jurvakainen S., Koivikko M. -L., Kahonen M., Leinonen E., Mykkanen T., Pohjola H., Riikonen K., Niittyvuopio A., Stenius A., Tapanainen P., Veijola R., Alar A., Jovio S., Korpela P., Makinen E., Hietanen L., Kivisto J., Kaar M. -L., Lehtimaki P., Mustila T., Popov E., Saatela S., Taittonen L., Ahtiainen K., Laaksonen N., Luoto M., Viitala J., Virransalo R., Nykanen P., Paajanen S., Parkkinen S., Pyrhonen H., Sarkka T., Aschemeier B., Bektas S., Biester T., Datz N., Deiss D., Fath M., Lupke K., Muller B., Nestoris C., Rothes S., Sadeghian E., Semler K., Arato A., Krikovszky D., Nobilis A., Szenasi J., Benevento D., Anguissola G. B., Biagioni M., Bizzarri C., Cherubini V., Ferrito L., Giordano C., Giorgetti C., Khazrai Y. M., Kyanvash S., Maddaloni E., Napoli A., Piergiovanni F., Pitocco D., Suraci T., Tabacco G., Valente L., Visalli N., Carboni M. B., Cavallo R., Cau V., Isola C., Ledda A., Loddo M., Mannu C., Pettinau M., Pisano S., Porceddu M., Putzu C., Rita A., Peters D., Schierloh U., Bisschoff M., Blonk L., Lappenschaar T., Manai B., Seesink M., Sperling-Conrad M., Verhagen M., Zoethout J. A., Basiak A., Chalas M., Chesiak M., Gramza A., Iwankiewicz J., Sieradzan E., Wikiera B., Ciechanowska M., Dziatkowiak H., Futona B., Gorska A., Glowacka-Wony M., Kaim I., Klich B., Starzyk J., Wolanin M., Tokarska L., Chucherco D., Deja G., Firek-Pedras M., Jarosz-Chobot P., Kalina M., Kutrowska-Adamusiak K., Minkina-Pedras M., Muchaka-Bianga M., Bodalski J., Mlynarski W., Szadkowska A., Cieslak A., Cypryk K., Dziatosz K., Jastzebowska J., Krysiak A., Szymanska U., Wilcznski J., Zawodniak-Szalapska M., Aguay A., Bilbao J. R., Chueca M., Cortazar A., Echarte G., Frutos T. G., Jimenez P., Martul P., Moreno A., Oyarzabal M., Rica I., Salgado Y., Martinez-Larrad M. T., Hawkins F. G., Hernandez R., Herranz L., Pallardo L. F., Deibarra L. S., Fernandez B. H., Luis J. L., Ortiz-Quintana L., Recarte P. P., Arnau D. R., Aronsson L., Boden S., Fredriksson J., Isacsson E., Johansson I., Karlsson E., Lock C., Sandstrom A. -M., Konefal M. S., Andreasson C., Dahlstrom U., Hanas R., Lundqvist K., Windell L., Jansson I., Karlsson A. -K., Lindbladh B., Odenman I., Pettersson C., Sundberg F., Sundqvist M., Aronsson S., Bellman I., Bengtsson A. -B., Lyden G. -B., Nilsson N. -O., Soderblom M., Unt C., Augustsson M., Bengtsson M., Fors H., Helmrich A., Johansson T. O., Andersson A. -C., Boiard-Stomlid A., Hellgren G., Kallsholm H., Lindqvist J., Nilsson M., Nordwall M., Stromstedt C., Ahsberg C., Lindh A., Lindhe C., Samuelsson C., Wiik A., Edenwall H., Ljumgcrantz M., Persson I. -B., Strigard E., Svensson B. -L., Aman J., Breivik G. -E., Detlofsson I. -L., Kroon M., Sarnblad S., Johansson C., Ilvered R., Lundberg A., Akesson K., Beccarelli A., Gadient M., Rappold-Amrein C., Schoenle E., Daftary A., Damagro-Elias M. E., Gilmour C., Klein M. B., Lain C., Salerno D., Smith M. E., Vats K., Pfaff D. J., Malone P., Mansfield P., Munns M., Nickel K., Pompilio K., Siemion W., Taculad R., Van Horn K., Zdanadewic M., Chambliss C., Jones J., Sadler M., Tanner-Blasiar M., Bell C., Camper N., Devaskar S., Devaskar U., Horowitz H., Rogers L., Shannahan R., Silk K., Bermudez Z., Colon R., Frazer T., Martinez-Nieves B., Torres J., Vega J., Chan M., Cook S., Goland R., Greenberg E., Jules N., Montes J., Nelson M., Parra-Valencia Z., Schachner H., Softness B., Kiviniemi M., Suomenin R., Alexander A., Hyrckowian E., Nichol L., Trucco M., Karjalainen E., Louhio T., Sarnesto A., Valtonen E., Davydova B., Helander S., Hamalainen J., Harkonen T., Joutsjoki L., Kararic M., Latva-Koivisto M., Lonn E., Nurmi T., Ollila I., Rinkinen J., Ronkainen M., Tukiainen H., Cederlof A., Kiikeri M., Tsupari S., Cheng R., Bryant K., Chan Y., Maezawa Y., Paltser G., Rasavi R., Tsui H., Winer S., Wu P., Yantha J., Pediatrics, Knip M., Akerblom H.K., Altaji E., Becker D., Bruining J., Castano L., Danne T., De Beaufort C., Dosch H.-M., Dupre J., Fraser W.D., Howard N., Ilonen J., Konrad D., Kordonouri O., Krischer J.P., Lawson M.L., Ludvigsson J., Madacsy L., Mahon J.L., Ormisson A., Palmer J.P., Pozzilli P., Savilahti E., Serrano-Rios M., Songini M., Taback S., Vaarala O., White N.H., Virtanen S.M., Wasikowa R., Mandrup-Poulsen T., Arjas E., Lernmark A., Laara E., Schmidt B., Hyytinen M., Koski K., Koski M., Merentie K., Pajakkala E., Reunanen A., Salonen M., Terhonen T., Virkkunen S., Cuthbertson D., Gainer B., Hadley D., Malloy J., Nallamshetty L., Shanker L., Bradley B., Lough G., Fraser W., Sermer M., Taback S.P., Franciscus M., Nucci A., Palmer J., Alahuhta K., Barlund S., Korhonen T., Kovanen L., Lehtonen E., Niinisto S., Pekkala M., Sorkio S., Toivanen L., Vahatalo L., Uusitalo U., Ohman T., Bongiorno R., Catteau J., Fraser G., Lloyd M., Crock P., Giles M., Siech K., See D.W., Brown C., Craig M., Johnston A., Bere L.J., Clarson C.L., Jenner M., McManus R., Renato N., Lovell M., Higo D., Kent N., Kwan J., Marshall C., Metzger D., Chanoine J.-P., Stewart L., Thompson D., Edwards A., Lange I., Mercer J., Pacaud D., Josephine H., Schwarz W., Stephure D.K., Boer J., Chatur T., Chick C., Couch B., Demianczuk N., Girgis R., Marks S., Ryan E., Thompson M., Dean H.J., Grant L., Hamelin K., LaForte J., Murphy L., Catte D., Schneider C., Sellers E.A.C., Woo V., Boland A., Clark H.D., Cooper T., Gruslin A., Karovitch A., Keely E., Malcolm J.C., Sauro V., Tawagi G.F., Andrighetti S., Arnold G., Barrett J., Blumer I., Daneman D., Donat D., Ehrlich R., Feig D., Gottesman I., Gysler M., Karkanis S., Kenshole A., Knight B., Lackie E., Lewis V., Martin M.J., Maxwell C., Oliver G., Panchum P., Shilletto N., Simone A., Skidmore M., Turrini T., Wong S., Allen C., Belanger L., Bouchard I., Ferland S., Frenette L., Garrido-Russo M., Leblanc M., Imbeault J., Morin V., Olivier G., Weisnagell J., Costain G., Dornan J., Heath K., MacSween M.-C., McGibbon A., Ramsay C., Sanderson F., Sanderson S., Benabdesselam L., Gonthier M., Huot C., Thibeault M., Laforte D., Legault L., Perron P., Armson A., Canning P., Cummings E.A., Ivanko V., McLeod L., Mokashi A., Scott K., Bridger T., Crane J., Crummell C., Curtis J.C., Dawson C., Joyce C., Newhook L.A., Newman S., Druken E., Begum-Hasan J., Breen A., Houlden R., Woods M., Carrson G., Kelly S., Martel M.J., Penner M., Sankaran K., Hardy-Brown K., King N., White R.A., Park M., Popkin J., Robson L., Coles K., Al Taji E., Cerna M., Cerny M., Francova H., Hainerova I., Kothankova H., Koukalova R., Krakorova V., Mendlova P., Sitova R., Stechova K., Vavrinec J., Vosahlo J., Zlatohlavkova B., Brazdova L., Faksova P., Gregorova D., Kantor L., Malkova K., Venhacova J., Venhacova P., Cipra A., Skvor J., Budejovice C., Tomsikova Z., Botkova-Krauseova H., Mockova A., Paterova P., Gogelova P., Kandrnalova J., Einberg U., Jakovlev U., Posiadlo S., Rannaste E., Raukas R., Riikjarv M.-A., Valla K., Astover V., Kirss A., Retpap J., Taht E., Tillmann V., Vahtra S., Heikkila M., Hirvasniemi M., Luopajarvi K., Johansson S., Kleemola P., Laukkanen E., Parkkola A., Pigg H.-M., Puttonen H., Renlund M., Salonen K., Suomalainen H., Tenkula T., Teramo K., Jarvenpaa A.-L., Hamalainen A.-M., Jussila R., Kiiveri S., Haavisto H., Holopainen S., Kupiainen H., Leeve T., Lumme K., Nironen T., Tenhola S., Tiilikainen T., Keinonen H., Lautala P., Salonen P., Vesanto M., Aspholm A.S., Asunta P., Ikavalko H., Jason E., Jaminki S., Kekki P., Koskinen M., Lehtimaki S., Lahde J., Makela M., Peltoniemi S., Poutiainen L., Ranta K., Salonsaari T., Sarviharju-Tujula S.-L., Selvenius J., Siljander H., Haanpaa P.-L., Holm C., Juutilainen A., Jarvelainen V., Kangaskolkka-Keskilohko A.-M., Laino E., Marjamaki L., Suominen E., Ylitalo S., Hokkanen M., Lounamaa R., Matikainen M., Nuuja A., Paalanen I., Puupponen A.R., Salo-Edwards H., Alanne S., Kultti T., Linjama H., Muhonen K., Vaaraniemi M., Talvitie T., Backman M., Hanhijarvi R., Koivula P., Lindstrom K., Martikainen A., Nurmi P., Bjork A., Huopio H., Komulainen J., Lehtomaki S., Muikku E., Pesola J., Sankilampi U., Arkkola T., Hekkala A., Jurvakainen S., Koivikko M.-L., Kahonen M., Leinonen E., Mykkanen T., Pohjola H., Riikonen K., Niittyvuopio A., Stenius A., Tapanainen P., Veijola R., Alar A., Jovio S., Korpela P., Makinen E., Hietanen L., Kivisto J., Kaar M.-L., Lehtimaki P., Mustila T., Popov E., Saatela S., Taittonen L., Ahtiainen K., Laaksonen N., Luoto M., Viitala J., Virransalo R., Nykanen P., Paajanen S., Parkkinen S., Pyrhonen H., Sarkka T., Aschemeier B., Bektas S., Biester T., Datz N., Deiss D., Fath M., Lupke K., Muller B., Nestoris C., Rothes S., Sadeghian E., Semler K., Arato A., Krikovszky D., Nobilis A., Szenasi J., Benevento D., Anguissola G.B., Biagioni M., Bizzarri C., Cherubini V., Ferrito L., Giordano C., Giorgetti C., Khazrai Y.M., Kyanvash S., Maddaloni E., Napoli A., Piergiovanni F., Pitocco D., Suraci T., Tabacco G., Valente L., Visalli N., Carboni M.B., Cavallo R., Cau V., Isola C., Ledda A., Loddo M., Mannu C., Pettinau M., Pisano S., Porceddu M., Putzu C., Rita A., Peters D., Schierloh U., Bisschoff M., Blonk L., Lappenschaar T., Manai B., Seesink M., Sperling-Conrad M., Verhagen M., Zoethout J.A., Basiak A., Chalas M., Chesiak M., Gramza A., Iwankiewicz J., Sieradzan E., Wikiera B., Ciechanowska M., Dziatkowiak H., Futona B., Gorska A., Glowacka-Wony M., Kaim I., Klich B., Starzyk J., Wolanin M., Tokarska L., Chucherco D., Deja G., Firek-Pedras M., Jarosz-Chobot P., Kalina M., Kutrowska-Adamusiak K., Minkina-Pedras M., Muchaka-Bianga M., Bodalski J., Mlynarski W., Szadkowska A., Cieslak A., Cypryk K., Dziatosz K., Jastzebowska J., Krysiak A., Szymanska U., Wilcznski J., Zawodniak-Szalapska M., Aguay A., Bilbao J.R., Chueca M., Cortazar A., Echarte G., Frutos T.G., Jimenez P., Martul P., Moreno A., Oyarzabal M., Rica I., Salgado Y., Martinez-Larrad M.T., Hawkins F.G., Hernandez R., Herranz L., Pallardo L.F., Deibarra L.S., Fernandez B.H., Luis J.L., Ortiz-Quintana L., Recarte P.P., Arnau D.R., Aronsson L., Boden S., Fredriksson J., Isacsson E., Johansson I., Karlsson E., Lock C., Sandstrom A.-M., Konefal M.S., Andreasson C., Dahlstrom U., Hanas R., Lundqvist K., Windell L., Jansson I., Karlsson A.-K., Lindbladh B., Odenman I., Pettersson C., Sundberg F., Sundqvist M., Aronsson S., Bellman I., Bengtsson A.-B., Lyden G.-B., Nilsson N.-O., Soderblom M., Unt C., Augustsson M., Bengtsson M., Fors H., Helmrich A., Johansson T.O., Andersson A.-C., Boiard-Stomlid A., Hellgren G., Kallsholm H., Lindqvist J., Nilsson M., Nordwall M., Stromstedt C., Ahsberg C., Lindh A., Lindhe C., Samuelsson C., Wiik A., Edenwall H., Ljumgcrantz M., Persson I.-B., Strigard E., Svensson B.-L., Aman J., Breivik G.-E., Detlofsson I.-L., Kroon M., Sarnblad S., Johansson C., Ilvered R., Lundberg A., Akesson K., Beccarelli A., Gadient M., Rappold-Amrein C., Schoenle E., Daftary A., Damagro-Elias M.E., Gilmour C., Klein M.B., Lain C., Salerno D., Smith M.E., Vats K., Pfaff D.J., Malone P., Mansfield P., Munns M., Nickel K., Pompilio K., Siemion W., Taculad R., Van Horn K., Zdanadewic M., Chambliss C., Jones J., Sadler M., Tanner-Blasiar M., Bell C., Camper N., Devaskar S., Devaskar U., Horowitz H., Rogers L., Shannahan R., Silk K., Bermudez Z., Colon R., Frazer T., Martinez-Nieves B., Torres J., Vega J., Chan M., Cook S., Goland R., Greenberg E., Jules N., Montes J., Nelson M., Parra-Valencia Z., Schachner H., Softness B., Kiviniemi M., Suomenin R., Alexander A., Hyrckowian E., Nichol L., Trucco M., Karjalainen E., Louhio T., Sarnesto A., Valtonen E., Davydova B., Helander S., Hamalainen J., Harkonen T., Joutsjoki L., Kararic M., Latva-Koivisto M., Lonn E., Nurmi T., Ollila I., Rinkinen J., Ronkainen M., Tukiainen H., Cederlof A., Kiikeri M., Tsupari S., Cheng R., Bryant K., Chan Y., Maezawa Y., Paltser G., Rasavi R., Tsui H., Winer S., Wu P., Yantha J., University of Zurich, and Knip, Mikael

Subjects
Male, Risk, medicine.medical_specialty, Casein, Breastfeeding, 030209 endocrinology & metabolism, 610 Medicine & health, 2700 General Medicine, Endocrinology and Diabetes, Disease-Free Survival, law.invention, Follow-Up Studie, Nutrition Policy, 03 medical and health sciences, 0302 clinical medicine, Randomized controlled trial, Double-Blind Method, SDG 3 - Good Health and Well-being, law, Internal medicine, Diabetes mellitus, medicine, Humans, Cumulative incidence, 030212 general & internal medicine, Child, Infant Nutritional Physiological Phenomena, Original Investigation, 2. Zero hunger, Type 1 diabetes, business.industry, Hazard ratio, Absolute risk reduction, Infant, Newborn, Caseins, General Medicine, ta3121, medicine.disease, Infant Formula, 3. Good health, Diabetes Mellitus, Type 1, Infant formula, 10036 Medical Clinic, Endokrinologi och diabetes, Female, business, Human, Follow-Up Studies
Abstract

IMPORTANCE Early exposure to complex dietary proteins may increase the risk of type 1 diabetes in children with genetic disease susceptibility. There are no intact proteins in extensively hydrolyzed formulas. OBJECTIVE To test the hypothesis that weaning to an extensively hydrolyzed formula decreases the cumulative incidence of type 1 diabetes in young children. DESIGN, SETTING, AND PARTICIPANTS An international double-blind randomized clinical trial of 2159 infants with human leukocyte antigen-conferred disease susceptibility and a first-degree relative with type 1 diabetes recruited from May 2002 to January 2007 in 78 study centers in 15 countries; 1081 were randomized to be weaned to the extensively hydrolyzed casein formula and 1078 to a conventional formula. The follow-up of the participants ended on February 28, 2017. INTERVENTIONS The participants received either a casein hydrolysate or a conventional adapted cows milk formula supplemented with 20% of the casein hydrolysate. The minimum duration of study formula exposure was 60 days by 6 to 8 months of age. MAIN OUTCOMES AND MEASURES Primary outcome was type 1 diabetes diagnosed according to World Health Organization criteria. Secondary outcomes included age at diabetes diagnosis and safety (adverse events). RESULTS Among 2159 newborn infants (1021 female [47.3%]) who were randomized, 1744 (80.8%) completed the trial. The participants were observed for a median of 11.5 years (quartile [Q] 1-Q3, 10.2-12.8). The absolute risk of type 1 diabetes was 8.4% among those randomized to the casein hydrolysate (n = 91) vs 7.6% among those randomized to the conventional formula (n = 82) (difference, 0.8%[95% CI, -1.6% to 3.2%]). The hazard ratio for type 1 diabetes adjusted for human leukocyte antigen risk group, duration of breastfeeding, duration of study formula consumption, sex, and region while treating study center as a random effect was 1.1 (95% CI, 0.8 to 1.5; P = .46). The median age at diagnosis of type 1 diabetes was similar in the 2 groups (6.0 years [Q1-Q3, 3.1-8.9] vs 5.8 years [Q1-Q3, 2.6-9.1]; difference, 0.2 years [95% CI, -0.9 to 1.2]). Upper respiratory infections were the most common adverse event reported (frequency, 0.48 events/year in the hydrolysate group and 0.50 events/year in the control group). CONCLUSIONS AND RELEVANCE Among infants at risk for type 1 diabetes, weaning to a hydrolyzed formula compared with a conventional formula did not reduce the cumulative incidence of type 1 diabetes after median follow-up for 11.5 years. These findings do not support a need to revise the dietary recommendations for infants at risk for type 1 diabetes. Funding Agencies|Eunice Kennedy Shriver National Institute of Child Health and Development (NICHD); National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health [HD040364, HD042444, HD051997]; Canadian Institutes of Health Research; Commission of the European Communities [QLK1-2002-00372]; European Foundation for the Study of Diabates/JDRF/Novo Nordisk; Academy of Finland (Centre of Excellence in Molecular Systems Immunology and Physiology Research) [250114]; Dutch Diabetes Research Foundation; Finnish Diabetes Research Foundation; JDRF

Published
2018

13. Anti-keratin antibodies in patients with juvenile idiopathic arthritis

Author

Hromadníková I, Vavrincova P, Stechova K, and Hridelova D

Subjects
Adult, Male, Adolescent, In Vitro Techniques, Middle Aged, Arthritis, Juvenile, Rats, Rheumatoid Factor, Child, Preschool, Immunoglobulin G, Animals, Humans, Keratins, Female, Child, Fluorescent Antibody Technique, Indirect, Autoantibodies
Abstract

We discuss the presence of anti-keratin antibodies (AKA) of the IgG class in patients with defined juvenile idiopathic arthritis (JIA).An indirect immunofluorescence test with rat oesophagus substrate was used for the detection and quantification of AKA antibodies in patients'sera.Overall 30/60 patients with JIA had sera positiveforAKA (50%, p=0.0005) ranging from 1:20 to 1:160 dilutions. Using the classification criteria for childhood idiopathic arthritis, AKA occurred in 2/7 patients with systemic disease (28.6%), in 13/30 patients with RF negative polyarthritis (43.3%, p=0.008) and in 12/18 RF positive polyarthritis (66.7%, p=0.002). AKA were also found in a small cohort of patients with oligoarthritis (1/3) and psoriatic arthritis (2/2). AKA positivity occurred in 3/26 healthy controls at a 1:20 dilution. The presence ofAKA was correlated as well as with the severity of the disease. Our study revealed that AKA was present overall in 16/29 patients (55.2%) with severe JIA and in 11/26 patients (42.3%) with non-severe disease. We also observed that AKA remained positive regardless of disease activity. AKA were detectable in 44.4% patients with active JIA and in 45.9% patients in the complete or near remission.Our data suggest that AKA are present in patients with JIA. However no correlation with severity or disease activity was observed.

Published
2001

14. Influence of maternal hyperglycaemia on cord blood mononuclear cells in response to diabetes-associated autoantigens

Author

Stechova, K, Spalovat, I, Durilova, M, Baratskovat, M, Cernys, M, Cerena, M, Pithova, D, Chudoba, D, Ullmanova, T, Faresjö, Maria, Stechova, K, Spalovat, I, Durilova, M, Baratskovat, M, Cernys, M, Cerena, M, Pithova, D, Chudoba, D, Ullmanova, T, and Faresjö, Maria

Abstract

Perfect maternal diabetes compensation is crucial for the outcome of the baby. However, little is known how hyperglycaemia influences the specific immune response. Furthermore, babies of type 1 diabetes (T1D) mothers have less risk of development T1D than babies with a T1D father. This study aimed to analyze the effect of maternal hyperglycaemia on newborns with focus on the response to diabetes-associated autoantigens. Populations: (1) Newborns of T1D mothers split into groups according to maternal diabetes compensation during the 3rd trimester: perfect (n = 15) or acceptable (n = 25) compensation. (2) newborns with T1D father (n = 12) (3) newborns with a mother treated for either gestational or type 2 diabetes (n = 10) (4) control newborns (n = 25). Spontaneous as well as diabetes-associated autoantigen-stimulated production of 23 cytokines and chemokines were tested using protein microarray. In addition, the influence of glucose on cytokine and chemokine responsiveness was analyzed in vitro. The study groups differed in their spontaneous as well as stimulated cytokine and chemokine spectra. A prominent Th1 response (high IFN-gamma) from autoantigen stimulation was observed especially in babies of T1D fathers (P = 0.001) and also in mothers with perfect diabetes compensation during the 3rd trimester (P = 0.016) in comparison with control newborns. By contrast, cord blood mononuclear cells cultivated in vitro in high glucose concentration decreased the diabetogenic stimulated Th1 cytokine response. Maternal ‘sweet’ as well as ‘autoimmune environment’ may both lead to lower occurrence of T1D within their offspring. Further studies will reveal the exact immunological mechanism of this observation.

Published
2009
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15. Switch from a dominant Th1-associated immune profile during the pre-diabetic phase in favour of a temporary increase of a Th3-associated and inflammatory immune profile at the onset of type 1 diabetes

Author

Rydén, A, Stechova, K, Faresjö, Maria, Rydén, A, Stechova, K, and Faresjö, Maria

Abstract

Background: Type 1 diabetes (T1D) is all autoimmune disease dominated by loss of self-tolerance resulting in depletion of the beta-cells. This Study aims to confirm previous observations of a dominant T-helper (Th)1-like profile during the period close to onset of disease. Further, to follow the immune response from onset to 2 years duration, the Study focused on spontaneous as well as autoantigen-induced immune profile. Methods: Peripheral blood mononuclear cells were collected 4 days and 1 and 2 years after diagnosis of T1D children, from healthy children carrying the human leukocyte antigen-risk genes and from high-risk children (ICA >= 20 IJDF units). Peripheral blood mononuclear cells were stimulated with glutamic acid decarboxylase (GAD(65)) and phytohaemagglutinin (PHA). Cytokines and chemokines were detected in cell-culture supernatants by protein microarray (naive T-cells; interleukin (IL)-7, Th1; interferon-gamma, turnout necrosis factor-beta, Th2; IL-5, Th3; transforming growth factor-beta, T-regulatory cell type 1; IL-10 and inflammatory cytokines; tumour necrosis factor-alpha, IL-6 and chemokines; monocyte chemoattractant protein-1, monokine upregulated by IFN-gamma) in relation to clinical outcome (C-peptide). Results: High-risk children showed a dominant Th1-associated profile with high spontaneous and GAD(65)-induced secretion. The mitogen PHA instead induced a Th2-associated response exclusively in high-risk children. In contrast, newly diagnosed T1D children showed a pronounced Th3-associated cytokine profile as well as a burst of inflammatory cytokines and chemokines secreted both spontaneously and by GAD(65) and PHA stimulation. The immune response to GAD(65) and PHA, however, diminished with duration of disease. Conclusion: A dominant Thl-associated immune profile was observed during the pre-diabetic phase. This Th1 dominance, however, diminished in favour of a temporary increase in a Th3-associated and inflammatory immune profile at the o

Published
2009
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16. The dynamic changes of zinc transporter 8 autoantibodies in Czech children from the onset of Type 1 diabetes mellitus

Author

Petruzelkova, L., primary, Ananieva-Jordanova, R., additional, Vcelakova, J., additional, Vesely, Z., additional, Stechova, K., additional, Lebl, J., additional, Dusatkova, P., additional, Sumnik, Z., additional, Coles, R., additional, Powell, M., additional, Furmaniak, J., additional, Rees Smith, B., additional, and Kolouskova, S., additional

Published
2013
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17. Protein microarray analysis as a tool for monitoring cellular autoreactivity in type 1 diabetes patients and their relatives

Author

Vrabelova, Z, Kolouskova, S, Böhmova, K, Faresjö, Maria, Sumnik, Z, Pechova, M, Kverka, M, Chudoba, D, Zacharovova, K, Stadlerova, G, Pithova, P, Hladikova, M, Stechova, K, Vrabelova, Z, Kolouskova, S, Böhmova, K, Faresjö, Maria, Sumnik, Z, Pechova, M, Kverka, M, Chudoba, D, Zacharovova, K, Stadlerova, G, Pithova, P, Hladikova, M, and Stechova, K

Abstract

Background: Autoreactive T cells have a crucial role in type 1 diabetes (T1D) pathogenesis.: Objectives: The aim of our study was to monitor the in vitro production of cytokines by peripheral blood mononuclear cells (PBMCs) after stimulation with diabetogenic autoantigens. Subjects: Ten T1D patients (tested at the time of diagnosis and 6 and 12 months later), 10 first-degree relatives of the T1D patients, and 10 controls underwent the study. Methods: PBMCs were stimulated with glutamic acid decarboxylase 65 (GAD65) amino acids (a.a.) 247-279, 509-528, and 524-543, proinsulin a.a. 9-23, and tyrosine phosphatase (islet antigen-2)/R2 a.a. 853-872. Interleukin (IL)-2, IL-4, IL-5, IL-6, IL-10, IL-13, interferon (IFN)-γ, tumor necrosis factor β, transforming growth factor β1, and granulocyte colony-stimulating factor (GCSF) were analyzed by protein microarray. Results: Differences in cytokine(s) poststimulatory and mainly in basal production were observed in all groups. The most prominent findings were in controls, the higher basal levels of IL-2, IL-4, IL-5, IL-13, and GCSF were observed when compared with relatives (p < 0.05, for all). After stimulation in controls, there was a significant decrease in IL-2, IL-13, GCSF, and IFN-γ (p < 0.05, for all). The group of relatives was the most variable in poststimulatory production. A strong correlation between cytokines production was found but groups differed in this aspect. Conclusion: By multiplex analysis, it may be possible, for example, to define the risk immunological response pattern among relatives or to monitor the immune response in patients on immune modulation therapy. © 2007 The Authors Journal compilation © 2007 Blackwell Munksgaard.

Published
2007
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18. Cord blood cytokine profile detection in neonates with T1D parents - Monitoring of cellular auto-reactivity using protein microarray

Author

Bohmova, K, Hladikova, Z, Cerny, M, Flajsmanova, K, Vrabelova, Z, Skramlikova, T, Spalova, I, Cerna, M, Chudoba, D, Pithova, P, Stadlerova, G, Bartaskova, D, Faresjö, Maria, Stechova, K, Bohmova, K, Hladikova, Z, Cerny, M, Flajsmanova, K, Vrabelova, Z, Skramlikova, T, Spalova, I, Cerna, M, Chudoba, D, Pithova, P, Stadlerova, G, Bartaskova, D, Faresjö, Maria, and Stechova, K

Abstract

Type 1 diabetes (T1D) is a great medical challenge and its incidence rises rapidly. T lymphocytes and their cytokine production are supposed to play a major role in T1D development. So far, there is no potent tool to recognize the early signs of cellular auto-reactivity which leads to β-cell damage. The naïve immune system of the newborn (not yet influenced by external factors) can be used as an important model for T1D pathogenesis studies. Cord blood samples of 22 healthy neonates born at term to a diabetic parent (T1DR) and 15 newborns with no family history of any autoimmune disease (controls) were collected. Determination of 23 cytokines was performed before and after the stimulation with diabetogenic autoantigens using protein microarray. We observed lower basal production of all detected cytokines in the T1DR group - granulocyte/macrophage colony-stimulating factor (GM-CSF) (P = 0.025), growth regulated protein (GRO) (P = 0.002), GRO-α (P = 0.027), interleukin (IL)-1-α (P = 0.051), IL-3 (P = 0.008), IL-7 (P = 0.027), IL-8 (P = 0.042), monocyte chemoattractant proteins (MCP)-3 (P = 0.022), monokine-induced by IFN-γ (MIG) (P = 0.034) and regulated upon activation normal T-cell express sequence (RANTES) (P = 0.004). Exclusively lower post-stimulative levels of G-CSF (P = 0.030) and GRO-α (P = 0.04) were observed in controls in comparison with the basal levels. A significant post-stimulative decrease in G-CSF (P = 0.030) and MCP-2 (P = 0.009) levels was observed in controls in comparison with T1DR neonates. We also observed the interesting impact of the risky genotype on the protein microarray results. Protein microarray seems to be a useful tool to characterize a risk pattern of the immune response for T1D also in newborns. © 2007 The Authors.

Published
2007
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20. Immune regulatory T cells in siblings of children suffering from type 1 diabetes mellitus

Author

Michalek, J, Vrabelova, Z, Hrotekova, Z, Kyr, M, Kolouskova, S, Faresjö, Maria, Stechova, K, Michalek, J, Vrabelova, Z, Hrotekova, Z, Kyr, M, Kolouskova, S, Faresjö, Maria, and Stechova, K

Abstract

Patients with type 1 diabetes are suffering from defects in immune regulatory cells. Their siblings may be at increased risk of type 1 diabetes especially if they are carriers of certain human leucocyte antigen (HLA) alleles. In a prospective non-randomized study, we intended to evaluate 31 healthy siblings of paediatric patients with type 1 diabetes and explore immune regulatory populations of CD4+CD25+ T cells and natural killer (NK) T cells. Tested siblings of type 1 diabetes patients were stratified according to the HLA-associated risk of possible diabetes development. Immune regulatory function of CD4+CD25+ T cells was tested in vitro. Significant differences in CD4+CD25+ but not in NK T cells have been identified. Siblings of type 1 diabetes patients carrying high risk HLA alleles (DQA1*05, DQB1*0201, DQB1*0302) had significantly lower number of immune regulatory CD4+CD25+ T cells than the age-matched healthy controls or siblings carrying low-risk HLA alleles (DQB1*0301, DQB1*0603, DQB1*0602). Regulatory function of CD4+CD25+ T cells demonstrated a dose-escalation effect. In siblings of type 1 diabetes patients, the defect in immune regulatory CD4+CD25+ T cells exists in association with genetic HLA-linked risk for type 1 diabetes. © 2006 The Authors.

Published
2006
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30. CD 127− and FoxP3+ Expression on CD25+CD4+ T Regulatory Cells upon Specific Diabetogeneic Stimulation in High-risk Relatives of Type 1 Diabetes Mellitus Patients.

Author

Vrabelova, Z., Hrotekova, Z., Hladikova, Z., Bohmova, K., Stechova, K., and Michalek, J.

Subjects
DIABETES, PEOPLE with diabetes, T cells, LYMPHOCYTES, CD4 antigen
Abstract

Abnormalities in CD4+CD25+ regulatory T cells (Treg) may contribute to type 1 diabetes (T1D) development. First-degree relatives of T1D patients are at increased risk especially when they carry certain HLA II haplotypes. Using two novel markers of CD4+CD25+ Treg (CD127− and FoxP3+ respectively), we evaluated number and function of Treg after specific stimulation with diabetogeneic autoantigens in 11 high-risk (according to HLA-linked risk) relatives of T1D patients and 14 age-matched healthy controls using a cytokine secretion assay based on interferon- γ (IFN- γ) production. High-risk relatives of T1D patients had significantly lower pre- and post-stimulatory number of CD127− Treg than that of healthy controls ( P < 0.05). Labelling Treg with FoxP3+ demonstrated similar trend but did not reach statistical significance. Although the stimulation with diabetogenic autoantigens did not lead to a significant change in number of Treg in both groups, the defective function of Treg was performed by significantly higher activation of diabetogeneic T cells in high-risk relatives of T1D patients compared to healthy controls ( P ≤ 0.02). Individuals at increased HLA-associated genetic risk for T1D showed defects in Treg. [ABSTRACT FROM AUTHOR]

Published
2008
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33. Dysfunction of peripheral somatic and autonomic nervous system in patients with severe forms of Crohn's disease on biological therapy with TNFα inhibitors-A single center study.

Author

Wasserbauer M, Mala S, Stechova K, Hlava S, Cernikova P, Stovicek J, Drabek J, Broz J, Pichlerova D, Kucerova B, Liskova P, Kral J, Bartuskova L, and Keil R

Subjects
Humans, Tumor Necrosis Factor-alpha therapeutic use, Autonomic Nervous System, Biological Therapy, Crohn Disease drug therapy, Crohn Disease epidemiology, Crohn Disease complications, Autonomic Nervous System Diseases, Peripheral Nervous System Diseases
Abstract

Objective: Crohn's disease (CD) can be associated with a wide range of extraintestinal manifestations (EIMs), including neurological ones. Published studies differ in their conclusions about the epidemiology and etiopathogenesis of neurological EIMs. The aims of this study were to demonstrate the presence and find risk factors of peripheral (somatic and autonomic) neuropathy patients with severe CD on anti-TNFα biological therapy., Material and Methods: A clinical examination focusing on detection of peripheral sensor-motor nervous dysfunction (including Sudoscan) and examination of autonomic nervous system dysfunction (using Ewing´s battery tests and spectral analysis) together with laboratory tests and collection of demographic data followed by administration of questionnaires were performed on a total of 30 neurologically asymptomatic outpatients with severe CD on anti-TNFα biological therapy., Results: Peripheral sensor-motor nervous function via clinical neurological examination was pathological in 36.7% and Sudoscan in 33.3% of cases. Statistically significant associations between vibration perception test and age, CD and biological therapy duration, body mass index and Crohn's Disease Activity Index were proved while statistically significant associations between temperature perception test and age and BMI were proved as well. Additionally, a decrease of total protein in a patient´s serum below the physiological cut-off in the 6 months prior to measurement was associated with a pathological result of a Sudoscan. Cardiovascular autonomic neuropathy based on Ewing´s battery tests was present in 56.7% of patients, no statistically significant risk factors were found. Our peripheral neuropathy questionnaire correlated with the results of the Sudoscan test and some tests of the clinical examination of peripheral sensor-motor nervous function (discriminatory contact perception test, temperature perception test)., Conclusions: This study demonstrated a relatively high prevalence of peripheral (especially autonomic) neuropathy and verified some risk factors for the development of peripheral somatic neuropathy in asymptomatic patients with severe form of CD on anti-TNFα biological therapy., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Wasserbauer et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Published
2023
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35. The impact of type 1 diabetes mellitus on male sexual functions and sex hormone levels.

Author

Hylmarova S, Stechova K, Pavlinkova G, Peknicova J, Macek M, and Kvapil M

Subjects
Adult, Depression epidemiology, Depression psychology, Diabetes Mellitus, Type 1 complications, Diabetes Mellitus, Type 1 metabolism, Diabetic Nephropathies etiology, Erectile Dysfunction metabolism, Erectile Dysfunction psychology, Glycated Hemoglobin metabolism, Humans, Hypoglycemic Agents therapeutic use, Insulin therapeutic use, Male, Quality of Life, Sex Hormone-Binding Globulin metabolism, Sexual Dysfunction, Physiological epidemiology, Sexual Dysfunction, Physiological metabolism, Sexual Dysfunction, Physiological psychology, Testosterone metabolism, Diabetes Mellitus, Type 1 epidemiology, Diabetic Nephropathies epidemiology, Erectile Dysfunction epidemiology
Abstract

Little is known about type 1 diabetes mellitus (T1DM) impact on the male sexual and reproductive functions. We aim to evaluate the influence of T1DM on male sexual function, quality of sexual life, and sex hormone levels. A total of 57 male patients aged 18 to 50 years (mean = 33) with T1DM (duration mean = 15 years) had a medical examination and completed a set of questionnaires - International Index of Erectile Function-5 (IIEF-5), Beck Depression Inventory (BDI) and Sexual quality of life questionnaire male (SQoL-M). The prevalence of erectile dysfunction was 28.1% (IIEF-5 ≤21). Patients without diabetic nephropathy had better erectile function (p = 0.008). Subjects with better glycemic control (HbA 1c <65 mmol/mol) had also better erectile function (p = 0.041). At least 8.8% patients had retrograde ejaculation. Blood serum levels of sex hormones were determined and compared to laboratory reference values of healthy men. Total testosterone level was not significantly changed, sex hormone binding globulin was higher (p < 0.001) and its level correlated with daily insulin dose adjusted to body weight (p = 0.008). Free androgen index and calculated free testosterone were lower (p = 0.013; p < 0.001), estradiol was not significantly changed, LH was higher (p < 0.001), FSH was unchanged, and prolactin was higher (p < 0.001). Prostate-specific antigen (PSA) negatively correlated with HbA 1c (p < 0.001). To conclude, we found significant changes in sexual functions and sex hormone blood concentrations that indicate impairment of sexual and reproductive functions in T1DM males.

Published
2020
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36. Sexual Dysfunction in Women Treated for Type 1 Diabetes and the Impact of Coexisting Thyroid Disease.

Author

Stechova K, Mastikova L, Urbaniec K, Vanis M, Hylmarova S, Kvapil M, and Pastor Z

Abstract

Introduction: More sexual problems are reported among people treated for diabetes; however, this situation is less explored in women than in men., Aim: To analyze the presence and causal links of female sexual dysfunction (FSD) among Czech women treated for type 1 diabetes., Methods: 40 women completed a national version of the Female Sexual Function Index (FSFI), Female Sexual Distress Scale-revised (FSDS-R), and Beck's Depression Inventory-II (BDI-II). A metabolic and endocrine analysis was done using blood samples. Data were statistically analyzed using SPSS v.24 and the R environment., Main Outcome Measures: Patient details (personal information, diabetes-related data, and sex history), sexual performance (the FSFI and FSDS-R scores), and level of depression (the BDI-II score) were measured., Results: FSD was present in 58% of the participants (based on the FSFI score), and 38% women declared significant sexual distress (according to their FSDS-R score). Even though only 4 women fulfilled the criteria for depression, we observed a strong association between BDI-II and FSFI (for total FSFI score P = .012, ρ = -0.394) resp. FSDS-R scores (P < .001, ρ = 0.552). Although we were not able to establish a clear direct connection between FSD and metabolic control, BDI-II scores were closely correlated with glycosylated hemoglobin (P = .009, ρ = 0.407). The duration of diabetes (based on FSDS-R: P = .046) but neither age nor the presence of chronic diabetic microvascular complications was associated with a higher FSD occurrence. We also observed an association between FSD and the presence of autoimmune hypothyroidism, even when successfully treated (FSDS-R: P = .009; FSFI: P = .067)., Conclusion: FSD is more common in women with type 1 diabetes than in healthy women, and coexisting thyroid autoimmune disease seems to exacerbate FSD. Women suffering from type 1 diabetes, and particularly those with additional endocrinopathies, should be actively screened for FSD. Stechova K, Mastikova L, Urbaniec K, et al. Sexual Dysfunction in Women Treated for Type 1 Diabetes and the Impact of Coexisting Thyroid Disease. Sex Med 2019;7:217-226., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2019
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37. Comprehensive Analysis of the Real Lifestyles of T1D Patients for the Purpose of Designing a Personalized Counselor for Prandial Insulin Dosing.

Author

Stechova K, Hlubik J, Pithova P, Cikl P, and Lhotska L

Subjects
Adult, Biomarkers blood, Blood Glucose metabolism, Blood Glucose Self-Monitoring, Diabetes Mellitus, Type 1 blood, Diabetes Mellitus, Type 1 diagnosis, Dietary Carbohydrates administration & dosage, Energy Metabolism, Exercise, Feeding Behavior, Female, Humans, Hypoglycemic Agents adverse effects, Insulin adverse effects, Insulin Infusion Systems, Male, Middle Aged, Pilot Projects, Proof of Concept Study, Time Factors, Treatment Outcome, Young Adult, Blood Glucose drug effects, Cell Phone, Diabetes Mellitus, Type 1 drug therapy, Drug Dosage Calculations, Hypoglycemic Agents administration & dosage, Insulin administration & dosage, Life Style, Mobile Applications, Postprandial Period
Abstract

Post-prandial hyperglycemia is still a challenging issue in intensified insulin therapy. Data of 35 T1D patients during a four-week period were analyzed: RT-CGM (real time continuous glucose monitoring) record, insulin doses, diet (including meal photos), energy expenditure, and other relevant conditions. Patients made significant errors in carbohydrate counting (in 56% of cooked and 44% of noncooked meals), which resulted in inadequate insulin doses. Subsequently, a mobile application was programmed to provide individualized advice on prandial insulin dose. When using the application, a patient chooses only the type of categorized situation (e.g., meals with other relevant data) without carbohydrates counting. The application significantly improved postprandial glycemia as normoglycemia was reached in 95/105 testing sessions. Other important findings of the study include: A high intake of saturated fat (median: 162% of recommended intake); a low intake of fiber and vitamin C (median: 42% and 37%, respectively, of recommended intake); an increase in overweight/obesity status (according to body fat measurement), especially in women (median of body fat: 30%); and low physical activity (in 16/35 patients). The proposed individualized approach without carbohydrate counting may help reach postprandial normoglycemia but it is necessary to pay attention to the lifestyle habits of T1D patients too.

Published
2019
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38. Lessons Learned from Implementing a New Testing/Educational Tool for Patients Using an Insulin Pump.

Author

Stechova K, Vanis M, Tuhackova M, Urbaniec K, and Kvapil M

Subjects
Adult, Blood Glucose, Diabetes Mellitus, Type 1 blood, Female, Humans, Hypoglycemic Agents administration & dosage, Insulin administration & dosage, Male, Middle Aged, Motivation, Personality, Surveys and Questionnaires, Diabetes Mellitus, Type 1 drug therapy, Health Knowledge, Attitudes, Practice, Hypoglycemic Agents therapeutic use, Insulin therapeutic use, Insulin Infusion Systems, Patient Education as Topic
Abstract

Background: To improve insulin pump therapy results, a special test for patients was devised. The model successfully used to achieve a license to operate different machines was followed., Methods: The test (a practice and a full run, with a time limit) contained 42 questions, each with four optional choices, and could be answered online. Patients could familiarize themselves with the whole question pool first. Patients could repeat a full run attempt if they failed and were offered focused remedial education. The study group composed of adults, 46 females, and 54 males, all treated for type 1 diabetes, 38/100 newly introduced to insulin pump therapy., Results: Eighty-five of 100 patients successfully completed their first full run attempt (80% or higher correct answers) and 3 of 100 on their second full run attempt; 12 of 100 patients were not able to succeed. The median of the test score was 2 mistakes (range 0-17 mistakes). The most problematic topics were diet and insulin regimens and their application. The crucial factor influencing the test score was the willingness to try practice run(s). Those who practiced had a significantly higher total test score with better results in 5 of 8 tested knowledge domains. Age and diabetes existing >15 years had an impact on the result, too. Both patients' and caregivers' opinions on the test were predominantly positive (or neutral)., Conclusions: The type of test introduced is a good tool for checking a patient's theoretical knowledge and indirectly revealing a patient's level of motivation.

Published
2018
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39. Not Only Glycaemic But Also Other Metabolic Factors Affect T Regulatory Cell Counts and Proinflammatory Cytokine Levels in Women with Type 1 Diabetes.

Author

Stechova K, Sklenarova-Labikova J, Kratzerova T, Pithova P, and Filipp D

Subjects
Adult, Cholesterol, HDL metabolism, Cholesterol, LDL metabolism, Diabetes Mellitus, Type 1 complications, Diabetes Mellitus, Type 1 drug therapy, Diabetes Mellitus, Type 1 metabolism, Diabetic Neuropathies etiology, Diabetic Neuropathies immunology, Female, Glycated Hemoglobin metabolism, Glycation End Products, Advanced metabolism, Humans, Hypoglycemic Agents administration & dosage, Insulin administration & dosage, Interleukin-1alpha immunology, Interleukin-6 immunology, Lymphocyte Count, Triglycerides metabolism, Tumor Necrosis Factor-alpha immunology, Vitamin D metabolism, Young Adult, Cytokines immunology, Diabetes Mellitus, Type 1 immunology, T-Lymphocytes, Helper-Inducer immunology, T-Lymphocytes, Regulatory immunology
Abstract

Type 1 diabetic (T1D) patients suffer from insulinopenia and hyperglycaemia. Studies have shown that if a patient's hyperglycaemic environment is not compensated, it leads to complex immune dysfunctions. Similarly, T1D mothers with poor glycaemic control exert a negative impact on the immune responses of their newborns. However, questions concerning the impact of other metabolic disturbances on the immune system of T1D mothers (and their newborns) have been raised. To address these questions, we examined 28 T1D women in reproductive age for the relationship between various metabolic, clinical, and immune parameters. Our study revealed several unexpected correlations which are indicative of a much more complex relationship between glucose and lipid factors (namely, glycosylated haemoglobin Hb1Ac, the presence of one but not multiple chronic diabetic complications, and atherogenic indexes) and proinflammatory cytokines (IL-1alpha and TNF-alpha). Regulatory T cell counts correlated with HbA1c, diabetic neuropathy, lipid spectra parameters, and IL-6 levels. Total T-helper cell count was interconnected with BMI and glycaemia variability correlated with lipid spectra parameters, insulin dose, and vitamin D levels. These and other correlations revealed in this study provide broader insight into the association of various metabolic abnormalities with immune parameters that may impact T1D mothers or their developing child.

Published
2017
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40. Personal Portable Devices in the Light of the Internet of Things.

Author

Lhotska L, Stechova K, and Pharow P

Subjects
Health Services, Humans, Internet, Wearable Electronic Devices
Abstract

Personal portable devices have already gained their position in health services. However, mobile technologies and Internet of Things open new areas of applications. The possibility to collect many data types continuously over long time intervals brings various questions that must be answered in the design process. We also discuss briefly the role of the user. We illustrate the complexity of the field by a case study of diabetes management.

Published
2017

41. T regulatory lymphocytes in type 1 diabetes: Impaired CD25 expression and IL-2 induced STAT5 phosphorylation in pediatric patients.

Author

Parackova Z, Kayserova J, Danova K, Sismova K, Dudkova E, Sumnik Z, Kolouskova S, Lebl J, Stechova K, and Sediva A

Subjects
Adolescent, Age Factors, Biomarkers, Case-Control Studies, Cell Differentiation, Child, Child, Preschool, Diabetes Mellitus, Type 1 diagnosis, Female, Forkhead Transcription Factors metabolism, Humans, Immunophenotyping, Infant, Interleukin-2 pharmacology, Interleukin-2 Receptor alpha Subunit metabolism, Lymphocyte Count, Male, Phosphorylation, STAT5 Transcription Factor, Signal Transduction, T-Lymphocytes, Regulatory cytology, Thymocytes cytology, Thymocytes immunology, Thymocytes metabolism, Diabetes Mellitus, Type 1 etiology, Diabetes Mellitus, Type 1 metabolism, Interleukin-2 metabolism, Interleukin-2 Receptor alpha Subunit genetics, T-Lymphocytes, Regulatory immunology, T-Lymphocytes, Regulatory metabolism
Abstract

T regulatory cells (Tregs) are essential for maintaining tolerance and preventing autoimmune diseases, such as type 1 diabetes (T1D). In our study, we investigated CD25 + FoxP3 + Tregs and thymic FoxP3 + Helios + Tregs in large cohorts of children with T1D at onset and with long-term T1D, and further in their relatives and healthy controls. We observed significantly decreased numbers of CD25 + FoxP3 + Tregs, but not FoxP3 + Helios + Tregs, in long-term patients compared with the control group and T1D onset. Furthermore, long-term T1D patients exhibited highly significant decrease of CD25 expression on both CD25 + FoxP3 + Tregs and FoxP3 + Helios + Tregs, independently on age or the duration of diabetes. A similar reduction of CD25 expression was also found in T1D relatives, more significant in those with positive autoantibodies. Low CD25 expression was associated with impaired signal transducer and activator of transcription 5 (STAT5) phosphorylation after IL-2 exposure. Our results show that the frequency of Tregs is altered in a large cohort of long-term T1D patients, a profound decrease in CD25 expression and altered IL-2 signaling are typical features of Tregs populations in long-term diabetic patients and their relatives.

Published
2016
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42. Aviation and technology in diabetes management.

Author

Stechova K, Stecha R, and Kvapil M

Subjects
Accidents, Aviation, Equipment Design, Humans, Man-Machine Systems, Patient Education as Topic standards, Aviation education, Aviation standards, Diabetes Mellitus psychology, Insulin Infusion Systems psychology
Published
2015
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43. Treated Autoimmune Thyroid Disease Is Associated with a Decreased Quality of Life among Young Persons with Type 1 Diabetes.

Author

Spirkova A, Dusatkova P, Peckova M, Kolouskova S, Snajderova M, Obermannova B, Stechova K, Hrachovinova T, Mares J, Cinek O, Lebl J, Sumnik Z, and Pruhova S

Abstract

Type 1 diabetes (T1D) in children and adolescents is relatively often accompanied by other immunopathological diseases, autoimmune thyroid disease (AITD) or celiac disease (CD). Our aim was to assess whether these conditions are associated with changes in the health-related quality of life (HRQOL) in pediatric patients with T1D. In a cross-sectional study we identified eligible 332 patients with T1D aged 8-18 years, of whom 248 (75%) together with their parents responded to the PedsQL Generic and Diabetes Modules. Compared to 143 patients without thyroid autoantibodies, 40 patients with a thyroxine-treated AITD scored lower in the overall generic HRQOL (P = 0.014), as well as in the overall diabetes-specific HRQOL (P = 0.013). After adjustment for age, gender, duration of diabetes, type of diabetes treatment, and diabetes control, this association remained statistically significant for the generic HRQOL (P = 0.023). Celiac disease was not associated with a change in the generic or diabetes-specific HRQOL (P = 0.07  and  P = 0.63, resp.). Parental scores showed no association with AITD or celiac disease, except a marginally significant decrease in the overall generic HRQOL (P = 0.039) in the T1D + AITD compared to T1D group. Our study indicates that, in pediatric patients with T1D, concomitant thyroxine-treated AITD is associated with lower quality of life.

Published
2015
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44. Maternal BMI and HDL as predictors of pregnancy outcome in women with type 1 diabetes.

Author

Ulmannova T, Bartaskova D, Spalova I, Zoban P, Vesely Z, and Stechova K

Subjects
Adolescent, Adult, Diabetes Mellitus, Type 1 complications, Female, Humans, Pre-Eclampsia blood, Pre-Eclampsia etiology, Pregnancy, Retrospective Studies, Young Adult, Body Mass Index, Cholesterol, HDL blood, Diabetes Mellitus, Type 1 blood, Pregnancy Outcome, Pregnancy in Diabetics blood
Abstract

Objective: Diabetes in pregnancy is associated with increased risks of maternal as well as foetal complications., Methods: Retrospective data on 96 women and their 96 newborns were anonymously statistically analysed to assess pregnancies of type 1 diabetes (T1D) women managed in our hospital in past nine years. The outcomes of the neonates were divided into three categories according to the clinical status, presence of congenital abnormalities and infant's treatment., Results: We found out that the outcome of newborn infants associated with maternal HbA1c before gestation as well as during the whole course of pregnancy (p < 0.02 for all). Surprisingly, neonatal outcome was strongly associated with the maternal BMI (p < 0.05). In our model, a lowering of BMI by one grade led to an 18% increase in the chance that the newborn will have no health problems. We did not observe an important worsening of chronic diabetic complications in mothers; however, regarding maternal clinical status, we found that preeclampsia occurrence was strongly and independently connected to HDL level (p < 0.01)., Conclusion: Our data demonstrate that lower pregestational BMI could substantially improve T1D mothers' pregnancy outcome. Lower HDL levels in T1D mothers during pregnancy correlate with higher risk of preeclampsia development.

Published
2014
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45. The cytokine production of peripheral blood mononuclear cells reflects the autoantibody profile of patients suffering from type 1 diabetes.

Author

Labikova J, Vcelakova J, Ulmannova T, Petruzelkova L, Kolouskova S, and Stechova K

Subjects
Autoantibodies immunology, Child, Child, Preschool, Female, Flow Cytometry, Glutamate Decarboxylase immunology, Humans, Interferon-gamma blood, Interleukin-17 blood, Male, T-Lymphocytes, Helper-Inducer immunology, T-Lymphocytes, Regulatory immunology, Autoantibodies blood, Diabetes Mellitus, Type 1 blood, Diabetes Mellitus, Type 1 immunology, Interferon-gamma biosynthesis, Interleukin-17 biosynthesis, Leukocytes, Mononuclear metabolism
Abstract

Type 1 diabetes (T1D) is an autoimmune disorder characterised by the immune-mediated destruction of insulin-producing pancreatic beta cells. The inflammatory process appears to be primarily mediated by pro-inflammatory Th1 lymphocytes, while the role Th17 cells in T1D is currently being investigated. T1D is characterised by the presence of autoantigen-specific autoantibodies. This study was conducted using patients with confirmed T1D and healthy control subjects. We examined the effect of the patient's autoantibody profile on peripheral blood mononuclear cell (PBMC) cytokine production following stimulation with the major diabetogenic autoantigens GAD65 and IA2. IFN-gamma and IL17 production was detected by ELISPOT and the ratio of basic cellular populations in PBMCs was measured by flow cytometry. We demonstrated a significant interaction between the patient's autoantibody profile and mode of stimulation. This suggests that autoantigen stimulation has a different effect on different groups of patients depending on their autoantibody profile. An increased production of IL17 was found in patients with high IA2 autoantibodies compared to patients with low levels of autoantibodies and healthy controls regardless of the mode of stimulation. The titre of IA2 autoantibodies positively correlates with the proportion of Tc lymphocytes and negatively correlates with the proportion of Th lymphocytes. Our results show that a patient's autoantibody profile reflects the type of cellular immune responses. It seems that the high titre of IA2 autoantibodies is related to increased production of IL17 and an increased proportion of Tc lymphocytes. This finding may be useful in designing immunointervention studies to prevent T1D., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Published
2014
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46. Experience with real time continuous glucose monitoring in stabilising fluctuating glycaemia during intensive care of the preterm infant of a diabetic mother.

Author

Stechova K, Cerny M, Brabec R, Ulmannova T, Bartaskova D, Spalova I, and Zoban P

Subjects
Adult, Diabetes Mellitus, Type 1, Female, Humans, Male, Monitoring, Physiologic, Pregnancy, Pregnancy in Diabetics, Blood Glucose, Infant, Premature blood, Intensive Care, Neonatal methods
Abstract

Objective: The newborns of diabetic mothers suffer from perinatal complications more frequently than the newborns of healthy women., Methods: We used for 7 days a real time continuous glucose monitoring system (RT-CGMS) to monitor glucose homeostasis and manage glucose administration in a premature newborn of a diabetic mother., Results: The boy was born at 35 + 5 gestational weeks with typical signs of diabetic fetopathy. RT-CGMS revealed 2 late hypoglycaemia episodes on the 2nd and 4th days. The sensor readings correlated well with glycaemia measured in the laboratory (r = 0.908, p = 0.005). To support conclusions of this case report, we attached the data of five other preterm newborns of diabetic mothers who were later successfully treated according to the RT-CGMS data as well., Conclusions: This approach allows timely response to glycaemia instability and is applicable even in preterm infants.

Published
2014
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47. Decreased dendritic cell numbers but increased TLR9-mediated interferon-alpha production in first degree relatives of type 1 diabetes patients.

Author

Kayserova J, Vcelakova J, Stechova K, Dudkova E, Hromadkova H, Sumnik Z, Kolouskova S, Spisek R, and Sediva A

Subjects
Adolescent, Adult, Cell Count, Child, Child, Preschool, Family, Female, Humans, Interferon-alpha blood, Leukocytes, Mononuclear drug effects, Leukocytes, Mononuclear metabolism, Ligands, Male, Oligodeoxyribonucleotides pharmacology, Young Adult, Dendritic Cells immunology, Dendritic Cells metabolism, Diabetes Mellitus, Type 1 immunology, Diabetes Mellitus, Type 1 metabolism, Interferon-alpha biosynthesis, Toll-Like Receptor 9 metabolism
Abstract

Objective: Dendritic cells (DCs) play an important role in pathogenesis of autoimmunity, including type 1 diabetes (T1D). In this study, we investigated DC subpopulations and their responses to TLR stimulation in T1D patients and their relatives., Methods: We analyzed the frequency of myeloid (mDCs) and plasmacytoid DCs (pDCs) in 97 T1D patients (69 onset, 28 long-term), 67 first-degree relatives, and 64 controls. We additionally tested the IFN-alpha production by pDCs upon stimulation with TLR 7, 8 and 9 agonists., Results: A lower number of mDCs and pDCs were found in T1D patients and their relatives. Of all the tested TLR ligands, only stimulation with CpG 2216 induced IFN-alpha production that was the highest in T1D relatives, except of autoantibody-negative relatives bearing the protective haplotypes., Conclusion: Our data demonstrate disturbances in DC number and function expressed most significantly in T1D relatives and point to a potential role of TLR9-induced IFN-alpha production in T1D development., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Published
2014
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48. The effect of diabetes-associated autoantigens on cell processes in human PBMCs and their relevance to autoimmune diabetes development.

Author

Vcelakova J, Blatny R, Halbhuber Z, Kolar M, Neuwirth A, Petruzelkova L, Ulmannova T, Kolouskova S, Sumnik Z, Pithova P, Krivjanska M, Filipp D, and Stechova K

Subjects
Adolescent, Adult, Autoantibodies immunology, Autoantibodies metabolism, Autoantigens metabolism, Child, Child, Preschool, Diabetes Mellitus, Type 1 genetics, Diabetes Mellitus, Type 1 metabolism, Female, Gene Expression, Humans, Leukocytes, Mononuclear metabolism, Male, Middle Aged, Prediabetic State genetics, Prediabetic State metabolism, Autoantigens immunology, Diabetes Mellitus, Type 1 immunology, Leukocytes, Mononuclear immunology, Prediabetic State immunology
Abstract

Type 1 Diabetes (T1D) is considered to be a T-helper- (Th-) 1 autoimmune disease; however, T1D pathogenesis likely involves many factors, and sufficient tools for autoreactive T cell detection for the study of this disease are currently lacking. In this study, using gene expression microarrays, we analysed the effect of diabetes-associated autoantigens on peripheral blood mononuclear cells (PBMCs) with the purpose of identifying (pre)diabetes-associated cell processes. Twelve patients with recent onset T1D, 18 first-degree relatives of the TD1 patients (DRL; 9/18 autoantibody positive), and 13 healthy controls (DV) were tested. PBMCs from these individuals were stimulated with a cocktail of diabetes-associated autoantigens (proinsulin, IA-2, and GAD65-derived peptides). After 72 hours, gene expression was evaluated by high-density gene microarray. The greatest number of functional differences was observed between relatives and controls (69 pathways), from which 15% of the pathways belonged to "immune response-related" processes. In the T1D versus controls comparison, more pathways (24%) were classified as "immune response-related." Important pathways that were identified using data from the T1D versus controls comparison were pathways involving antigen presentation by MHCII, the activation of Th17 and Th22 responses, and cytoskeleton rearrangement-related processes. Genes involved in Th17 and TGF-beta cascades may represent novel, promising (pre)diabetes biomarkers.

Published
2013
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49. Case report: type 1 diabetes in monozygotic quadruplets.

Author

Stechova K, Halbhuber Z, Hubackova M, Kayserova J, Petruzelkova L, Vcelakova J, Kolouskova S, Ulmannova T, Faresjö M, Neuwirth A, Spisek R, Sediva A, Filipp D, and Sumnik Z

Subjects
Autoimmunity, Child, Preschool, Diabetes Mellitus, Type 1 genetics, Female, Humans, T-Lymphocytes, Regulatory immunology, T-Lymphocytes, Regulatory metabolism, Diabetes Mellitus, Type 1 immunology, Quadruplets
Abstract

Type 1 diabetes (T1D) is an autoimmune disease characterized by the lack of insulin due to an autoimmune destruction of pancreatic beta cells. Here, we report a unique case of a family with naturally conceived quadruplets in which T1D was diagnosed in two quadruplets simultaneously. At the same time, the third quadruplet was diagnosed with the pre-diabetic stage. Remarkably, all four quadruplets were positive for anti-islet cell antibodies, GAD65 and IA-A2. Monozygotic status of the quadruplets was confirmed by testing 14 different short tandem repeat polymorphisms. Serological examination confirmed that all quadruplets and their father suffered from a recent enteroviral infection of EV68-71 serotype. To assess the nature of the molecular pathological processes contributing to the development of diabetes, immunocompetent cells isolated from all family members were characterized by gene expression arrays, immune-cell enumerations and cytokine-production assays. The microarray data provided evidence that viral infection, and IL-27 and IL-9 cytokine signalling contributed to the onset of T1D in two of the quadruplets. The propensity of stimulated immunocompetent cells from non-diabetic members of the family to secrete high level of IFN-α further corroborates this conclusion. The number of T regulatory cells as well as plasmacytoid and/or myeloid dendritic cells was found diminished in all family members. Thus, this unique family is a prime example for the support of the so-called 'fertile-field' hypothesis proposing that genetic predisposition to anti-islet autoimmunity is 'fertilized' and precipitated by a viral infection leading to a fully blown T1D.

Published
2012
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50. Is there any relationship between cytokine spectrum of breast milk and occurence of eosinophilic colitis?

Author

Durilova M, Stechova K, Petruzelkova L, Stavikova V, Ulmannova T, and Nevoral J

Subjects
Case-Control Studies, Female, Humans, Infant, Infant, Newborn, Interferon-gamma analysis, Interleukin-18 analysis, Male, Th1 Cells immunology, Transforming Growth Factor beta1 analysis, Colitis etiology, Cytokines analysis, Eosinophilia etiology, Milk, Human chemistry
Abstract

Aim: The aim of our study was to analyse cytokine composition of human milk and its relationship to the development of eosinophilic colitis (EC)., Methods: Cytokines were measured by ELISA method in breast milk of 20 mothers of infants who developed EC and 20 controls., Results: We found significantly higher concentrations of interferon-gamma (IFN-gamma) (Th1 cytokine) in breast milk received by EC infants compared to controls (p = 0.0004). In contrary, IL-18 (Th1-inducing cytokine) was significantly higher in breast milk received by healthy infants comparing to EC infants (p = 0.001). Regulatory cytokine transforming growth factor beta1 (TGF-beta1) showed higher concentrations in breast milk received by healthy infants, although the difference from EC group was not significant (p = 0.072)., Conclusion: The results of our study showed that infants with EC were receiving breast milk with a possibly risky cytokine pattern indicating cytokine imbalance, impaired immunoregulation and the early Th1 shift., (© 2010 The Author(s)/Journal Compilation © 2010 Foundation Acta Paediatrica.)

Published
2010
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