Fernando Magro1, Eduardo Rodrigues-Pinto2, Rosa Coelho3, Patrícia Andrade3, João Santos-Antunes4, Susana Lopes3, Claudia Camila-Dias5, Guilherme Macedo3. 1. 1] Department of Gastroenterology, Centro Hospitalar São João, Porto, Portugal [2] IBMC-Institute for Molecular and Cell Biology, University of Porto, Porto, Portugal [3] The first two authors contributed equally to this work. 2. 1] Department of Gastroenterology, Centro Hospitalar São João, Porto, Portugal [2] The first two authors contributed equally to this work. 3. Department of Gastroenterology, Centro Hospitalar São João, Porto, Portugal. 4. 1] Department of Gastroenterology, Centro Hospitalar São João, Porto, Portugal [2] Department of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal. 5. CIDES-Department of Health Information and Decision Sciences, Faculty of Medicine, University of Porto, Porto, Portugal.
Abstract
OBJECTIVES: Crohn's disease (CD) induces cumulative structural damage, initially characterized by a non-stenosing non-penetrating behavior (B1) with progression over time to a fibro-stenosing (B2) and/or penetrating phenotype (B3). Our aim was to assess the long-term evolution of disease behavior of CD and determine what factors predict phenotype progression. METHODS: This was a study based on prospectively collected data from a CD database in an inflammatory bowel disease outpatient clinic. B1 corresponds to a non-stenosing non-penetrating disease, B2 to a stenosing behavior, and B3 to a penetrating one. RESULTS: Seven hundred and thirty-six patients with CD (368 female) were followed up for 12.3 years (± 8.4), with 87.0% of them exhibiting B1 phenotype at diagnosis. Of these patients, 28.5% progressed to B2 phenotype and 23.5% to B3. Fifty percent of the patients started azathioprine treatment before phenotype change and 13.9% started anti-tumor necrosis factor-α (anti-TNFα) treatment before phenotype change. Monotherapy with azathioprine before phenotype change as well as combination therapy with azathioprine/anti-TNFα before phenotype change delayed disease progression (B1-B2 or B3) in comparison with patients who did not receive treatment (P<0.001). The hazard ratio (HR) for disease progression was lower for both monotherapy with azathioprine (HR: 0.15, P<0.001) or combination therapy with anti-TNFα (HR: 0.33, P<0.001). Upper gastrointestinal tract involvement, male gender, and steroid use were associated with an early progression of phenotype from B1 to B2 or B3 (P<0.001). The HR for disease progression was higher in patients who used steroids without criteria of dependence or resistance (HR: 2.67, P<0.001) and was even higher in patients with criteria of dependence or resistance (HR: 6.44, P<0.001). Longer delays between CD diagnosis and beginning of therapy with azathioprine and/or anti-TNFα were associated with disease progression. The longer the duration of treatment, the less likely the disease progression. CONCLUSIONS: Monotherapy with azathioprine before behavior change as well as combination therapy with azathioprine and anti-TNFα before behavior change delays phenotype progression of CD, whereas upper gastrointestinal tract involvement, male gender, and steroid use with or without criteria of steroid dependence are associated with a higher risk for disease progression.
OBJECTIVES:Crohn's disease (CD) induces cumulative structural damage, initially characterized by a non-stenosing non-penetrating behavior (B1) with progression over time to a fibro-stenosing (B2) and/or penetrating phenotype (B3). Our aim was to assess the long-term evolution of disease behavior of CD and determine what factors predict phenotype progression. METHODS: This was a study based on prospectively collected data from a CD database in an inflammatory bowel diseaseoutpatient clinic. B1 corresponds to a non-stenosing non-penetrating disease, B2 to a stenosing behavior, and B3 to a penetrating one. RESULTS: Seven hundred and thirty-six patients with CD (368 female) were followed up for 12.3 years (± 8.4), with 87.0% of them exhibiting B1 phenotype at diagnosis. Of these patients, 28.5% progressed to B2 phenotype and 23.5% to B3. Fifty percent of the patients started azathioprine treatment before phenotype change and 13.9% started anti-tumor necrosis factor-α (anti-TNFα) treatment before phenotype change. Monotherapy with azathioprine before phenotype change as well as combination therapy with azathioprine/anti-TNFα before phenotype change delayed disease progression (B1-B2 or B3) in comparison with patients who did not receive treatment (P<0.001). The hazard ratio (HR) for disease progression was lower for both monotherapy with azathioprine (HR: 0.15, P<0.001) or combination therapy with anti-TNFα (HR: 0.33, P<0.001). Upper gastrointestinal tract involvement, male gender, and steroid use were associated with an early progression of phenotype from B1 to B2 or B3 (P<0.001). The HR for disease progression was higher in patients who used steroids without criteria of dependence or resistance (HR: 2.67, P<0.001) and was even higher in patients with criteria of dependence or resistance (HR: 6.44, P<0.001). Longer delays between CD diagnosis and beginning of therapy with azathioprine and/or anti-TNFα were associated with disease progression. The longer the duration of treatment, the less likely the disease progression. CONCLUSIONS: Monotherapy with azathioprine before behavior change as well as combination therapy with azathioprine and anti-TNFα before behavior change delays phenotype progression of CD, whereas upper gastrointestinal tract involvement, male gender, and steroid use with or without criteria of steroid dependence are associated with a higher risk for disease progression.
Authors: Steven F G Jeuring; Vince B C Biemans; Tim R A van den Heuvel; Maurice P Zeegers; Wim H Hameeteman; Mariëlle J L Romberg-Camps; Liekele E Oostenbrug; Ad A M Masclee; Daisy M A E Jonkers; Marieke J Pierik Journal: Am J Gastroenterol Date: 2018-01-09 Impact factor: 10.864
Authors: Iago Rodríguez-Lago; Javier Del Hoyo; Alexandre Pérez-Girbés; Alejandro Garrido-Marín; María José Casanova; María Chaparro; Agnès Fernández-Clotet; Jesús Castro-Poceiro; María José García; Sara Sánchez; Rocío Ferreiro-Iglesias; Iria Bastón; Marta Piqueras; Lola Esteba I Bech de Careda; Raquel Mena; Cristina Suárez; Joaquín Poza Cordón; Alicia López-García; Lucía Márquez; Maite Arroyo; Erika Alfambra; Mónica Sierra; Noelia Cano; Pedro Delgado-Guillena; Víctor Morales-Alvarado; Juan Carlos Aparicio; Iván Guerra; Carolina Aulló; Olga Merino; Laura Arranz; María Araceli Hidalgo; Jordina Llaó; Rocío Plaza; Gema Molina; Paola Torres; Pablo Pérez-Galindo; María Giselle Romero; Claudia Herrera-deGuise; Edisa Armesto; Francisco Mesonero; Santiago Frago-Larramona; José Manuel Benítez; Marta Calvo; María Del Carmen López Martín; Ainara Elorza; Alejandro Larena; Elena Peña; María Del Carmen Rodríguez-Grau; Jaime de Miguel-Criado; Belén Botella; José Antonio Olmos; Laura López; Urko Aguirre; Javier P Gisbert Journal: United European Gastroenterol J Date: 2020-07-28 Impact factor: 4.623