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ENFERMEDAD
INFLAMATORIA
INTESTINAL
CARLOS J. PECH LUGO R3MI
BIBLIOGRAFIA
 Enfermedad inflamatoria intestinal: realidad en México. Dr. Edder René Sandoval G, Dr.
Francisco Bosques Padilla. Rev Gastroenterol Mex,Vol. 73, Supl. 2, 2008.
 Epidemiología y características clínicas de la colitis ulcerosa crónica idiopática en el
noreste de México. Bosques-Padilla FJ, Sandoval-García et al. Rev Gastroenterol Mex,Vol.
76, Núm. 1, 2011.
 Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio
Fiocchi. Nature Reviews. Gastroenterology and Hepatology.Volume 13. January 2016.
 Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al.
Journal of Inflammation Research 2014:7 113–120.
 Inflammatory Bowel Disease: An overview of immune Mechanism and Biological
treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
 Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–
1605.
 Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest
Med Sur Mex, January-March 2016; 23 (1): 10-20.
BIBLIOGRAFIA
 Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-
25.
 A Review of Crohn’s Disease. Philip Hendy and Ailsa Hart. European Medical Journal.
Gastroenterology. December 2013.
 Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists.
Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428.
 The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created
using GRADE methodology. Fernando Gomollón , Santiago García-López et al.
Gastroenterol Hepatol. 2013.
 Clinical practice guidelines for the medical management of nonhospitalized ulcerative
colitis:TheToronto Concensus. Brain Bressler et al. Gastroenterology 2015.Vol. 148, No. 5
 Inflamatory Bowel Disease. Worl Gastroenterology Organization. Update 2015.
 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil.Therapeutic Advances in
Gastroenterology. 2015,Vol 8(6) 352-359.
DEFINICIÓN
NATURE 2016
Condición inflamatoria crónica del tracto gastrointestinal que
incluye dos entidades clínicas principales : Enfermedad de Crohn y
Colitis Ulcerativa.
WGO 2015
Grupo de condiciones inflamatorias, crónicas e idiopáticas que
incluyen EC y CU que comparten características clínicas y
patológicas.
Inflamatory Bowel Disease. Worl Gastroenterology Organization. Update 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13.
January 2016.
EPIDEMIOLOGIA
 Mayor incidencia norte de Europa, Reino Unido y EEUU
 Asia 0.54 – 3.44 casos por cada 100,000 habitantes.
 Australia 7.6 -25.2 casos por cada 100,000 habitantes.
 Europa 8.7 – 11.8 casos por cada 100,000 habitantes.
 Mayor prevalencia en áreas urbanas vs rurales y en zonas con alto nivel
socioeconómico.
 Pico de presentación en tercera década de la vida.
Inflamatory Bowel Disease. Worl Gastroenterology Organization. Update 2015.
EPIDEMIOLOGIA
 México 2.3 – 3.6 casos por cada 10,000 pacientes.
 INCMNSZ diagnóstico de 76 casos por año.
 CUCI 52% mujeres y 48% hombres .
 80% pacientes diagnosticados entre tercera y quinta década de la vida.
Enfermedad inflamatoria intestinal: realidad en México. Dr. Edder René Sandoval G, Dr. Francisco Bosques Padilla. Rev Gastroenterol Mex, Vol. 73, Supl. 2, 2008.
Epidemiología y características clínicas de la colitis ulcerosa crónica idiopática en el noreste de México. Bosques-Padilla FJ, Sandoval-García et al. Rev Gastroenterol Mex, Vol. 76, Núm. 1, 2011.
FISIOPATOLOGÍA
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
FACTORES
PREDISPONENTES EII
Ambiente
Microbiota
Respuesta
Inmune
Genética
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
AMBIENTE
 Estilos de vida.
 Consumo excesivo de proteína de leche, proteína animal, ácidos
grasos poliinsaturados.
 Exposición a antibióticos en la infancia.
 Cuadros de gastroenteritis repetitivos.
 Tabaquismo.
 Poca disponibilidad deVitamina D (ingesta y/o exposición solar). CD
 Higiene en hogar y accesibilidad de agua sanitizada. “Hipótesis de la
higiene”
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20.
Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25.
MICROBIOTA
 Dysbiosis
 Saccharomyces cerevisiae
 EscherichiaColi
 Pseudomona fluorecens
 Aumento de Bacteroides y Proteobacterias, disminución de
Firmicutes (lactobacilos, clostridios)
Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
MICROBIOTA
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
MICROBIOTA
Microbe associated molecular patterns (MAMPs)
Pathogen associated molecular patterns (PAMPs)
Toll like receptors (TLRs)
NOD like receptors (NLR)
Moco, defensinas, IgA, Reg IIIγ
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
GENÉTICA
(GWAS) 163 loci: 110 (EII); 30 (EC) y 23 (CU)
Variantes del gen codificador NOD2 (reconocimiento
bacteriano y supresión de IL-10)
Gen ILR23R, ATG16L1 e IRGM (EC) por defectos de
fagocitosis.
ABCD1/MDR1 (CU) por alteración de protección a
xenobióticos.
Polimorfismo deTLR4 (EC)
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
RESPUESTA
INMUNE
INMUNIDAD INNATA
 Neutrófilos, Monocitos, Macrófagos y Células dentríticas
 Células epiteliales, endoteliales y mesenquimales
INMUNIDADADAPTATIVA
 Activación general de respuesta humoral
 Producción alterada de inmunoglobulinas
 Anticuerpos anticitoplasmáticos (50-90% de los pacientes)
 Anticuerpos anti glicanos.
 Alteraciones en célulasT
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
MACRÓFAGOS
Clasificación como M1 y M2
En mucosa intestinal sana son anérgicos.
EC expresan CD14, CD33, CD68, CD205 y CD209
Producción de IL-6, IL-23 ,TNF e IFNγ
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
CÉLULAS
DENTRÍTICAS
Incluyen tejido mieloide, plasmocitoide y residente.
Función primaria de monitorizar el microambiente
circulante con reactividad inmune.
Inducen tolerancia o incitan respuesta
inflamatoria
En EC expresan niveles aumentados deTLr2 yTLR4
comparado con mucosa intestinal sana.
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
CÉLULAST
EFECTORAS
PreviamenteTh1 asociada a EC (IL-12, IFNγ) yTH2
asociada a CU (IL-5 e IL-13).
Actualmente descubrimiento de IL-17 porTh17 con
respuesta sobrepuesta e interrelacionada de estas.
Th1 Th2 Th17
T
reg
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
CÉLULAST
REGULADORAS
Primordiales para desarrollo de tolerancia ante antígenos
seguros
Potenciación de célulasT reguladores se ha visto beneficio en
EC y CU.
CD4+, CD25+ encontradas en mucosa normal de ratones que
disminuyen concentración durante exacerbación de
enfermedad.
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
ASESINAS
NATURALESY
CÉLULAS
LINFOIDES
Células asesinas naturales (NK), CélulasT asesinas
(NKT) y Células linfoides innatas (ILCs).
Producción de IL-17 e IL-22 por ILCs.
La mucosa en CU aumento de expresión de NKT tipo II.
Genes asociados con transcripción de ILCs defectuosos
sugieren papel en EII.
Estudios realizados en animales.
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
APOPTOSIS
CÉLULAST
Normalmente en lámina propia las célulasT sufren
apoptosis.
En EC son resistentes a este proceso.
Tumour supresor geneTP53 alterado.
Acumulación y replicación acumulada de célulasT
activadas relevante en inmunopatogénesis de EII.
Mecanismo postulado para uso de Infliximab y
Adalimumab.
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
ENFERMEDA
DECROHN
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
COLITIS
ULCERATIVA
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
OTRASVÍAS
PATOGÉNICAS
Células epiteliales (alteración en presentación de antígenos, inmunorregulación)
Disminución de expresión de PPAR γ en pacientes con CU pero no en EC.
Sistema nervioso entérico por liberación de neuropéptidos (substancia P,
péptido vasoactivo intestinal, agonistas del receptor opioide µ y galanina.
Estado proinflamatorio en obesidad.
Inflamasomas (producción de caspasas, IL-8, IL.18)
micro RNAs
DAMPs , MAMPs.
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.
Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
CARACTERÍSTICAS
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
ENFERMEDAD DE
CROHN
CUADRO
CLÍNICO
Diarrea crónica
Pérdida de peso
Sangrado gastrointestinal bajo
Dolor abdominal
Obstrucción intestinal
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
CLASIFICACIÒN
CLASIFICACIÓN DE MONTREAL
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
LABORATORIO
Biometría hemática completa.
Pruebas de función renal.
Pruebas de función hepática.
Marcadores de inflamación (PCR,VSG).
Coprológico y coproparasitoscópico.
Coprocultivo
(ASCA) Ac- Saccharomyces cerevisiae (+) S52% y E64%
(p-ANCA) Ac- Anticitoplasma de neutrófilos (–) S92% y E94%
(Anti-OMpC) Porina de E. Coli 46% de adultos con EC
Calprotectina y Lactoferrina S 93% E 96%
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
ENDOSCOPIA
 Ileocolonoscopía con toma de biopsias “gold estándar”
 Cápsula endoscópica (no provee diagnóstico histopatológico)
 Úlceras aftosas, lineales y profundas, “cobblestones”, fisuras,
seudopólipos.
 Estudio normal no excluye diagnóstico (27% enfermedad localizada ìleo
terminal)
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
IMAGENOLOGIA
Fluoroscopía/Enteroclisis ( bario, gastrografin)
Radiografía simple de abdomen
EnteroTomografía (S 76% y E 84%)
Entero Resonancia (S 78% y E 85%)
Ultrasonido (S 85% y E 98%) *operador dependiente*
Se puede detectar inflamación de mucosa, estenosis, dilatación colónica,
fístulas y abscesos.
Combinación de métodos aumenta S y E.
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
ENTEROCLISIS
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
IMAGENOLOGIA
ENTEROTAC
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
IMAGENOLOGIA
ENTERO RNM
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
ESCALA DE
ACTIVIDAD/SEVERI
DAD
Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605.
Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
COLITISULCERATIVA
CUADRO
CLÍNICO
Diarrea crónica
Urgencia y tenesmo
Sangrado gastrointestinal bajo
Dolor abdominal
Fiebre (casos severos)
Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25.
Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5
The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
LABORATORIO
Biometría hemática completa.
Pruebas de función renal.
Pruebas de función hepática.
Marcadores de inflamación (PCR,VSG).
Coprológico y coproparasitoscópico.
Coprocultivo (C. difficile, campylobacter, E. Coli )
(ASCA) Ac- Saccharomyces cerevisiae (+)
(p-ANCA) Ac- Anticitoplasma de neutrófilos (+) **
Calprotectina y Lactoferrina S 93% E 96%
Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25.
Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5
The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
IMAGEN
Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25.
Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5
The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
ENDOSCOPIA
Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25.
Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5
The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
DIAGNÓSTICO
Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25.
Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5
The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
ESCALAS
CLASIFICACIÓN/
SEVERIDAD
Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25.
Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5
The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
HISTOPATOLOGÍA
HISTOPATOLOGIA
Al menos 2 biopsias de 5 sitios diferentes incluyendo: Íleon terminal,
recto y mucosa aparentemente normal.
Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
ESPECÍFICOS PARA EC
• Ileítis
• Metaplasia antral (pilórica) en íleon
• Granulomas (excluirTb)
• Inflamación parcheada con predominio de
histiocitos
• Aftas y fisuras
ESPECÍFICOS DE CU
• Inflamación rectal con criptitis y microabscesos
• Apariencia pseudovellosa de fragmentos
inflamados
• Distorción arquitectural extensa.
HISTOPATOLOGIA
Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
HISTOPATOLOGIA
Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
HISTOPATOLOGIA
Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
Inflamatory Bowel Disease. Worl Gastroenterology Organization. Update 2015.
TRATAMIENTO
TRATAMIENTO
MÉDICO
• Corticosteroides
• 5- Aminoacilatos (sulfasalazina, sulfapiridina, 5-
ácido aminosalicílico)
• Antimetabolitos (azatioprina, 5- mercaptopurina,
metotrexate)
• AntiTNF (infliximab, adalimumab)
• Anti α4- integrina (natalizumab)
QUIRÚRGICO
• Resección quirúrgica
• Laparoscopía
Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015
Inflamatory Bowel Disease. World Gastroenterology Organization. Update 2015.
MEDICO
Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015
Inflamatory Bowel Disease. World Gastroenterology Organization. Update 2015.
MEDICO
Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015
Inflamatory Bowel Disease. World Gastroenterology Organization. Update 2015.
QUIRÚRGICO
La mayor parte de los pacientes tendrán una resección
dentro de los primeros 10 años posterior al diagnóstico.
Recomendado para pacientes con falla al manejo
farmacológico
Recurrencia de obstrucción intestinal, desnutrición o
complicaciones sépticas.
Alta recurrencia de enfermedad 28-45% en 5 años y 36-
61% a 10 años.
Laparoscopía (complicaciones 12%) y cirugía abierta
(complicaciones 18%)
Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015
Inflamatory Bowel Disease. World Gastroenterology Organization. Update 2015.
COMPLICACIONES
Enfermedad de Crohn
• Asociación EC y malignidad bien documentada.
• Incidencia 1.7 a 2.5 veces más que en población
general.
• Se recomienda seguimiento cada 1-3 años.
Colitis Ulcerativa
• Riesgo acumulado de 2%, 8% y 18% a los 10, 20
y 30 años de diagnóstico respectivamente para
CU.
• Incidencia de hasta 14.8 veces más que en
población general.
• Seguimiento con biopsias, colonoscopía
posterior a 8 años de diagnóstico.
Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120
Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015

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Enfermedad inflamatoria intestinal

  • 2. BIBLIOGRAFIA  Enfermedad inflamatoria intestinal: realidad en México. Dr. Edder René Sandoval G, Dr. Francisco Bosques Padilla. Rev Gastroenterol Mex,Vol. 73, Supl. 2, 2008.  Epidemiología y características clínicas de la colitis ulcerosa crónica idiopática en el noreste de México. Bosques-Padilla FJ, Sandoval-García et al. Rev Gastroenterol Mex,Vol. 76, Núm. 1, 2011.  Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology.Volume 13. January 2016.  Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120.  Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015.  Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590– 1605.  Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20.
  • 3. BIBLIOGRAFIA  Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713- 25.  A Review of Crohn’s Disease. Philip Hendy and Ailsa Hart. European Medical Journal. Gastroenterology. December 2013.  Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428.  The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013.  Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis:TheToronto Concensus. Brain Bressler et al. Gastroenterology 2015.Vol. 148, No. 5  Inflamatory Bowel Disease. Worl Gastroenterology Organization. Update 2015.  Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil.Therapeutic Advances in Gastroenterology. 2015,Vol 8(6) 352-359.
  • 4. DEFINICIÓN NATURE 2016 Condición inflamatoria crónica del tracto gastrointestinal que incluye dos entidades clínicas principales : Enfermedad de Crohn y Colitis Ulcerativa. WGO 2015 Grupo de condiciones inflamatorias, crónicas e idiopáticas que incluyen EC y CU que comparten características clínicas y patológicas. Inflamatory Bowel Disease. Worl Gastroenterology Organization. Update 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 5. EPIDEMIOLOGIA  Mayor incidencia norte de Europa, Reino Unido y EEUU  Asia 0.54 – 3.44 casos por cada 100,000 habitantes.  Australia 7.6 -25.2 casos por cada 100,000 habitantes.  Europa 8.7 – 11.8 casos por cada 100,000 habitantes.  Mayor prevalencia en áreas urbanas vs rurales y en zonas con alto nivel socioeconómico.  Pico de presentación en tercera década de la vida. Inflamatory Bowel Disease. Worl Gastroenterology Organization. Update 2015.
  • 6. EPIDEMIOLOGIA  México 2.3 – 3.6 casos por cada 10,000 pacientes.  INCMNSZ diagnóstico de 76 casos por año.  CUCI 52% mujeres y 48% hombres .  80% pacientes diagnosticados entre tercera y quinta década de la vida. Enfermedad inflamatoria intestinal: realidad en México. Dr. Edder René Sandoval G, Dr. Francisco Bosques Padilla. Rev Gastroenterol Mex, Vol. 73, Supl. 2, 2008. Epidemiología y características clínicas de la colitis ulcerosa crónica idiopática en el noreste de México. Bosques-Padilla FJ, Sandoval-García et al. Rev Gastroenterol Mex, Vol. 76, Núm. 1, 2011.
  • 8. Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 9. FACTORES PREDISPONENTES EII Ambiente Microbiota Respuesta Inmune Genética Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 10. AMBIENTE  Estilos de vida.  Consumo excesivo de proteína de leche, proteína animal, ácidos grasos poliinsaturados.  Exposición a antibióticos en la infancia.  Cuadros de gastroenteritis repetitivos.  Tabaquismo.  Poca disponibilidad deVitamina D (ingesta y/o exposición solar). CD  Higiene en hogar y accesibilidad de agua sanitizada. “Hipótesis de la higiene” Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20. Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25.
  • 11. MICROBIOTA  Dysbiosis  Saccharomyces cerevisiae  EscherichiaColi  Pseudomona fluorecens  Aumento de Bacteroides y Proteobacterias, disminución de Firmicutes (lactobacilos, clostridios) Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
  • 12. MICROBIOTA Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 13. MICROBIOTA Microbe associated molecular patterns (MAMPs) Pathogen associated molecular patterns (PAMPs) Toll like receptors (TLRs) NOD like receptors (NLR) Moco, defensinas, IgA, Reg IIIγ Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 14. GENÉTICA (GWAS) 163 loci: 110 (EII); 30 (EC) y 23 (CU) Variantes del gen codificador NOD2 (reconocimiento bacteriano y supresión de IL-10) Gen ILR23R, ATG16L1 e IRGM (EC) por defectos de fagocitosis. ABCD1/MDR1 (CU) por alteración de protección a xenobióticos. Polimorfismo deTLR4 (EC) Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 15. RESPUESTA INMUNE INMUNIDAD INNATA  Neutrófilos, Monocitos, Macrófagos y Células dentríticas  Células epiteliales, endoteliales y mesenquimales INMUNIDADADAPTATIVA  Activación general de respuesta humoral  Producción alterada de inmunoglobulinas  Anticuerpos anticitoplasmáticos (50-90% de los pacientes)  Anticuerpos anti glicanos.  Alteraciones en célulasT Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 16. MACRÓFAGOS Clasificación como M1 y M2 En mucosa intestinal sana son anérgicos. EC expresan CD14, CD33, CD68, CD205 y CD209 Producción de IL-6, IL-23 ,TNF e IFNγ Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 17. CÉLULAS DENTRÍTICAS Incluyen tejido mieloide, plasmocitoide y residente. Función primaria de monitorizar el microambiente circulante con reactividad inmune. Inducen tolerancia o incitan respuesta inflamatoria En EC expresan niveles aumentados deTLr2 yTLR4 comparado con mucosa intestinal sana. Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 18. CÉLULAST EFECTORAS PreviamenteTh1 asociada a EC (IL-12, IFNγ) yTH2 asociada a CU (IL-5 e IL-13). Actualmente descubrimiento de IL-17 porTh17 con respuesta sobrepuesta e interrelacionada de estas. Th1 Th2 Th17 T reg Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 19. CÉLULAST REGULADORAS Primordiales para desarrollo de tolerancia ante antígenos seguros Potenciación de célulasT reguladores se ha visto beneficio en EC y CU. CD4+, CD25+ encontradas en mucosa normal de ratones que disminuyen concentración durante exacerbación de enfermedad. Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 20. ASESINAS NATURALESY CÉLULAS LINFOIDES Células asesinas naturales (NK), CélulasT asesinas (NKT) y Células linfoides innatas (ILCs). Producción de IL-17 e IL-22 por ILCs. La mucosa en CU aumento de expresión de NKT tipo II. Genes asociados con transcripción de ILCs defectuosos sugieren papel en EII. Estudios realizados en animales. Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 21. APOPTOSIS CÉLULAST Normalmente en lámina propia las célulasT sufren apoptosis. En EC son resistentes a este proceso. Tumour supresor geneTP53 alterado. Acumulación y replicación acumulada de célulasT activadas relevante en inmunopatogénesis de EII. Mecanismo postulado para uso de Infliximab y Adalimumab. Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 22. Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 23. ENFERMEDA DECROHN Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 24. COLITIS ULCERATIVA Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 25. OTRASVÍAS PATOGÉNICAS Células epiteliales (alteración en presentación de antígenos, inmunorregulación) Disminución de expresión de PPAR γ en pacientes con CU pero no en EC. Sistema nervioso entérico por liberación de neuropéptidos (substancia P, péptido vasoactivo intestinal, agonistas del receptor opioide µ y galanina. Estado proinflamatorio en obesidad. Inflamasomas (producción de caspasas, IL-8, IL.18) micro RNAs DAMPs , MAMPs. Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015. Inmunopathogenesis of IBD: current state of the art. Heitor S. P. de Souza and Claudio Fiocchi. Nature Reviews. Gastroenterology and Hepatology. Volume 13. January 2016.
  • 26. CARACTERÍSTICAS Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20
  • 28. CUADRO CLÍNICO Diarrea crónica Pérdida de peso Sangrado gastrointestinal bajo Dolor abdominal Obstrucción intestinal Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 29. CLASIFICACIÒN CLASIFICACIÓN DE MONTREAL Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 30. LABORATORIO Biometría hemática completa. Pruebas de función renal. Pruebas de función hepática. Marcadores de inflamación (PCR,VSG). Coprológico y coproparasitoscópico. Coprocultivo (ASCA) Ac- Saccharomyces cerevisiae (+) S52% y E64% (p-ANCA) Ac- Anticitoplasma de neutrófilos (–) S92% y E94% (Anti-OMpC) Porina de E. Coli 46% de adultos con EC Calprotectina y Lactoferrina S 93% E 96% Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 31. ENDOSCOPIA  Ileocolonoscopía con toma de biopsias “gold estándar”  Cápsula endoscópica (no provee diagnóstico histopatológico)  Úlceras aftosas, lineales y profundas, “cobblestones”, fisuras, seudopólipos.  Estudio normal no excluye diagnóstico (27% enfermedad localizada ìleo terminal) Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 32. IMAGENOLOGIA Fluoroscopía/Enteroclisis ( bario, gastrografin) Radiografía simple de abdomen EnteroTomografía (S 76% y E 84%) Entero Resonancia (S 78% y E 85%) Ultrasonido (S 85% y E 98%) *operador dependiente* Se puede detectar inflamación de mucosa, estenosis, dilatación colónica, fístulas y abscesos. Combinación de métodos aumenta S y E. Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 33. ENTEROCLISIS Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 34. IMAGENOLOGIA ENTEROTAC Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 35. IMAGENOLOGIA ENTERO RNM Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 36. ESCALA DE ACTIVIDAD/SEVERI DAD Crohn’s disease. Daniel C Baumgart, William J Sandborn. Seminar. Lancet 2012; 380: 1590–1605. Crohn´s disease. Review and current concepts. Deyanira Kúsulas-Delint et al. Rev Invest Med Sur Mex, January-March 2016; 23 (1): 10-20 Crohn´s disease: a clinical update. Francis Ha and Hanan Khalil. Therapeutic Advances in Gastroenterology. 2015, Vol 8(6) 352-359
  • 38. CUADRO CLÍNICO Diarrea crónica Urgencia y tenesmo Sangrado gastrointestinal bajo Dolor abdominal Fiebre (casos severos) Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25. Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5 The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
  • 39. LABORATORIO Biometría hemática completa. Pruebas de función renal. Pruebas de función hepática. Marcadores de inflamación (PCR,VSG). Coprológico y coproparasitoscópico. Coprocultivo (C. difficile, campylobacter, E. Coli ) (ASCA) Ac- Saccharomyces cerevisiae (+) (p-ANCA) Ac- Anticitoplasma de neutrófilos (+) ** Calprotectina y Lactoferrina S 93% E 96% Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25. Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5 The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
  • 40. IMAGEN Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25. Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5 The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
  • 41. ENDOSCOPIA Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25. Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5 The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
  • 42. DIAGNÓSTICO Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25. Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5 The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
  • 43. ESCALAS CLASIFICACIÓN/ SEVERIDAD Ulcerative Colitis. Silvio Danese, M.D., and Claudio Fiocchi, M.D. N Engl J Med 2011;365:1713-25. Clinical practice guidelines for the medical management of nonhospitalized ulcerative colitis: The Toronto Concensus. Brain Bressler et al. Gastroenterology 2015. Vol. 148, No. 5 The GETECCU clinical guideline for the treatment of ulcerative colitis: A guideline created using GRADE methodology. Fernando Gomollón , Santiago García-López et al. Gastroenterol Hepatol. 2013
  • 45. HISTOPATOLOGIA Al menos 2 biopsias de 5 sitios diferentes incluyendo: Íleon terminal, recto y mucosa aparentemente normal. Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
  • 46. ESPECÍFICOS PARA EC • Ileítis • Metaplasia antral (pilórica) en íleon • Granulomas (excluirTb) • Inflamación parcheada con predominio de histiocitos • Aftas y fisuras ESPECÍFICOS DE CU • Inflamación rectal con criptitis y microabscesos • Apariencia pseudovellosa de fragmentos inflamados • Distorción arquitectural extensa. HISTOPATOLOGIA Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
  • 47. HISTOPATOLOGIA Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
  • 48. HISTOPATOLOGIA Clinical Aspects of Idiopathic Inflammatory Bowel Disease, a review for pathologists. Hwajeong Lee, MD; Maria Westerhoff et al. Arch Pathol Lab Med.2016;140:413–428
  • 49. Inflamatory Bowel Disease. Worl Gastroenterology Organization. Update 2015.
  • 51. TRATAMIENTO MÉDICO • Corticosteroides • 5- Aminoacilatos (sulfasalazina, sulfapiridina, 5- ácido aminosalicílico) • Antimetabolitos (azatioprina, 5- mercaptopurina, metotrexate) • AntiTNF (infliximab, adalimumab) • Anti α4- integrina (natalizumab) QUIRÚRGICO • Resección quirúrgica • Laparoscopía Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120 Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015 Inflamatory Bowel Disease. World Gastroenterology Organization. Update 2015.
  • 52. MEDICO Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120 Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015 Inflamatory Bowel Disease. World Gastroenterology Organization. Update 2015.
  • 53. MEDICO Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120 Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015 Inflamatory Bowel Disease. World Gastroenterology Organization. Update 2015.
  • 54. QUIRÚRGICO La mayor parte de los pacientes tendrán una resección dentro de los primeros 10 años posterior al diagnóstico. Recomendado para pacientes con falla al manejo farmacológico Recurrencia de obstrucción intestinal, desnutrición o complicaciones sépticas. Alta recurrencia de enfermedad 28-45% en 5 años y 36- 61% a 10 años. Laparoscopía (complicaciones 12%) y cirugía abierta (complicaciones 18%) Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120 Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015 Inflamatory Bowel Disease. World Gastroenterology Organization. Update 2015.
  • 56. Enfermedad de Crohn • Asociación EC y malignidad bien documentada. • Incidencia 1.7 a 2.5 veces más que en población general. • Se recomienda seguimiento cada 1-3 años. Colitis Ulcerativa • Riesgo acumulado de 2%, 8% y 18% a los 10, 20 y 30 años de diagnóstico respectivamente para CU. • Incidencia de hasta 14.8 veces más que en población general. • Seguimiento con biopsias, colonoscopía posterior a 8 años de diagnóstico. Inflammatory bowel disease: clinical aspects and treatments. Marc Fakhoury et al. Journal of Inflammation Research 2014:7 113–120 Inflammatory Bowel Disease: An overview of immune Mechanism and Biological treatments. Bruno Rafael Ramos de Mattos et al. Mediators of inflammation. Volume 2015

Editor's Notes

  1. La colonización temprana es esencial para el desarrollo y maduración del sistema inmune(consumo de leche, comida e higiene así como otros factores)
  2.  estudio de asociación del genoma completo (en inglés, GWAS (Genome-wide association study) o WGAS (Whole genome association study) es un análisis de una variación genética a lo largo de todo el genoma humano con el objetivo de identificar su asociación a un rasgo observable. IRGM, a human immunity-related GTPase, confers autophagic defence against intracellular pathogens by an unknown mechanism
  3. Células inmunológicas como las primeras y no inmunológicas.
  4. Clasificados en razón de su patrón de secreción de citosinas
  5. TP53 inhibe el reciclaje de céluas T, evitando la expansión de las mismas.
  6. Damage associated molecular paterns (DAMPs)
  7. Musculoesqueléticos 20% Mucosa oral y piel 10% Hepatobiliar 5% Ocular 5% Metabólicas
  8.  anti-Saccharomyces Cerevisiae (ASCA) Anemia secundario a deficiencias (VitB12, Hierro), Leucocitosis Hipoalbuminemia
  9.  GASTROGRAFIN: amidotrizoato sódico (D.C.I.) y 66 g de amidotrizoato de meglumina (D.C.I.). Sacarina sódica 85 mg VENTAJA DE USG Y RNM es menor exposición a radiación.
  10. Fig. 4: (a) Imágenes de enteroclisis donde se observa un patrón en empedrado por convergencia de úlceras lineales y fisuras transversales (flecha). (b) y (c) El cambio de calibre lleno simple nos muestra (b) el área de estenosis y (c) con doble contraste el patrón nodular de la mucosa.
  11. : Enfermedad activa en un paciente a través de los años. (a) Corte coronal de ETC que revela enfermedad activa de EC en íleon, con engrosamiento de la pared y realce en el borde mesentérico, adenomegalias y proliferación fibroadiposa, en el año 2009 durante un episodio agudo de dolor abdominal. (b) Dos años más tarde, se observa persistencia del engrosamiento mural, adenomegalias y aumento del diámetro del ciego. (c) y (d) Cortes axiales de TC con contraste donde se muestra el engrosamiento mural del asa, presentando la típica imagen en tiro al blanco. Signos: engrosamiento mural, reconocido por el espesor parietal mayor de 3 mm (la densidad de la pared intestinal debería ser igual a la densidad de los músculos intrapélvicos), pérdida de la estratificación (flechas blancas) y realce mucoso en el que se reconoce aumento de la captación de contraste de la capa interna (flecha hueca).
  12. En caso de afectación colon distal con ANCAS negativos puede ser difícil diferenciar, Colitis indeterminada. Sucede del 10-15% de los casos.
  13. Aspecto final de la colitis ulcerosa con esa apariencia rígida, carente de haustración por la contracción mantenida de la muscularis mucosa.
  14. core 0=normal; endoscopic remission. (B) Score 1=mild; erythema, decreased vascular pattern, mild friability. (C) Score 2=moderate; marked erythema, absent vascular pattern, friability, erosions. (D) Score 3=severe; spontaneous bleeding, ulceration. Images courtesy of El
  15. A, Normal colonic mucosa. B, Crypt distortion (yellow arrow) and basal lymphoplasmacytosis (red arrow) in chronic active colitis. C, Paneth cell metaplasia (arrow) and unevenly spaced crypts in the left colon. D, Pyloric gland metaplasia (arrow) in the terminal ileal biopsy of Crohn disease (hematoxylin-eosin, original magnification
  16. A, Typical macroscopic features of ulcerative colitis, with diffuse mucosal edema, erythema, and ulceration involving distal and transverse colon, with a sharp demarcation between the diseased and uninvolved segments. B, Scanning magnification view shows that the disease is superficial and confined within the mucosa, with intact submucosa and muscularis propria. C, Cecal involvement in a left-sided ulcerative colitis. D, Crypt rupture–associated granuloma in ulcerative colitis with neutrophils and mucin. It is closely associated with a damaged crypt (hematoxylin-eosin, original magnifications
  17. Mencionar las microcápsulas