2. Enfermedad inflamatoria
intestinal (EII): definición
• Describe dos condiciones idiopáticas:
colitis ulcerosa crónica inespecífica (CUCI)
enfermedad de Crohn
• CUCI: inflamación crónica de la mucosa del
colon.
• Crohn: Inflamación transmural en cualquier
parte del TD de la boca al ano. Tipicamente
produce granulomas, fisuras, fístulas.
Una definición operativa en México:
DISENTERÍA RESISTENTE
A LOS IMIDAZÓLICOS.
Aceptada por los expertos,
pero no validada cientificamente.
3. ¿QUÉ SON
“GASTRITIS/COLITIS”?
• “ITIS” = inflamación.
• Término anatomopatológico.
• Infiltración de neutrófilos = aguda. Linfocitos
y células plasmáticas=crónica.
• Edema, cambios en las glándulas.
• Múltiples causas. En colon, correlación con
hallazgos endoscópicos.
4. La EEI es diferente en México
• Tenemos más enfermedades
inflamatorias además de CUCI y Crohn.
• A pesar de que ha disminuido su
frecuencia, la amibiasis sigue en la mente
del médico.
• Algunos médicos diagnostican “colitis”
en casos de disfunción.
5. La EEI es diferente en México
• CUCI y, sobre todo, Crohn, son poco
frecuentes.
• Algunos patológos sobrediagnostican
“colitis inespecífica”.
• Tal vez para permitir a algunos médicos
diagnosticar “CUCI”.
• Se agregan dos “nuevas”: colitis
colagenosa y colitis linfocítica.
6. IMPORTANCIA EN MÉXICO
• Poco interés de los investigadores: artículos
originales en 5 años en la RGEM: 2,
revisión: 1, foto clínica: 1.
• “Temas de Medicina Interna” Vol2,#4, 1993
el artículo sobre EII no menciona a México.
• Tampoco el capítulo del “Gastroenterología”
de Villalobos.
7. IMPORTANCIA EN MÉXICO
• CUCI: 3-5 veces más frecuente que Crohn, Tb y
linfoma intestinal. 1.3-1.6/1000 admisiones hospital.
• En el INCMNSZ se estudiaron en forma
prospectiva 14 pacientes con actividad moderada
de CUCI en 10 meses. (RGEM 1993;58:210)
• En el Hospital de Especialidades del CMN siglo
XXI del IMSS tienen 94 pacientes en control por
CUCI. (RGEM 2002;67:179)
8. IMPORTANCIA EN MÉXICO
(INCMNSZ)
• CUCI: 3-5 veces más frecuente que Crohn, Tb y
linfoma intestinal. 1.3-1.6/1000 admisiones hospital.
• En el INCMNSZ se estudiaron en forma
prospectiva 14 pacientes con actividad moderada
de CUCI en 10 meses. (RGEM 1993;58:210)
• En el Hospital de Especialidades del CMN siglo
XXI del IMSS tienen 94 pacientes en control por
CUCI. (RGEM 2002;67:179)
0
1
2
3
4
5
6
7
C
U
C
I
C
R
O
H
N
Tb
IN
T
L
IN
FO
M
A
1970-74
1975-79
1980-84
1985-89
(J Jacobo y cols RGEM1990;55:298R)
*p=0.0002
*
9. (reproduced with permission, the AGA Teaching Project, 1992)
Distribución geográfica de la EII
Máxima
frecuencia
de EEI
10. EII: EPIDEMIOLOGÍA
(UPTODATE 11-05)
• “incidencia”/100mil: 1-10: Crohn
3-15: CUCI
• “prevalencia”/100mil: 20-100 Crohn
50-80: CUCI
• Geografía: NORTE > SUR
• Edad al inicio: “pico”: 15-30
segundo “pico” (Crohn): 50-80
• Sexo: H = M
11. EII: EPIDEMIOLOGÍA
(UPTODATE 11-05)
• Raza: blancos > negros > “hispanos”
• Etnia: judíos > no judíos
• Tabaco: asociado a Crohn
protege en CUCI
• Apendicectomía: puede proteger en CUCI
13. (reproduced with permission from Wells Medical Ltd, Binder 1993)
Frecuencia según edad y sexo
Frecuencia de CUCI/año/105 Frecuencia de Crohn
Inci
den
cia
a
nual
In
cid
enc
ia
anu
al
EDAD EDAD
14. (reproduced with permission from Wells Medical Ltd, Binder 1993)
Cambio en la frecuencia
Colitis ulcerosa
CrohnF
re
c
u
e
n
ci
a/
a
año
15. Raza y EII
Grupo étnico
Prevalencia
(por 105
)
(after Kurata et al, 1992)
0
10
20
30
40
50
White Black Hispanic Asian Otherblanco negro “hispano” asiático otro
16. EII: Teorías etiológicas
• Genética.
• Tabaco: protege en Cuci
aumenta la frecuencia en Crohn.
• Dieta. Conservadores. Carregenina.
• Infección: micobacterias, virus.
• Inmunológica.
• Sicológica (?).
17. EII: ¿causa común?
DATOS A FAVOR DE PATOGENIA COMÚN
• Distribución similar de edad, sexo, raza.
• Manifestaciones no GE similares.
• Cambios histológicos similares en algunos.
• Anormalidades inmunológicas comunes.
• Frecuencia y agrupación familiar relacionadas.
• Hallazgos patológicos de ambas en el mismo
paciente.
19. CUCI CLÍNICA CROHN
• Diarrea con sangre
(disentería resistente al
metronidazol).
• Fiebre.
• Cólicos.
• Pérdida de peso.
• Pujo, urgencia, tenesmo,
frecuencia.
• Ataque al estado general.
• Diarrea.
• Dolor abdominal.
• Hemorragia.
• Fiebre.
• Pérdida de peso.
• Fístulas.
• Enfermedad perianal.
• Ataque al estado general.
20. DIAGNÓSTICO DE EII
EN TODOS LOS CASOS CON CLÍNICA
SUGESTIVA:
1. TACTO RECTAL.
2. ENDOSCOPIA.
3. BIOPSIA.
EN ALGUNOS CASOS, COLON POR
ENEMA Y OTRAS DE IMAGEN.
21.
22.
23.
24.
25. CUCI: COMPLICACIONES
• SÓLO INTESTINALES.
• COLITIS FULMINANTE (RARA).
• MEGACOLON TÓXICO. Perforación.
• CÁNCER.
Cuadro desde la infancia,
involucra todo el colon,
casi siempre activo,
más de 10 años de evolución.
30. (reproduced with permission, Schiller et al, 1986)
CROHN: ENDOSCOPIA
EMPEDRADO PÓLIPOS LESIONES
INFLAMATORIOS
DISCONTINUAS
31. (reproduced with permission
from McGraw-Hill)
(courtesy of Dr Sten Norby
Rasmussen, Denmark)
CROHN: RADIOLOGÍA
COLITIS DE CROHN ILEON TERMINAL
(signo de la cuerda)
32. Crohn: enfermedad perianal
Localizacion de los
abscesos anorectales
Colgajos cutáneos
Fístula anal
Esfínter
externo
absceso
rectoElevador
del ano
recto
fístula
34. Tratamiento farmacológico
• Ácido 5-amino salicílico. Tratamiento inicial
La azulfidina (salicilazosulfapiridina) es más
barata pero tiene más efectos secundarios por
la sulfapiridina.
Los otros derivados, que son sólo ácido 5-amino
salicílico, deben iniciase a dosis alta (3-4 g al
dia en 3 dosis) y reducirla según respuesta, a la
más baja que mantenga la remision.
35. Tratamiento farmacológico
• Esteroides.
Potentes, rápidos, por ambas vias. Efectos
secundarios graves sólo a largo plazo. Iniciar si
no hay respuesta a 5-asa.
La budesonida tiene menos efectos secundarios:
9 mg -> 6 mg -> 3 mg.
La prednisona se inicia a 40-60 mg/dia o 1mg/kg.
-> bajar 5 mg por semana después de la
inducción de la remisión.
No deben usarse como mantenimiento una vez
obtenida la remisión.
37. Tratamiento farmacológico
• Biológicos (infliximab).
Anticuerpo quimérico monoclonal contra el
factor de necrosis tumoral alfa.
Efectivo en Crohn con fístulas y en CUCI que no
responde a los otros tratamientos.
5 mg/Kg IV/2 horas a las 0-2-6 semanas y c/8
semanas si induce remisión.
Es muy caro y tiene muchos efectos nocivos.
38. Indicaciones de cirugía
• Perforación.
• Megacolon.
• Hemorragia.
• Enfermedad crónica debilitante.
• Riesgo de cáncer.
• Falta de respuesta al tratamiento médico.
40. EII: RIESGO DE CÁNCER
(adapted from Hamilton, 1985, with permission)
COLITIS ULCEROSA
CROHN%
Ca
colo
rectal
Años de enfermedad
Editor's Notes
24. Geographical distribution of IBD
The incidence of IBD is greatest in the ‘developed’ world and lowest in the ‘developing’ world. However, in recent years the incidence of IBD appears to have been leveling off in developed countries, while beginning to increase in the developing world. There has been a rise in the incidence and prevalence of Crohn’s disease in the USA and Western Europe in recent decades.
26. Incidence of IBD with respect to age and sex
The onset of both ulcerative colitis and Crohn’s disease usually occurs in young adulthood, with both sexes equally affected (Pettit & Irving 1992; Shanahan & Targan 1989). While the prevalence of IBD increases as the population ages, the incidence of UC (ulcerative colitis) also increases in men over the age of 65 years (Binder 1993). An epidemiological study in the USA found a higher incidence of Crohn’s disease in women than in men up to the age of 80 years (Kurata et al, 1992).
27. Patterns of IBD incidence in previous decades
The incidence of ulcerative colitis has remained stable for many years at approximately 8/105, with a prevalence of approximately 96/105 (Hay & Hay 1992).
The incidence of Crohn’s disease has been increasing in Western societies over the past 20–50 years, and is currently estimated at approximately 5/105 with a prevalence of 60/105 (Hay & Hay 1992).
25. Ethnic prevalence of IBD
IBD may be genetically determined since certain ethnic groups have an increased prevalence of the disease. An epidemiological study in the USA found that the prevalence of Crohn’s disease was highest in Whites, followed by Blacks, while Asians and Hispanics had much lower rates of disease (Kurata et al, 1992). Other studies have found an increased prevalence of IBD in Ashkenazi Jews, while the disease is virtually unknown in Bedouin Arabs (Lashner & Kirsner, 1992; Podolsky, 1991).
Figure 10-16. Idiopathic ulcerative colitis. A, The radiographic features of acute idiopathic ulcerative colitis. The disease characteristically begins in the rectum and extends to the ascending colon. There is diffuse ulceration of the entire colon in this patient. Notice the shortening of the colon and the loss of normal haustral pattern. The terminal ileum is spared and is normal. B, A close-up view of the rectosigmoid area. Notice the granular appearance of the mucosa. The earliest radiologic lesion identified in ulcerative colitis is the granular appearance caused by edema and the superficial ulceration in this disease. The air-contrast examination is the most sensitive examination for the early manifestations of inflammatory bowel disease.
Figure 10-16. Idiopathic ulcerative colitis. A, The radiographic features of acute idiopathic ulcerative colitis. The disease characteristically begins in the rectum and extends to the ascending colon. There is diffuse ulceration of the entire colon in this patient. Notice the shortening of the colon and the loss of normal haustral pattern. The terminal ileum is spared and is normal. B, A close-up view of the rectosigmoid area. Notice the granular appearance of the mucosa. The earliest radiologic lesion identified in ulcerative colitis is the granular appearance caused by edema and the superficial ulceration in this disease. The air-contrast examination is the most sensitive examination for the early manifestations of inflammatory bowel disease.
Figure 4-1. Endoscopic features of active ulcerative colitis. Findings include diffusely erythematous, edematous, and granular mucosa with areas of submucosal hemorrhage and, when severe, frank mucopurulent exudate. Inflammation invariably begins in the rectum and extends proximally for varying extents. The chronicity of the process is suggested by the loss of colonic haustrations; otherwise, the endoscopic picture is nonspecific and could be consistent with acute infectious colitis, chronic ulcerative or Crohn's colitis, or any number of other specific causes of colitis. A, Mild distal ulcerative colitis with diffuse erythema and friability well demarcated from the normal mucosa more proximally is depicted. B, This example shows moderately severe ulcerative colitis with irregular, inflamed, ulcerated mucosa and a patchy exudate.
Figure 4-9. Microscopic features of the specimen shown in Figure 4-8. A, There is diffuse acute and chronic inflammation with architectural distortion and destruction of some glands, depletion of mucin from goblet cells, and crypt abscesses. Inflammation is limited to the mucosa. B, A higher power microscopic feature showing diffuse inflammation and a crypt abscess.
6. Anatomical location of ulcerative colitis
Ulcerative colitis usually extends proximally from the rectum in a continuous fashion. The extent of proximal spread varies, but ulcerative colitis is always confined to the colon with the exception of occasional mild inflammation of the most distal part of the terminal ileum (backwash ileitis Pettit & Irving 1992; Podolsky 1991; Shanahan & Targan 1989)
3. Endoscopic features of ulcerative colitis
In ulcerative colitis the mucosa is erythematous and friable. Blood mucus, pus and shallow ulceration may be present. In long-standing ulcerative colitis’ the mucosa has a granular appearance and there may be pseudopolyps.
Mild disease: Friable mucosa, loss of normal vascular pattern, fine granular texture, small haemorrhages when mucosa is touched.
Moderate disease: Gross pitting of the mucosa, purulent exudate, spontaneous bleeding.
Severe disease: Areas of ulceration surrounding islands of inflammatory tissue, profuse bleeding, purulent exudate.
15. Anatomical location of Crohn’s disease
Unlike ulcerative colitis, Crohn’s disease can affect any part of the gastrointestinal tract. The most common site of involvement is the terminal ileum and caecum. Approximately 40% of patients have disease confined to the small intestine, 30% have colonic disease only, and the remaining 30% have involvement of both the small and large intestines (Pettit & Irving 1992; Podolsky 1991). The inflamed segments are discontinuous, with areas of normal bowel separating diseased sections (skip lesions) (Pettit & Irving 1992; Shanahan & Targan 1989).
13. Endoscopic appearance of Crohn’s disease
In Crohn’s disease, the inflamed mucosa may have a ‘cobblestone’ appearance (a), and pseudopolyps are sometimes present (b). Areas of normal mucosa between inflamed segments (skip lesions) are also typical of Crohn’s disease (c). Granulomas may be present, distinguishing Crohn’s disease from ulcerative colitis.
14. Radiological features of Crohn’s disease
A barium enema may demonstrate discontinuous colonic changes, including skip lesions and small ulcerations at irregular nodules (a). In patients with small intestinal involvement, the characteristic ‘string sign’ may be seen, which results from severe narrowing of the intestinal lumen (b). In more advanced disease, longitudinal ulcers and fistulous tracts may be visible, together with narrowing and rigidity.
17. Perianal complications of Crohn’s disease
Perianal involvement occurs in up to 50% of patients with Crohn’s disease. Perianal complications include fistulae, abscesses and skin tags. These are often presenting symptoms.
37. Post-operative recurrence of Crohn’s disease
The rate of recurrence of Crohn’s disease after surgery is high (Hellers, 1979). In one study, 1 year after surgery, rates were estimated at 72% (Rutgeerts et al, 1984). Although surgery is unlikely to provide a cure for Crohn’s disease, it can relieve symptoms and complications (Lee & Papaioannou 1980). Recent studies (Loch et al, 2000), have demonstrated that Pentasa is effective at maintaining remission in CD patients who have small bowel surgery.
18. Risk of cancer with Crohn’s disease
Like ulcerative colitis, Crohn’s disease increases the risk of colorectal cancer. The incidence appears to be lower than it is with ulcerative colitis, but nevertheless, the incidence of both small and large bowel cancer is greater in patients with Crohn’s disease than it is in the general population (Glickman 1987). The cumulative incidence of colorectal cancer in patients with Crohn’s disease and ulcerative colitis increases over time (Hamilton 1989).
A Swedish study of 1655 patients found an overall risk of colorectal cancer of 2.5%, which was increased to 5.6% in patients with Crohn’s disease of the colon alone (Ekbom et al 1990).
