DIAGNÓSTICO NO INVASIVO DE CIRROSIS E...
Transcript of DIAGNÓSTICO NO INVASIVO DE CIRROSIS E...
DIAGNÓSTICO NO INVASIVO
DE CIRROSIS
E HIPERTENSIÓN PORTAL
Salvador Augustin Hepatología-Medicina Interna
Hospital Vall d’Hebron, Barcelona
5º Curso de Residentes AEEH 30-31 Octubre 2015
Diagnóstico No Invasivo
Cirrosis / Hipertensión portal
i. Para qué el diagnóstico de cirrosis/HTP
ii. Diagnóstico NO invasivo HOY
iii. Hacia dónde vamos
Diagnóstico No Invasivo
Cirrosis / Hipertensión portal
i. Para qué el diagnóstico de cirrosis/HTP
ii. Diagnóstico NO invasivo HOY
iii. Hacia dónde vamos
Para qué el diagnóstico de
cirrosis/HTP
1. Cribado de complicaciones
• Varices
• HCC
2. Pronóstico
• Decisiones prácticas
• Estudios
3. Interpretar los síntomas y signos del paciente
Diagnóstico No Invasivo
Cirrosis / Hipertensión portal
i. Para qué el diagnóstico de cirrosis/HTP
ii. Diagnóstico NO invasivo HOY
iii. Hacia dónde vamos
Qué nospermiten HOY los métodos
diagnósticos no invasivos
1. Evitar exploraciones invasivas
– FGS (DESCARTAR varices)
– HVPG (ASUMIR CSPH)
2. Identificar precozmente cirrosis “oculta”
3. Estadiar al paciente (estudios)
ii. Cómo
¿Cómo EVITAR endoscopia de cribado
VARICES?
- Métodos NO invasivos: DESCARTAR VNT
- Mejor COMBINACIONES de métodos: LSPS,
VRS, ANTICIPATE
- Riesgo aceptable : <5% VNT
N All
varices
VNT Classification rule All varices
NPV
VNT
NPV
Varices
missed
VNT
missed
Endoscopies
avoided
Augustin, et al 49 10% 0 LSM<25
LSM<25+Pla≥150
93%
100%
100%
100%
7%
0
0
0
61%
20%
Montes, et al 85 45%* 20% LSM<20
LSM<20 and/or Pla>120
90%
100%
-
100%
9.5%
0
-
0
25%
15%
Ding, et al 271 - 10% LSM<25+Pla≥100 - 100% - 0 39%
ANTICIPATE 379 42% 15% LSM<25+Pla≥100
LSM<25+Pla≥150
79%
86%
95%
96.5%
21%
14%
5%
3.5%
45%
23%
Elastografía-cACLD
¿Cómo EVITAR endoscopia de cribado
VARICES?
Fibroscan (LSM) + plaquetas
ANTICIPATE STUDY
N 23%
VNT 3.5%
N 34%
VNT 12%
N 57%
VNT 9%
N 43%
VNT 23%
N 12%
VNT 17%
N 31%
VNT 25%
379 patients with endoscopy
LSM ≥25 kPa LSM <25 kPa
Plat ≥ 150 000 Plat < 150 000 Plat ≥ 150 000 Plat < 150 000
393 patients with compensated cirrhosis
Abraldes et al., EASL 2015
ANTICIPATE STUDY
N 45%
VNT 5%
N 12%
VNT 24%
N 57%
VNT 9%
N 43%
VNT 23%
N 24%
VNT 17%
N 19%
VNT 29%
379 patients with endoscopy
LSM ≥25 kPa LSM <25 kPa
Plat ≥ 100 000 Plat < 100 000 Plat ≥ 100 000 Plat < 100 000
393 patients with compensated cirrhosis
Abraldes et al., EASL 2015
Baveno VI
SESSION 1 – Screening and surveillance ; invasive and non invasive methods
IDENTIFICATION OF PATIENTS WITH cACLD WHO CAN SAFELY AVOID SCREENING ENDOSCOPY
• Patients with a liver stiffness < 20 kPa and with
a platelet count > 150,000 have a very low risk of having varices requiring treatment, and can avoid screening endoscopy (3,B)
Patients with presumed/confirmed compensated cirrhosis
Routine blood tests (platelet count), abdominal ultrasound (US), liver stiffness (LS)
Non-Valid LS LS <25 kPa LS >=25
N=20 CSPH 16/20=80%
Normal
Plt+US
Low Plt
and/or Spleno
CSPH
3/5=60%
CSPH
13/15=87%
ASSUME CSPH
RULE 2: You can ASSUME CSPH in ALL patients with LS>=25 kPa (
in those with Non-Valid LS measurement and Platelet <
150000/mm3 & splenomegaly) (67 patients represent 67/182=37% of the studied population, if only patients with valid LS are considered; 67
15=82 patients,
who represent 82/202=41% of the studied population, including patients with non-valid LS;)
1CSPH: Clinically significant portal hypertension; *Low platelet count <150000/mm3; ¥ Splenomegaly is defined as spleen diameter >12 cm at abdominal ultrasound;
Fig. 5. ANTICIPATE : NON-INVASIVE ASSESSMENT OF CSPH
N=115 CSPH 45/115=39%
N=67 CSPH 64/67=96%
Normal
Plt+US
Low Plt
or
Spleno
Low Plt
and
Spleno
CSPH
5/34=16%
CSPH
13/35=37%
CSPH
27/46=59%
Baveno VI
SESSION 1 – Screening and surveillance ; invasive and non invasive methods
DIAGNOSIS OF CSPH IN PATIENTS WITH cACLD
• In patients with virus-related cACLD non-invasive methods are sufficient to rule-in CSPH, defining the group of patients at risk of having endoscopic signs of PH. The following can be used (3, B): – Liver stiffness by TE (≥20-25 kPa) alone or combined to Plt and
spleen size – Imaging showing collateral circulation
• The diagnostic value of TE for CSPH in other etiologies remains to be ascertained (5, D)
Elastografía-cACLD
cACLD-LC
CLINICAL DIAGNOSIS
LIVER BIOPSY
TRANSIENT ELASTOGRAPHY
Cirrosis oculta – concepto cACLD
Elastografía-cACLD
Estudio N F/kPa %
Roulot, 2011 1190 ≥8
>13
7,5
0,76
Baba, 2011 423 ≥F2 14,3
Wong, 2012 922 ≥9,6 1,62
Fung, 2014 2493 ≥8,7
≥10,3
1,2
0,17
You, 2015 159 ≥F2
≥8
7
1,9
Koelher, 2015 3041 ≥8
≥13
5,6
0,6
Mayoría NAFLD
Cirrosis oculta – Población general
1% Población general LS>10
59% NAFL
7% NASH incompleto / fibrosis
leve 7% NASH fibrosis avanzada
73%
NAFLD
Kwok, et al. Gut 2015
NAFLD – DIABETES
(China)
CAP >222 dB/m
LS >9.5 kPa
Cirrosis oculta – Poblaciones de riesgo
Elastografía-cACLD
Estudio PRECISED
CONTROLES DIABÉTICOS
No Enfermedad Hepática aparente
Probable NASH / fibrosis leve
Probable NASH / Fibrosis avanzada
10-15% POBLACIÓN
DIABÉTICA TIENE
FIBROSIS
AVANZADA
NAFLD – DIABETES
(Barcelona) LS >10 kPa
Cirrosis oculta – Poblaciones de riesgo
Elastografía-cACLD
AMONG PATIENTS WITH UNSUSPECTED CIRRHOSIS:
Augustin, et al
Augustin, et al
Chen, et al
Chen, et al ANTICIPATE
*LSM≥13-13.6 kPa
* NO SIGNS OF CIRRHOSIS
AMONG PATIENTS WITH LSM≥13-13.6 kPa:
n=173
*8%
n=702
*14%
n=54 n=270 n=221
*24% *37% *15%
*10%
n=2876 Kim, et al
Cirrosis oculta – Población Hepatópatas
CLINICAL STAGE Adv.CHR. L.D. EARLY
COMPENSATED
CIRRHOSIS
LATE
COMPENSATED
CIRRHOSIS
DECOMPENSATED
CIRRHOSIS
LIVER
BIOLOGY
HISTOLOGY F3 F4 F4 F4
HVPG
(mmHg) <5 5 10
ELASTOGRAPH
Y (kPa) 8.5/
10 13,6 25
VARICES
SYMPTOMS ASYMPTOMATIC ASYMPTOMATIC ASYMPTOMATIC
(Varices)
HYPERDYNAMIC
CIRCULATION
DEFINING
FEATURE
Fibrosis,
Angiogenesis Scar, X-linking
Acellular scar,
nodules,
microthrombosis
Insoluble scar,
microthrombosis
LIVER
INFLAMMATION LIVER
SCAR 1) HVPG>10 = CSPH
2) HYPERDYNAM.
CLINICAL
DECOMPENSATION
CARCINOGENESI
S
Diagnóstico No Invasivo
Cirrosis / Hipertensión portal
i. Para qué el diagnóstico de cirrosis/HTP
ii. Diagnóstico NO invasivo HOY
iii. Hacia dónde vamos
Mittal, Clin Gastro Hepatol 2015
86%
72%
58%
0
10
20
30
40
50
60
70
80
90
100
Virus OH NAFLD
Cirrosis AP
N=1419 HCC
(VA – USA)
2. HCC – WHEN to start screening
Cost-effectiveness
Tsochatzis et al., NHS Health Tech Assess 2015 Armstrong et al., Q Med J 2013
How to do it
(combination of methods)
3. Detect Occult Cirrhosis
82-83% Prog. LENTOS (> 7 años)
Prog. RÁPIDOS (<6 años)
17%
18%
Singh et al., Clin Gastro Hepatol 2015; McPherson et al. J Hepatol 2015
4. Identify rapid progressors
Spleen stiffness:
• Basal: 37,4 kPa (17,3-75)
• 4 wk: 33,3 kPa (13,9-75)
• 12 wk: 31,9 kPa (11,8-75)
P = 0,09 P = 0,05
Elastografía-cACLD
Datos preliminares internos, sept. 2015
5. Response to therapies
HCV therapy – Changes in portal pressure
Physical Methods
Serologic Markers
Imaging
Clinical Data
SIGNOS ROJOS EN V. ESOFAGICAS
Combining Methods
Take-Home Messages
• Evitar exploraciones invasivas
– FGS (DESCARTAR varices)
– HVPG (ASUMIR CSPH)
• Detección precoz cirrosis “oculta”
• Redefinición del concepto clínico de cirrosis
Impacto Métodos No Invasivos
i. Para qué
3. Estudios
HVPG ≥10
HVPG<10
Pacientes Outcomes
Ripoll et al., Gastroenterology 2007
Groszmann et al., NEJM 2005
Development
of new
TOOLS
Non-Invasive Methods Hepatic venous pressure gradient (HVPG)
Development
of new
IDEAS
What we talk about when we talk about cirrhosis
PROGNOSIS - RISKS
“Now there are many where before there was one…”
Robic et al. J Hepatol 2011
-100 Px -16 meses -65% CH -HVPG ≥10: 51% -Varices: 72% de CH -No tratamiento -41% alguna complicación
Elastografía-cACLD
Impacto elastografía-Pronóstico