Transcript J Parenter Enteral Nutr

Nutrition and liver
cirrhosis
萬芳醫院營養室
江詩雯
2005.03.03
Influence of the metabolic complications of liver
cirrhosis on dietary intake
Nurdan T
Med Sci Monit 2000; 6 :1223-1226
Nutritional therapy in cirrhosis
Giulio M, Rebecca M, Federica A and Giampaolo B
J Gast Hepa 2004; 19 :S401-405
Post-feeding hyperammonaemia in patients with
transjugular intrahepatic portosystemic shunt and
liver cirrhosis: role of small intestine ammonia release
and route of nutrition administration
Plauth M, Roske AE, Romaniuk P, Roth E, Ziebig R and Lochs H
Gut 2000; 46 :849-855
Fatty liver
www.gicare.com/ pated/gifs/elv0004.gif
www.gutfeelings.com/ CRLIVER.JPG
Normal healthy liver, surface is smooth
Sever cirrhosis, surface is very nodular
and uniform
www.gihealth.com/ newsletter/34/two_livers.jpg
liver inflammation
liver necrosis
pain
nausea
vomiting
anorexia
constipation
Wt loss
fatigue
nutrition metabolism
hypoglycemia
portal pressure
ascites
venous pressure
edema
EV
hormone metabolism
bilirubin metabolism
splenomegaly
anemia
leukopenia
thrombocytopenia
erectile dysfunction
menstrual disorders
jaundice
bilirubinemia
intestinal bile
total liver failure
HE
coma
death
urobilingen
bleeding
Vit. K absorption
clay-colored stool
dark urine
Complications of liver cirrhosis
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Portal hypertension
Esophageal varices (EV)
Ascites
Hyperammonaemia
Hepatic encephalopathy (HE)
Hepatorenal syndrome
www.bio.ri.ccf.org/ Henderson/port.html
www.murrasaca.com/ Hepaticirrosis.htm
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Malnutrition is an early and typical aspect
of hepatic cirrhosis.
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70% of p’t with cirrhosis have signs of
PT/Cal malnutrition.
Lautz et al. 1992
Crawford et al. 1994
Prijatmoko et al. 1993
Way to lead malnutrition
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food intake (anorexia, nausea, drugs)
malabsorption
energy and PT requirement
paracenthesis induced PT loss
complications
Malnutrition
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mortality (35% v.s. 16% in normal-fed p’t)
complications : ascites (44% v.s. 24%)
Lautz et al. 1992
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p’t with advanced liver disease should be
recommended a diet providing adequate
calories, proteins, minerals and vitamines.
Dietary supplementation is much essential in
CLD, which can decrease malnutrition,
infections and sepsis happened.
Nompleggi and Bonkovsky 1994
p’t with cirrhosis can be observed early
postprandial hyperinsulinemia, which results
in early satiety and decrease hunger via
cholecystokinin (CCK).
 It directly actions on the brain.
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Richardson et al. 1994
Nutrition in the complications of liver
cirrhosis
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Calories (Cal)
Fat
Protein (PT)
Carbohydrate (CHO)
Sodium (Na)
Fluid
Vitamins
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Total Cal=REE*1.2 or 30 kcal/kg
Fat=30-35% of total Cal
PT=1g/kg/d
HE :10-20g/d (3-5d
m.
5-10g)
ESPEN Consensus group : req. 1-1.5g/kg/d
low PT diet may worsen HE
Plauth et al. 1997
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CHO=remainder of the Cal requirement
Nurdan 2000
HE
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Vegetable PT :
1.
intraluminal pH
2.
3.
ammonia secretion
transit time
suggest 30-40g/d
Nurdan 2000
Na : not exceed 2g(88mmol)/d
 Daily sodium intake :
130 (mmol/kg) * wt change (kg/d) + 24h urinary
Na (mmol/d) – 10 (mmol/d)
 Tense ascites : 40mmol/d
 Na free diet : energy, PT, lean body mass
 Na intake should be restricted before fluid
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Way to lead Na depletion
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NSAID
Vasopression analogues
Large volume paracentesis without volume
expansion
Diuretic therapy
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Fluid : no need to restrict at the beginning
Vitamins : supplement water and fat
solutable vit.(B1, B12, folate, A, D, E, K)
Alb.:
(1)p’t don’t receive alb. had significantly more
distrubances in electrocyte, PRA and
creatinine level than those who received it.
no difference in survival
(2)iv. filtered to ascitic fluid and doesn’t
remain in the intravascular compartment.
Furthermore cause alb. degeneration and
be harmful in PT deficiency states.
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iv BCAAs in cirrhosis with acute
encephalopathy
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Riggio et al. 1982
7 controlled studies
Wahren et al. 1983
et al. 1985
BCAAs group v.s. glucose or nonMichel
selective
AA
Cerra et al. 1985
Fiaccadori et al. 1985
soln. or lipid groups
Strauss et al. 1986
Vilstrup et al. 1990
BCAAs was gave for 2-6 d
Post treatment observation period : 4-16 d
201(BCAAs) v.s. 179(isocaloric group)
No statistically significant in survival
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Certainly BCAAs don’t worsen encephalopathy
and may be safely used to maintain an
adequate PT intake in subjects at risk of altered
mental state.
Plauth et al. 1997
BCAAs may be easily used as energy sources,
thus improving nitrogen balance and have a
beneficial on anorexia.
Panella et al. 1987
Tessair et al. 1996
Laviano et al. 1997
Davidson et al. 1999
Oral BCAAs in cirrhosis with or without
chronic encephalopathy
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Oral BCAAs are generally used in athletes
Eriksson et al. 1982
9 controlled studies
Sieg et al. 1983
Simko et al. 1983
BCAAs (7-30g), alcoholic cirrhosisMcGhee
(29-90%),
et al. 1983
Horst et al. 1984(8latent encephalopathy (0-79%), lactulose
Guarnieri et al. 1984
Christie et al. 1985
100%)
Fiaccadori et al. 1988
BCAAs supplementation can onlyMarchesini
be et al. 1990
recommended in p’t at high risk of
encephalopathy
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A multicenter, randomized study, > 1 yr,
174 p’t
(a) BCAA supplementation group
(b) maltodextrins group (equicaloric)
Non-BCAA group
(c) lactoalbumin group (equicaloric/nitrogenous)
Long term BCAA supplementation
increases survival time and prevents
to decrease hospital admission rates.
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BCAA-enriched formulations can be useful
in p’t who are intolerant to PT and
malnourished, which can improve PT
synthesis and reduce post injury catabolism.
Nompleggi and Bonkovsky 1994
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BCAA-enriched soln. increased serum alb.
also reduced morbidity and improved the
Poon et al, 2004
quality of life.
BCAAs strongly activate mTOR signaling in
liver, which is the cellular nutrition sensor
for PT translation initiation. Nishitani et al, 2004
Transjugular Intrahepatic
Portosystemic Shunt
(TIPS)
Hepatic vein
Expandable stent
Portal vein
www.med-ars.it/ galleries/gastro16.htm
Liver cirrhosis, ascites, hepatorenal syndrome
Small intestine mucosa extracts glutamine
from arterial blood for metabolism of enterocytes
and releases ammonia into portal vein
TIPS
hyperammonaemia
Hepatic encephalopathy
Methods
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Enteral AA infusion (TIPS : 5/8)
Parenteral AA infusion (TIPS : 3/8)
ND tube (2mL/kg/h)
Drugs: tobramycin 80mg, colistin 100mg,
amphotericin B 500mg qid to reduce
ammonia production from intestinal
bacterial
CHO:182g/L
Ammoniagenic AA :
Fat:56g/L
Glycine & Gln.
NaCl:170mmol/L
Gln. : 274
μmol/kg/h
Provide Cal substrates and
maintain hormonal response,
mucosal perfusion comparable
Infusion
over
Enteral or parenteral
AA infusion
-10 -5 0
15
30
60
90
120
180
Blood was sampled in triplicant and then
centrifugated and deproteinisated/
Analysis for ammonia and Gln.
240
min
Methods
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Arterial blood
Superior mesenteric venous (SMV) blood
Data are given as mean (SEM)
Values were calculated as area under the curve
of venous-arterial differences
Two tailed t test
SPSS and Excel
P <0.05
EN
ammonia
Gln.
157
60
74
PN
ammonia
Gln.
115
ammonia
Gln.
ammonia SMV-artery
166
107
65
85
50
62
Gln.
SMV-artery
ammonia
EN
Gln.
PN
EN
PN
ammonia
Gln.
Results
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Small intestine is a source of post-feeding
hyperammonaemia in liver cirrhosis.
EN is associated with higher degree of
systemic hyperammonaemia than
isonitrogenous PN in cirrhosis and TIPS p’t.
Discussion
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TIPS can be used to control variceal
haemorrhage or ascites, but aslo
associated with an increased risk of HE.
Ochs et al, 1995
Nolte et al,1998
Somberg et al, 1994
Jalan et al, 1997
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None of p’t had worsening of their mental
state when feeding a substantial nitrogen
load of 40.5g of AA/ 75kg BW within 120
min.
Staedt et al, 1993
PT test meals in cirrhosis
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Gln. 5.9g (14.5% of total AA) as more
ammoniagenic than other AA and capable
of inducing HE.
Gln. as a potentially essential PN in
malnourished cirrhotic p’t deserves further
clarification.
Conclusion
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Gln. metabolism of small intestine is a
source of increased portal ammonia
concentrations and that post-feeding
hyperammonaemia is caused.
PN feeding should be regarded as superior
to EN in cirrhotic p’t.
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Rossi-Fanelli F, Riggio O, Cangiano C, Cascino A, De Conciliis D, Merli M, Stortoni M, Giunchi G.
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Child-Pugh score
score
1
2
3
Alb.
Bilrubin
Ascites
>3.5
<2
Absent
3.5-2.8
2-3
MildModerate
<2.8
>3
Severe/
Refractory
HE
Absent
Mild (I-II)
Severe (III-IV)
PT
prolongation
<4 sec.
(<1.7)
4-6 sec.
(1.7-2.3)
>6 sec.
(>2.3)
Interpretation:
Class A: 5-6
Class B: 7-9
Class C: 10-15
BCAAs and amyotrophic lateral sclerosis
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active glutamate dehydrogenase (deficient in
ALS, also called Lou Gehrig’s disease
double-blind trial
26g/d of BCAA supplements help ALS p’t
Plaitakis et al, 1988
maintain muscle strength
a larger study was ended early when people
using BCAAs not only failed to improve, but
experienced higher death rates than the
placebo group
The Italian ALS Study Group 1993
Thanks for your attention!!