Nutrition and liver cirrhosis

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Nutrition and liver cirrhosis

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• 2005.03.03

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Influence of the metabolic complications of liver
cirrhosis on dietary intakeNurdan TMed Sci
Monit 2000 6 1223-1226Nutritional therapy in
cirrhosisGiulio M, Rebecca M, Federica A and
Giampaolo BJ Gast Hepa 2004 19
S401-405Post-feeding hyperammonaemia in
patients with transjugular intrahepatic
portosystemic shunt and liver cirrhosis role of
small intestine ammonia release and route of
nutrition administrationPlauth M, Roske AE,
Romaniuk P, Roth E, Ziebig R and Lochs HGut
2000 46 849-855
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Fatty liver
www.gicare.com/ pated/gifs/elv0004.gif
www.gutfeelings.com/ CRLIVER.JPG
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Normal healthy liver, surface is smooth and
uniform
Sever cirrhosis, surface is very nodular
www.gihealth.com/ newsletter/34/two_livers.jpg
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liver inflammation
liver necrosis
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Complications of liver cirrhosis

• Portal hypertension
• Esophageal varices (EV)
• Ascites
• Hyperammonaemia
• Hepatic encephalopathy (HE)
• Hepatorenal syndrome

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www.bio.ri.ccf.org/ Henderson/port.html
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www.murrasaca.com/ Hepaticirrosis.htm
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• Malnutrition is an early and typical aspect of
  hepatic cirrhosis.
• 70 of pt with cirrhosis have signs of PT/Cal
  malnutrition.

Lautz et al. 1992 Crawford et al. 1994 Prijatmoko
et al. 1993
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Way to lead malnutrition

• food intake (anorexia, nausea, drugs)
• malabsorption
• energy and PT requirement
• paracenthesis induced PT loss
• complications

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Malnutrition

• mortality (35 v.s. 16 in normal-fed pt)
• complications ascites (44 v.s. 24)

Lautz et al. 1992
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• pt 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
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• pt 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.

Richardson et al. 1994
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Nutrition in the complications of liver cirrhosis

• Calories (Cal)
• Fat
• Protein (PT)
• Carbohydrate (CHO)
• Sodium (Na)
• Fluid
• Vitamins

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• Total CalREE1.2 or 30 kcal/kg
• Fat30-35 of total Cal
• PT1g/kg/d
• HE 10-20g/d (3-5d 5-10g)
• ESPEN Consensus group req. 1-1.5g/kg/d
• low PT diet may worsen HE
• CHOremainder of the Cal requirement

m.
Plauth et al. 1997
Nurdan 2000
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HE

• Vegetable PT
• 1. intraluminal pH
• 2. ammonia secretion
• 3. transit time
• suggest 30-40g/d

Nurdan 2000
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• 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

• 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)

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• Alb.
• (1)pt dont 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 doesnt
• 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
Riggio et al. 1982 Wahren et al. 1983 Michel et
al. 1985 Cerra et al. 1985 Fiaccadori et al.
1985 Strauss et al. 1986 Vilstrup et al. 1990

• 7 controlled studies
• BCAAs group v.s. glucose or non selective AA
  soln. or lipid groups
• 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 dont worsen encephalopathy and
  may be safely used to maintain an adequate PT
  intake in subjects at risk of altered mental
  state.
• BCAAs may be easily used as energy sources, thus
  improving nitrogen balance and have a beneficial
  on anorexia.

Plauth et al. 1997
Panella et al. 1987 Tessair et al. 1996 Laviano
et al. 1997 Davidson et al. 1999
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Oral BCAAs in cirrhosis with or without chronic
encephalopathy

• Oral BCAAs are generally used in athletes
• 9 controlled studies
• BCAAs (7-30g), alcoholic cirrhosis (29-90),
  latent encephalopathy (0-79), lactulose (8-100)
• BCAAs supplementation can only be recommended in
  pt at high risk of encephalopathy

Eriksson et al. 1982 Sieg et al. 1983 Simko et
al. 1983 McGhee et al. 1983 Horst et al.
1984 Guarnieri et al. 1984 Christie et al.
1985 Fiaccadori et al. 1988 Marchesini et al. 1990
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• A multicenter, randomized study, gt 1 yr,
• 174 pt
• (a) BCAA supplementation group
• (b) maltodextrins group (equicaloric)
• (c) lactoalbumin group (equicaloric/nitrogenous)

Non-BCAA group
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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 pt
  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 quality of
  life.
• BCAAs strongly activate mTOR signaling in liver,
  which is the cellular nutrition sensor for PT
  translation initiation.

Poon et al, 2004
Nishitani et al, 2004
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Transjugular Intrahepatic Portosystemic Shunt
(TIPS)
Hepatic vein
Expandable stent
Portal vein
www.med-ars.it/ galleries/gastro16.htm
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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
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Methods

• 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

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Methods

• 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 lt0.05

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EN
ammonia
Gln.
157
60
74
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PN
ammonia
Gln.
115
38
ammonia
Gln.
39
ammonia
Gln.
SMV-artery
SMV-artery
40
ammonia
Gln.
EN
EN
PN
PN
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ammonia
Gln.
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Results

• 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 pt.

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Discussion

• 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 pt had worsening of their mental state
  when feeding a substantial nitrogen load of 40.5g
  of AA/ 75kg BW within 120 min.
• PT test meals in cirrhosis

Staedt et al, 1993
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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 pt deserves further
  clarification.

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Conclusion

• 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 pt.

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Child-Pugh score
InterpretationClass A 5-6 Class
B 7-9 Class C 10-15
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BCAAs and amyotrophic lateral sclerosis

• active glutamate dehydrogenase (deficient in ALS,
  also called Lou Gehrigs disease
• double-blind trial
• 26g/d of BCAA supplements help ALS pt 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

Plaitakis et al, 1988
The Italian ALS Study Group 1993
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