Nutrition and liver cirrhosis

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 portal pressure venous pressure hypoglycemia ascites splenomegaly anemia leukopenia edema EV hormone metabolism bilirubin metabolism total liver failure thrombocytopenia erectile dysfunction menstrual disorders jaundice bilirubinemia intestinal bile clay-colored stool dark urine bleeding Vit. K absorption HE coma death urobilingen Complications of liver cirrhosis       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  Malnutrition is an early and typical aspect of hepatic cirrhosis.  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      food intake (anorexia, nausea, drugs) malabsorption energy and PT requirement paracenthesis induced PT loss complications Malnutrition   mortality (35% v.s. 16% in normal-fed p’t) complications : ascites (44% v.s. 24%) Lautz et al. 1992   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.  Richardson et al. 1994 Nutrition in the complications of liver cirrhosis        Calories (Cal) Fat Protein (PT) Carbohydrate (CHO) Sodium (Na) Fluid Vitamins    Total Cal=REE*1.2 or 30 kcal/kg Fat=30-35% of total Cal PT=1g/kg/d m. HE :10-20g/d (3-5d 5-10g) ESPEN Consensus group : req. 1-1.5g/kg/d low PT diet may worsen HE Plauth et al. 1997  CHO=remainder of the Cal requirement Nurdan 2000 HE  Vegetable PT : 1. 2. 3. intraluminal pH 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  Way to lead Na depletion     NSAID Vasopression analogues Large volume paracentesis without volume expansion Diuretic therapy   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.  iv BCAAs in cirrhosis with acute encephalopathy       Riggio et al. 1982 7 controlled studies Wahren et al. 1983 et al. 1985 BCAAs group v.s. glucose or nonMichelet al. 1985 AA selective Cerra 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   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     Oral BCAAs are generally used in athletes Eriksson et al. 1982 9 controlled studies Sieg et al. 1983 BCAAs (7-30g), alcoholic cirrhosisSimko etetal. 1983 (29-90%), McGhee al. 1983 Horst et al. 1984 latent encephalopathy (0-79%), lactulose (8Guarnieri et al. 1984 Christie et al. 1985 100%) Fiaccadori et al. 1988 Marchesini BCAAs supplementation can only be et al. 1990 recommended in p’t at high risk of encephalopathy     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.  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   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     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 Enteral or parenteral AA infusion Infusion over -10 -5 0 15 30 60 90 120 180 240 min Blood was sampled in triplicant and then centrifugated and deproteinisated/ Analysis for ammonia and Gln. 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 <0.05 EN ammonia Gln. 157 60 74 PN ammonia Gln. 115 ammonia Gln. ammonia SMV-artery Gln. SMV-artery 166 107 65 85 50 62 ammonia Gln. EN PN EN PN ammonia Gln. 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 p’t. 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   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   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   Gln. metabolism of small intestine is a source of increased portal ammonia concentrations and that post-feeding hyperammonaemia is caused. 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(>2.3) Class C: 10-15 Interpretation: Class A: 5-6 Class B: 7-9 BCAAs and amyotrophic lateral sclerosis     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!!