0.23 EFFECT OF LIPID INFUSION ON PLASMA AMINO ACID PATTERN IN LIVER CIRRHOSIS, M.Muscaritoli,

C.Cangiano,A.Cascino,F.Ceci and F.Rossi Fanelli. (III Department of Internal Medicine,

University "La Sapienza" of Rome,ITALY).

The alteration in plasma Amino Acid (AA) pattern observed in chronic liver failure (CLF),

with low Branched Chain AA and high Aromatic AA (AAA) are thought to be consequent toin-

creased muscle catabolism and in turn responsible for Hepatic Encephalopathy (HE). Gluco-

se has been demonstrated to reduce AAA levels acting as protein sparing,promptly availa-

ble energy source. The effect of exogenous lipids has not been evaluated, despite the

widely frequent use of fat emulsion in TPN formulas.

350 ml IntralipidRlO% were infused during 3 hr. in 13 cirrhotics and 10 healthy controls.

Plasma AA were assayed before and after the infusion. A mean decrease of 10% occurredfor

all AA except Alanine (ALA) and Free Tryptophan (F.TRP). Ala decreased significantly in

cirrhotics and controls. F.TRP rose significantly in cirrhotics. The ratio F.TRP/Sneut-

ral AA (NAA) with may better predict brain TRP levels was found higher in cirrhoticsthan

in controls and rose significantly upon Intralipid infusion only in cirrhotics.

TIME &A(umol/dl) F.TRP(pmol/dl) Ratio F.TRP/BNAA

Controls 0 34.63 + 9.05 0.41 + 0.16 0.007 + 0.004

180' 27.96 5 6.54 ** 0.44 : 0.18 0.011 : 0.006

0 Cirrhotics

34.59 T 9.00 0.88 T 0.34 * 0.014 IO.005 *

180' 27.26 5 5.44 ** 1.27 ; 3.62 ** 0.023 + 0.014 **

Mean values + SD. Minimal significance pdO.05; - *) vs Controls, **) vs time 0. - - In conclusion the slight decrease observed in all AA levels is probably due to diluition

effect whereas the decrease of ALA is likely due to its decreased peripheral production

or increased conversion into glucose.The potential risk of precipitating HE by increasing

F.TRP should not be overlooked when lipids are infused to decompensated cirrhotics.

0.24 AMINO ACID CLEARANCE IN TWO GROUPS OF PATIENTS WITH LIVER CIRRHOSIS, FINDINGS IN MODERATE

AND SEVERE HEPATIC INSUFFICIENCY. H. Leweling, E. Helm, U. Staedt, J.-P. Striebel, B. Klein (Dept. of Pathophysiology, Medical Clinic I Mannheim, University of Heidelberg,FRG)

The question of whether the elimination rates of amino acids (AA) from plasma are related to the degree of hepatic failure has not yet satisfactorily been investigated. - There- fore, AA clearance rates were determined in 8 healthy volunteers (groupA),,in 12 patients

with moderate (group B), and in 14 with severe hepatic insufficiency (classification cri- terion: plasma methionine concentration). A branched-chain AA (BCAA)-enriched AA solution

(0.08 g AA x kg-l x h-l) and glucose (1.35 kcal x kg-' x h-l) were continuously infused by means of automatic pumps. The AA clearance was calculated as the ratio between the in- fusion rate and the steady state concentrations. - The clearance rate of the total of the AA was 98.4 ml x kg-' x min-1 in group A but reached only 50.1 (p IO.001) and 55.4 (p I 0.001) in groups B and C, respectively. With the exception of the BCAA, all AA were eli-

minated significantly more slowly in groups B and C. In terms of the percentage values, the BCAA therefore had higher clearance rates in the patients; this was more evident in group C than in group B. Furthermore, a significant positive correlation (r = 0.57; p I

;.Olj between the BCL clearance and.the degree of hyperauunonemia could be established. Groun A Grout B Grout, C

Valine [Xl 5.0 + '0.2 6.3 + b.3.. 7.0 + b.3*** n.s. Isoleucine [Xl 10.4 7 0.6 14.8 7 0.8.. 18.0 5 0.8**** Leucine Is.1 9.4 + 0.5 13.1 T 0.7*e 16.3 5 0.7..mH Ammonia [ug/dll 59 + 7 122 T 14 0.0 200 7 21 l *.+ - - _

BCAA clearance rates and venous plasma ammonia concentrations (mean+SEM). l /*significant- ly different from group A/B. "p5b.05; l */**p<O.OI; l ** ~10.001 (U-test). Conclusion: Nutritional theraov of cirrhotic patients should provide relatively large

quantities of BCAA. The increased clearance rate of BCAA in ciinical states with pronoun- ced hyperammonemia is compatible.with the hypothesis that hyperammonemia intensifies the utilisation of BCAA (provided that the arterial ammonia level largely parallels the venous level).

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