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Resting energy expenditure (REE) in patients with alcoholic liver cirrhosis (ALC): Relationships with malnutrition and liver fallure
0.27
RESTINGENERGYEXPENDITURE(REE) IN PATIENTS VITH ALCOHOLIC LIVER CIRRHOSIS(ALC) : RELATIONSHIPS WIl’H MALNUTRITION ANDLIVER FAILURE. R. Pierrugues, H. Michel. Clinique des Maladies de 1’Appareil Digestif, HBpital
Saint-Eloi,
Patients
with
higher
mortality
-Aim excretion
:
This
liver
The
of
the
cent
of
to
be hypermetabolic,
Pugh
standard
out
lean
disease
and
:
11 to
body to
mass;
the
We measure
was
measure 2)
to
REE in
thirty
similar
(1728
index,
and
the
and
abnormal
+
indirect
the
and
323
and
energy
malnutr-itio”
failure
Cal/day). was
arm muscle
The
to
and probably
relate
expenditurelmg
assessed
and without
severity by
circumference
severity
of
liver
a
REE to
creatinine
creatinine
to
the
of
abnormal (<
alcohol
the triceps
90 p cent
untake
liver
disease
skinfold of
the
for
two weeks.
was
evaluated
thickness
standard
(< 40 p
value).
disease REE/creat
(mg)
= 5)
1522
T 238
1.83
+ 0.52
Child
B (n
= 11)
1374
+ 243
1.62
+ 0.63
1497 ; 376
REE and nutritional
2.05 ; 0.75
patients
“wished
co”clusio”
(“=lO)
1269
patients(n.20)
:
the
RFE a”d REE/creat
were not significantly
different
the
between
three
groups.
status
REE (Kcals) malnurished
1550
hypermetabolic
REE/creat
+ 308 :
271
status
in
1.86
+ 0.67
REE was significantly decreased in malnourished ALC (p < 0.05) but REE/creat
1.86
:
was
ALC is
(mg)
0.71
independent of
the the
same liver
in
the
two groups.
failure
and
of
the
nutri-
status.
PARNTWAL
Richard,
malnutrition
(22 me” 8 women - mea” age 56 + 10) with ALC who
renal
A (n
tional
their
calorimetry
estimated
patients
bleeding
value)
Child C (n = 14)
0.28
FXE by
ChLld
well
explain
status.
PxEE (Kcals)
I”
would
:
REE and
2)
which
relate
nutritional
gastrointestinal
intake
Child
the
Results 1)
carried
of
septicemy,
nutritional
using
was
index
and methods
Patients
were free
thought
France
and morbidity.
an
of
Yontpellier,
ALC are
study
as
severity
34059
NUTRITION
C. Nszelof,
A!BXIATED
AH. Gorski.
LIVER
IN QIILDEN WITHUMSIM LOSS OF INTESTINE. 0. Mpital dss Enfants Malades. Paris. France.
DISEASE
C. Riaour.
Goulat.
6.
Cholestatic liver disease is .$ well known complication of paranters nutrition (PN) in which numerous factors are involvad. Ws carried out .s study in 6 children on long tarn hems PN for 6.1 + 3.4 yssrs (Z-llyrsl. All patients unleruant a large small bwsl resection after total volvulus of with a msan sge of 11.5 + 4 yrs. the gut, leaving then with 12.5 + 10 cm of small bowl and no ileocascal valve in = S). Oallblsdw was ram+sd include daily intskes o 260 + 92mg/Kg nitrogsn in all cases. PN. during the 6 months before liver assessawrt. and 192 + 52 KJ/Kg of non pkotein energy with 0 to 40 1 as fat owlsion (Introlipid i sbi). Were psrformd needle (1,6 mm) and liver function tests including : bilirubin fbili), liver biopsy using hepafix transaminases CT@& TGP). alkaline phosphstsses (Ap) and ganla glutsmyl trsnspsptidase (9GTPl. mild to sward in RESULTS : Light microscopic examination of liver spscimsn shobmd l constant steatosis. inflannation : severe (n = 21. mild (n - 3). l intensity, l Kupffer cells hyperplesie. *portal and pariportal portal and periportal fibrosis : severe fn = 21. mild fn =-31 Dr absent in = 2. l iron pigmsnt dsposition fn = 5), l no portal bile ductular prollfmrstion. aithatt lipid Yith lipid kral II=3 n=5 21 + 14 Bili uDl/l 26.6 + 17 < I7 04 + 45 0 - 20 TWU 32 + 7 72 + 40 5 - 20 TWU 54 + 21 408 2 149 96 - 260 221 + 110 Ap u 6GTPU
1e+
F1bm.L
+(“=3).0(“=2)
52 + 9
11
++
(n=Z)
S - 38 0 +
mrtal
intttial
++ ln=21
+(“=3).0(“=2)
++
: :
absent
mild : swsrd
in children with massive loss of intsstins on long term PN. show : 1) constant liver This results. disease with biological and histological involverent ; 2) APandGGTP are the best indicators : 3) lfV*r of fibrosis and portal disease variable but remains limited despite long term PN : 4) ths lntsnsity inflanaation sssms related to PN duration but also to PN composition in terms of lipids.
24
RESTINGENERGYEXPENDITURE(REE) IN PATIENTS VITH ALCOHOLIC LIVER CIRRHOSIS(ALC) : RELATIONSHIPS WIl’H MALNUTRITION ANDLIVER FAILURE. R. Pierrugues, H. Michel. Clinique des Maladies de 1’Appareil Digestif, HBpital
Saint-Eloi,
Patients
with
higher
mortality
-Aim excretion
:
This
liver
The
of
the
cent
of
to
be hypermetabolic,
Pugh
standard
out
lean
disease
and
:
11 to
body to
mass;
the
We measure
was
measure 2)
to
REE in
thirty
similar
(1728
index,
and
the
and
abnormal
+
indirect
the
and
323
and
energy
malnutr-itio”
failure
Cal/day). was
arm muscle
The
to
and probably
relate
expenditurelmg
assessed
and without
severity by
circumference
severity
of
liver
a
REE to
creatinine
creatinine
to
the
of
abnormal (<
alcohol
the triceps
90 p cent
untake
liver
disease
skinfold of
the
for
two weeks.
was
evaluated
thickness
standard
(< 40 p
value).
disease REE/creat
(mg)
= 5)
1522
T 238
1.83
+ 0.52
Child
B (n
= 11)
1374
+ 243
1.62
+ 0.63
1497 ; 376
REE and nutritional
2.05 ; 0.75
patients
“wished
co”clusio”
(“=lO)
1269
patients(n.20)
:
the
RFE a”d REE/creat
were not significantly
different
the
between
three
groups.
status
REE (Kcals) malnurished
1550
hypermetabolic
REE/creat
+ 308 :
271
status
in
1.86
+ 0.67
REE was significantly decreased in malnourished ALC (p < 0.05) but REE/creat
1.86
:
was
ALC is
(mg)
0.71
independent of
the the
same liver
in
the
two groups.
failure
and
of
the
nutri-
status.
PARNTWAL
Richard,
malnutrition
(22 me” 8 women - mea” age 56 + 10) with ALC who
renal
A (n
tional
their
calorimetry
estimated
patients
bleeding
value)
Child C (n = 14)
0.28
FXE by
ChLld
well
explain
status.
PxEE (Kcals)
I”
would
:
REE and
2)
which
relate
nutritional
gastrointestinal
intake
Child
the
Results 1)
carried
of
septicemy,
nutritional
using
was
index
and methods
Patients
were free
thought
France
and morbidity.
an
of
Yontpellier,
ALC are
study
as
severity
34059
NUTRITION
C. Nszelof,
A!BXIATED
AH. Gorski.
LIVER
IN QIILDEN WITHUMSIM LOSS OF INTESTINE. 0. Mpital dss Enfants Malades. Paris. France.
DISEASE
C. Riaour.
Goulat.
6.
Cholestatic liver disease is .$ well known complication of paranters nutrition (PN) in which numerous factors are involvad. Ws carried out .s study in 6 children on long tarn hems PN for 6.1 + 3.4 yssrs (Z-llyrsl. All patients unleruant a large small bwsl resection after total volvulus of with a msan sge of 11.5 + 4 yrs. the gut, leaving then with 12.5 + 10 cm of small bowl and no ileocascal valve in = S). Oallblsdw was ram+sd include daily intskes o 260 + 92mg/Kg nitrogsn in all cases. PN. during the 6 months before liver assessawrt. and 192 + 52 KJ/Kg of non pkotein energy with 0 to 40 1 as fat owlsion (Introlipid i sbi). Were psrformd needle (1,6 mm) and liver function tests including : bilirubin fbili), liver biopsy using hepafix transaminases CT@& TGP). alkaline phosphstsses (Ap) and ganla glutsmyl trsnspsptidase (9GTPl. mild to sward in RESULTS : Light microscopic examination of liver spscimsn shobmd l constant steatosis. inflannation : severe (n = 21. mild (n - 3). l intensity, l Kupffer cells hyperplesie. *portal and pariportal portal and periportal fibrosis : severe fn = 21. mild fn =-31 Dr absent in = 2. l iron pigmsnt dsposition fn = 5), l no portal bile ductular prollfmrstion. aithatt lipid Yith lipid kral II=3 n=5 21 + 14 Bili uDl/l 26.6 + 17 < I7 04 + 45 0 - 20 TWU 32 + 7 72 + 40 5 - 20 TWU 54 + 21 408 2 149 96 - 260 221 + 110 Ap u 6GTPU
1e+
F1bm.L
+(“=3).0(“=2)
52 + 9
11
++
(n=Z)
S - 38 0 +
mrtal
intttial
++ ln=21
+(“=3).0(“=2)
++
: :
absent
mild : swsrd
in children with massive loss of intsstins on long term PN. show : 1) constant liver This results. disease with biological and histological involverent ; 2) APandGGTP are the best indicators : 3) lfV*r of fibrosis and portal disease variable but remains limited despite long term PN : 4) ths lntsnsity inflanaation sssms related to PN duration but also to PN composition in terms of lipids.
24