Nutritional support to hepatic failure patients is challenging and requires experience, skill, careful planning and meticulous follow-up. It is indeed an attempt to replenish the lost power of one of the most vital organs we possess

Rao Nanjunda, Mr Ananth

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Hepatic Failure: Role for biochemists and nutrition experts

Ananth Nanjunda Rao

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Published Quarter ly
Mangalore, S outh I ndia
I S S N 0972-5997
Volume 1;  I s sue 1;  January -  March 2002
S hor t  Communicat ion
H epat ic F ai lur e:  R ole for  biochemis t s  and nut r i t ion exper t s
Anant h N
Depar tment of B iochemis try, Center  for  Bas ic S ciences , Mangalore -  575004 , I NDI A.
Email:  gmcs f@operamail.com
Cit at ion:  Ananth N. Hepatic Failure:  Role for  biochemis ts  and nutr ition exper ts . Online J Health All ied
S cs . 2002; 1: 2
U R L :  http: //www.oj has .org/is sue1/2002-1-2.htm
Open Acces s  Ar chive:  http: //cogpr ints .ecs .soton.ac.uk/view/subj ects /OJHAS .html
T he liver  is  the larges t gland of the human body.
S ometimes  refer red to as  the " great chemical
factory"  of the body, the liver  creates , regulates , and
s tores  a var iety of subs tances  used by the
gas trointes tinal sys tem and it serves  a number  of
impor tant diges tive functions . T he liver  also plays  a
maj or  role in the regulation of blood sugar . T he liver
synthes izes  dis solves , and s tores  amino acids ,
protein, and fat. I t s tores  several impor tant vitamins
like B-12 and Vitamin A. T he liver  also disposes  of
cellular  was te and breaks  down harmful subs tances
like alcohol, dispos ing them into the bile.
Acute inj ury to the liver  due to causes  such as
hepatitis , tox ins , encephalopathy and chronic liver
failure are well-documented causes  of a very near ly
fatal manifes tation termed " Hepatic Failure"  (HF).
Owing to the multitude of functions  that the organ
performs , the management and treatment of HF
poses  a true challenge to a clinician and a biochemis t
/ nutr ition exper t put together . Pinning down the
under lying cause with a battery of tes ts  and
inves tigations  ass is ts  the clinician for  diagnos is  and
mos tly the prognos is  of the condition, s ince mor tality
rate is  very high in HF.
S imultaneous ly, a biochemis t / nutr ition exper t
needs  to think on the lines  of S uppor tive Nutr itional
T herapy. S ince the liver  eventually metabolizes  all
nutr ients  adminis tered either  parenterally or
enterally, HF poses  a formidable challenge. I t is  bas ic
to review br iefly the metabolic derangements  in HF
before cons ider ing Nutr itional S uppor t. Mos t of such
changes  are mediated by cytokines  whose roles  have
yet to be clear ly defined.
1. Hyper insulinemia, a consequence of decreased
hepatic clearance results  in hyperglycemia and
per ipheral insulin res is tance.
2. Decreased synthes is  of I GF 1 causes  exces s ive
protein catabolism and a reduced glycogenes is .
3. A low insulin: glucagon ratio changes  the normal
" milieu inter ior "  of the cells .
4. Lipid metabolism represents  an accelerated
s tate of s tarvation and leads  to depletion of fat
s tores  and es sential fatty acid deficiency.(1)
5. Decreased activity of hepatic lipoprotein lipase
and mild hyper tr iglycer idemia ensue.
6. Protein synthes is  is  decreased as  is  true with
every hepatocellular  disorder . An increase in
ammonia production due to glutamine ox idation
(2) may aggravate encephalopathy, bacter ia
contr ibuting to very ins ignificant amounts  of
ammonia.
HF has  a well-defined relation with ammonia levels
and neurotransmitter s . (3) Ammonia metabolism
pr imar ily occurs  in the hepatic tis sue and secondar ily
in the muscle tis sue. Due to muscle was ting in HF,
ammonia metabolism in the muscle is  diminished
and excess  ammonia cros ses  the blood-brain bar r ier .
T he ammonia thus  having entered the cranial space
combines  with glutamic acid resulting in the
formation of Glutamine, a reaction catalysed by the
enzyme Glutamine synthetase. Glutamine then acts
as  a predispos ing factor  to the cerebral edema that
follows . (4)
T he biological amines  produced as  a result of
decarboxylation of selected amino acids  such as
tyros ine, tryptophan are the phys iologically
s ignificant neurotransmitter s . However , amines  such
as  phenylethylamine, tr yptamine which are not the
" true"  neurotransmitter s  also result from the proces s
and are normally cleared by the liver . I n HF, these
" false"  neurotransmitter s  are not cleared by the liver
and get access  to the brain.
T hus , bear ing all these metabolic derangements  in
mind, a biochemis t mus t ins titute a Nutr itional
S uppor t to suit the delicate sys tem. Protein energy
malnutr ition is  common in HF (5) and more so with a
his tory of alcoholism. I n all such cases , appropr iate
nutr itional intervention and suppor t should be
ins tituted as  ear ly as  pos s ible. Cor rections  for
hemodynamic parameter s  and electrolytes  need to
be paid equal attention too.
Route of adminis tration should not pose a problem if
the phys iology of the gut is  normal. However , a
combination of routes  such as  enteral, oral and
parenteral may be used.
Guidelines  for  Nutr itional S uppor t in HF are defined
by the European S ociety for  Parenteral and Enteral
Nutr ition (ES PEN). (6) Protein requirements  are
increased in HF (7) and mus t be ins tituted as  a par t
of the Nutr itional S uppor t along with neomycin which
helps  to lower  the ammonia burden by reducing the
activity of the synthetase. (8) Branched chain amino
acids  mus t be provided as  a par t of the
supplementation and the protein feed could range
from 0.6 g / kg body weight upto 1.5 / kg body
weight depending on the grade of HF.
Deficiencies  of both water  and fat-soluble vitamins
are known. T hough commercial vitamin supplements
may provide suppor t, adequacy may s til l be
ques tionable. T hiamin and Vitamin K deficiency are
well documented. T hiamin deficiency leads  to lactic
acidos is  and may manifes t as  conges tive hear t
failure.(9) A dose of up to 50 mg per  day has  been
recommended.
HF has  been associated with Z inc deficiency.(10)
Parenteral supplementation up to 600 mg of sulfate
salt /day has  been found to be appropr iate. Other
trace elements  that need to be supplemented are
S elenium, Copper  and Manganese.
With reference to electrolytes , mild sodium
res tr iction has  been recommended. Adequate
Potas s ium, Magnes ium and Phosphates  have to be
provided.
Calor ie requirements  have been es timated at 25-30
non-protein Kcal/kg/day. Only carbohydrate sources
mus t be used for  parenteral nutr ition. Adminis tration
of intravenous  fats  have also been attempted.(11)
Enteral route for  fats  is  not recommended s ince
malabsorption is  common in HF.
A careful follow-up for  such cases  is  absolutely
es sential. S erum tr iglycer ide es timations  need to be
performed regular ly alongs ide per iodic
determinations  of glucose, Prothrombin time,
electrolytes  and trace elements .
CONCL U S I ON
I n conclus ion, nutr itional suppor t to HF patients  is
challenging and requires  exper ience, s kill,  careful
planning and meticulous  follow-up. I t is  indeed an
attempt to replenish the los t power  of one of the
mos t vital organs  we pos ses s .
R E F E R E NCE S :
1. Cabre, E, Abad-Lacruz, A, Nunez, M.C etal:
T he relation of plasma polyunsaturated fatty
acid deficiency with survival in advanced liver
cir rhos is :  a multivar iate analys is . Am J Gas tr .
1993;  88: 718.
2. James , J.H, Jeppson, B ., Z iparo, V. and
Fisher , J.E.:  Hyperammonemia, plasma
aminoacid imbalance and blood-brain
aminoacid transpor t:  a unified theory of
por tal- sys temic encephalopathy. Lancet.
1979;  2: 772.
3. Hawkins , R.A., Mans , A.M.,:  B rain metabolism
in encephalopathy caused by
hyperammonemia. Adv Exp Med B iol. 1994;
368: 11.
4. T akahashi, H., Koehler , R., Brudiolos , S .W.,
and T rays tman, R.J.:  I nhibition of brain
glutamine accumulation prevents  cerebral
oedema in hyperammonsemic rats . Am J
Phys iol. 1991;  261: H 825.
5. Marsano, L. and McClain, C.J.:  Nutr ition and
alcoholic liver  disease:  JPEN, 15: 337, 191.
6. Plauth, M., Mer li, M., Kondrup, J., etal:  ES PEN
guidelines  for  nutr ition in liver  disease and
transplantation. Clin Nutr . 1997;  16: 43.
7. S war t, G.R., van den Berg, J.W.O.,
Wattinema, J.L., etal:  Elevated protein
requirements  in cir rhos is  of the liver
inves tigated by whole body protein turnover
s tudies . Clin S ci. 1988;  75:  101.
8. Hawkins , R.A., Jes sey, J., Mans , A.M., Cheid,
A. and De Joseph , M.R.:  Neomycin reduces
the intes tinal production of ammonia from
glutamine. Adv Exp Med B iol. 1995;  368: 125.
9. Les lie, D., Gherghiade, M.:  I s  there a role for
thiamine supplementation in the management
of hear t failure? Am Hear t J. 1996;  131: 1248-
50.
10. McClain, C.J., Mar sano, L., Burk, R.F. and
Bacon,B.:  T race elements  in liver  disease.
S emin Liv Dis . 1991;  18: 321.
11. Muscuratoli, M., Cangiano, C., cascino, A.
etal:  Exogenous  lipid clearance in
compensated liver  cir rhos is , JPEN. 1986;
10: 599.


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Hepatic Failure: Role for biochemists and nutrition experts

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