Nutritional Management of Liver Disease

1
Nutritional Management of Liver Disease
2

• Review the functions of the liver
• Review diseases of the liver
• Major complications of liver disease
• Nutritional features of end stage liver disease
• Nutritional management of end stage liver disease
• Nutritional response to hepatic transplantation
• Nutritional management of non alcoholic fatty
  liver disease (NAFLD)
• Hepatitis C

3
Functions of the Liver

• Major role of the liver is the regulation of
  solutes in the blood that affect the functions of
  other organs for example the brain, heart,
  muscle and kidneys
• Strategically placed such that all blood passing
  from the small intestine must travel through the
  liver

4
Functions of the Liver

• Storage and metabolism of macronutrients such as
  protein, carbohydrates and lipids
• Metabolism of micronutrients vitamins and
  minerals
• Metabolism and excretion of drugs and toxins
  endogenous and exogenous

5
Role of the Liver in Nutrient Metabolism

• Storage and metabolism of macronutrients such as
  protein, carbohydrates and lipids
• Carbohydrate
• Storage of carbohydrate as glycogen
• Gluconeogenesis
• Glycogenolysis

6
Role of the Liver in Nutrient Metabolism

• Protein
• Synthesis of serum proteins e.g. albumin
• Synthesis of blood clotting factors
• Formation of urea from ammonia
• Oxidation of amino acids
• Deamination or transamination of amino acids

7
Role of the Liver in Nutrient Metabolism

• Fat
• Hydrolysis of triglycerides, cholesterol and
  phospholipids to fatty acids and glycerol
• Formation of lipoproteins
• Ketogenesis

8
Role of the Liver in Nutrient Metabolism

• Fat
• Fat storage
• Cholesterol synthesis
• Production of bile necessary for digestion of
  dietary fat

9
Role of the Liver in Nutrient Metabolism

• Vitamins
• Site of the enzymatic steps in the activation of
  vitamins thiamine
• pyridoxine
• folic acid
• vitamin D(25 hydroxycholecalciferol)
• Site of the synthesis of carrier proteins for
  vitamins A, B12, E

10
Role of the Liver in Nutrient Metabolism

• Storage site for fat soluble vitamins A, D, E,
  K, B12
• Minerals
• Storage site for copper iron and zinc

11
Diseases of the Liver

• Hepatitis
• Inflammation of hepatocytes
• Reversible
• Precipitants include
• Viral infections such as hepatitis A, B, C
• Drugs such as paracetamol
• Some herbal preparations
• Alcohol

12

• Fatty Liver
• Infiltration of the liver by fat
• Possible causes include
• alcohol
• obesity
• type 2 diabetes mellitus
• hyperlipidaemia
• sudden rapid weight gain
• hepatitis C
• TPN

13
NAFLD (Non Alcoholic Fatty Liver Disease)

• Resembles alcohol induced fatty liver
• Occurs in people who do not abuse alcohol
• Has the potential to progress to cirrhosis and
  liver failure

14
Non Alcoholic Fatty Liver Disease (NAFLD)

• Simple steatosis
• Steatohepatitis (NASH)
• Fibrosing steatohepatitis
• Cirrhosis

15
Non Alcoholic Fatty Liver Disease (NAFLD)

• Risk Factors include
• Overweight
• Obesity
• Central Obesity

16
Non Alcoholic Fatty Liver Disease (NAFLD)

• Factors involved in the development of NAFLD
• Lifestyle
• Weight gain
• Weight loss
• Reduced activity
• Childhood and adult obesity
• Type 2 diabetes

17
Non Alcoholic Fatty Liver Disease (NAFLD)

• The major underlying risk factor for the
  development of NAFLD is insulin resistance

18
NAFLD (Non Alcoholic Fatty Liver Disease)

• Prevalence of obesity in patients with NAFLD
  reported between 30 and 100
• Prevalence of type 2 diabetes in patients with
  NAFLD reported between 10 and 75
• Prevalence of hyperlipidaemia in patients with
  NAFLD reported between 20 and 92

19
NAFLD - Symptoms

• Often asymptomatic of liver disease at time of
  diagnosis
• Fatigue or malaise and/or a feeling of fullness
  or discomfort on the right side of the abdomen

20
NAFLD - Symptoms

• Mild to moderate elevation of the enzymes
• aspartate amino transferase
• alanine amino transferase
• Diagnosis confirmed on biopsy

21

• Cirrhosis
• Refers to chronic scarring of the liver
• Clearly delineated nodules form within the liver
  which contain connective tissue
• This leads to a significant reduction in liver
  function

22

• Fulminant Hepatic Failure
• Sudden massive necrosis of hepatocytes
• The patient rapidly becomes encephalopathic and
  comatosed
• Causes may be viral or a reaction to a drug such
  as paracetamol, sulphathiazone or some herbal
  remedies

23

• Autoimmune liver diseases
• Diseases of the biliary tract and include primary
  sclerosing cholangitis (PSC) and primary biliary
  cirrhosis (PBC)
• PSC often occurs in association with ulcerative
  colitis
• Serum cholesterol levels may be elevated and
  unresponsive to medication or dietary manipulation

24
Alcoholic liver disease

• Alcohol is toxic to the liver
• Caused by chronic alcohol abuse
• All stages of the disease process hepatitis,
  fatty liver fibrosis and cirrhosis

25
Alcoholic liver disease

• Cessation of alcohol may result in recovery in
  the early stages of liver disease
• Cessation of alcohol in patient with cirrhosis
  may result in an improvement in liver function
  and may also result in a slowing down of the
  disease progression

26
Wilsons Disease

• Copper storage disease
• May result in cirrhosis if untreated
• First presentation often in adults who present
  with cirrhosis

27
Wilsons Disease

• If detected in childhood management involves
  penecillamine which acts to bind Cu in the GIT
• Value of dietary Cu restriction debatable in
  children of no value in adults in the presence
  of cirrhosis

28

• Hepatic tumours
• Often occur in association with Hepatitis B or
  Hepatitis C
• Occur independently
• Include hepatocellular carcinomas,
  cholangiosarcoma (bile duct tumours)

29
Portal Hypertension

• Occurs as a result of fibrous infiltration of the
  liver which in turn causes increased pressure in
  the portal vein
• This pressure continues back through the system
  to the abdominal capillaries which then leak
  serous fluid into the abdominal cavity due to
  this increased pressure and low serum albumin
  levels

30
Portal Hypertension

• Surgical interventions may be undertaken to
  alleviate this pressure (TIPSS). There are risks
  associated with these procedures infection,
  failed shunts, encephalopathy

31
Cirrhosis

• Compensated i.e. well controlled
• or
• Decompensated i.e. symptomatic

32
Decompensated cirrhosis

• Symptoms of portal hypertension include
• Ascites and/or peripheral oedema
• Jaundice
• Oesophageal and/or gastric varices
• Encephalopathy
• Hepatorenal failure
• Malnutrition

33

• Ascites
• Refers to the accumulation of fluid in the
  abdominal cavity
• It contains protein, sodium and potassium
• It is considered to be an active metabolic unit

34

• Jaundice
• Refers to the yellow colour seen in patients with
  liver disease
• It is caused by high circulating levels of
  bilirubin
• Severe itching may be present. May be alleviated
  by Questran/cholestyramine or by phenergan

35

• Varices
• Distended/engorged veins that can occur at any
  point in the venous system of the GIT
• May bleed readily as patients with end stage
  liver disease (ESLD) have poor coagulation
  secondary to impaired synthesis of clotting
  factors

36

• Encephalopathy
• Impaired mental state that results in impaired
  mentation and coordination
• May result in coma
• Believed to be caused by increases in plasma
  ammonia and other nitrogenous waste products
• These toxins cross the blood brain barrier and
  interfere with neuromuscular function and
  behaviour

37

• Precipitants of encephalopathy include
• Peritoneal infection (subacute bacterial
  peritonitis SBP)
• GIT bleeding
• Poor compliance with lactulose (marketed as
  Duphalac) therapy
• Nitrogen overload
• Fluid and electrolyte imbalance
• Medications
• Acid-base imbalance

38
There are four classifications of encephalopathy

• Grade1. foetor, impaired
  coordination, tremor, altered
  handwriting, reduced attention span,
  mild confusion, mood swings and altered
  sleep pattern
• Grade 2. asterixis (impaired ability to draw a
  star), slurred speech, ataxia inappropriat
  e behaviour, lethargy, impaired memory and
  mild disorientation

39
Classifications of encephalopathy cont

• Grade3. bizarre behaviour, confusion,
  moderate to severe disorientation,
  uncharacteristic anger, paranoia, somnolence,
  stupor and muscle rigidity
• Grade 4. comatosed, dilated pupils

40
Nutritional Management of Liver Disease

• Early Stages of Liver Disease
• No specific dietary management
• Healthy diet according to healthy eating
  guidelines
• Beware of miracle cures

41
Acute Hepatitis

• High protein/high energy intake required to
  promote hepatocyte regeneration
• Fat restriction contraindicated
• Nausea/anorexia
• Consider oral supplementation such as glucose
  polymers, fruit based high protein drinks, or
  high protein/ high energy drinks in the presence
  of nausea/anorexia
• Caution against herbal remedies as some may be
  harmful and most have no scientific basis

42
Nutritional Features of End Stage Liver Disease

• Look malnourished
• Low se protein levels
• albumin, prealbumin, transferrin, retinol
  binding protein, insulin like growth factor-1
• Vitamin deficiencies
• thiamine, vit A, D, E
• Mineral deficiencies
• Zn, Mg, Cu, Ca

43
Nutritional Features of Liver Disease

• Weight and BMI do not reflect true nutritional
  status (ascites and/or oedema)
• Oral intakes are not necessarily poor
• Exhibit features of protein energy malnutrition

44
Nutritional Assessment of patients with ESLD

• Weight?
• Weight history?
• Protein markers of nutritional status?
• Descriptive history of wasting?
• Skinfolds?
• Intake?
• Appetite?

45
Nutritional Assessment of patients with ESLD

• SGA for patients with liver disease (Hasse)
• Anthropometry
• Food history
• Nausea
• Anorexia
• Taste changes
• Diarrhoea
• Early satiety
• Functional capacity
• Grip strength

46
Malnutrition in End Stage Liver Disease

• Changes in Macronutrient Metabolism
• Energy
• Fat
• Protein

47
Nutritional Management of End Stage Liver Disease

• Energy Requirements
• Patients with compensated cirrhosis do not appear
  to need modification of their energy intakes
• Patients with decompensated liver disease require
  35 40 non protein kcals/kg/day
• Ascites is a viable metabolic unit
• Plauth M, Merlim, Kondrup J, Weimann A, Ferenci
  P, Muller MJ.ESPEN Guidelines for Nutrition in
  Liver Disease and Transplantation. Clinical
  Nutrition 1997 16 43-55

48
Nutritional Management of End Stage Liver Disease

• Energy
• Energy expenditure currently there are no
  metabolic equations which are able to estimate
  accurately the energy requirements of the patient
  with ESLD.
• Harris-Benedict, Schofields and Muller all
  underestimate the energy requirements of this
  group
• Indirect calorimetry

49
Nutritional Management of End Stage Liver Disease

• Glycogen storage
• Reduced glycogen storage capacity
• Unable to tolerate periods of prolonged fasting
  increased protein breakdown in periods of
  prolonged fasting

50
Nutritional Management of End Stage Liver Disease

• Fat
• Altered fat synthesis
• Lipids are oxidised as a preferential substrate
• Increased lipolysis
• Active mobilisation of lipid stores

51
Decompensated Liver Disease

• Fat restriction contraindicated in most patients
• Symptoms of fat intolerance such as steatorrhoea,
  abdominal pain or nausea following a high fat
  intake are rare. If present fat modification may
  be necessary

52
Nutritional Management of End Stage Liver Disease

• Protein
• Protein turnover in cirrhotic patients is normal
  or increased
• Stable cirrhotics have increased protein
  requirements¹?²
• Stable cirrhotic patients are capable of
  achieving positive nitrogen balance during
  aggressive nutritional support regime¹?²
• ¹Kondrup J, Neilsen K et al. Effect of long term
  refeeding on protein metabolism in patients with
  cirrhosis of the liver. Br J Nutr 1997 77
  197-212
• ²Swart, GR et all. Minimal protein requirements
  in liver cirrhosis determined by nitrogen balance
  measurements at three levels of protein intake.
  Clin Nutr 1989 8 329-336

53
Nutritional Management of End Stage Liver Disease

• Protein
• Protein turnover in cirrhotic patients is normal
  or increased
• Stable cirrhotics have increased protein
  requirements¹?²
• Stable cirrhotic patients are capable of
  achieving positive nitrogen balance during
  aggressive nutritional support regime¹?²
• ¹Kondrup J, Neilsen K et al. Effect of long term
  refeeding on protein metabolism in patients with
  cirrhosis of the liver. Br J Nutr 1997 77
  197-212
• ²Swart, GR et all. Minimal protein requirements
  in liver cirrhosis determined by nitrogen balance
  measurements at three levels of protein intake.
  Clin Nutr 1989 8 329-336

54
Nutritional Management of End Stage Liver Disease

• Protein
• Protein refeeding showed a 30 increase in
  protein synthesis
• Protein refeeding did not show a significant
  increase in protein degradation
• Kondrup J, Neilsen, K,and Anders J. Effect of
  long term refeeding on protein metabolism in
  patients with cirrhosis of the liver. Br J
  Nutrition (1997), 77, 197-212

55
Nutritional Management of End Stage Liver Disease

• Protein
• Patients with cirrhosis have been shown to have
  high protein requirements to maintain positive
  nitrogen balance
• Konrup J, Nielsen K, Juul A. Effect of long-term
  refeeding on protein metabolism in patients with
  cirrhosis of the liver. Br. J. Nutr. 1997 77
  197-212

56
Nutritional Management of End Stage Liver Disease

• Protein
• The protein restricted diets used traditionally
  have probably arisen historically from the
  response to a dietary protein load seen in
  cirrhotic patients who have some form of
  portocaval shunt surgery

57
Nutritional Management of End Stage Liver Disease

• Protein requirements in episodic hepatic
  encephalopathy
• 62 patients with acute encephalopathy assessed
  32 excluded
• 30 patients randomised into two groups
• All patients received lactulose enema and then
  identical oral neomycin dosage
• Cordoba J, Lopez-Hellin J et al. Normal protein
  diet for episodic hepatic encephalopathy results
  of a randomised study. J of Hepatology 41 2004)
  38-43

58
Nutritional Management of End Stage Liver
Disease

• 20 patients completed study
• 5 patients in each arm dropped out 4 deaths in
  each. Group A additional variceal bleed group
  B additional voluntary abandon

59
Nutritional Management of End Stage Liver Disease

• 2 groups 15 in each group
• 14 days
• Group A 0g protein/day for 3 days. Protein
  increased incrementally to 1.2g protein/kg/day
• Group B 1.2g protein/kg/day
• Protein synthesis and breakdown studied at day 2
  and day 14

60
Nutritional Management of End Stage Liver Disease

• Day 2
• Increased protein breakdown in protein restricted
  group
• No statistically significant difference in
  protein synthesis

61
Nutritional Management of End Stage Liver Disease
62
Nutritional Management of End Stage Liver Disease

• Restricting protein intake did not have any
  positive effect on the evolution of episodic
  hepatic encephalopathy

63
Nutritional Management of End Stage Liver Disease

• Protein
• Protein restriction is contra - indicated for
  patients with decompensated cirrhosis
• Recommended protein intake for cirrhotics is 1.0
  1.5g protein/kg/day¹
• Dietary protein restriction does not appear to be
  of any benefit in episodic hepatic
  encephalopathy²
• ¹Plauth M, Merlim, Kondrup J, Weimann A, Ferenci
  P, Muller MJ.ESPEN Guidelines for nutrition in
  Liver Disease and Transplantation. Clinical
  Nutrition 1997 16 43-55²
• ²Cordoba J, Lopez-Hellin J et al. Normal protein
  diet for episodic hepatic encephalopathy results
  of a randomised study. J of Hepatology 41 2004)
  38-43

64
Nutritional Management of End Stage Liver Disease

• Does the type of protein matter?

65
Nutritional Management of End Stage Liver Disease

• Amino Acids in Encephalopathy
• Patients with advanced liver disease have an
  altered ratio of branched chain amino (leucine
  valine, isoleucine) acids to aromatic amino acids
  (phenylalanine, tyrosine)
• Aromatic amino acids are catabolised in the liver
  and their metabolism is impaired in cirrhosis
  resulting in an increase in circulating levels of
  AAAs

66
Nutritional Management of End Stage Liver Disease

• Amino Acids in Encephalopathy
• Branched chain amino acids (BCAA) are metabolised
  predominantly in the skeletal muscle and fat
• Plasma BCAA levels fall due to their utilisation
  as an energy substrate and a substrate in
  gluconeogenesis

67
Nutritional Management of End Stage Liver Disease

• Amino Acids in Encephalopathy
• The alteration in the ratio of BCAAAAA has been
  proposed as an aetiological factor in the
  development of encephalopathy
• Fischer JE, Rosen HM, Ebeid AM et al. The effect
  of normalisation of plasma amino acids on
  hepatic encephalopathy in man. Surgery. 1976 Jul.
  80 (1) 77-91.

68
Nutritional Management of End Stage Liver Disease

• Amino Acids in Encephalopathy
• Marchesini et al carried out a multicentre double
  blind randomised trial in which BCAA
  supplementation was compared with an isocaloric
  casein supplementation in 64 patients with
  encephalopathy
• G Marchesini, FS Dioguardi, GP Bianchi et al.
  Long- term oral branched chain amino acid
  treatment in chronic hepatic encephalopathy. J of
  Hepatol, 1990 1192-101

69
Nutritional Management of End Stage Liver Disease

• 16/34 patients in the BCAA group regained normal
  mental state compared with 9/30 in the casein
  treated group (plt0.05)
• After 6 months on BCAA treatment nitrogen balance
  improved and was suggestive of decreased nitrogen
  catabolism in the BCAA treated group
• G Marchesini, FS Dioguardi, GP Bianchi et al.
  Long- term oral branched chain amino acid
  treatment in chronic hepatic encephalopathy. J of
  Hepatol, 1990 1192-101

70
Nutritional Management of End Stage Liver Disease

• Long-term oral BCAA supplementation(6 months)
  resulted in an increase in body weight
• G Marchesini, FS Dioguardi, GP Bianchi et al.
  Long- term oral branched chain amino acid
  treatment in chronic hepatic encephalopathy. J of
  Hepatol, 1990 1192-101

71
Nutritional Management of End Stage Liver Disease

• 15 centres over up to 15.5 months
• 174 patients with Childs B or C cirrhosis
• Marchesini G, Bianchi G, Merli M et al.
  Nutritional supplementation with branched chain
  amino acids in advanced cirrhosis a double blind
  randomised trial. Gastroenterology
  20031241792-1801

72
Nutritional Management of End Stage Liver Disease

• Methods
• Three types of nutritional supplements. Each 10g
  package supplied
• 14.4g BCAA/day (leucine, isoleucine, valine and
  saccharose providing 37.5 kcal)
• 2.1g lacto-albumin/day (lacto-albumin, saccharose
  and mannitol providing 33.6 kcal)
• 2.4g maltodextrose/day (maltodextrose, saccharose
  providing 34.9 kcal)

73
Nutritional Management of End Stage Liver Disease

• Methods
• All subjects were instructed to take 2 packets
  three times daily dissolved in 200ml water half
  an hour before meals
• Patients were maintained on self selected diet.
  No new dietary restrictions were recommended or
  prescribed
• Standard therapies (albumin, diuretics,
  lactulose) were allowed but registered

74
Nutritional Management of End Stage Liver Disease

• Results
• 115 patients remained in the study
• 59 patients were withdrawn for a variety reasons
• Death
• Deterioration in liver function
• Non-compliance (palatability, nausea,
  gastrointestinal discomfort and diarrhoea)
• Psychiatric disease

75
Nutritional Management of End Stage Liver Disease

• Results
• Patients treated with BCAAs were admitted to
  hospital less frequently
• 195 days in BCAA group
• 327days in L-ALB group and
• 520days in M-DXT group
• Length of stay varied within the treated groups
• 0-24 days in BCAA group
• 0-31 days in the L-ALB group
• 0-77 days in the M-DXT group

76
Nutritional Management of End Stage Liver Disease

• Results
• Improved triceps skinfold thickness in the BCAA
  group
• Improved midarm fat area in the BCAA group
• Reduction in the prevalence and severity of
  ascites in the BCAA group
• Shift towards better scoring of health only in
  the BCAA group
• M-DXT supplementation therapy did not require
  increase in insulin therapy

77
Nutritional Management of End Stage Liver Disease

• Results
• Total bilirubin levels decreased in the BCAA
  group and increased in the M-DXT group
• Improvement in the CTP score in the BCAA group
• CTP was stable in the L-Alb group and M-DXT group
• Reduced prevalence of anorexia in the BCAA group

78
Nutritional Management of End Stage Liver Disease

• To summarise
• There are benefits to routinely supplement
  patients with advanced cirrhosis with branched
  chain amino acids
• Patient compliance

79
Nutritional Management of End Stage Liver Disease

• Current Criteria for use of Oral BCAA
  Supplementation at RPAH
• chronic encephalopathy
• frequent hospital admissions due to
  encephalopathy
• severe depletion of fat and muscle stores
• elevated blood sugar levels

80
Nutritional Management of End Stage Liver Disease

• Does the timing or frequency of meals of meals
  matter?

81
Nutritional Management of End Stage Liver Disease

• Reduced glycogen storage capacity

82
Nutritional Management of End Stage Liver Disease

• Eating Pattern
• Swart and Zillikens demonstrated that spreading
  food intake and inclusion of a late evening meal
  significantly improved nitrogen balance in
  cirrhotics
• Swart G, Zillikens M. Effect of a late evening
  meal on nitrogen balance in patients with
  cirrhosis of the liver Med J 1989299 1202-3

83
Nutritional Management of End Stage Liver Disease

• Eating Pattern
• A modified eating pattern should be recommended
  to all patients with ESLD.
• This would include eating at regular intervals
  perhaps 5-7 small HP/HE meals/snacks per day
• Include a pre-bedtime HP/HE snack to provide
  substrate for the liver to work with during sleep
  (supplements)

84
Ascites

• Patients with ascites usually have a high total
  body sodium but often have a low se sodium
• Generally have a poor intake secondary to
  abdominal distension
• Early Satiety
• Delayed gastric emptying
• Frequent snacking important to achieve high
  energy intake

85
Ascites

• Sodium restricted diet. Most common restriction
  is a no added salt diet which can range between
  50Mm Na and 100Mm Na
• Diuretics. Most commonly used are Lasix and
  Aldactone.
• Salt substitutes contraindicated due to potassium
  sparing effect of aldactone

86
Ascites

• Fluid restriction
• Moderate (1500ml )to severe ( 800ml)
• 800ml used to treat intractable ascites
  unresponsive to diuretic therapy or when diuretic
  therapy no longer possible due to compromised
  renal function
• Dont measure custards, ice cream

87
Oesophageal Varices

• Varices can occur at any point along the GIT
• Oesophageal varices may bleed easily and bleeding
  further compromises the patient's nutritional
  status

88
Oesophageal Varices

• Varices can occur at any point along the GIT
• Oesophageal varices may bleed easily and bleeding
  further compromises the patient's nutritional
  status

89
Oesophageal Varices

• Following an oesophageal bleed the patient will
  be nil by mouth
• Varices will be banded
• Oral intake recommenced when patients condition
  stabilises

90
Oesophageal Varices

• When allowed to eat patients should be advise to
• Eat carefully and avoid large bolus of food which
  might dislodge a clot
• Avoid over distension of the stomach which might
  lead to regurgitation or vomiting
• Avoid foods with sharp bones that might be
  accidentally swallowed

91
Diabetes in Liver Disease

• Patients with ESLD may present with impaired
  glucose tolerance. This may be due to a number
  of factors
• Depleted hepatic glycogen stores
• Impaired glucose tolerance
• Hyperinsulinaemia
• Insulin resistance

92
Diabetes in Liver Disease

• Management involves diabetic education without
  restriction of energy intake
• Insulin therapy
• BCAA supplementation has been shown to facilitate
  control of blood sugar levels in patients with
  ESLD

93
Nutritional Management of End Stage Liver Disease

• Achieve and maintain high energy intake(35-40 non
  protein kcal/kg/day)
• Achieve and maintain a high protein
  intake(1.0-1.5g/kg/day)
• Avoid unnecessary fat restriction
• Encourage frequent snacking

94
Nutritional Management of End Stage Liver Disease

• Restrict dietary sodium intake in the presence of
  ascites and/or oedema
• Restrict fluid intake to assist in the management
  of ascites/oedema associated with hyponatraemia

95
Nutritional Management of End Stage Liver Disease

• Consider branched chain amino acid
  supplementation
• Significant pre-bedtime snack

96
Nutritional Response to Hepatic Transplantation
97
Hepatotoxicity of Herbal Remedies

• Herbs are potent medicines
• The community is increasingly seeking out
  alternative or natural therapies
• Patients with hepatitis C frequently seek out
  alternative therapies

98
Hepatotoxicity of Herbal Remedies

• Important to be aware of the possible harmful
  effects of herbs
• Some herbs are hepatotoxic and patients with
  known liver disease should avoid using them

99
Nutritional Management of NAFLD

• Treatment centres around reducing insulin
  resistance
• Dietary intervention
• Increased physical activity
• Metformin

100
Nutritional Management of NAFLD

• Weight loss strategies in presence of
  overweight/obesity. Weight loss results in
  improved lipid and carbohydrate metabolism.
• Weight loss must be slow. Rapid weight loss
  results in worsening liver function tests and
  hepatomegaly
• Rapid weight loss may promote or worsen NAFLD,
  NASH and may result in liver failure

101
Nutritional Management of NAFLD

• Normal weight subjects dietary and
  pharmacological treatment of altered lipid and
  /or carbohydrate metabolism
• In overweight individuals with elevated
  aminotransferase levels weight loss of 10 or
  more corrects aminotransferase levels and
  decreases hepatomegaly

102
Nutritional Management of NAFLD

• Modification in lifestyle which involves weight
  reduction and regular exercise are the mainstay
  of treatment and prevention of NAFLD

103
Nutritional Management of NAFLD

• Summary
• There is no quick fix and there are no gimmicks
  for the consumer
• Weight control
• Increased exercise/physical activity
• Good Diabetic control
• Manage lipid abnormalities