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NUTRITION in COPD

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NUTRITION in COPD Dr. T lay YARKIN 25.04.2008 TOPICS Terminology Prevalence in COPD Effect on prognosis Potential mechanisms of malnutrition in COPD Therapeutic ... – PowerPoint PPT presentation

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Title: NUTRITION in COPD


1
NUTRITION in COPD
  • Dr. Tülay YARKIN
  • 25.04.2008

2
TOPICS
  • Terminology
  • Prevalence in COPD
  • Effect on prognosis
  • Potential mechanisms of malnutrition in COPD
  • Therapeutic interventions

3
TERMINOLOGY
  • Malnutrition a state of nutrition in which a
    deficiency or excess of energy, protein, and
    other nutrients causes measurable adverse effects
    on tissue/body form and function, and clinical
    outcome
  • Undernutrition deficient energy or protein
    intake or absorption (protein energy
    malnutrition)
  • Wasting involuntary loss of body weight and
    decline of muscle strength. (is not etiologically
    or pathologically different from undernutrition)
  • Sarcopenia a state of loss of muscle mass
    specifically occurring in bedridden, immobile or
    elderly patients

4
Severe Nutritional Risk
  • As the presence of at least one of the following
    criteria
  • weight loss gt1015 within 6 months,
  • BMI lt18.5 kg/m2,
  • Serum albumin lt30 g/l (with no evidence of
    hepatic or renal dysfunction).

5
Cachexia
  • Wasting in life-threatening diseases such as
    cancer, AIDS, COPD, and advanced organ failure
    where it is defined by a documented
    non-intentional weight loss of more than 6 in
    the previous 6 months, accompanied by catabolic
    conditions and resistance to increased substrate
    intake.

6
Pulmonary Cachexia Syndrome
  • Malnutrition associated with advanced lung
    disease
  • Associated with an accelerated decline in
    functional status
  • The prevalence in COPD pts 20-40
  • An independent predictor of mortality

7
Association Between Nutritional Status and
Prognosis in COPD
  • Wilson et al. (Am. Rev. Respir. Dis.1989) In a
    study of 779 men moderate to severe
    COPD,described body weight for height and
    all-cause mortality as inversely related
  • Gray-Donald et al (Am. J. Respir. Crit. Care Med
    1996) In a study of 348 patients with severe
    COPD, found low BMI to be a strong predictor of
    death from respiratory causes

8
All causes of mortality
COPD-related mortality
9
semistarvation
cachexia
muscle atrophy
normal nutr. muscle atrophy


semistarvation
cachexia
Median survival was less in pts with cachexia and
muscle atrophy than in pts with semistarvation or
no impairment (plt.001)
Cachexia was more prevalent in GOLD stage IV than
in stage II or III (plt.001)
10
Underweight increased with increasing severity of
COPD, especially in women
Mean FFMI 16.0 kg/m² for women, 18.7 kg/m² for
men FFMI decreased with increasing severity of
COPD Prevalence of a low FFMI depended on cut
points
11
Among subjects in stages 3 and 4 with normal BMI,
approximately 50 had low FFMI
In the group with normal BMI, a low FFMI was also
associated with mortality
12
Mechanisms of Malnutrition in COPD
13
CHRONIC ILLNESS
Starvation
PROTEIN-ENERGY MALNUTRITION
ACUTE ILLNESS Infections Sepsis Hospitalization Re
spiratory failure
HYPOALBUMINEMIA STRESS-related CATABOLISM
Inflammatory response
Increased infection rate Gut dysfunction Hormonal
response Increased metabolic rate
14
Malnutrition is multifactorial in COPD
Genetik Predispozisyon
15
Increased Metabolism
  • Basal metabolism in COPD pts does not follow the
    expected age-related decline seen in normal
  • REE is found to be 10 higher than normal
  • Hypermetabolism depends on increased WOB The
    cost of energy for breathing is 10 times higher
    in COPD pts (N 36-72cal/g)
  • The oxygen cost of exercise is higher Due to
    fibre-type shift in skeletal muscle from type I
    to II
  • Despite hypermetabolism, COPD pts have a reduced
    caloric intake

16
associated GI problems
lost of apetit
dyspnea
infections
Powerty
Insufficient nutrient intake
Prolonged starvation
Enhanced glycogenolysis Depletion of glycogen
stores within 1-2d
Intense gluconeogenesis Mobilization of fat and
protein muscle stores
17
Inflammation
  • Any acute or chronic inflammation can contribute
    to weight loss
  • Elevated TNF-a is associated with cachexia
  • sICAM ve soluble TNF reseptors are elevated and
    inversely correlate with caloric intake
  • Inflammatory immune activation (higher levels of
    IL-6, and an increased IL-16/IL-10 ratio)
  • Acquired GH resistance, and insulin resistance

18
Acute Attacks
  • Infection
  • Systemic inflammatory response
  • Hospitalization
  • Developing respiratory failure
  • Intensive care and invasive mechanical
    ventilation

19
Genetic Predisposition
  • Studies about genes encoding proinflammatory
    molecules have been performed
  • A -511 polymorphism in the IL-1ß gene has been
    found strongly correlated with cachexia
  • (Broekhuizen et al. Am J Clin Nutr 200582)
  • CC genotype associated with cachexia
  • TT genotype was not associated
  • CT genotype had an intermediate
  • association
  • The association with IL-1ß is tantalising !!

20
Genetic Predisposition
  • Another polymorphism associated with cachexia is
    in the bradykinin reseptor (Hopkinson et al. Am J
    Clin Nutr 200683)
  • ACE gene polimorphism related to the muscle
    strenght (Hopkinson et al. AJRCCM 2004, Gosker et
    al. AJRCCM 2004)
  • No polymorphism have been found in TNF-a and IL-6
    gen (Broekhuizen et al. Am J Clin Nutr 200582)

21
Therapeutic Nutritional Approach
22
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23
Malnutrition is multifactorial in COPD
24
Main Therapeutic Interventions
  • Nutrition
  • Exercise
  • Oxygen
  • Anti-inflammatory drugs
  • Anabolic hormones
  • Suggested or tested treatments
  • Wagner PD Eur Respir J 2008

25
Nutrition
  • What is the role for nutritional enhancement?
  • Is it effective on prognosis or quality of life?
  • Which preparations should be given?
  • Should it be started in the earlier stages?
  • What is the role of appetite stimulation?
  • Anabolic steroids?
  • Should the vitamines and the
  • other micronutrients be added?

26
Prestratification
Depleted
non-depleted
Randomization
Nutrition Anabolic st
Placebo
Placebo
Nutrition
Nutrition
Nutrition Anabolik st
Exercise
Exercise
Primary outcome
  • Weight
  • Fat-free mass
  • Maximal insp mouth pressure
  • 12 minute walking distance

48 mo
2 mo
Secondary outcome
Overall mortality
27
Nutritional intervention resulted in a
significant increase in weight, fat-free mass,
and fat-mass, whereas no significant changes in
any of these parameters was seen in the placebo
group Relative to a similar body weight gain as
the group receiving nutritional support only,
the anabolic steroids group showed a larger
increase in fat-free mass and maximal inspiratory
mouth pressure without causing adverse side
effects No significant difference between the
treatments on survival was shown
28
Cochrane Database of Systematic Reviews 2005,
Issue 2. Art. No. CD000998
  • Nutritional support had no significant effect on
    anthropometric measures, lung function or
    exercise capacity in patients with stable COPD
  • Although some quality of life indices gave
    significant findings, these results were from a
    single small unblinded study and restricted to
    certain domains of health status measurements
  • More work in this particular area is needed to
    establish whether supplementation can lead to
    subjective benefits in quality of life

29

Effects of High- and Low-Carbohydrate Meals
  • Hughson and Kowalchuk (Respir Physiol 1981 46)
    demonstrated that normal young female subjects on
    a low CHO diet had a lower VCO2 and respiratory
    exchange ratio (R) than did those on a high CHO
    diet
  • Frankfort and Fischer (Chest 1991100) suggested
    that meals with higher fat and lower CHO content
    are less likely to impair the work performance of
    patients with CAO than are meals with a lower fat
    and higher CHO content

30
The Effects of High-fat and Highcarbohydrate Diet
Loads on Gas Exchange and Ventilation in COPD
Patients and Normal Subjects Kuo et al.

Chest 1993104
31
P lt 0.05
- - - CH-rich Fat-rich
? CH-rich Fat-rich
Differences between post- and preprandial
shortness of breath score on a VAS after
consumption of a nutritional supplement
RQ postprandially and during exercise after a
nutritional supplement
32
Recommendations
  • Mixed carbohydrate-fat diets in which fat
    comprises 20-40 of the total calories should be
    preferred
  • The use of very high fat (gt40) or very low fat
    (lt15) diets is not recommended
  • Very high fat is poorly tolerated and can result
    diarrhea and abdominal discomfort
  • Very low fat increases CO2 production and does
    not deliver enough essential fatty acids

33
Exercise
  • Inactive older patients demonstrate significantly
    greater loss of muscle mass
    (Klitgaard. Acta Physiol Scand 199014041)
  • Physical activity influences myocyte protein
    synthesis
  • Regular exercise improves the effectiveness of
    nutritional therapy and stimulates appetite
    (Schols. Clin Chest Med 200021753)

34
Anti-inflammatory Drugs
  • N-acetyl cysteine To reduce oxidative stress
    markers and to improve exercise endurance time
  • Eicosapentaenoic acid To reduce proteolysis
    inducing factor
  • Inhaled steroids and bronchodilators As
    modulators of inflammation and thereby as agents
    to prevent or reverse cachexia
  • (Wagner PD. ERJ 200831492)

35
Anabolic Hormones
  • Treatment with GH and insuline-like GH have been
    studied in COPD pts Fat-free body mass was
    increased without any benefits to skeletal muscle
    function
    (Burdet.Am J Respir Crit
    Care Med 1997)
  • Anabolic steroids (nandrolone and oxandrolone)
    have similar outcomes (Creutzberg. Chest
    2003 Yeh. J Am Geriatr Soc 2003)
  • GH-releasing factor (ghrelin) has been found to
    increase FFM and increase the distance patients
    can cover in the 6-min walk test
    (Lainscak Intern Med 2006 Nagaya. Chest 2005)

36
Ancillary Treatments
  • NPPV appears to result in a gain in total body
    mass (Budweiser. Respir Care
    200651126)
  • Creatine supplementation has been reported to
    produced increased FFM and to lead to improved
    muscle strength (Fuld. Thorax 200560531)
  • There is some evidence that a diet rich in
    omega-3 PUFA improves skeletal muscle function in
    COPD (Matsuyama. Chest 20051283817)
  • ACE inhibition has also been suggested as a
    treatment for cachexia (Wagner PD. Eur Respir J
    2008)

37
General Princeples
  • Adequate calories to meet basal energy
    expenditure
  • Small, frequent meals with nutrient-dense foods
    (eg, eggs)
  • Meals requiring little preparation (eg,
    microwaveable)
  • Rest before meals
  • Daily multivitamins
  • Megestrol acetate trial to increase appetite

38
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39
CONCLUSIONS
  • Malnutrition is a common problem in COPD pts
  • It is associated with an accelerated decline in
    functional status and an independent predictor
    for murtality
  • Due to the multifactorial mechanism, treatment
    should have several components
  • Further studies are necessary in the treatment of
    pulmonary cachexia

40
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