British Medical Bulletin (1981) Vol. 37, No. 1, pp.

19-24

BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS WA Coward&PGLunn

but they do not, in any way, distinguish causes in the same
manner that the term protein-energy malnutrition quite
specifically suggests a dietary cause.
We can therefore make clinical distinctions between kwashi-
THE BIOCHEMISTRY AND orkor and marasmus, but the object of many experimental
PHYSIOLOGY OF KWASHIORKOR studies, and of dietary surveys in different parts of the world,
has been to find differences in their dietary aetiology. It is well
AND MARASMUS known that it is necessary to feed experimental animals
unrestricted amounts of diets low in protein to produce a
W A COWARD PhD syndrome resembling kwashiorkor; restricting the intake of any
diet will result in severe wasting. Survey work in Uganda
P G LUNN PhD (Whitehead et al. 1977) also showed that, when diets with a
wide range of protein: energy ratios are available within a
University of Cambridge
and community, it is the children who habitually consume diets from
Medical Research Council the low end of the range (protein: energy, 0.04-0.06) who are at
Dunn Nutritional Laboratory, Cambridge risk of developing kwashiorkor. These observations contrast
with others typified by those of Gopalan (1968). He showed
that, in Indian children eating cereal-based diets with a relatively
Concepts and definitions: protein-energy malnutrition, constant protein: energy ratio (0.08), either kwashiorkor or
kwashiorkor and marasmus marasmus could emerge if energy intakes were low. Taking
Adaptation to a deficiency of energy: the pathogenesis of extreme views would therefore suggest that kwashiorkor and
marasmus marasmus represent different aspects of the same disease (as the
Failure of adaptation to protein deficiency: the pathogenesis
term protein-energy malnutrition suggests) or that they are
of kwashiorkor
Pathogenesis of intermediate forms of protein-energy different diseases with distinguishable aetiologies.
malnutrition Protagonists of each idea have ample support for their
Regulation of body fluid volumes in protein-energy arguments but it is unrewarding to initiate a discussion of the
malnutrition aetiology of kwashiorkor and marasmus by emphasizing one
a The distribution of extracellular fluid volume theory to the exclusion of the other. A more realistic approach
b Sodium and water balance is to accept that each idea makes a worthwhile contribution in a
c Membrane defects and the sodium pump
worldwide context but that causes can differ in individual,
Plasma proteins in kwashiorkor and marasmus
References regional circumstances.

It is just four years since Alleyne et al. (1977) published their 2 Adaptation to a Deficiency of Energy: the Pathogenesis
comprehensive treatise on protein-energy malnutrition. In this of Marasmus
paper we will focus on a few developments in biochemistry and
physiology that we believe are important for our understanding It is now widely accepted that the severe wasting seen in
of how the clinical features of the disease emerge in children marasmic children represents the end-product of metabolic
subjected to a hostile environment and inadequate diet. adaptation to an inadequate energy intake, mediated by changes
in hormonal pattern. Although a child is not clinically identified
as a case of marasmus until weight-for-age falls below 60%, the
1 Concepts and Definitions: Protein-Energy Malnutrition,
relevant metabolic changes can be detected, within a community
Kwashiorkor and Marasmus
where marasmus occurs, well before this stage is reached.
In recent years it has been customary to use the term Whitehead et al. (1977) and Lunn et al. (1979a) showed that
"protein-energy malnutrition" to describe a group or spectrum fasting plasma cortisol and growth hormone (GH) levels were
of diseases that often affect children living in poor communities high but insulin concentrations were low in Gambian children
in most developing countries. The expression suggests impor- with faltering growth rates, and insulin: cortisol ratios were
tant concepts. These are that inadequate intakes of energy or strongly correlated with growth velocities (Lunn et al. 1979a).
protein, or both, are causative factors and that there is a The changes seen when children are admitted to hospital
continuous connection in terms of biochemistry and physiology (reviewed by Alleyne et al. 1977) are only more exaggerated
between the extreme forms of protein-energy malnutrition, examples of the same pattern.
which are kwashiorkor and marasmus. A reduction in plasma insulin concentration is a normal
For comprehensive clinical descriptions of the two syndromes response to a reduced food intake and extremely low values are
the reader may refer to Alleyne et al. (1977), but for the present seen in marasmic children admitted to hospital. Cahill (1970)
it will be sufficient to use a series of internationally accepted suggested that a decreased level of this hormone is the main
definitions suggested by a Wellcome Trust Working Party regulator for the release of energy metabolites from endogenous
(Lancet, 1970). The crucial diagnostic features are the degree sources. Raised plasma cortisol concentrations will augment
of body wasting and the presence of oedema. Thus, when the effect on the mobilization of skeletal muscle protein,
Harvard weight standards (Stuart & Stevenson, 1959) are used, releasing amino acids for gluconeogenesis and perhaps for the
children of 60-80% expected weight-for-age are called cases of hepatic synthesis of plasma proteins. Adipose tissue
kwashiorkor if oedema is present. Below 60% the diagnosis is mobilization will be enhanced by changes in GH concentra-
marasmic kwashiorkor if they have oedema or marasmus if tions, and free fatty acids will become available as alternative
oedema is absent. These definitions have the merit of simplicity sources of energy (Parra et al. 1973).

19

Vol. 37 No. 1

where children can develop either kwashiorkor orkor. becomes easier to understand. 1977). Lunn et al. Philbrick & Hill. marasmus because they fail. However. as values 3 Failure of Adaptation to Protein Deficiency: the will be influenced by the duration and severity of the clinical Patbogenesls of Kwashlorkor phase of the illness. If the excess energy is not removed. 1979). or marasmus on identical diets. hied. 1977). Bull. endemic. information on thyroid hormone concentrations was obtained. blood Although plasma cortisol concentrations are elevated • in glucose concentrations will tend to rise and result in hyper. 1973). Kajubi & Okel. since lowering the basal metabolic rate described as apathetic and anorexic and the hormone profile is will conserve the meagre supplies of energy available. 1974.BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS W A Coward & P G Lunn Reductions in the plasma concentration of thyroid hormones cance of a high variability in the unrelated individual require- have also been reported for marasmic children admitted to ments for protein and energy. to produce including albumin and apo-proteins for (J-lipoprotein synthesis. Data from Jordan determine the kind of protein-energy malnutrition that even. 1968. Fasting plasma insulin concentrations in these GH concentration is elevated and thyroid hormone concentra- children were higher than in children who had recovered from tions are either normal or reduced (Alleyne et al. that there are other more (Coward et al. The impaired glucose tolerance (Vance et al. Children with all forms of protein-energy malnutrition have a When the low protein content of a diet limits growth there poor insulin response to a glucose load (Alleyne et al. 20 Br. In general. feedback stimulus for GH release (Mohan & Jaya Rao. but there are some features not Plasma cortisol and GH levels were not elevated. anorexia and hypoglycaemia. If true. (1973) showed that this response occurs Enwonwu & Sreebny. assessed by plasma albumin concentrations (Pimstone el al. 1971. 1973) that impaired somatomedin production might cause a Waterlow (1974) has previously pointed out the likely signifi. The course taken may ultimately faster return to a normal insulin respose. 1968). 1977). 1971) tually develops (see MacLean & Graham. but a number of possibilities are (James & Trayhurn. Lunn el al. then the situation described by Gopalan somatomedin concentrations are low in children with kwashi- (1968) in India. Although plasma to low-protein diets. There need. It must be a relative excess of energy. already in short supply. because of in- Rats do not respond to low-protein diets in this way and adequate food intakes. malnutrition. By promoting muscle protein found in marasmic children with the same degree of anorexia synthesis. high insulin concentrations will deplete the plasma of and infection. 1974). the appearance of kwashiorkor in children who. cortisol values are often elevated complete source of information on the hormonal profiles of and correlate with the degree of wasting and the severity of pre-school children living in an area where kwashiorkor is intercurrent infections (Abbassy et al. 1968) and Turkey (Giirson & Saner. (1973). These non-essential amino acids typical of the developmental phases of results suggest that a defect in the adrenals' ability to produce kwashiorkor (Grimble & Whitehead. 1973. (Hopkins et al. they are usually lower than those insulinaemia and fat deposition. effect. even when energy intakes could be argued that this might be expected in a child whose are lower than recommended requirements. might otherwise be expected to become instead have a much reduced plasma insulin concentration marasmic. very different from that which existed earlier in his illness but much more like that found in marasmus. 1967). 1979). problem of adaptation is how to deal with the energy excess. amounts of cortisol adequate for adaptation to protein-energy Hypoalbuminaemia could lead to defects in body fluid homo. There is also an inverse relationship Edozien. 1981) also exists in the response of children discussed by Pimstone et al. We believe. Thus the rat is a poor model for kwashiorkor and a few days of feeding meals containing protein (Pimstone el al. 1970). (1973) in Uganda remains the most are reduced but can be normal. 1977). 1967. 1977) and a markedly elevated tri-iodothyronine likely explanations (see section 4). However. Locking away cortisol may be a feature of kwashiorkor. is the one adopted. hospital (Alleyne et al. 1979) can this adaptation between GH levels and the severity of protein deficiency as be overcome. 1981 . and by inhibiting Synacthen (synthetic P'~24 adrenocorticotrophic hormone) gluconeogenesis will cause an accumulation of alanine and other results in a poor response (Jaya Rao et al. Tulp et al. it would explain to a fatty liver. however. only by feeding diets virtually free of protein (Edozien. There can be only two options: energy can be stored as fat or it potassium supplementation of rehabilitation diets results in a can be removed by oxidation. in South African children. children with kwashiorkor. and stimulation of the adrenal cortex with essential amino acids. and much higher than those found in Gambian changes described are in most cases the expected responses to pre-school children of the same age (Whitehead et al. Fiorotto & Coward. be no hypoglycaemic stress and consequently no shown that short-term fasting in healthy subjects results in elevation of plasma cortisol or GH to cause wasting. The considerable variation that exists between reports is not surprising. and deficiencies in (J-lipoprotein synthesis dietary ideas we have already outlined. 1968). but this was not found to be the case in Egyptian children school children indicates that the first of these possible pathways (Carter et al. 1979). The mechanisms we have discussed are clearly similar to 1968. The malnutrition. This latter Plasma GH concentrations are high in children with response enables the animals to "burn-off' any energy excess kwashiorkor and are not reduced by glucose loads (Pimstone et and will prevent the development of changes we have described al. (1975) have shown that. 1978. there is no evidence to support the suggestion (Grant el al. Robinson et al. Anthony & even after a single meal. metabolism is geared to survival. This view is substantially different from the eostasis and oedema. indicate that adding chromium to the diet produces a similar The endocrine pattern in non-hospitalized Ugandan pre. but no fully understood. 1968). 1975. Mann et al. from an early stage. plasma insulin concentrations The study of Lunn et al. level (Edozien et al. 1968). and certainly it has been therefore. it has been demonstrated that they fall after in children. Jaya Rao (1974) essential amino acids in muscle when protein intake is low is proposed that some children develop kwashiorkor rather than likely to produce a fall in hepatic synthesis of export proteins. if the mechanisms regulating plasma GH concentrations in kwashi- considerable degree of individual variation to over-eating orkor have not been identified. This change can be regarded as A child admitted to hospital with kwashiorkor is usually an effective adaptation. The those involved in the development of obesity and.

ments with sheep (Rabinowitz et al. At this stage any (M Fiorotto & W A Coward. or protein deficiencies. In these cir- metabolic features of marasmus. However. 37 No. control over the distribution of extracellular fluid volume will be Finally. They observed that. For example. as a result of the alternating dominance of energy leadingly large. it is prevent plasma volume contraction but. plasma albumin concentrations will fall kwashiorkor can develop. activity in oedematous malnourished rats but not in non- This represented a proportionally larger change in interstitial oedematous animals. interstitial volume expansion will occur. published data show that renal plasma flow (RPF) and glomerular filtration rate (GFR) are decreased but. 1979). (1975a) found increased plasma renin content of interstitial fluid that matched the changes in plasma. Srikantia (1968) postulated a role for antidiuretic 21 Vol. when plasma protein rates in malnourished children but plasma concentrations were concentrations fall in protein-deficient rats. although Van der water filtration. al. BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS WA Coward & P G Lunn Since plasma GH concentrations rise only in the terminal stages lost. the homoeostatic mech. sodium retention could result from a The Distribution of Extracellular Fluid Volume elevated plasma aldosterone levels and increased plasma renin Coward & Fiorotto (1979) and Fiorotto & Coward (1979) activity but. 1968). it is more insistence that changes in plasma albumin concentration are likely that non-nutritional factors modulate the effects of the functionally important in the development of kwashiorkor and diet. While protein-energy malnutrition have elevated plasma renin ac- this adaptation to hypoproteinaemia is effective over a large tivities. the concept that children with kwashiorkor are over-hydrated We have also recently suggested (Lunn et al. they are not specifically associated with the presence The appearance of oedema in malnourished children is an of oedema in children (Alleyne. cumstances the task is to identify the reasons for phases of oedema and hypoproteinaemia have appeared precipitously as a sodium retention in malnourished children. 4 Pathogenesis of Intermediate Forms of Protein-Energy 1977) show that this is the case. effects of diet and accelerate wasting in children developing marasmus. further early pathogenesis of this disease. In addition. 1 . At the tubular level. Furthermore. Klahr & Alleyne (1973) identified factors that causes of such losses are a measles infection or the presence of could impair the ability of malnourished children to excrete intestinal helminths. because in normal animals the Westhuysen et al. Active renal salt and water retention might then occur to of the development of kwashiorkor (Lunn et al. in the face of the unlikely that GH-mediated changes are directly involved in the circulation's reduced ability to hold retained fluid. contradicting much of the Malnutrition earlier work. but Fiorotto and W A Coward. result of an increased gastrointestinal loss of plasma proteins. by the recognition that the contribution of albumin to the total A conventional view was outlined by Whitehead & Lunn colloid osmotic pressure of plasma (>50%) is greater than that (1979). interstitial fluid protein oedema was present. Worthington et range of plasma protein concentrations. marasmic kwashiorkor might emerge The development of these ideas was stimulated by an (Whitehead & Alleyne. 1979b) that and suggests that. However. With only one exception (Srikantia. Alternatively. when plasma monkeys fed low-protein diets and found elevated levels when protein concentration is reduced by half. in practice. (1977) measured plasma aldosterone concentrations in anism does not possess infinite gain because. evidence for a specific association with the believe that the most important factors are those that determine presence of oedema is ambiguous. This idea indicates that blood and plasma volumes will be reduced in kwashiorkor and the most recent observations with labelled erythrocytes (Viart. The differences could be attributed to different We have suggested that the endocrine response to a diet can methodologies. preventing excessive those with kwashiorkor. sodium loads. because albumin synthesis admitted to hospital with oedema have the underlying rates are unalterably low (Patrick. again. idea begins with kwashiorkor. and it is theoretically volumes measured with protein-bound tracers could be mis- possible that. a normal balance of normal in children with marasmus and elevated in only half of transcapillary colloid osmotic pressures. 1973). 1975b) showed that children suffering from plasma: interstitial fluid concentration ratio is about 2. but our own serial studies with baboons concentrations reach values close to zero. not In a review of the effects of protein-energy malnutrition on compensated for by increased rates of protein synthesis. We believe that many children with the development of oedema. in preparation) showed that further reduction in plasma protein content will produce an changes in aldosterone concentration and plasma renin activity imbalance of the transcapillary forces and the organism's can precede the appearance of oedema by many months. was maintained by a reduction in the colloid Westhuysen et al. Superimposed on these. experi- example of a failure of homoeostasis that specifically dis. two distinctly different views can now be low-protein diets and are not associated with evidence of identified. excessive salt and water retention. 1972). the same group of workers (Van der fluid protein concentration. or perhaps complementary. while these 5 Regulation of Body Fluid Volumes In Protein-Energy changes will undoubtedly limit the potential for salt and water Malnutrition excretion. Migeon et al. in preparation) have shown that until recently little progress had been made in identifying its reductions in RPF and GFR are early effects of feeding cause. irrespective of the presence of oedema. the distribution of extracellular fluid between the vascular and (1973) found either normal or increased aldosterone secretion interstitial spaces. Likely renal function. 1973) and baboons (M tinguishes kwashiorkor from other forms of malnutrition. 1967). severe wasting could be induced in b Sodium and Water Balance children who are otherwise likely to present as cases of The alternative. but other abnormalities occur and elevate plasma glucocorticoid concentrations will alter the their importance has to be considered. It was proposed that the incidence of infections that of any other plasma protein. Viart suggested that in malnutrition plasma determine how available nutrients are used. when a malnourished child develops sodium there may be another important way in which marasmic and water retention.

secondly. Observations made by Patrick et al. Our general view is that malnutrition because of its rapid response to refeeding in there is a need to separate the influence of those factors malnourished children. marasmic children fed high-energy diets increase their are likely to be less ambiguous. (1971) showed that low transferrin concentrations were could cause increased fractional sodium resorption. and in these circumstances other indices of malnutrition However. the the interstitium and cells. In this way it is possible to build normal children. al. since the plasma con- tubule cell physiology in malnutrition. we can describe the "sensitivity" of a particular Patrick (1979) commented on the significance of changes in protein in malnutrition without simultaneously considering membrane permeability and the activity of the sodium pump in nutrient intake or the final form of malnutrition that emerges.23-30 of thiiBuBttm. changes in its plasma environment in the renal medulla needed for salt and water concentration should be meaningful in terms of the ultimate reabsorption in later segments. 1978. S « Nirumg* R«o. Furthermore. because their concentrations are greatly 1 1 See Golden & Golden. other workers report even indicators of nutritional status (Ingenbleek et al. malnutrition. Bull. However. In the first instance it should be responsive to synthesis would lead to the dissipation of the hypertonic changes in nutrient intake and. It is the transport rates of sodium in kwashiorkor.—ED.and substrate-dependent component) but (Kaplay. and in protein deficiency reduced rates of urea for malnutrition. the problem of the relationship of these and Reeds & Laditan (1976) extended this observation to changes to dietary and environmental causes of kwashiorkor. The connection between these observations and those 6 Plasma Proteins in Kwashiorkor and Marasmus showing that fractional sodium reabsorption can be decreased in malnourished oedematous children (Alleyne. in experimental animals (Olusi et al. 1965. Thus excessive sodium and pathology of protein-energy malnutrition. produce substantial changes in rates of plasma protein synthesis. 1979) may be relevant. malnourished children can complicate the situation to the extent (1978) illustrate the problem. 1979) and erythrocytes synthesis (the diet. 1971.—ED. 1980) that measurement of plasma protein concentrations for the assess- hypoproteinaemia and low plasma oncotic pressure in the ment of nutritional status. remains. a thermogenic response involving nourished children although albumin concentrations were not increased sodium pumping might be relevant Others have also advocated the use of plasma transferrin It will be clear that we are some way from integrating all these concentration as a most sensitive index of protein-energy observations into a concise framework. 31-36 of this Bulletin. essentially because urine osmolality is regulative physiology will be able to explain these findings. if we accept water losses could be prevented only by reductions in RPF and that a low plasma albumin concentration specifically contri- GFR. higher values in oedema-free marasmic children (Hansen et al. where the functional significance c Membrane Defects and the Sodium Pump of changes in the concentration of a plasma protein is In following up lines of thought developed by Metcoff (1975). Ingenbleek et al. 22 Br. three plasma proteins results obtained for erythrocytes. Fondu et al. Delpeuch et al. but before discussing them it is peritubular capillaries would limit sodium reabsorption in the necessary to develop a concept that describes an ideal marker proximal tubules. the latter workers Trace element deficiencies1 could provide the link (Patrick. 1980). Wright & Briggs (1979) have recently reviewed the butes to oedema formation. however. PP. if mirrored at the level of the renal tubule. but it is suggested that centration of any protein is dependent not only on rates of findings for leucocytes (Patrick.and length-for-age in under- significant dietary component. (1969). rates of intravascular- leucocytes it was shown that there were dramatically increased extravascular exchange and the degree of hydration. ouabain-sensitive Na-K adenosinetriphosphatase activity is thyroxine-binding prealbumin (TBPA) and retinol-binding pro- increased (compared with normal and recovery values) in tein (RBP). 1981 . 1980). pp. showed that serum transferrin concentrations were linearly 1980) or. There associated with a poor prognosis in children with kwashiorkor. In these circumstances the manner in which convenient to classify children according to their albumin the kidney regulates salt and water balance in relationship to concentration and to relate other biochemical changes to these intake may not have the precision of response available in values (Whitehead et al. Delpeuch et al. and sensitivity to reduced protein intake responsible for the distribution of body water between plasma. never elevated in malnourished children. The protein-energy malnutrition. 1972. are compatible with these McFarlane et al. 1975). but this idea has not been 1965). up a comprehensive picture of the development and resolution of kwashiorkor. In contrast to this situation. Children with kwashiorkor can that a decrease in transferrin concentration caused by mal- lose their oedema and decrease their total body water from 77% nutrition can be masked by an increase due to a lack of iron to 63% of body weight when they are fed diets not known to (Ismadi et al. which could be balance between these processes that determines whether the achieved only by an increase in membrane permeability to concentration of a specific protein reflects the degree of sodium and subsequent stimulation of the sodium pump. recognized. hied. Thus. However. and those controlling the general frequency with which iron-deficiency anaemia2 occurs in degree of hydration. For also on utilization and catabolism. 1975. It could be argued (Fiorotto. where it was found that have consistently attracted attention: these are transferrin. if an energy intake in excess of requirements is a related to deficits in weight. total body water from 64% to over 70% of body weight in 14 Plasma RBP and TBPA have also been proposed as sensitive days but oedema does not appear. It is unlikely that changes in only one aspect of universally accepted. it is clear that its measurement is evidence for the existence of a mechanism by which GFR in a useful in communities where kwashiorkor is the predominant single nephron is regulated by the composition or rate of flow of form of malnutrition. Nichols et There are a multitude of reports on the usefulness of the al. There is no information on this aspect of renal This strategy is inevitably empirical. kwashiorkor but not in marasmus. McFarlane et al. 1975. (1970) and Gabr et observations and. We have therefore often found it distal tubule fluid. 1973) is not clear. BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS W A Coward & P G Lunn hormone in oedema formation. 1973). include those with marasmus.

pp. peaking at 3 result of infection. The immunoglobulins (IgA. Ingenbleek Y.1313-1319 Coward W A S Fiorotto M (1979) Proc. but suggests that proteinase have recently investigated RBP and TBPA in children suffering inhibitor levels determine the extent to which a malnourished the combined effects of vitamin A deficiency and protein-energy child can mobilize endogenous proteins to provide amino acids malnutrition and have shown that. Makoui T & Switzer B R (1978)/. Niehaus N. Hay R W. Fiorotto M & Coward W A (1979) Br. Becker D & Pimstone B L (1973) Arch. London colloquium held in Cambridge. most concisely outlined by Schelp et are equally low in kwashiorkor.501-514 Clin. Nutr. Chim. marasmus and marasmic kwashiorkor. with an energy therapy. The theory. This result therefore indicates that RBP synthesis is less affected in marasmus than in We recognize that marasmus. 63. 39.917-919 203-211 Edozien J C.J. When proteinase inhibitor levels are high as a protein with the ligand retinol attached) increased. / . 101. Large et al. Soc. orkor. novel idea.106-109 108. albumin) essential for injection with vitamin A. 2. Thailand (Schelp et al. Brinkman G L & Bowie M D (1965) S. 37 No. but it needs related to the accumulated surplus of native RBP in the liver experimental investigation and further studies on malnourished before dosing. following intramuscular for the synthesis of proteins (e. diet-dependent although we may have an adequate knowledge of how and why proteins were subdivided into those that increased in concentra. Coward W A. awakening an interest in the latter disease. even though only a lipoprotein and complement). Clin. 1. Med. IgG and IgM) were gap rather than a protein gap. 1 . Ada. children with marasmic to disturbances in homoeostasis such as those found in kwashiorkor had intermediate values. Arnold. Susheela T P & Narasinga Rao B S (1971) Indian J. Churchill. Olson (1975) found it possible to distinguish view (McLaren. However.61-67 Fiorotto M (1980) Studies on oedema/unction in experimental protein-energy Ismadi S D. 43. University of London 216-221 Alleyne G A O (1967) Pediatrics (Springfield) 39. De Visscher M & De Nayer P (1972) Lancet. Med. 1977. April 1967). For (prothrombin. 1979) attach crucial 1979) indicate that TBPA and RBP concentrations are sensitive metabolic importance to changes in the plasma concentration of to changes in either energy or protein intake and this finding a1-antitrypsin and a1-antichymotrypsin in the development of supports the observations that TBPA and RBP concentrations malnutrition. In this respect. many aspects of the biochemistry and tion when only 1 g protein/kg body weight per day was fed physiology of kwashiorkor have not yet been explained.596-600 Carter J P. Nutr. Nutr. University of Cambridge 59. Nutr. is most important. Hyg. Edozien J C (1968) Nature (London) 220. 42. It was not possible convincingly minority of the world's malnourished children are likely to suffer to relate these differences in responsiveness to normal fractional from it. Trop. Ransome-Kuti O & Majaj A S (1968) Am. Child. (3. De Nayer P & De Visscher M (1975) Enwonwu C O & Sreebny L M (1971)/. Med.631-648 Grant D B. Schrieck Van den H-G. 38. transferrin. 1978. Zeitoun M M & Ragab M (1967)/. Res. 282. 105.918-921 Patwardhan V N (1968) Am. since vitamin A deficiency inhibits the release of children in other developing countries. Mar M-H. This is an intriguing. recognizes that kwashiorkor and marasmus are marasmus (Smith et al. J. (1978). Trop. RBP from the liver. Pediatr.115—126 491-195 Delpeuch F. Nutr. nutritional problem most frequently encountered by doctors In reviewing the relationship between diet and plasma protein working in developing countries. Clin. Nuxr. is the kwashiorkor. It would be wrong to suggest stresses interact to produce the diseases identified as kwashi- that RBP and TBPA are better indices than albumin concentra.51-59 Hansen J D L. 21. Mikhail M. (1980) metabolically distinct diseases. e d Calorie Alleyne G A O. / . malnutrition (Thesis for PhD degree). proconvertin.1581-1587 23 Vol. identified as diet-independent plasma proteins. Abd-FJ-Hadi K. J. so the authors considered that the peak concentrations provided some measure of the liver's ability to synthesize RBP from the outset. attention are the plasma proteinase inhibitors.g. Fondu P. Ogunshina & Hussain different indices from the dietary and metabolic points of view. Stanfield J P & Whitehead R G (1977) deficiencies and protein deficiencies.87-95. Dis. marasmic kwashiorkor and al. marasmus appears. Workers in metrically.400-411 Gopalan C (1968) In: McCance R A & Widdowson E M. The peak levels were lowest in kwashi. 21-31 13.J. plasma levels of holo-RBP (native homoeostasis. Clin. Jamaican children (Thesis for MD degree). 38. J. London Anthony L E & Edozien J C (1975) / . CahiU G F Jr (1970) New Engl. or to their sites of synthesis.375-379 Hopkins L L Jr. (1980) have also shown that TBPA concentrations decrease Another group of proteins that has recently attracted with increasing severity of malnutrition assessed anthropo. El-Hawary M F S & El-Dali M. 1974) that in a universal context it is necessary groups of proteins on the basis of the responsiveness to dietary to appreciate that a lack of nutrients in general. Elucidation of the mechanisms involved will not only or absolute rates of synthesis. Mandelbaum I M & Vis H L (1979) Am. However. Kattab A. 49—58 (Proceedings of a Protein-energy malnutrition. Picou D I. Nutr. 1767-1776 Ingenbleek Y. 74. Afr. B Gholmy A & GrimbleR F & Whitehead R G (1970) Lancet. Hambley J. Med. Nutr.(1971) / . REFERENCES Abbassy A S. we accept the concentrations. Experimental studies on obese women (Shetty et al. but will also provide a more complete usefulness of an index for malnutrition is defined only in terms of understanding of how nutritional and other environmental sensitivity to a dietary change. Nutr. BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS WA Coward & P G Lunn reduced in malnourished children admitted to hospital and tion and more appropriate to suggest instead that they are rapidly return to normal with refeeding. RBP and TBPA) and those this reason we have biased our discussions towards re- requiring larger protein intakes (albumin. The values achieved are kwashiorkor. but lead to improvements in the prevention and treatment of the differences illustrate the difficulties that exist when the nutritional disease. 21.195-202 Gurson C T & Saner G (\91\)Am. Whitehead R G & Lunn P G (1977) Br. rather than kwashiorkor. Cornu A & Chevalier P (1980) Br. Davis I T .721-722 Alleyne G A O (1965) Renal and cardiac function In severely malnourished Gabr M. it is possible that a balanced relationship hours after treatment. Nutr. Clin. between proteinases and their inhibitors is destroyed. 668-675 48. this leads orkor and highest in marasmus. 32. Nutr. 24. J. J. 1975).

28. Calorie McLaren D S (1974) Lancet. Klish W. London Mann M D.J. 230-232 1. 32. Med. Migasen* P. J. J. Protein-calorie malnutrition. Endocrine aspects of malnutrition: marasmus.302-303 Reeds P J & LadiUn A A O (1976) Br. pp. Adcock K J. 2. Barbezat G. Thanangkul O. 34. Bull. (1973) 24 Br. 65-85. 1. Pimpantha R.1729-1731 363-398* Viart P (1977) Am. Leitzmann C. Afr. Kanengoni E. Med. J. 203-211 (Proceedings of a MacLean W C Jr & Graham G G (1979). Nutr. 4. Schreura W H P & Supawan V (1977) Lunn P G. Buchanan K D & Williams R H (1968) /. 71. Becker D J & Hansen J D L (1973) pp. Nutr. /. Br.J.Nutr. Med. Bull. Med. Shoji E S. J.349-354 Ogunshina S O & Hussain M A (1980) Am. 21. Textbook of 33.. 1981 .69-76 Olusi S O. ed. Nutr. J. Nutr. 365-367 Nutr. Whitehead R G. 2. Robinson H.451-456 73-84 Schelp F P. Academic Press. Cole T J & Austin S (1979t) Br. Clin. Soc. 709-711 1333-1334 Jaya Rao K S. ed. Protein-calorie malnutrition. Kerr D & Picou D (1973) pp. 28.1200-1201 Pimstone B L. Migasen* P. 32. Int. 30.438-^44 Shetty P S. Dis. 39. (1975b) S. Beitins I Z. Thanangkul O & Olson R E (1980) Br.579-584 Rabinowitz L. Nutr. Lab.794-800 Waterlow J C (1974) Lancet. Hazlewood C F & Viteri F (1973) pp.255-263 Large S. 43.188-207 Lancet (1970) 2. Soc. J. Garcia G. Nulr. 2. Whitehead R G. J. ed. Nutr. Meyers C. Reddy S. 33. Nutr. Watrasiewicz K E. 49. Kowarski A & Graham G G (1973) In: Gardner LI Vance J E. Freedland R A & Avery E H (1973) Klahr S & Alleyne G A O (1973) Kidney Int. Stuart H C & Stevenson S S (1959) In: Nelson W E.393--W2 Schdp F P. Thanangkul O. Pongpaew P. Clin. Suttajit M. ed. Nutr. J. Dls. 38. Parra A. New York Whitehead R G & Lunn P G (1979) Proc. PA Metcoff J (1975) In: Olson R E.1217 Smith F R.63-66 Ada.107-116 Whitehead R G. McFarlane H. Neal G. Med. Clin. 37. Garza C. Clin. 73-90* Kaplay S S (1978) Am. 27. 72. Cuellar A Soc.4m. 399—424 (Proceedings of a Van der Westhuysen J M. R. 31. Nutr.43-^8 Pimstone B. Child. Academic Press. Adeshina H. Child. Clin.958-1006 Patrick J. Osunkoya B O & Adesina H (1975) Clin.55-61 pediatrics. Nutr. 49. Argote R M. Soc. Chim. 1. Kimzey S L. Pimstone B L. 12-61.189-195 & Nichols B L (1973) pp. 31. 290-297 kwashlorkor and psychosocial deprivation. Churchill. J. Hansen J D L & Murray P (1967) Lancet. Lunn P G A Rutishauser I (1977) Trans R. Glover J. Clin.4m. Gunther R A. Lunn P G. 29. April 1967).417-424 Phflbrick D J & Hill D C (1974) . Med. held in May 1973). 73. Pongpaew P & Migasena P (1979) Am. /. Philadelphia. pp. Nutr. 1. Med Bull.93-96 deficiencies and protein deficiencies. Pimstone B L & Hansen J D L (1975) Br. Clin. Reddy S. 31-43* Worthington B S. J. symposium. 45-72* 43.Med. Trop. Whitehead R G & Alleyne G A O (1972) Br. 41. Danforth E Jr & Horton E S (1979) /. Cocks T. 27. CA J. Jones J J & Van Niekerk C H (1975a) S. Coward W A.72-79 275-297.482^*87 Kajubi S K & Okel R M (1974) Am. J. Clin. 16.1799-1803 Mohan P S & Jaya Rao K S (1979)^rcA.Hyg. Supawan V. Hyg.813-818 ' For full bibliographic*] daaflj tec Migeon et at. Becker D J.712 Olson R E (1975) In: Olson R E. Nutr.61-68 751-760 Patrick J (1980) Lancet. Hay R W & Baker B A (1973) Br. Ahmed S I & Jacobton K L (1977) Nutr. Saunders. 38. Whitehead R G & Coward W A (1979b) Trans. 732-738 (1970) Br. 7th ed. 2. Jones J J & Van Niekerk C H Nichols B L. 129-141 Kidney Int. J.31-38 399-422 Schelp F P. Clin. Jung R T & James W P T (1979) Lancet. New York 1321-1332 Migeon C J. Alvarado 1. Whitehead R G. Rev. Coward W A & Lunn P G (1973) Lancet. 4. Cooke A R & Akene J R E (1975) Am. 109. Srikantia S G & Gopalan C (1968) Arch. Kroc Foundation. Cooke A & Gumey J M (1969) Lancet. Krupp P P. J. Goodman D S & Olson McFariane H. pp. Nutr. Canseco L./. & Amacher P. 62. Trop. Nutr.BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS W A Coward & P G Lunn James W P T & Trayhurn P (1981) Br.J. 38. 59. 3. Seakins A & Picou D I M (1978) Br. McFarlane H. pp. Nutr. Tulp O L. Suskind R.1415-1422 Med.766-767 Wright F S & Briggs J P (1979) Physiol. Nutr. Jaya Rao K S (1974) Lancet. Nutr. Hansen J D L & Murray P (1968) Am. 36. Santa Ynez. Clin.62-64 Van der Westhuysen J M. Afr. Reeds P J. Barbezat G. Patrick J (1979) Proc. Adcock K J. Jackson A A.268-270 Srikantia S G (1968) In: McCtnce R A & Widdowson E M. Pongpaew P & Schreurs W H P (1978) Am. Clin.1381-1387 colloquium held in Cambridge. Rep. Lunn P G. pp. ed.

Sign up to vote on this title
UsefulNot useful