A kwashiorkor case due to the use of an exclusive rice milk diet to treat atopic dermatitis.

Although several cases of severe hypoalbuminemia resulting from rice milk have been described in the past, today the use of rice milk without nutritional counseling to treat eczema is still a continuing, poor practice. We describe a kwashiorkor case in an infant with severe eczema exclusively fed with rice milk. It is well documented that rice milk is not a sufficient protein source. Moreover, only a small portion of eczema is triggered by food allergy. In conclusion this case raises the importance of managing dietary changes facing food allergies with responsibility for specialized consensus among pediatricians, nutritionists, endocrinologists and allergists all of them specialist professionals.

A tragic case of atopic eczema: malnutrition and infections despite multivitamins and supplements.

Eczema is a common childhood atopic condition and treatment is with emollients, topical corticosteroids and avoidance of possible triggers. S. aurues colonization is a common complication. During exacerbation, intensification of treatment is needed to relieve the child from the miserable symptoms of pruritus and sleep disturbance. Systemic antibiotics against S. aureus may be required. We report an infant with eczema who presented with a generalised rash, cardiac arrest and septic shock. Kwashiorkor-like protein energy malnutrition was noted presumably due to deviated dietary practice. Childhood eczema is an eminently treatable atopic disease. Extreme alternative therapy seems not to be efficacious and may even be associated with grave sequelae.

Aflatoxins and growth impairment: a review.

Aflatoxins, fungal toxins produced by Aspergillus flavus and Aspergillus parasiticus in a variety of food crops, are well known as potent human hepatocarcinogens. Relatively less highlighted in the literature is the association between aflatoxin and growth impairment in children. Foodborne aflatoxin exposure, especially through maize and groundnuts, is common in much of Africa and Asia--areas where childhood stunting and underweight are also common, due to a variety of possibly interacting factors such as enteric diseases, socioeconomic status, and suboptimal nutrition. The effects of aflatoxin on growth impairment in animals and human children are reviewed, including studies that assess aflatoxin exposure in utero and through breastfeeding. Childhood weaning diets in various regions of the world are briefly discussed. This review suggests that aflatoxin exposure and its association with growth impairment in children could contribute a significant public health burden in less developed countries.

The effects of aflatoxin B1 on the development of kwashiorkor in mice.

Seventy Swiss albino mice (6-week-old male) were selected for the investigation into aflatoxin B1's role in the cause of kwashiorkor. The mice were divided randomly into four groups. They were grouped within each group by being fed either low or normal protein level diets supplemented with very small amounts of aflatoxin B1 (0.5 microg/day). The control groups were fed aflatoxin B1-free diets containing either normal or low protein levels. All groups were monitored for 7 weeks. The increase in body weight was found to be low in groups I and II, given diets contaminated with aflatoxin B1. Although groups II and IV, which were given low dietary protein, showed remarkable decreases in serum total protein and albumin levels (group II: total protein 4.1 +/- 0.1 g/dL, albumin 2.6 +/- 0.8 g/dL and group IV: total protein 4.6 +/- 1.3 g/dL, albumin 2.8 +/- 0.82 g/dL) when compared with the groups fed a normal dietary protein level (group I: total protein 5.9 +/- 1.3g/dL, albumin 3.4 +/- 0.7g/dL and group III: total protein 5.4 +/- 1.6g/dL, albumin 3.5 +/- 1.2g/dL; P < 0.05). The statistical difference between these two groups was found not to be significant (P > 0.05). However, decreases in total protein and albumin levels were a little more prominent in group II. In addition, histopatological changes of the liver was remarkable in the group fed a low protein diet and aflatoxin B1 when compared with the group fed only a low protein diet and no aflatoxin B1. More significantly, however, was the increase in liver weight in both groups fed a low protein diet (groups II and IV). Our conclusion is that aflatoxin B1 could not have contributed to the development of kwashiorkor.

Aflatoxin exposure and its relationship to kwashiorkor in African children.

The urinary excretion of aflatoxins in normal children from a periurban area, as well as those hospitalized with kwashiorkor and marasmus was assessed. In no case was aflatoxin isolated from the urine. It is concluded that aflatoxin exposure is unusual in this population and that aflatoxins do not play a primary role in the pathogenesis of kwashiorkor.

Nondairy-creamer-induced kwashiorkor: 5-year follow-up.

Failure to thrive may not be a result of organ disease, physical abuse, or intentional neglect. We describe an infant who developed kwashiorkor with a high-fat, low-protein, nondairy coffee creamer diet. The elimination diet was administered on the advice of a family friend for a facial rash. The child presented at 10 months of age with decreased weight for height, rash, hepatomegaly, edema, hypoproteinemia, hypoalbuminemia, anemia, hypoglycemia, and evidence of hepatic sequestration of lipids. A rapid recovery of biochemical abnormalities was evident on reinstitution of a full diet. An intellectual assessment at age 5 years showed normal results.

Reduction in vitro of red cell glutathione reproduces defects of cellular sodium transport seen in oedematous malnutrition.

Red cells in oedematous malnutrition (kwashiorkor) have an increased sodium content, 'leakiness' to sodium and enhanced sodium pumping. In non-oedematous malnutrition (marasmus) there is a reduction in the sodium pump activity. The explanation has hitherto been unknown but the glutathione content of red cells is low in kwashiorkor and normal in marasmus. We artificially lowered the glutathione content of normal red cells to values characteristic of mild oedematous malnutrition, using the enzyme inhibitors bischloronitrosourea (BCNU) and buthionine sulfoximine (BSOX). After preincubation, the cells were washed to remove the inhibitors and oxidized glutathione. Cellular content of sodium and potassium, and 86Rb influx were then measured. The reduction in glutathione reproduced the abnormalities of sodium content and flux observed in kwashiorkor. We suggest that oxidant stress in kwashiorkor, by reducing cellular glutathione, may affect cell membrane electrolyte transport. This may act through alterations in membrane sulfhydryl groups. Glutathione depletion may therefore play an important role in the clinical picture and natural history of oedematous malnutrition and may have relevance to other conditions where oxidant stress occurs.

Reduction in vitro of red cell glutathione reproduces defects of cellular sodium transport seen in oedematous malnutrition

Red cells in oedematous malnutrition (kwashiorkor) have an increased sodium content, 'leakiness' to sodium and enhanced sodium pumping. In non-oedematous malnutrition (marasmus) there is a reduction in the sodium pump activity. The explanation has hitherto been unknown but the glutathione content of red cells is low in kwashiorkor and normal in marasmus. We artifically lowered the glutathione content of normal red cells to values characteristic of mild oedematous malnutrition, using the enzyme inhibitors bischloronitrosourea (BCNU) and buthionine sulfoximine (BSOX). After preincubation, the cells were washed to remove the inhibitors and oxidized glutathione. Cellular content of sodium and potassium, and 86Rb influx were then measured. The reduction in glutathione reproduce the abnormalities of sodium content and flux observed in kwashiorkor. We suggest that oxidant stress in kwashiorkor, by reducing cellular glutathione, may affect cell membrane electrolyte transport. This may act through alterations in membrane sulfhydryl groups. Glutathione depletion may therefore play an important role in the clinical picture and natural history of oedematous malnutrition and may have relevance to other conditions where oxidant stress occurs. (AU)

The influence of aflatoxins on child health in the tropics with particular reference to kwashiorkor.

Aflatoxins are common environmental hazards in all the underdeveloped countries of the tropics where they commonly contaminate food. They are toxic to most species of animals and are among the most powerful carcinogenic agents known. The liver is the principal target for toxicity. Metabolic derangements caused by aflatoxins include depression of protein and enzyme synthesis, disorder of lipid metabolism and immunological suppression. The aetiology and pathogenesis of kwashiorkor remains somewhat obscure. Similarities in the geographical and climatic prevalence of kwashiorkor and aflatoxins and similarities in the metabolic derangements caused by aflatoxins and those observed in kwashiorkor, prompted investigation of the relationship between aflatoxin and kwashiorkor in the Sudan and elsewhere in Africa. Analysis of foods from markets and in homes revealed widespread aflatoxin contamination. Aflatoxins were found more frequently and at higher concentrations in the serum of children with kwashiorkor than in those with other types of malnutrition or in normal children. Aflatoxicol, a metabolite of aflatoxin B1 was detected in serum in kwashiorkor and marasmic kwashiorkor but not in normally nourished children and only once in marasmus. Autopsy liver samples from West and Southern Africa have shown aflatoxins in all cases of kwashiorkor but not in marasmus. These findings establish relationships between aflatoxin and kwashiorkor the nature of which remains obscure but includes the possibility of a causal association.

Aflatoxins and kwashiorkor. Epidemiology and clinical studies in Sudanese children and findings in autopsy liver samples from Nigeria and South Africa.

The aetiology and pathogenesis of kwashiorkor remains obscure. Clinical and epidemiological studies are in progress in Sudan to determine whether aflatoxins play a role in the pathogenesis of kwashiorkor. Local foods are screened for their aflatoxin content and children with kwashiorkor and age and sex matched children with marasmus and with normal nutrition are being investigated for aflatoxins in their blood and urine. Autopsy liver samples of children with kwashiorkor and other nutritional disorders in Nigeria and South Africa have been examined for their aflatoxin content. Aflatoxins are detected using two dimensional thin layer chromatography and high performance liquid chromatography. Results to date on over 350 children studied show that aflatoxins occur more frequently and at higher concentrations in the sera of children with kwashiorkor than in children with marasmus or in normal children. Urinary excretion of aflatoxins in kwashiorkor appears to be less than in other groups. In the autopsy liver samples, aflatoxins have been detected in all kwashiorkor livers but not in livers from marasmic children. These findings seem to implicate aflatoxins in the pathogenesis of kwashiorkor. If this is confirmed it would have very wide implications for the management and prevention of kwashiorkor.