World Health Organization and knowledge translation in maternal, newborn, child and adolescent health and nutrition.

The World Health Organization (WHO) has a mandate to promote maternal and child health and welfare through support to governments in the form of technical assistance, standards, epidemiological and statistical services, promoting teaching and training of healthcare professionals and providing direct aid in emergencies. The Strategic and Technical Advisory Group of Experts (STAGE) for maternal, newborn, child and adolescent health and nutrition (MNCAHN) was established in 2020 to advise the Director-General of WHO on issues relating to MNCAHN. STAGE comprises individuals from multiple low-income and middle-income and high-income countries, has representatives from many professional disciplines and with diverse experience and interests.Progress in MNCAHN requires improvements in quality of services, equity of access and the evolution of services as technical guidance, community needs and epidemiology changes. Knowledge translation of WHO guidance and other guidelines is an important part of this. Countries need effective and responsive structures for adaptation and implementation of evidence-based interventions, strategies to improve guideline uptake, education and training and mechanisms to monitor quality and safety. This paper summarises STAGE's recommendations on how to improve knowledge translation in MNCAHN. They include support for national and regional technical advisory groups and subnational committees that coordinate maternal and child health; support for national plans for MNCAHN and their implementation and monitoring; the production of a small number of consolidated MNCAHN guidelines to promote integrated and holistic care; education and quality improvement strategies to support guidelines uptake; monitoring of gaps in knowledge translation and operational research in MNCAHN.

Difference between kwashiorkor and marasmus: Comparative meta-analysis of pathogenic characteristics and implications for treatment.

Kwashiorkor and marasmus are two clinical syndromes observed in severe acute malnutrition. In this review, we highlighted the differences between these two syndromes by reviewing the data comparing kwashiorkor and marasmus in literature, combined with recent microbiological findings and meta-analysis. Depletion of antioxidants, vitamins and minerals were more severe in kwashiorkor than marasmus. This was consistent with the severe and uncontrolled oxidative stress associated with the depletion of gut anaerobes and the relative proliferation of aerotolerant gut pathogens. This relative proliferation and invasion of gut microbes belonging to the aerotolerant Proteobacteria phylum and pathogens suggested a specific microbial process critical in the pathogenesis of kwashiorkor. Liver mitochondrial and peroxisomal dysfunction could be secondary to toxic microbial compounds produced in the gut such as ethanol, lipopolysaccharides and endotoxins produced by Proteobacteria, particularly Klebsiella pneumoniae, and aflatoxin produced by Aspergillus species. The gut-liver axis alteration is characterized by oedema and a fatty and enlarged liver and was associated with a dramatic depletion of methionine and glutathione, an excessive level of free circulating iron and frequent lethal bacteraemia by enteric pathogens. This was consistent with the fact that antibiotics improved survival only in children with kwashiorkor but not marasmus. The specific pathogenic characteristics of kwashiorkor identified in this review open new avenues to develop more targeted and effective treatments for both marasmus and/or kwashiorkor. Urgent correction of plasma glutathione depletion, alongside supply of specific essential amino acids, particularly methionine and cysteine, early detection of pathogens and an antibiotic more efficient than amoxicillin in supressing gut Proteobacteria including K. pneumoniae, and probiotics to restore the human gut anaerobic mature microbiota could save many more children with kwashiorkor.

Malnutrition Predisposes to Endotoxin-Induced Edema and Impaired Inflammatory Response in Parenterally Fed Piglets.

BACKGROUND: Poor nutrition status is common among hospitalized children and children in low-income countries and may be associated with increased susceptibility to edema and infections. We hypothesized that poor nutrition status, established with a suboptimal composition of parenteral nutrition (PN), predisposes to endotoxemia-induced edema, oxidative stress, and dysregulated immune responses. METHODS: Using a 2 × 2 factorial design, 3-day-old piglets (n = 40) were given either optimal or suboptimal composition of PN for 7 days and then infused with either saline or lipopolysaccharide (LPS) for 9 hours to induce an acute-phase reaction. Abdominal tissue edema and blood markers of immunity, inflammation, and oxidative stress were assessed. RESULTS: Piglets receiving suboptimal nutrition showed signs of malnutrition with restricted growth, signs of inflammation (elevated C-reactive protein [CRP], interleukin-6, and serum amyloid A levels), oxidative stress (lower erythrocyte glutathione/hemoglobin and α-tocopherol/cholesterol ratios), and liver dysfunction (increased liver weight and blood bilirubin levels). Perirenal edema was more excessive in malnourished LPS-infused animals, relative to healthy LPS-infused control animals (P < .01). Malnutrition reduced the inflammatory response to LPS (lower CRP, tumor necrosis factor-α, haptoglobin, and neutrophil to lymphocyte ratio) but did not influence LPS-induced oxidative stress markers. CONCLUSIONS: We conclude that endotoxemia and malnutrition in combination lead to acute-phase hyporesponsiveness and perirenal edema in piglets. This finding may have implications for pediatric patients that suffer from malnutrition, as their response to bacterial infections may differ substantially from patients of normal nutrition status.

Severe acute malnutrition and mortality in children in the community: Comparison of indicators in a multi-country pooled analysis.

OBJECTIVES: This study aims to describe the mortality risk of children in the community who had severe acute malnutrition (SAM) defined by either a mid-upper arm circumference (MUAC) <115mm, a low weight-for-height Z-score (WHZ) <-3 or both criteria. METHODS: We pooled individual-level data from children aged 6-59 months enrolled in 3 community-based studies in the Democratic Republic of the Congo (DRC), Senegal and Nepal. We estimate the mortality hazard using Cox proportional hazard models in groups defined by either anthropometric indicator. RESULTS: In total, we had 49,001 time points provided by 15,060 children available for analysis, summing to a total of 143,512 person-months. We found an increasing death rate with a deteriorating nutritional status for all anthropometrical indicators. Children identified as SAM only by a low MUAC (<115mm) and those identified only by a low WHZ (Z-score <-3) had a similar mortality hazard which was about 4 times higher than those without an anthropometric deficit. Having both a low MUAC and a low WHZ was associated with an 8 times higher hazard of dying compared to children within the normal range. The 2 indicators identified a different set of children; the proportion of children identified by both indicators independently ranged from 7% in the DRC cohort, to 35% and 37% in the Senegal and the Nepal cohort respectively. CONCLUSION: In the light of an increasing popularity of using MUAC as the sole indicator to identify SAM children, we show that children who have a low WHZ, but a MUAC above the cut-off would be omitted from diagnosis and treatment despite having a similar risk of death.

Severely malnourished children with a low weight-for-height have similar mortality to those with a low mid-upper-arm-circumference: II. Systematic literature review and meta-analysis.

BACKGROUND: The WHO recommended criteria for diagnosis of sever acute malnutrition (SAM) are weight-for-height/length Z-score (WHZ) of <- 3Z of the WHO2006 standards, a mid-upper-arm circumference (MUAC) of < 115 mm, nutritional oedema or any combination of these parameters. A move to eliminate WHZ as a diagnostic criterion has been made on the assertion that children with a low WHZ are healthy, that MUAC is a "superior" prognostic indicator of mortality and that adding WHZ to the assessment does not improve the prediction of death. Our objective was to examine the literature comparing the risk of death of SAM children admitted by WHZ or MUAC criteria. METHODS: We conducted a systematic search for reports which examined the relationship of WHZ and MUAC to mortality for children less than 60 months. The WHZ, MUAC, outcome and programmatic variables were abstracted from the reports and examined. Individual study's case fatality rates were compared by chi-squared analysis and random effects meta-analyses for combined data. RESULTS: Twenty-one datasets were reviewed. All the patient studies had an ascertainment bias. Most were inadequate because they had insufficient deaths, used obsolete standards, combined oedematous and non-oedematous subjects, did not report the proportion of children with both deficits or the deaths occurred remotely after anthropometry. The meta-analyses showed that the mortality risks for children who have SAM by MUAC < 115 mm only and those with SAM by WHZ < -3Z only are not different. CONCLUSIONS: As the diagnostic criteria identify different children, this analysis does not support the abandonment of WHZ as an important independent diagnostic criterion for the diagnosis of SAM. Failure to identify such children will result in their being denied treatment and unnecessary deaths from SAM.

Severely malnourished children with a low weight-for-height have a higher mortality than those with a low mid-upper-arm-circumference: III. Effect of case-load on malnutrition related mortality- policy implications.

BACKGROUND: Severe acute malnutrition (SAM) is diagnosed when the weight-for-height Z-score (WHZ) is <-3Z of the WHO2006 standards, or a mid-upper-arm circumference (MUAC) of < 115 mm or there is nutritional oedema. Although there has been a move to eliminate WHZ as a diagnostic criterion we have shown that children with a low WHZ have at least as high a mortality risk as those with a low MUAC. Here we take the estimated case fatality rates and published case-loads to estimate the proportion of total SAM related deaths occurring in children that would be excluded from treatment with a MUAC-only policy. METHODS: The effect of varying case-load and mortality rates on the proportion of all deaths that would occur in admitted children was examined. We used the same calculations to estimate the proportion of all SAM-related deaths that would be excluded with a MUAC-only policy in 48 countries with very different relative case loads for SAM by only MUAC, only WHZ and children with both deficits. The case fatality rates (CFR) are taken from simulations, empirical data and the literature. RESULTS: The relative number of cases of SAM by MUAC alone, WHZ alone and those with both criteria have a dominant effect on the proportion of all SAM-related deaths that would occur in children excluded from treatment by a MUAC-only program. Many countries, particularly in the Sahel, West Africa and South East Asia would fail to identify the majority of SAM-related deaths if a MUAC only program were to be implemented. Globally, the estimated minimum number of deaths that would occur among children excluded from treatment in our analyses is 300,000 annually. CONCLUSIONS: The number, proportion or attributable fraction of children excluded from treatment with any change of current policy are the correct indicators to guide policy change. CRFs alone should not be used to guide policy in choosing whether or not to drop WHZ as a diagnostic for SAM. All the criteria for diagnosis of malnutrition need to be retained. It is critical that methods are found to identify those children with a low WHZ, but not a low MUAC, in the community so that they will not remain undetected.

Severely malnourished children with a low weight-for-height have a higher mortality than those with a low mid-upper-arm-circumference: I. Empirical data demonstrates Simpson's paradox.

BACKGROUND: According to WHO childhood severe acute malnutrition (SAM) is diagnosed when the weight-for-height Z-score (WHZ) is <-3Z of the WHO2006 standards, the mid-upper-arm circumference (MUAC) is < 115 mm, there is nutritional oedema or any combination of these parameters. Recently there has been a move to eliminate WHZ as a diagnostic criterion on the assertion that children meeting the WHZ criterion are healthy, that MUAC is universally a superior prognostic indicator of mortality and that adding WHZ to the assessment does not improve the prediction; these assertions have lead to a controversy concerning the role of WHZ in the diagnosis of SAM. METHODS: We examined the mortality experience of 76,887 6-60 month old severely malnourished children admitted for treatment to in-patient, out-patient or supplementary feeding facilities in 18 African countries, of whom 3588 died. They were divided into 7 different diagnostic categories for analysis of mortality rates by comparison of case fatality rates, relative risk of death and meta-analysis of the difference between children admitted using MUAC and WHZ criteria. RESULTS: The mortality rate was higher in those children fulfilling the WHO2006 WHZ criterion than the MUAC criterion. This was the case for younger as well as older children and in all regions except for marasmic children in East Africa. Those fulfilling both criteria had a higher mortality. Nutritional oedema increased the risk of death. Having oedema and a low WHZ dramatically increased the mortality rate whereas addition of the MUAC criterion to either oedema-alone or oedema plus a low WHZ did not further increase the mortality rate. The data were subject to extreme confounding giving Simpson's paradox, which reversed the apparent mortality rates when children fulfilling both WHZ and MUAC criteria were included in the estimation of the risk of death of those fulfilling either the WHZ or MUAC criteria alone. CONCLUSIONS: Children with a low WHZ, but a MUAC above the SAM cut-off point are at high risk of death. Simpson's paradox due to confounding from oedema and mathematical coupling may make previous statistical analyses which failed to distinguish the diagnostic groups an unreliable guide to policy. WHZ needs to be retained as an independent criterion for diagnosis of SAM and methods found to identify those children with a low WHZ, but not a low MUAC, in the community.

Change in quality of malnutrition surveys between 1986 and 2015.

BACKGROUND: Representative surveys collecting weight, height and MUAC are used to estimate the prevalence of acute malnutrition. The results are then used to assess the scale of malnutrition in a population and type of nutritional intervention required. There have been changes in methodology over recent decades; the objective of this study was to determine if these have resulted in higher quality surveys. METHODS: In order to examine the change in reliability of such surveys we have analysed the statistical distributions of the derived anthropometric parameters from 1843 surveys conducted by 19 agencies between 1986 and 2015. RESULTS: With the introduction of standardised guidelines and software by 2003 and their more general application from 2007 the mean standard deviation, kurtosis and skewness of the parameters used to assess nutritional status have each moved to now approximate the distribution of the WHO standards when the exclusion of outliers from analysis is based upon SMART flagging procedure. Where WHO flags, that only exclude data incompatible with life, are used the quality of anthropometric surveys has improved and the results now approach those seen with SMART flags and the WHO standards distribution. Agencies vary in their uptake and adherence to standard guidelines. Those agencies that fully implement the guidelines achieve the most consistently reliable results. CONCLUSIONS: Standard methods should be universally used to produce reliable data and tests of data quality and SMART type flagging procedures should be applied and reported to ensure that the data are credible and therefore inform appropriate intervention. Use of SMART guidelines has coincided with reliable anthropometric data since 2007.

The Effect of Random Error on Diagnostic Accuracy Illustrated with the Anthropometric Diagnosis of Malnutrition.

BACKGROUND: It is often thought that random measurement error has a minor effect upon the results of an epidemiological survey. Theoretically, errors of measurement should always increase the spread of a distribution. Defining an illness by having a measurement outside an established healthy range will lead to an inflated prevalence of that condition if there are measurement errors. METHODS AND RESULTS: A Monte Carlo simulation was conducted of anthropometric assessment of children with malnutrition. Random errors of increasing magnitude were imposed upon the populations and showed that there was an increase in the standard deviation with each of the errors that became exponentially greater with the magnitude of the error. The potential magnitude of the resulting error of reported prevalence of malnutrition were compared with published international data and found to be of sufficient magnitude to make a number of surveys and the numerous reports and analyses that used these data unreliable. CONCLUSIONS: The effect of random error in public health surveys and the data upon which diagnostic cut-off points are derived to define "health" has been underestimated. Even quite modest random errors can more than double the reported prevalence of conditions such as malnutrition. Increasing sample size does not address this problem, and may even result in less accurate estimates. More attention needs to be paid to the selection, calibration and maintenance of instruments, measurer selection, training & supervision, routine estimation of the likely magnitude of errors using standardization tests, use of statistical likelihood of error to exclude data from analysis and full reporting of these procedures in order to judge the reliability of survey reports.

Developing food supplements for moderately malnourished children: lessons learned from ready-to-use therapeutic foods.

Ready-to-use therapeutic foods (RUTFs) are solid foods that were developed by changing the formulation of the existing liquid diet, F-100, recommended by the World Health Organization (WHO) for the rapid catch-up phase of the treatment of children suffering from severe acute malnutrition (SAM). The resulting products proved highly effective in promoting weight gain in both severely and moderately wasted children and adults, including those infected with HIV. The formulation of the existing RUTFs, however, has never been optimized to maximize linear growth, vitamin and mineral status, and functional outcomes. The high milk content of RUTFs makes it an expensive product, and using lower quantities of milk seems desirable. However, the formulation of alternative, less expensive but more effective versions of RUTF faces difficult challenges, as there are uncertainties regarding the effect in terms of protein quality, antinutrient content, and flatulence factors that will result from the replacement of current dairy ingredients by less expensive protein-rich ingredients. The formulation of alternative RUTFs will require further research on these aspects, followed by efficacy studies comparing the future RUTFs to the existing formulations.

Evolution of nutritional management of acute malnutrition.

Wasting, kwashiorkor and stunting are not usually due to either protein or energy deficiency. Treatment based upon this concept results in high mortality rates, and failure of treated children to return physiologically to normal. They become relatively obese with insufficient lean tissue. Preventive strategies have also failed. Wasting and stunting are primarily due to deficiency of type II nutrients and kwashiorkor probably due to deficiency of several type I nutrients that confer resistance to oxidative stress. Modern dietary treatments are based upon the F75 formula whilst the child is sick without an appetite, followed by F100 for rapid gain of weight. Derivative, ready-to-use therapeutic foods (RUTF) allow treatment of large numbers of children at home, are preferred by mothers and dramatically improve coverage. Children are indentified by screening in the community and treated before complications arise, using simple protocols. Successful treatment of the sick children with severe malnutrition not only depends upon these products, but appropriate management of complications. The physiology of the malnourished child is completely different from the normal child and many drugs and treatments that are safe in children with normal physiology are fatal for the malnourished child. In particular, the diagnosis and management of diarrhea and dehydration is different in the malnourished child. Giving standard treatment frequently leads to circulatory overload and death from heart failure. The challenge now is to find successful local ways to prevent malnutrition and achieve nutritional security. Until prevention works, we have to rely on fortified foods for treatment and convalescence from illness.

Proposed recommended nutrient densities for moderately malnourished children.

Recommended Nutrient Intakes (RNIs) are set for healthy individuals living in clean environments. There are no generally accepted RNIs for those with moderate malnutrition, wasting, and stunting, who live in poor environments. Two sets of recommendations are made for the dietary intake of 30 essential nutrients in children with moderate malnutrition who require accelerated growth to regain normality: first, for those moderately malnourished children who will receive specially formulated foods and diets; and second, for those who are to take mixtures of locally available foods over a longer-term to treat or prevent moderate stunting and wasting. Because of the change in definition of severe malnutrition, much of the older literature is pertinent to the moderately wasted or stunted child. A factorial approach has been used in deriving the recommendations for both functional, protective nutrients (type I) and growth nutrients (type II).

Reduced production of sulfated glycosaminoglycans occurs in Zambian children with kwashiorkor but not marasmus.

BACKGROUND: Kwashiorkor, a form of severe malnutrition with high mortality, is characterized by edema and systemic abnormalities. Although extremely common, its pathophysiology remains poorly understood, and its characteristic physical signs are unexplained. OBJECTIVE: Because kwashiorkor can develop in protein-losing enteropathy, which is caused by a loss of enterocyte heparan sulfate proteoglycan (HSPG), and previous observations suggest abnormal sulfated glycosaminoglycan (GAG) metabolism, we examined whether intestinal GAG and HSPG are abnormal in children with kwashiorkor. DESIGN: Duodenal biopsy samples collected from Zambian children with marasmus (n = 18), marasmic kwashiorkor (n = 8), and kwashiorkor (n = 15) were examined for expression of HSPG, GAGs, and immunologic markers and compared against reference samples from healthy UK control children. GAG and HSPG expression density and inflammatory cell populations were quantitated by computerized analysis. RESULTS: The kwashiorkor group was less wasted and had a lower HIV incidence than did the other groups. All duodenal biopsy samples showed inflammation compared with the histologically uninflamed control samples. Biopsy samples from marasmic children had greater inflammation and greater CD3+ and HLA-DR (human leukocyte antigen DR)-positive cell densities than did samples from children with kwashiorkor. Expression of both HSPG and GAGs was similar between marasmic and well-nourished UK children but was markedly lower in children with kwashiorkor in both the epithelium and lamina propria. Although underglycosylated and undersulfated, epithelial syndecan-1 protein was normally expressed in kwashiorkor, which confirmed that abnormalities arise after core protein synthesis. CONCLUSIONS: Intestinal HSPG loss occurs in kwashiorkor, which may precipitate protein-losing enteropathy to cause edema. If occurring systemically, impaired HSPG expression could cause several previously unexplained features of kwashiorkor. We speculate that a genetic predisposition to reduced HSPG biosynthesis may offer a contrasting selective advantage, by both diminishing protein catabolism during transient undernutrition and protecting against specific infectious diseases.

Nutritional associations with bone loss during the menopausal transition: evidence of a beneficial effect of calcium, alcohol, and fruit and vegetable nutrients and of a detrimental effect of fatty acids.

BACKGROUND: The menopausal transition is characterized by rapid bone loss. Few data exist on the role of nutrition. OBJECTIVE: The objective of the study was to ascertain which dietary factors influence perimenopausal skeletal loss. DESIGN: A longitudinal study was conducted of 891 women aged 45-55 y at baseline and 50-59 y at follow-up 5-7 y later. Bone mineral density (BMD) was measured by using dual-energy X-ray absorptiometry at the lumbar spine and femoral neck (FN). Nutrient intakes were assessed after the baseline visit and 5 y later, by using the same food-frequency questionnaire. RESULTS: After adjustment for energy intake and other confounders, higher intakes of calcium were correlated with change in FN BMD (ie, reduced loss) (r = 0.073, P < 0.05), and the intake of modest amounts of alcohol was associated with less lumbar spine bone loss (P < 0.01 for quartile of alcohol intake). Greater FN BMD loss was associated with increased intake of polyunsaturated fatty acids (r = -0.110, P < 0.01), monounsaturated fatty acids (r = -0.069, P < 0.05), retinol (r = -0.067; P < 0.05), and vitamin E (r = -0.110; P < 0.01). The latter 2 nutrients were highly correlated with polyunsaturated fatty acids. For premenopausal women, calcium and nutrients found in fruit and vegetables (vitamin C, magnesium, and potassium) were associated with FN BMD, and calcium, vitamin C, and magnesium were associated with change in FN BMD. CONCLUSIONS: Although menopausal status and hormone replacement therapy use dominate women's bone health, diet may influence early postmenopausal bone loss. Fruit and vegetable intake may protect against premenopausal bone loss.

Antenatal factors in the development of the lumbar vertebral canal: a magnetic resonance imaging study.

STUDY DESIGN: The lumbar vertebral canal was measured in two cohorts of 10-year-old children (n = 161) using magnetic resonance imaging (MRI) and compared with obstetric records. OBJECTIVE: To investigate whether there are identifiable obstetric factors that determine the size of the lumbar vertebral canal. SUMMARY OF BACKGROUND DATA: The most rapid period growth for the lumbar vertebral canal is between 12 and 32 weeks in utero, with the midsagittal diameter of L1-L4 already 70% of adult dimension at birth. Therefore, adverse antenatal factors during this critical growth period may be expected to affect the size of the canal. METHODS: The canal size was measured from axial MRI sections taken through each lumbar vertebra (L1-L5) at the pedicular level of 84 children. Relations with obstetric data, prospectively collected in a neonatal database, were sought. The relation of low birthweight and canal size was further investigated in a second cohort of children (n = 77). RESULTS: The canal size, particularly the midsagittal diameter and the cross-sectional area, was found to be significantly reduced by low birthweight (with growth retardation in utero being a more important factor than length of gestation), low placenta weight, and lower socioeconomic class. Smoking during pregnancy significantly reduced the perimeter at L3 (P = 0.032) and L5 (P = 0.031), and also the cross-sectional area at L3 (P = 0.030) and L5 (P = 0.016). CONCLUSIONS: This study showed that, for this group of children, the size of the lumbar vertebral canal was reduced by low birthweight, with maternal smoking as an added adverse factor. Therefore, good antenatal care and maternal education may help to reduce the risk of spinal stenosis in adult life.

Urinary collagen cross-links as biochemical markers of growth: an evaluation of biological variables.

AIM: To investigate the validity of urinary pyridinium cross-links (pyridinoline and deoxypyridinoline) as markers of growth in healthy children. METHODS: Three pilot studies (P1-P3) were conducted to investigate the time of day, the minimal duration within a day, and how many times per week urine samples needed to be collected to obtain representative values of cross-link excretion in normal children 3-5 years of age. The results were used to design a 4-month longitudinal protocol to evaluate whether pyridinium cross-links could be used as markers of growth velocity. RESULTS: Mean differences from 24-hour values were only between 1 and 4% for urinary cross-links (nmol/h) in overnight 12-hour collections. Three consecutive collections were required for weekly output estimates with a maximum error of 10% in >90% of the children. During the 4-month longitudinal study, the regression equation of height velocity on pyridinoline and deoxypyridinoline excretion explained approximately 60% of the variance in the subgroup of subjects who provided three complete urinary collections per observation period. No relationship was observed when the cases with fewer or incomplete collections were included in the analysis. Cross-link values collected at baseline were of no use to predict height velocity at 4 months. CONCLUSIONS: Urinary pyridinium cross-links correlate with the growth velocity in healthy children when using an appropriate urinary collection protocol. However, their predictive value in this population is negligible.

Glyoxalase I activity in erythrocytes from severely malnourished children

The enzyme glycoxalase I (glyox I) is involved in metabolic detoxification, and requires glutathione (GSH) as a cofactor. Given the low concentration of whole blood GSH in children with oedematous malnutrition, it is possible that the function of this pathway may be compromised in these children. Glyox I activity was therfore assayed in erythocytes taken from 133 severely malnourished children and 21 age-matched controls. The mean values (ñSEM) for the marasmic group (marasmus: 105 ñ 4/u/gm Hb) and the group with kwashiorkor (Kwash: 103 ñ 4/u/gm Hb) were not significantly different from controls (cont: 104 ñ 2u/gm HB)>. In the group with marasmic-kwashiorkor (M-K: 88 ñ 4u/g Hb) Glyox I activity was significantly lower in controls (p < 0.005), as well as in children with marasmus (p < 0.005), and kwashiorkor (p < 0.05). Enzyme activity was lower than normal in 45 per cent of the MK group. Seven children died subsequent to admission; in five cases Glyox I activities were exceedingly low. There was a weak positive correlation between Glyox I activity and whole blood levels of GSH (r=0.215). We conclude that Glyox I activity is relatively unaffected in malnutrition, except in those with M-K and especially those who do not survive the acutely malnourished state

Pathology of the lungs in childhood malnutrition in Jamaica: light and electron microscopy

The autopsy records of 115 children with severe protein-energy malnutrition were reviewed. Sections of the lung histology showed evidence of bacterial pneumonia in 49 per cent of cases. An additional 18 per cent showed bronchitis, bronchiolitis or interstitial pneumonitis. Aspiration of gastric contents was evident in 10 per cent of cases; 6 per cent showed pulmonary oedema and congestion. In the remaining cases, no lung pathology was identified (17 per cent ). In 8 cases, rapid autopsy examination permitted fixation of lung tissue for electron microscopy. These included 4 cases of bronchopneumonia, one of which was associated with viral pneumonia. Another interstitial pneumonitis, probably of viral aetiology, was also studied. Both these virus-associated cases showed loss of type I pneumocytes and hyperplasia of type II pneumocytes. Another patient with herpes simplex hepatitis showed necrotic emboli in pulmonary capillaries with virions, as well as colonies of interstitial bacteria. One patient with acute pulmonary oedema displayed severe endothelial cell swelling on electron microscopy. In one case, there was no evidence of respiratory changes, apart from desquamation of type I pnuemocytes. Useful information can be obtained on the fine structure of the lung, using samples taken soon after death.