Growth, Body Composition, and Metabolism
Updated November 2007
I. INTRODUCTION
Recommendation:
Clinicians should perform an annual nutritional assessment as part of routine care for all HIV-infected children (see Table 1).
As effective therapies for HIV infection have become available, there has been a shift in the types of clinical problems confronting HIV-infected patients and their medical providers. Disturbances in growth, body composition, and metabolism have emerged as important issues in research and clinical care of perinatally HIV-infected children and adolescents. Behaviorally infected adolescents are more likely to have problems resembling those seen in adults with HIV, including the metabolic and lipid disturbances related to ARV therapy, especially HAART. Many uncertainties concerning the cause, long-term consequences, and optimal management of all of these problems remain. Abnormalities in growth and body composition and related nutritional, endocrine, and gastrointestinal alterations are discussed in this chapter. In addition, disturbances in lipid, glucose, and lactic acid metabolism are described.
Click here to view Table 1: Elements of a Nutritional and Dietary Assessment
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II. GROWTH ABNORMALITIES IN PERINATALLY HIV-INFECTED CHILDREN AND ADOLESCENTS
Recommendations:
Clinicians should obtain weight and height (or length) measurements every 3 to 4 months until children have reached full adult height.
Clinicians should assess children who are experiencing suboptimal growth for potentially reversible causes of poor growth.
Abnormalities in somatic growth may appear in several patterns. Progressive stunting (decreased height for age), wasting (decreased weight for height), and decreased weight with stunting (decreased weight for age) are the most common abnormalities in postnatal growth. Growth retardation is often apparent within 3 to 4 months after birth.1,2 The magnitude of height and weight impairment increases with age. As with other childhood chronic diseases, sexual maturation is often delayed in HIV-infected children with growth abnormalities.
Monitoring growth is an important aspect of clinical care of HIV-infected children and adolescents (see Appendices A and B). Weight and height (or recumbent length for children <24 months) should be determined in a standardized manner by trained personnel using calibrated scales and stadiometers or measuring boards. Some clinicians also assess and monitor trends in body mass index [BMI = body wt (kg)/ht (m)2]. To date, body mass index (BMI) measurements have not been widely applied in HIV-infected children.
When a child's growth fails to consistently follow a normal height- and weight-for-age curve, additional assessment of growth using height velocity derived from 6- or 12-month measurements should be performed. Growth velocity in less than the third percentile is generally considered an indication of growth failure. Growth failure, by this criterion, is a significant prognostic factor for disease progression and death, independent of CD4 count. Typically, HIV-infected children with growth failure are short for age but normally proportioned, with normal weight-for-height ratios. Growth charts are available on the Centers for Disease Control and Prevention (CDC) website at: www.cdc.gov/growthcharts/.
Multiple factors may cause or contribute to growth failure in HIV-infected children (see Figure 1). These factors may cause decreased calorie or nutrient intake, increased energy utilization, or increased losses from vomiting or diarrhea; they may be organic, psychosocial, or even iatrogenic in nature. Reversible causes of growth failure should be sought and treated.
A number of abnormalities in body composition have been described in HIV-infected children. In contrast to patterns observed in undernourished children in which initial depletion of fat stores is typical, HIV-infected children with growth failure preferentially deplete lean or fat-free body mass (FFM) with relative sparing of body fat. FFM has a marked impact on disease progression and death. In one study, HIV-infected children with the lowest quantities of FFM had a 5-fold increase in the risk of death.3
Obtaining body composition measurements to determine FFM should be considered to provide additional information on overall nutritional status and on overall prognosis. If validated laboratory-based methods, such as dual energy x-ray absorptiometry (DEXA) or underwater weighing, are not available, anthropometrics, such as mid-arm circumference and skin-fold measurements, yield meaningful results when standardized methods are used by a skilled consistent observer (see Appendix B). Bioelectrical impedance analysis (BIA) may also be used.
Inadequate weight gain or frank weight loss (i.e., wasting) also occurs in HIV-infected children but less commonly than statural growth failure. Recent CDC surveillance data regarding AIDS wasting syndrome indicate an increase in its relative prevalence as an AIDS-related condition in children.4 AIDS wasting syndrome is defined as chronic diarrhea and either weight loss of >10% of body weight or deceleration in weight gain resulting in downward "crossing" of two SD lines for age when weight is plotted on standard growth curves.
Click here to view Figure 1: Causes of Malnutrition
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III. RESTORATION OF GROWTH
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A. Energy Intake
Recommendations:
Clinicians should carefully evaluate the dietary intake of children with growth failure or wasting syndrome, and dietary counseling should be provided by a health professional with expertise in pediatric nutrition.
Clinicians should increase total caloric intake as needed for growth, and potential causes of growth failure should be treated when possible.
Caloric intake should be nutritionally balanced: 50%-55% of total calories from carbohydrate; 15%-20% from protein; and 20%-30% from fat (with <10% of total calories as saturated fatty acids).
HIV-infected children may require a greater number of calories to grow than the recommended dietary allowances for healthy children of the same age. Accurately assessing basal dietary intake is difficult in children, especially when not all meals or food taken throughout the day are consumed at home. Three-day food records can provide excellent results when completed properly. Another option is 24-hour recall using food models and measuring devices.
The Dietary Reference Intakes, which are composed of Recommended Dietary Allowances (RDAs) or when RDAs are unknown, Adequate Intakes (see Appendix C), may be used as a starting point to determine the caloric needs of an HIV-infected child. However, these allowances should be increased as needed to obtain adequate growth. Furthermore, dietary intake for children with growth failure may not be sufficient to meet metabolic demands and to sustain normal growth. Several studies performed before the availability of potent ARV medications demonstrated that increasing the nutritional intake in children with HIV-associated growth failure by use of supplemental enteral and tube feedings improves weight but has no effect on linear growth or lean body mass (i.e., arm muscle circumference). Nonetheless, measures for improving intake are recommended for children with growth abnormalities that are not due to other reversible causes.
Approaches used for improving dietary intake include nutritional counseling to maximize the caloric density of food and use of age-appropriate dietary supplement beverages in between meals. Adolescents should use adult supplements. Appendix D lists commonly used supplement beverages. Supplemental nocturnal feedings through nasogastric or gastrostomy tubes may also be indicated when other efforts to increase the caloric intake are unsuccessful. Teaching older children to use a small nasogastric tube each night to permit the administration of nocturnal supplemental feedings has been successful for some patients. Patients with gastrostomy tubes should be monitored for site-specific problems with the tube, as well as patency issues.
Appetite stimulants have been used to improve dietary intake in HIV-infected children. Although none has been officially approved for use in children, megestrol acetate, dronabinol, and periactin have all been used with some success. Megestrol acetate is approved for appetite stimulation in HIV-infected adults at a dose of 800 mg/day. No formal pediatric dosing studies have been performed, but the per-kilogram equivalent of the above dose would be 10 to 15 mg/kg/day. Concerns regarding the use of megestrol acetate include some reports suggesting that the weight gain consists of fat without improvement in lean tissue. In addition, megestrol acetate may cause potentially life-threatening adrenal suppression and hypertension.5 There are no pediatric dosing recommendations and little reported experience for dronabinol, which is an appetite stimulant used commonly in HIV-infected adults. Side effects of dronabinol include central nervous system abnormalities, including mood alteration. Periactin, a medication approved as an antihistamine, has also been used "off-label" for appetite stimulation in some HIV-infected patients. Overall, the need for these interventions in children has been considerably reduced since the introduction of HAART.
Oral or gastrointestinal tract lesions, such as oral and esophageal herpes and candidiasis and aphthous ulcers, may result in decreased intake in children or adolescents. Medication side effects, such as circumoral paresthesias and diarrhea, may also result in decreased dietary intake (see Table 2).
Any cause of vomiting or diarrhea, which can be primary causes of growth failure, may precipitate fear of eating and induce inadequate intake. Occasionally, an ill parent may be unable to prepare nutritious meals for a child or may be unable to obtain adequate food because of loss of income or benefits. Some caregivers may lack information on appropriate nutrition and may allow the child to eat an overabundance of less nutritious "junk" food. Psychosocial issues may also cause decreased intake; for example, children moved from one home to another may fail to eat adequately because of depression or simply because of a different cooking style of the new caregiver.
Click here to view Table 2: Common ARV Side Effects That May Affect Appetite and Nutrition
B. Viral Suppression
Recommendation:
Clinicians should assess the ARV regimen of patients with poor growth and high viral load to ensure optimal efficacy of the ARV regimen.
Poor growth may be an indication of poorly controlled HIV infection. Several studies confirm the central role of the level of HIV replication in growth and body composition disturbances. In one study, growth velocity, the quantity of FFM, and dietary intake were inversely related to viral load.6 The mechanism by which HIV replication impedes growth has not been established.
A key question awaiting further study is whether suppression of viral replication restores energy homeostasis and growth. Studies of the impact of potent suppressors of HIV replication in reversing deficits in height and body composition abnormalities are underway. Treatment with PI-containing ARV regimens has been reported to have a significant effect on weight and weight-for-height ratios and a marginal effect on height.6,7 A potentially important issue is whether HIV treatments, many of which have significant gastrointestinal toxicities (e.g., nausea, vomiting, diarrhea), negatively affect appetite and dietary intake, resulting in a blunting of growth improvement potentially achieved through viral suppression.
C. Micronutrients
Recommendations:
Clinicians should prescribe multivitamin and mineral supplements for HIV-infected children with growth problems but should be careful of the potential for overdose.
Clinicians should ensure that any micronutrient supplements that are used conform to the specific RDA for age.
The clinician should obtain a history of use of over-the-counter supplements and herbal supplements.
Infections (including HIV infection itself, as well as opportunistic infections) often lead to decreased intake and absorption of vitamins and minerals, along with increased use and excretion; thus, micronutrient status is impaired. Decreased micronutrient status may in turn lead to impairment in antibody production, T lymphocyte function, and phagocytic bactericidal capacity. At the same time, the acute phase response alters several serum micronutrient levels (especially those of iron, zinc, and vitamin A) such that it is difficult to clinically assess micronutrient status during acute and chronic infection. Nevertheless, a number of observational studies have shown that micronutrient deficiencies as measured by serum levels (vitamin A, zinc) or decreased intake (folate; vitamins C, E, B complex; iron) are associated with poor growth, HIV progression, and death, especially in developing countries.8
Clinicians should be aware that micronutrient excess, as well as deficiency, may also cause harm. Several micronutrients (e.g., vitamins A and D, iron) seem to have a "U-shaped" curve of risk versus dose.9,10 For example, repletion of iron deficiency restores certain immune functions, but iron overload is associated with more rapid HIV progression in both retrospective clinical trials and cross-sectional observational studies.10 Iron overload may also contribute to risk of opportunistic infection and malignancy.10 Antioxidant vitamins (vitamins A, E, C, and beta-carotene) and vitamin D may be harmful when taken in excess.
Given the difficulty of practically determining micronutrient status and the risks of both under- and overdosage of vitamins and minerals, it is reasonable to prescribe standard multivitamin and mineral supplements for HIV-infected children and adolescents with poor growth. Clinicians should ensure that such supplements comply with dietary reference intakes for age and gender (see Appendix C). A careful history of over-the-counter, herbal, or alternative medication intake should be obtained to prevent overdose of vitamins and minerals.
D. Anabolic Agents
Recommendation:
Anabolic agents should only be prescribed for children in consultation with a pediatric HIV specialist.
Anabolic agents have been used successfully for restoring lean tissue mass in adults with AIDS wasting; however, there is limited experience with using anabolic agents for treating HIV-associated growth failure in pediatric patients. In a small study of nine HIV-infected children (age range, 4-14 years), limited data suggested that oxandrolone reversed wasting when given for 3 months.11 Other anabolic steroids have been used in adults and adolescents, as has growth hormone. Adult dosing should be used for adolescents in Tanner stage IV. The safety and efficacy of anabolic steroids and other hormone therapies has not been established. The use of such therapies in HIV-infected children with growth failure should be limited to children who are not growing despite adequate attempts to remedy a reversible cause and suppress viral load. They should be prescribed in consultation with a pediatric HIV Specialist.
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IV. NEUROENDOCRINE DISORDERS AND GROWTH
Recommendations:
In patients with unexplained growth failure, clinicians should obtain thyroid function tests.
Clinicians should refer patients to an endocrinologist when growth failure remains unexplained after initial evaluation or when the evaluation suggests an endocrine abnormality.
Although no single endocrine abnormality is consistently encountered in HIV-associated growth failure, a number of neuroendocrine abnormalities with the potential to affect anabolism and growth frequently occur in HIV-infected children. Estimates of the occurrence of primary and secondary thyroid abnormalities vary widely from 0 to 18%.12 Abnormalities in the circadian secretory pattern of thyroid stimulating hormone also are reported. Data concerning adrenal function are derived from small studies and are inconsistent. Some investigators have reported abnormal basal cortisol levels.13 Adrenal suppression may also occur in this population as a result of medications (e.g., prednisone, megesterol).
Decreased growth hormone secretion has also been reported, but primary growth hormone deficiency is encountered only occasionally.14 Basal growth hormone and stimulated growth hormone levels are normal in most HIV-infected children. Insulin-like growth factor (IGF)-1 has variably been reported as normal or reduced; however, in these studies, overall nutritional status, which influences IGF-1 levels, was not taken into account. Endocrine tests should be performed on a case-by-case basis in HIV-infected children and adolescents.
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V. ASSOCIATION OF GROWTH ABNORMALITIES WITH GASTROINTESTINAL INFECTIONS AND MALABSORPTION
Recommendations:
Clinicians should carefully screen HIV-infected children with poor growth for gastrointestinal infection and malabsorption.
When lactose and fat intolerance is suspected, the clinician should consult with a pediatric gastroenterologist for screening and diet adjustment.
Gastrointestinal disease, including infections and malabsorption, are highly prevalent in HIV-infected children. The role of subclinical gastrointestinal disease in contributing to abnormal growth is uncertain. Malabsorption of carbohydrates, fat, and protein are reported but not clearly associated with growth failure.15 Diarrhea commonly occurs in children receiving ARV medications, especially PIs. Nelfinavir causes diarrhea in as many as 30% of children receiving it. The significance of medication-induced diarrhea on nutrient absorption is not known.
Gastrointestinal infections may also cause malabsorption in HIV-infected children. These infections include Cryptosporidium, microsporidia, Mycobacterium avium complex, cytomegalovirus, and multiple other agents.
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VI. LIPODYSTROPHY AND ABNORMALITIES OF LIPID METABOLISM
Recommendation:
Clinicians should screen serum cholesterol, triglycerides, low-density lipoprotein, and high-density lipoprotein in HIV-infected children initiating HAART, 3 to 6 months after initiation, and approximately every 6 months thereafter. Abnormal results warrant repeat studies performed in the fasting state (see Tables 3 and 4).
Since the introduction of HAART, several additional body composition and metabolic abnormalities of potential long-term clinical significance have been described in HIV-infected adults and children. Abnormalities in regional fat distribution, variably involving wasting of subcutaneous fat in arms, legs, and face, and accumulation of dorsal cervical, neck, breast, and trunk (visceral) fat have been referred to as lipodystrophy. These disfiguring and potentially stigmatizing body shape changes are frequently accompanied by alterations in lipid levels and insulin resistance, which, in non-HIV-infected populations, are associated with elevated coronary artery disease risk. It is important to note that insulin resistance and abnormal blood lipid profiles can also occur in the absence of physical changes.
Although the frequency and severity of these disorders seem to be reduced in younger age groups, lipodystrophy does occur in children. Simultaneous increases in visceral abdominal fat and wasting of extremity fat, changes that are uncharacteristic for prepubertal children, are detectable in HIV-infected children receiving HAART. HIV-infected children receiving HAART may also have elevated serum triglycerides and cholesterol that can potentially increase long-term coronary artery disease risk. Larger studies taking place over longer time periods are required to better evaluate the prevalence of these abnormalities and associated risk factors.
It is not clearly understood whether lipodystrophy and associated metabolic disturbances are the direct effect of therapy or paradoxical effects of the immunologic recovery that accompanies successful therapy. Currently available data regarding the role of direct ARV drug effects on lipodystrophy are conflicting.16-19 Several studies indicate that abnormally high levels of serum triglycerides and cholesterol (both total and low-density lipoprotein cholesterol) are associated with the use of HAART. However, elevated triglyceride or cholesterol levels have been noted even prior to the use of HAART. If suitable alternatives are available, changing the ARV regimen may be considered for patients with lipodystrophy or marked abnormal blood lipids. Discontinuation of PIs may or may not result in reversal or improvement of these abnormalities.
The significance of body fat and metabolic abnormalities in long-term coronary artery disease risk and whether changes are due to disease or therapy will not be fully understood until results are available from further investigation. With improved survival, perinatally infected children who begin lifelong ARV therapy in infancy may be at greater risk for accelerated atherosclerosis. Given the potential for adverse outcome and the availability of effective means of reducing cholesterol, routine monitoring of serum cholesterol seems warranted in HIV-infected children receiving ARV medications. There are few data from which to derive clinical recommendations concerning the optimal frequency of screening for elevated cholesterol and triglycerides.
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VII. MANAGEMENT OF HIV-INFECTED CHILDREN WITH ABNORMAL CHOLESTEROL
Recommendations:
Clinicians should use dietary and behavioral interventions to manage HIV-infected children and adolescents with abnormal cholesterol. Monitoring and dietary management should be in accordance with the guidelines published by the American Academy of Pediatrics (for adolescents, the Adult AIDS Clinical Trials Group Preliminary Guidelines).20,21
Clinicians should consider the use of pharmacologic interventions for patients with markedly abnormal cholesterol; however, there is the potential for drug-drug interactions, particularly between ARV agents and bile acid sequestering agents.
Clinicians should refer HIV-infected children with borderline or high cholesterol to a pediatric nutritionist or dietitian.
Abnormal cholesterol test results (see Table 3) should be confirmed with repeat measurements performed in the fasting state. HIV-infected children with borderline or high cholesterol should receive the same dietary, behavioral, and pharmacologic interventions that are recommended for use in non-HIV-infected children and adolescents.20-22 These interventions seem to be safe and effective in HIV-infected adults with hypercholesterolemia associated with PI therapy. Bile acid sequestrants should be avoided because of associated gastrointestinal upset and interference with absorption of other medications. At this time, optimizing ARV therapy and diet should remain the primary consideration. Changing ARV medications should only be considered if suitable alternatives with a high likelihood of successful viral suppression are available. Referral to a pediatric nutritionist or dietitian should be considered.
Click here to view Table 3: Classification of Cholesterol Levels in Children
Because there is considerable variability in some children, any abnormal lipoprotein analysis should be repeated so that an average LDL cholesterol level can be calculated. The average LDL cholesterol level determines the steps for risk assessment and treatment. Management of elevated LDL cholesterol determinations is described in Table 4.
Click here to view Table 4: Management of Hypercholesterolemia in HIV-Infected Children and Adolescents
After an adequate trial of 6 to 12 months of diet therapy, drug therapy should be considered for non-HIV-infected children >10 years of age whose LDL cholesterol level remains >190 mg/dL (or >160 mg/dl in the presence of risk factors such as low HDL cholesterol, diabetes mellitus, hypertension, or family history of premature cardiovascular disease).21,22 In the absence of specific data, it seems reasonable to apply these guidelines to HIV-infected children and adolescents as well. Pharmacologic agents are not recommended for routine use in children and adolescents, except in consultation with both a lipid specialist and pediatric HIV Specialist.
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VIII. ABNORMALITIES OF GLUCOSE METABOLISM
Recommendation:
Clinicians should screen for risk factors for diabetes mellitus, including obesity and family history.
The presence of insulin resistance, characterized as decreased sensitivity to insulin during insulin tolerance tests or decreased glucose tolerance during oral glucose tolerance tests, is now well documented in HIV-infected adults receiving treatment. Although data suggest that a direct effect of HAART is an important causative factor in alterations in glucose metabolism, the etiology of insulin resistance is most likely multifactorial.17,18 Insulin resistance also may be found in patients not receiving HAART. Alterations in insulin sensitivity secondary to the body composition changes of lipodystrophy may also be involved. Increased visceral adipose tissue and decreased subcutaneous adipose tissue are both indirect promoters of insulin resistance.
Studies of insulin resistance are not available in HIV-infected children. Without support of evidence from clinical studies, it is difficult to recommend routine screening for abnormalities in glucose and insulin homeostasis for HIV-infected children without additional risk factors for insulin resistance. Clinicians should, however, carefully screen for risk factors for diabetes (e.g., obesity, family history).
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IX. BONE DISORDERS
Bone abnormalities in the setting of HIV infection have been recently reported. HIV-infected children may experience bone disorders at a higher rate than children without HIV infection, both in relation to the infection itself and to complications of ARV therapy. HIV-infected children and adults have decreased bone mineral content and an increased incidence of avascular necrosis.23,24 It remains unclear if these findings are related to HIV disease, the effects of ARV therapy, or other factors, such as glucocorticosteroid use or sickle cell anemia. Regardless of the cause, interruption of normal bone mineral accrual during childhood, which is a critical period in which >50% of ultimate adult bone mass is accumulated, is likely to increase the risk of osteoporosis and related complications. Current data do not support routine screening of bone mineral density. In HIV-infected children with knee pain, radiography can be used to exclude avascular necrosis of the femoral head.
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REFERENCES
1. McKinney RE, Robertson JW, Duke Pediatric AIDS Clinical Trials Unit. Effect of human immunodeficiency virus infection on the growth of young children. J Pediatr 1993;123:579-582.
2. Saavedra J, Henderson RA, Perman JA, et al. Longitudinal assessment of growth in children born to mothers with human immunodeficiency virus infection. Arch Pediatr Adolesc Med 1995;149:497-502.
3. Fontana M, Zuin G, Plebani A, et al. Body composition in HIV-infected children: Relations with disease progression and survival. Am J Clin Nutr 1999;69:1282-1286.
4. Lindgren ML, Steinberg S, Byers RH. Epidemiology of HIV/AIDS in children. Pediatr Clin N Am 2000;47:1-20.
5. Stockheim JA, Daaboul JJ, Yogev R, et al. Adrenal suppression in children with the human immunodeficiency virus treated with megestrol acetate. J Pediatr 1999;134:368-370.
6. Arpadi SM, Cuff PA, Kotler DP, et al. Growth velocity, fat-free mass, and energy intake are inversely related to viral load in HIV-infected children. J Nutr 2000;130:2498-2502.
7. Miller TL, Mawn BE, Orav EJ, et al. The effect of protease inhibitor therapy on growth and body composition in human immunodeficiency virus type-1infected children. Pediatrics 2001;107:e77.
8. Duggan C, Fawzi W. Micronutrients and child health: Studies in international nutrition and HIV infection. Nutr Rev 2001;59:358-369.
9. Dreyfuss ML, Fawzi WW. Micronutrients and vertical transmission of HIV-1. Am J Clin Nutr 2002;75:959-970.
10. Weinberg GA, Boelaert JR, Weinberg ED. Iron and HIV infection. In: Micronutrients and HIV Infection. Friis H, ed. Boca Raton, FL: CRC Press LLC, 2002:135-157.
11. Fox-Wheeler S, Heller L, Salata CM, et al. Evaluation of effects of oxandrolone on malnourished HIV-infected pediatric patients. Pediatrics 1999;104:e73.
12. Hirschfeld S, Laue L, Cutler GB Jr, et al. Thyroid abnormalities in children infected with human immunodeficiency virus. J Pediatr 1996;128:70-74.
13. Oberfield SE, Cowan L, Levine LS, et al. Altered cortisol response and hippocampal atrophy in pediatric HIV disease. J Acquir Immune Defic Syndr Hum Retrovirol 1994;7:57-62.
14. Jospe N, Powell KR. Growth hormone deficiency in an 8 year-old girl with human immunodeficiency virus infection. Pediatrics 1990;86:309-312.
15. Miller TL, Orav EJ¸ Martin SR, et al. Malnutrition and carbohydrate malabsorption in children with vertically transmitted human immunodeficiency virus 1 infection. Gastroenterology 1991;100:1296-1302.
16. Arpadi, SM, Cuff PA, Horlick M, et al. Lipodystrophy in HIV-infected children is associated with high viral load and low CD4+-lymphocyte count and CD4+-lymphocyte percent at baseline and use of protease inhibitors and stavudine. J Acquir Immun Defic Syndr 2001;27:30-34.
17. Martinez E, Mocroft A, Garcia-Viejo MA, et al. Risk of lipodystrophy in HIV-1-infected patients treated with protease inhibitors: A prospective cohort study. Lancet 2001;357:592-598.
18. Behrens G, Dejam A, Schmidt H, et al. Impaired glucose tolerance, beta cell function and lipid metabolism in HIV patients under treatment with protease inhibitors. AIDS 1999;13:F63-F70.
19. Carr A. HIV protease inhibitor-related lipodystrophy syndrome. Clin Infect Dis 2000;30(Suppl 2):S135-S142.
20. Dubé MP, Sprecher D, Henry WK, et al. Preliminary guidelines for the evaluation and management of dyslipidemia in adults innfected with human immunodeficiency virus and receiving antiretroviral therapy: Recommendations of the Adult AIDS Clinical Trials Group Cardiovascular Disease Focus Group. Clin Infect Dis 2000;31:1216-1224.
21. American Academy of Pediatrics, Committee on Nutrition. Cholesterol in childhood. Pediatrics 1998;101:141-147.
22. National Cholesterol Education Program. Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents. Pediatrics 1992;89:525-584.
23. Gaughan DM, Mofenson LM, Hughes MD, et al. Osteonecrosis of the hip (Legg-Calvé-Perthes disease) in human immunodeficiency virus-infected children. Pediatrics 2002;109:e74.
24. Tebas P, Powderly WG, Claxton S, et al. Accelerated bone mineral loss in HIV-infected patients receiving potent antiretroviral therapy. AIDS 2000;14:F63-F67.
APPENDIX A
METHODOLOGIES FOR MEASURING BODY COMPOSITION
Click here to view Table A-1: Methodologies for Measuring Body Composition
APPENDIX B
ANTHROPOMETRIC MEASUREMENT GUIDELINES
General Rules for Measurement Techniques:
- Always document measurement conditions. For example, indicate the scale used, whether a length or height measure was taken, or if a child was unstable or moving during the measurement.
- Calibrate equipment according to individual facility policy.
- Remember that accuracy of measurements is directly dependent on subject cooperation.
- Measurements of weight, height/length, and head circumference should be plotted on NCHS growth charts and followed closely, monitoring trends.
- Compare current measurements with prior ones, checking for consistency. If current measurements are inconsistent with the previous ones, measurements should be repeated during the visit.
Weight- Use an electronic scale or beam scale with nondetachable weights.
- Zero scale prior to each measure. Calibrate scales when needed.
- Weigh infants and young children lying down with infants only wearing a dry diaper during measurement and small children in a gown or very light clothing.
- Weigh children who can stand on a beam scale, preferably ones with “handle bars” for support. Calm children down and reduce their movement as much as possible for accurate measurements. Children should only be wearing a gown or very light clothing.
- For children too large for the infant scale who have disabilities that prevent them from standing on a beam scale, using a bed scale is most accurate. However, if equipment is not available, a staff member or caretaker can hold the child on a beam scale, take his/her own weight on the same scale, and subtract to calculate the child’s estimated body weight. When using this method, take the average of two measures and make note that this method was used.
Length- Measure children’s recumbent length up to 24 months of age and, for those unable to stand, up to 36 months of age on a calibrated length board with a stable headboard and a sliding footboard.
- Two people are required to perform an accurate length measurement. One person holds the head in place with two hands while the other slides the footboard and takes the reading. The child's foot should be flat against the footboard with toes pointing straight upward and legs should be straight at the time of measurement.*
* If a child has hypertonicity and cannot be held in the above position, other forms of measurement, such as recumbent lengths (performed while contractures are stretched), supra pubic symphysis-to-crown height, sitting heights, or arm span, should be performed.
Height- Once a child is >24 months of age and can stand upright, stature is measured using a calibrated stadiometer.
- For best results, measure child while he/she wears a gown or clothing in which one can visualize body position. Children need to stand with bare feet close together, body and legs straight, arms at sides, relaxed shoulders, and head, back, buttocks, and heels up against the wall or shaft of the stadiometer.
- Instruct child to look straight ahead and stand tall, keeping heels on the ground.
- Bring headboard down to top of the child’s head while at eye-to-eye level with child and record measure to nearest 0.1 cm.
Head Circumference- Measure head circumference in children regularly at routine physical examination appointments up until 36 months of age or according to study parameters.
- Have infant or child sit on caregiver’s lap or stand if capable.
- Remove any hair pieces that could interfere with measurement.
- Place non-stretchable measuring tape just above the eyebrow and ears and straight around the occipital bulge in the back of the child's head.
- Compress hair with tape and record measure to the nearest 0.1 cm.
Mid-Arm Circumference- Use a non-stretchable centimeter tape, with millimeters delineated. On the non-dominant arm bent at a 90-degree angle with palm facing up, mark the midpoint between the acromium and olecranon processes. Make sure clothing is pushed up above the shoulder or removed if interfering with arm tissue.
- Measure the distance around the arm at the mark and record to the nearest 0.1 cm.
Triceps Skinfold Thickness- Grasp vertical fold of fat about 1 to 2 cm above the midpoint using forefinger and thumb.
- Measure skinfold with calipers at the midpoint after needle stabilizes while continuing to hold the fold with hand.
- Average three measures.
- Edematous tissue and very squirmy children are two main factors that prevent accuracy of this measurement.
- Measure to the nearest 0.5 millimeter.
Mid-Arm Muscle Circumference- Use the following equation to calculate mid-arm muscle circumference:
MAMC = MAC - (TSF x 3.14)/10
MAMC = Mid-arm Muscle Circumference in cm
MAC = Mid-arm Circumference in cm
TSF = Triceps Skinfold in mm
Modified from Nutrition Guidelines for HIV-Infected Children, Pediatric AIDS Clinical Trials Group, April 29, 1998.
Click here to view Table B-1: Percentiles of Upper Arm Circumference and Estimated Upper Arm Muscle CircumferenceClick here to view Table B-2: Percentiles for Triceps SkinfoldClick here to view Table B-3: Body Mass Index Norms (Percentile Values of Body Mass Index*)
APPENDIX C
RECOMMENDED ENERGY INTAKE FOR HEALTHY CHILDREN
Click here to view Table C-1: Recommended Energy Intake for Healthy Children
APPENDIX D
SELECTED NUTRITIONAL SUPPLEMENTS FOR TODDLERS, YOUNG CHILDREN, AND ADOLESCENTS
Click here to view Table D-1: Selected Nutritional Supplements for Toddlers and Young Children
Click here to view Table D-2: Selected Nutritional Supplements for Adolescents
APPENDIX E
STEP-ONE AND STEP-TWO DIETS
Click here to view Table E-1: Step-One Diet
The Step-Two diet requires detailed assessment of current eating patterns and instruction by a physician, registered dietitian, registered nurse, nutritionist, or other appropriately trained health professional. This eating pattern requires careful planning to ensure adequacy of nutrients, vitamins, and minerals.
Click here to view Table E-2: Step-Two Diet