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Original Studies |
Section of Pediatric Hematology and Oncology (K.N., H.H.), the Section of Growth and Reproduction (K.H., J.M.), and the Pediatric Nutrition Unit (K.F.M.), The Juliane Marie Center, Rigshospitalet, DK-2100 Copenhagen; and the Research Department of Human Nutrition and Center for Advanced Food Studies, Royal Veterinary and Agricultural University (K.F.M., C.M.), DK-1958 Frederiksberg, Denmark
Address all correspondence and requests for reprints to: Dr. Karsten Nysom, Kurvej 16, DK-2880 Bagsværd, Denmark. E-mail: nysom{at}dadlnet.dk
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Body mass index [BMI; weight (kilograms)/height (meters)2] is considered the best weight-height index in both children and adults, regarding independence of height, correlation with body fat content (fatness), and prediction of mortality (2). An elevated BMI (overweight) in childhood and adolescence increases the risk of overweight in adulthood (3, 4). Overweight in childhood (5), adolescence (6), and adulthood (7, 8) is associated with excessive morbidity and mortality. In industrialized countries, the prevalence of overweight has increased over the last decades (9).
Impaired GH secretion is common after cranial irradiation for childhood ALL (10). GH-deficient children (11) and adults (12) are fat, even when matched for BMI. Consequently, BMI is probably a less valid measure of fatness in survivors of childhood ALL than in the background population. Excessive overweight after childhood ALL has been reported frequently (13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25), but only two groups measured the body composition directly (25, 26).
We measured the BMI and the whole body percent fat of 95 survivors of childhood ALL, examined how these variables varied with previous therapy, and tried to identify risk factors for excessive fatness after ALL treatment.
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Subjects and Methods |
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From the population-based Danish Cancer Registry (27), 304 ALL patients were identified who were, at most, 14 yr old when diagnosed between 1970 and 1990 (inclusive) while residing in eastern Denmark. On January 1, 1993, 11 patients were still receiving therapy, 127 had died, and 4 emigrants were lost to follow-up.
Of 162 eligible patients, 128 (79%) participated in the present study. Thirty-two patients declined to participate for personal reasons, 1 was pregnant, and 1 had a relapse before being studied. To study fatness after standard ALL therapy, we excluded 24 patients treated for a relapse, 1 treated for a second malignancy, and 6 others treated with bone marrow transplantation or mediastinal irradiation. Two participants were too young to be compared with adequate reference values. This leaves 95 patients off therapy in first remission of ALL for the present analysis.
Four participants were of non-European ethnicity: one was from India, one was from Egypt, one had an Egyptian mother and a Danish father, and one had a Danish mother and a Palestinian father. One participant was born after 26 weeks gestation, but had no known sequelae from this. Another participant had recently gone through precocious puberty without receiving adequate therapy. At the time of the study, one participant was undernourished due to a long standing esophageal stricture, and one used beclomethasone inhalations for asthma.
The median age of the participants was 4.0 yr at diagnosis (range, 0.5–14.8 yr), 7.0 yr at completion of therapy (range, 3.5–19.7 yr), and 16.2 yr at the time of the study (range, 6.1–34.2 yr). The median length of follow-up was 10.7 yr from diagnosis (range, 3.4–23.4 yr) and 7.6 yr from completion of therapy (range, 1.2–18.3 yr).
The participants had been treated with multiagent chemotherapy as described previously (28). All had received corticosteroids: 27 received dexamethasone (median cumulative dose, 340 mg/m2; range, 180–2,400), and 93 received other corticosteroids, mainly prednisone (median cumulative dose, 5,600 mg/m2 prednisone; range, 200–31,900). Doses of corticosteroids other than prednisone and dexamethasone were corrected to prednisone equivalent doses; for some multiple regression analyses, doses of dexamethasone were also corrected to prednisone equivalent doses (1 mg prednisone was considered equivalent to 0.15 mg dexamethasone, 0.8 mg methylprednisolone, or 4 mg hydrocortisone). All participants received a median of 10 intrathecal methotrexate injections (range, 4–25), 67 received a median of 4 intermediate or high dose methotrexate infusions (range, 3–8), and 60 received doxorubicin, daunorubicin, or both (median cumulative dose, 197 mg/m2; range, 23–301).
Thirty-nine participants received prophylactic cranial irradiation in doses of 15 Gy (n = 3), 18 Gy (n = 19), or 24 Gy (n = 17), mostly (n = 34) in 2-Gy fractions. None received irradiation to any other field.
Regarding cranial irradiation and corticosteroid therapy, all but 4 participants could be assigned to 1 and only 1 of 3 groups: group I, treated with prednisone but without cranial irradiation and dexamethasone (n = 53; 26 males and 27 females; median age, 4.0 yr at diagnosis, 17.0 yr at follow-up; median dose of prednisone, 6600 mg/m2); group II, treated with prednisone and cranial irradiation but without dexamethasone (n = 15; 6 males and 9 females; median age, 4.3 yr at diagnosis, 16.1 yr at follow-up; median dose of prednisone, 7700 mg/m2); and group III, treated with prednisone, cranial irradiation, and dexamethasone (n = 23; 16 males and 7 females; median age, 3.4 yr at diagnosis, 8.8 yr at follow-up; median dose of prednisone, 2200 mg/m2; median dose of dexamethasone, 320 mg/m2).
Anthropometry
BMI was measured by experienced staff. Data at diagnosis, cessation of therapy, 1-yr intervals thereafter up to 10 yr after cessation of therapy, and follow-up examination were compared with French reference values (29). The French reference values and unpublished Danish reference values based on 32,500 measurements from 0- to 45-yr-old subjects examined between 1967–1985 have 10th, 50th, and 90th percentiles close to each other for both genders throughout the age range studied (figure not shown), and the mean BMI z-score of the Danish sample based on the French reference values is 0.03 (Nysom, K., unpublished manuscript).
Body composition assessment
Whole body fat mass and total mass were determined at follow-up examination between October 1992 and May 1995 by dual energy x-ray absorptiometry using a 1000/W scanner (Hologic, Inc., Waltham, MA). Whole body percent fat was calculated as fat mass divided by total mass. In adults, the coefficients of variation for the 1000/W scanner is 1.8% for percent fat (30).
Control groups
Whole body percent fat measurements were compared with local reference values for children and adolescents (n = 343; age, 6–19 yr) (31, 32) or young adults (n = 120; 40 men and 80 women; age, 20–38 yr) (Mølgaard, C., unpublished data). The latter group consisted of healthy staff members or university students and follow-up of 41 adolescents examined by us previously (31) [mean height: 182.7 cm (SD, 5.9) in men, 169.1 cm (SD, 6.9) in women; weight: 77.2 kg (SD, 9.1) in men, 63.9 kg (SD, 7.2) in women; BMI: 23.1 kg/m2 (SD, 2.3) in men, 22.4 kg/m2 (SD, 2.7) in women].
BMI at follow-up was compared with data from the same group and with data from 485 20- to 29-yr-old subjects from a population study examined between 1991–1994 (33).
Hormone assessment
The GH axis was tested in all except five participants by arginine infusion as described previously (34). In brief, after overnight fasting, GH secretion was stimulated by arginine infusion, and blood samples were drawn at 0, 30, 60, 90, 120, and 150 min. Until November 1993 (n = 58), samples were analyzed with an enzyme-linked immunosorbent assay using a monoclonal antibody (Norditest, Novo Nordisk, Gentofte, Denmark) with a cut-off value of 2.04 µg/L in children (<18 yr of age) and 1.22 µg/L in adults. From November 1993 (n = 32), a time-resolved fluoroimmunometric assay (Delfia, Wallac, Inc., Turku, Finland), with a cut-off value of 15 mU/L in children and 9 mU/L in adults, was used. At follow-up, three participants (one male) received GH therapy.
Data analysis
Results were analyzed as age- and sex-specific z-scores. The z-scores for BMI and percent fat were calculated with the LMS method of Cole and Green (35). Percent fat z-scores for the two men who were 30 yr or older were based on predicted values for 30-yr-old men, because only three control men were older than 30 yr. A t test was used to test for mean z-scores different from 0 and to test for different mean z-scores in two groups. To test for z-score differences between three or four groups, an ANOVA with a Tukey correction of the significance level was used. Changes in BMI after cessation of therapy were studied by analysis of covariance: a common linear trend was superimposed on an individual base level, regarded as a random effect. Thus, the individual level was regarded as the realization of a normally distributed variate with mean of zero. The corresponding variance describes the variation of BMI among patients. Finally, a measurement error must be included, in brief: BMI = common trend + individual level + measurement error.
After the removal of trend, a test for autocorrelation between successive measurements in individual patients was performed. Finally, the analysis was repeated for the three treatment subgroups described above. Simple and multiple linear regression was used to examine the relation between percent fat (in z-scores) and previous therapy, sex, age at diagnosis and follow-up, and length of follow-up. P < 0.05 was considered statistically significant. BMI and percent fat z-scores larger than 1.28, corresponding to the 90th percentile of a normal distribution, were considered increased. At 20 yr of age, the 90th percentile of the French BMI reference values (29) is 25.0 kg/m2 in men and 24.3 kg/m2 in women. Data were analyzed with SAS computer software (SAS Institute, Cary, NC) (36).
Ethics
All participants and the parents of the children younger than 18 yr gave their written informed consent. The study was in accordance with the Helsinki II declaration and was approved by the local medical ethics committee of Copenhagen and Frederiksberg, Denmark (Approval KF V92–097).
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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]. It increased
significantly during therapy (estimated increase, 0.84; CI, 0.56–1.11)
to 0.66 (CI, 0.46–0.85) at cessation of therapy. After cessation of
therapy, the mean BMI remained largely unchanged (Fig. 1; P
= 0.07 for trend, tending to indicate a weak decrease), and at
follow-up, it was significantly above the predicted value (Table 1). The mean BMI was, however, also
significantly above the predicted value in local control groups
examined during the same years as the patients (Table 1); BMI did not
differ significantly between patients and dual energy x-ray
absorptiometry controls (P = 0.07, by t
test; P = 0.25, by ANOVA) or between 26 patients older
than 20 yr and population study controls (mean z-scores, 0.14 and 0.20;
P = 0.76, by t test; P =
0.64, by ANOVA).
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shows the BMI of three groups of
patients according to cranial irradiation and corticosteroid therapy.
At cessation of therapy, the group treated with dexamethasone tended to
have higher BMI than the other two groups, but CIs were wide (Fig. 2),
and consequently, the BMI at diagnosis, cessation of therapy, and
follow-up and the increase from diagnosis to cessation of therapy did
not differ significantly among the three groups (P =
0.90, 0.21, 0.46, and 0.41, respectively).
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). This was caused by increased percent fat in the two groups of
patients treated with cranial irradiation with or without dexamethasone
(Table 1). In regression analysis, increased percent fat was
significantly related to GH insufficiency (estimated regression
coefficient 0.84; CI, 0.19–1.49; r2 = 0.07;
P = 0.01) or cranial irradiation (estimated regression
coefficient, 0.81; CI, 0.35–1.27; r2 = 0.12;
P = 0.0008), but GH insufficiency and cranial
irradiation were not both significant in the same model
(P = 0.19 and 0.015). The radiation dose was not
significant (15–18 vs. 24 Gy; P = 0.40) in
a model including cranial irradiation. The cumulative doses of
prednisone or corticosteroids were significant when added to the model
based on cranial irradiation, but these significant relationships
disappeared when one patient who had received the highest cumulative
dose of prednisone was excluded. Sex, age at diagnosis, length of
follow-up, age at follow-up, the number of intermediate or high dose
methotrexate infusions, the number of intrathecal methotrexate
injections, and the cumulative dose of anthracyclines were never
statistically significant (P = 0.15–0.98) when added
to the two significant models, one variable at a time.
Percent fat and BMI z-scores at follow-up were significantly related
(r2 = 0.49; P = 0.0001), but the
95% confidence interval for predicting individual percent fat z-scores
from BMI were more than 3 z-scores wide (Fig. 3). For a given BMI, patients treated
with cranial irradiation had an increased percent fat z-score compared
with the remaining patients (estimated difference, 0.73; CI,
0.40–1.06). Twenty-five patients (26%; CI, 18–36%) had a BMI
z-score and 25 patients (26%; CI, 18–36%) had a percent fat z-score
larger than 1.28, corresponding to the 90th percentile of reference
values.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Several reports describe BMI (13, 14, 15, 16, 17, 18, 19) or other fatness-related anthropometric variables (20, 21, 22, 23, 24) after treatment for childhood ALL. In contrast, only 2 reports describe more direct fat mass measurements. Using dual energy x-ray absorptiometry, Warner et al. (25) found significantly increased whole body percent fat in 21 girls, but not in 14 boys, an average of 7 yr after ALL treatment including cranial irradiation. The BMI of control boys was increased compared with local reference values; this may explain why boys treated for ALL were not fatter than controls. The percent fat of 21 patients treated without cranial irradiation for other malignancies was similar to that of sibling controls. Warner et al. only presented sex-specific results, but the percent fat of normal children also varies with age (32). Therefore, the fatness of our patients and that of the patients of Warner et al. were not comparable. Brennan et al. found an increased degree of fatness in adult survivors of childhood ALL (26). Their findings are, however, not comparable with ours because results were compared with data for BMI-matched controls rather than unselected controls. Excessive fatness was related to more severe GH deficiency at follow-up (26).
In the present study, a higher percent fat was associated with cranial irradiation or GH insufficiency, and percent fat was normal in patients treated without cranial irradiation. Cranial irradiation is a risk factor for GH insufficiency after childhood ALL (37), so the influence of these two risk factors could not be separated. The degree of fatness was, however, more closely associated with cranial irradiation than with GH insufficiency. This may be because we stimulated the GH secretion of adults with arginine rather than with the recently recommended insulin hypoglycemia (38), because we classified the GH secretion of patients based on one stimulation test rather than two, or because factors other than GH associate cranial irradiation with excess fatness. Children (11) and adults (12) who are GH deficient for other reasons than childhood ALL therapy are fat. We were unable to identify any other patient or treatment characteristics that were significantly related to percent fat.
Excess fatness develops if energy intake exceeds energy expenditure, if endocrine disturbances or inactivity redistribute the body mass toward reduced lean body mass and increased fat mass, or both. Reduced resting energy expenditure does not seem to cause excess fatness after childhood ALL; at diagnosis, the resting energy expenditure is increased in patients with a large tumor burden, but is normal in others (39). Once a remission is obtained, the resting energy expenditure normalizes (39) and remains normal during maintenance therapy (40). Several years after cessation of ALL therapy, the resting energy expenditure is similar to that in controls (41) or slightly lower (42). Adjusted for a reduced lean body mass, the resting energy expenditure of GH-deficient adults is also normal (43, 44).
Warner et al. found that energy expenditure during exercise (25) and physical activity level (41) were reduced in ALL survivors treated with cranial irradiation, but normal in patients treated for other malignancies without cranial irradiation. Reilly et al. (42) reported that habitual physical activity was also reduced in ALL survivors treated without cranial irradiation, and energy expended on habitual physical activity was significantly inversely correlated with BMI changes during the following 6 months. Physical inactivity has also been associated with overweight in normal children (45, 46). GH-deficient adults have a reduced exercise capacity (47), so the reduced physical activity after childhood ALL may at least partly be caused by GH deficiency.
Psychosocial consequences of leukemia and its treatment, such as overprotection or mood disturbances (48), may cause less physical activity after childhood ALL. In the present study, however, percent fat differed considerably between treatment groups, so either psychosocial factors played only a minor role or their severity was related to previous therapy (e.g. cranial irradiation). Cranial irradiation may also have damaged the leptin feedback loop between adipose tissue and the central nervous system (26), or cranial irradiation may be associated with reduced energy expenditure in some unknown way. In a previous study (16), BMI was increased both in patients treated with cranial irradiation and in patients treated without irradiation but with more methotrexate doses, suggesting that both of these types of central nervous system prophylaxis cause obesity (16). In the present study, however, fatness was related to cranial irradiation, but not to the number of methotrexate doses.
Warner et al. suggested that reduced energy expenditure during low intensity exercise (25) and reduced physical activity level (41) after childhood ALL were caused by cardiac damage from anthracyclines. However, they never examined the relationship between anthracycline dose and fatness directly (25, 41). Most of their ALL patients had received cumulative anthracycline doses of 90–270 mg/m2, but patients treated for other malignancies had normal percent fat, energy expenditure, and physical activity level despite the fact that nearly half of them (9 of 21) had received a median of 300 mg/m2 of anthracyclines (25, 41). Sophisticated methods can detect subclinical cardiac abnormalities in patients treated with low doses of anthracyclines (49, 50), but clinical anthracycline cardiotoxicity 10 yr after cumulative doses around 200 mg/m2 is rare (51). In the present study, percent fat and cumulative anthracycline dose were not significantly related. Consequently, it seems unlikely that anthracycline cardiotoxicity caused the excessive fatness of our patients.
Although our patients had an increased percent body fat, their BMI differed only marginally from that of nearly 1000 controls from the same region examined during the same period. Another Danish study (19) recently found a mean BMI z-score of 0.61 at attainment of final height, which increased significantly to 1.27 4 yr later. We found no such tendency for a higher BMI in older patients. In the other Danish study and in studies from The Netherlands (16) and the United States (14), BMI z-scores at follow-up tended to be more elevated than in our patients. The 3 previous studies did, however, all use reference values that were based on measurements made 10–20 yr before patients were measured, and the studies did not include recently examined local control groups. In industrialized countries, the average BMI and the prevalence of overweight have increased over the last decades (9), and the use of old reference values, random variation, and, perhaps, variation in the use and dose of cranial irradiation probably explain why our BMI findings do not agree fully with those of others.
Cranial irradiation was a risk factor for increased BMI in some previous studies (13, 15, 24, 25), but like two other studies (16, 19) we found no significant relationship between BMI and cranial irradiation. Consequently, the majority of unirradiated patients in the present study could not explain the limited BMI abnormalities. Dexamethasone has also been associated with more overweight after ALL therapy than prednisone (16, 24), but in our analyses, neither percent fat nor BMI at follow-up was significantly related to the use of dexamethasone.
Different frequencies and severities of GH insufficiency and the resulting body composition changes probably explain why BMI did not differ significantly among our three treatment groups despite their significantly different percent fat values. This may also explain why BMI was not significantly related to cranial irradiation (16, 19) or GH status (19) in some previous studies, and it emphasizes an important limitation of using BMI as a proxy for fatness after childhood ALL.
Some of our participants were of non-European ethnicity, and a few others may have had abnormal body composition for other reasons. When these participants were excluded from the analysis, results were, however, only minimally altered, and conclusions were essentially the same (data not shown).
In conclusion, 11 yr after diagnosis of childhood ALL, the whole body percent fat was significantly increased, and one in four patients was fat. A higher percent fat was related to cranial irradiation or GH insufficiency, but not to sex, the cumulative doses of anthracyclines or corticosteroids, or the type of corticosteroid used.
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Acknowledgments |
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Footnotes |
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Received June 29, 1999.
Accepted September 17, 1999.
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