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*Substance via MeSH
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*Growth Disorders
The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 4 1075-1079
Copyright © 1998 by The Endocrine Society

Original Articles

Comparison of Final Heights of Growth Hormone-Treated Vs. Untreated Children with Idiopathic Growth Failure

John G. Buchlis, Lydia Irizarry, Brian C. Crotzer, Barbara J. Shine, Laura Allen and Margaret H. MacGillivray

Department of Pediatrics, University at Buffalo School of Medicine and Children’s Hospital of Buffalo, Buffalo, New York 14222

Address all correspondence and requests for reprints to: John G. Buchlis, M.D., Division of Endocrinology, Children’s Hospital, 219 Bryant Street, Buffalo, New York 14222.

Abstract

We measured adult heights (Ht) of 94 healthy GH-sufficient children (peak GH > 10 ng/mL, polyclonal RIA) whose Ht at presentation were more than 2 SD below the mean for chronological age, with normal weight-to-Ht ratios, normal body proportions, and pathologic growth velocity for chronological age. Group 1 (n = 36, 6 females) received standardized doses (0.3 mg/kg·week) of GH (mean duration = 41 months), while group 2 (n = 58, 17 females) received no treatment.

Our conclusion was that the mean final Ht SD score in the GH-treated group (-1.5) was significantly greater than in the untreated group (-2.1); P < .001. Genetic predisposition to short stature was evident in both groups: the midparental Ht SD score was -1.1 in the treated and -1.0 in the untreated group. Midparental Ht was met or exceeded by 42% of the GH-treated group but only 15% of the untreated group. Final Ht was not significantly different from predicted Ht, except from GH-treated girls, who exceeded their predicted Ht. Although the mean Ht gains (6.8 cm in girls and 3 cm in boys) were modest and variable, GH treatment provided significantly better Ht outcomes for the majority of children with idiopathic growth failure.

BEFORE 1980, pituitary GH (pGH) was administered exclusively to GH-deficient (GHD) children who were unresponsive to two pituitary stimulation tests. Subsequently, many investigators studied the effects of GH in very short children who were GH sufficient (by provocative testing) and were growing at a subnormal velocity for their age. Various names were given to these short children; i.e. normal variant short stature, idiopathic short stature (ISS), constitutional delay of growth and puberty (CDGP), GH neurosecretory dysfunction, idiopathic growth failure, and non-GHD short stature (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17). Left untreated, many of these short children have failed to reach their midparental target Ht, whereas others have had acceptable Ht outcomes (3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13). Although GH treatment of non-GHD short children has been reported to improve Ht in the short term, opinions differ as to its impact on final Ht (18, 19, 20, 21). Also, there is controversy about the costs, risks, and ethics of administering GH to healthy, very short children for whom an endocrine disorder is undocumented or equivocal (22, 23).

The purpose of our study was to determine whether rGH treatment improved adult Ht outcomes of 36 healthy children with idiopathic growth failure, compared with 58 untreated controls, followed in a single institution. All participants were poorly growing children with Ht greater than 2 SD below the mean at first evaluation in childhood, and all had normal GH responses to two pituitary provocative tests. The Ht outcomes of the two groups were compared with each other, as well as with their midparental and predicted Ht (PH).

Materials and Methods

The study participants consisted of 94 children with idiopathic growth failure, who were followed from childhood to adulthood at The Children’s Hospital of Buffalo. Our population closely resembles children classified as ISS (17). Group 1 (30 males, 6 females) received rGH treatment (0.3 mg/kg per week, divided and given daily by sc injection). The duration of rGH treatment (mean ± SD) was 41 ± 14 months. Group 2 (41 males, 17 females) received no sex hormones or other treatment. Many of the untreated controls were patients who were tested, but not treated, during the PGH era.

The entry criteria for the participants were: 1) Ht SD score more than 2 SD below the mean for chronological age (CA) at initial endocrine evaluation; 2) growth velocity < 5 cm/yr; 3) normal birth weight (Wt) and length; 4) normal Wt-to-Ht ratio; 5) absence of chronic disease or skeletal dysplasia; 6) bone age (BA) delay; 7) normal karyotype (girls mainly); and 8) peak GH >= 10 ng/mL after two standard GH-provocative tests. GH was measured by RIA (polyclonal antibody). BA was determined by the Greulich and Pyle method, and predicted adult Ht was calculated using Bailey-Pinneau tables (24).

All subjects were older than 20 yr when they were recruited for measurement of final adult Ht. Females had a documented BA > 14 yr or growth rates < 2 cm/yr. All males had a BA reading in excess of 16.5 yr. All patients treated with rGH had final Ht measured by the investigators using a stadiometer. Of the 58 untreated subjects, 15 had Ht measured by their primary care physician. Genetic target Ht was calculated from self-reported parental Ht. The anthropometric data are expressed as SD scores based on the normative data of Hanes (25).

Statistical analysis was performed using Wilcoxon matched-pairs, Signed-ranks tests, Mann-Whitney U, {chi}-square, and Pearson corre-lations.

Results

The two groups at referral were similar for the following characteristics (mean ± SD): age, Ht SD score, Wt SD score, BA SD score, predicted Ht SD score, and midparental Ht SD score. In both groups, the delay in Ht and BA SD scores were greater than the delay in Wt SD score (Table 1Go).


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  		Table 1. Baseline data

 
In the GH-treated subjects (Group 1), the baseline age (mean ± SD) was 11.9 ± 2.8 yr, and 78% were prepubertal. The remainder were in early puberty (Tanner 2). The 6 girls in Group 1 were prepubertal, and their age (9.7 ± 1.6 yr) was younger than the boys (12.4 ± 2.8). At referral, the males and females had similar Ht SD scores (-2.9 ± 0.6 and -2.7 ± 0.7), Wt SD scores (-1.2 ± 0.8 and -1.1 ± 0.5), and BA SD scores (-3.0 ± 1.3 and -2.4 ± 1.3), respectively.

In group 2 (untreated), the baseline age (mean ± SD) for the 41 males (12.7 ± 2.8 yr) was similar to the 17 females (12.2 ± 1.3). Fifty-six percent were prepubertal, 24% were Tanner 2, and the rest were Tanner 3. The Ht SD score and BA SD score for the males (-2.9 ± 0.8 and -3.3 ± 1.5) were not significantly different from those for the females (-3.0 ± 0.6 and -2.5 ± 1.8). The influence of genetic short stature was similar for the two groups. The midparental Ht SD score for the treated children (group 1) was -1.1 ± 0.9, compared with that of the untreated subjects (-1.0 ± 0.7).

The Ht outcome data is summarized in Table 2Go and discussed under the following headings:


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  		Table 2. Outcome data

 
Adult Ht of treated vs. untreated groups

The adult Ht SD score in the treated group (-1.5 ± 0.8) was significantly greater than that in the untreated group (-2.1 ± 1.0); P < 0.01 (Fig. 1Go). The final Ht SD score was improved by 1.4 in the treated group vs. 0.8 in the untreated group. Females seemed to benefit more from rGH treatment. Girls treated with rGH were 6.8 cm taller than the untreated controls. In contrast, males treated with rGH were 3.0 cm taller than the untreated controls (Table 2Go).



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  		Figure 1. 70% of the rGH-treated group reached the third percentile, 42% reached or exceeded midparental Ht, and none fell below the lowest midparental Ht SD score. Only three patients reached (whereas none exceeded) an average adult Ht. In contrast, 48% of the untreated group had adult Ht SD scores that reached the third percentile, and 35% fell below the lowest midparental Ht SD score. Only one patient reached an average adult Ht.

 
Final Ht in both groups correlated positively with baseline Ht, midparental Ht, and PH (P < 0.01), but did not correlate significantly with baseline CA, Wt, or BA.

Adult Ht vs. midparental Ht

The adult Ht SD score of the entire treated group (-1.5 ± 0.8) was not significantly different from the midparental Ht SD score (-1.1 ± 0.9); P = 0.05.

In contrast, the adult Ht SD score for the untreated group (-2.1 ± 1.0) was significantly less than the midparental Ht SD score (-1.0 ± 0.7); P < 0.001 (Table 2Go).

Males treated with rGH achieved a mean adult Ht that was only 2 cm less than midparental Ht (167.7 vs. 169.8, respectively); P = 0.08. In contrast, untreated males had a final Ht that was 7 cm below mean midparental Ht (164.7 vs. 171.7, respectively); P < 0.001 (Table 2Go).

Females treated with rGH achieved a mean adult Ht that was 2.4 cm less than mean midparental Ht (154.8 vs. 157.2, respectively); P = 0.46. In contrast, untreated females reached a mean final Ht that was 8.2 cm less than mean midparental Ht (148.0 vs. 156.2, respectively); P < 0.01 (Table 2Go).

A significantly greater number of children treated with rGH (42%) achieved or exceeded midparental Ht, compared with the untreated group (15%); P < 0.01 (Fig. 1Go).

Adult Ht vs. PH

Within each group, the mean adult Ht SD score was not significantly different from the predicted Ht SD score, except for the treated females, who reached a mean adult Ht SD score of -1.3; this was significantly greater than their predicted Ht SD score (-2.0) (Table 2Go). A greater percentage of ISS children (63%), treated with rGH, achieved or exceeded PH, compared with the untreated ISS children (47%); but this difference did not reach statistical significance.

Discussion

Opinions differ as to the prognosis for adult Ht in children with idiopathic growth failure. Much of the disagreement relates to the lack of precision in classifying very short, slowly growing children and to the selection of short children with both normal and abnormal growth rates. The names applied often suggest an innocent condition: ISS, normal variant short stature, CDGP, and nonendocrine short stature (1, 2, 3, 4, 5, 6, 7, 8, 9, 10). Whereas some of the children seem to have a combination of genetic short stature and constitutional growth delay, others seem to have a growth disorder based on their pathologic growth rates and Ht. The existing confusion will not be clarified until we have more precise methods for subdividing short children into homogenous groups.

In other studies pertaining to adult Ht of patients with untreated ISS, Ht outcomes were compared with predicted and midparental target Ht (Table 3Go). In most instances, mean final Ht was similar to PH and less than genetic target Ht (4, 5, 6, 8, 12). The range of mean final Ht SD scores was between -0.7 and -2.7 for males and between -0.6 and -2.5 for females. At baseline, the starting Ht SD were between -1.9 and -3.4. Girls had a worse prognosis for adult stature in three studies; the probable cause was the earlier onset of puberty in females, compared with males (4, 9, present study). Also, children with markedly delayed BA were likely to have their adult Ht overpredicted (3). Bramswig observed that the prognosis for adult Ht was good if both parents had normal Ht. In contrast, if one or both parents were short (father < 165 cm; mother < 155 cm) the child’s potential for growth was compromised (7). The adult Ht of our untreated control patients are similar to those observed by Albanese and colleagues. The prognosis for these children to reach an average adult Ht was observed to be less than 2% (9, 10). Only 5% of males in the Albanese study and 15% of our control group reached midparental Ht. The variability observed in the Ht outcomes of the studies shown in Table 3Go probably is caused by differences in the selection criteria for patients and differences in underlying etiology.


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  		Table 3. Height outcomes of untreated ISS patients

 
In most of the investigations that have evaluated the benefits of GH treatment in children with ISS, the Ht outcomes were compared mainly with midparental Ht and PH, and seldom to untreated controls (Table 4Go). The present study focused on comparing the final Ht of rGH-treated vs. untreated children with ISS. Also, the Ht outcomes in the two groups were compared with midparental and PH. We observed significantly better Ht outcomes in the rGH-treated group, compared with untreated controls. However, the Ht gains were modest and variable. Nevertheless, 70% of the rGH-treated group reached the third percentile and 42% reached or exceeded midparental Ht; only three patients reached (whereas none exceeded) an average adult Ht. The distribution of adult Ht SD scores in the rGH-treated group was similar to the range of the midparental Ht SD scores, and none fell below the lowest midparental Ht SD score (Fig. 1Go). The mean final Ht SD score in the rGH-treated group was not significantly different from the midparental or predicted Ht SD scores. In contrast, 48% of the untreated group had adult Ht SD scores that reached the third percentile, and 35% fell below the lowest midparental Ht SD score. Only one patient reached an average adult Ht (Fig. 1Go). When rGH-treated males and females were compared with their untreated counterparts, treated girls gained more mean Ht (6.8 cm) than treated boys (3 cm). These findings are similar to those previously reported (17). Genetic factors seemed to have a major impact on the Ht outcomes of our entire population of short children; approximately 90% of the midparental Ht SD scores fell below the average adult Ht. When genetic predisposition to short stature is taken into consideration, it becomes apparent that rGH therapy was beneficial, because all of the treated population reached adult Ht that were compatible with genetic endowment, whereas one-third of the untreated group did not.


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  		Table 4. Height outcomes of children with ISS after GH treatment

 
How do the adult Ht of our rGH-treated ISS population compare with the final Ht of similarly treated GHD children? Blethen reported a mean adult Ht SD score of -0.7 in 121 GHD children who had received 0.3 mg per kilogram per week rGH for approximately 8 yr (26). In a recent outcome study of our own GHD children (n = 95), treated exclusively with rGH for 3.8 yr, the mean adult Ht SD score was -1.4 (27). Other reports have documented that final Ht SD scores after GH treatment ranged from -1.4 to -4.7, with the worst outcomes seen in GHD children who had received low doses and interrupted GH treatment during the PGH era (14, 28). On the basis of this comparison, we concluded that Ht outcomes after rGH treatment in our ISS population (mean Ht SD = -1.5) compared favorably with those seen in rGH-treated GHD children. Adult Ht above the 3rd percentile were attained in 87% of the GHD population in the Blethen study vs. 70% in our ISS children. The mean baseline Ht SD score in our ISS patients (-2.9) was similar to those reported by Blethen (-3.0) and MacGillivray (-2.8) in GHD children. However the ISS and GHD groups had different genetic influences (midparental Ht SD score in ISS = -1.1 vs. -0.3 in GHD) (27). Also, etiology in the GHD group was more homogeneous than in the ISS group. When all factors were taken into consideration, the efficacy of GH treatment in the GHD and ISS populations was similar.

Very short, slowly growing GH-sufficient children whose Ht are more than 2 SD below the mean for CA are a far greater challenge to pediatric endocrinologists than is the child with documented GH deficiency. Reassurance about Ht outcomes based on initial BA and Ht may not be justified because of inaccuracies in Ht prediction methods. Our data indicate that final Ht without treatment will fall below genetic target Ht in most of these children and that their chance of reaching an average adult Ht is almost negligible. We observed that rGH treatment seemed to improve Ht outcomes in some (but not all) children. Until there is wider availability of genetic tests for mutations in the genes for GH and the GH receptor, treatment decisions will depend on clinical judgment (29, 30). Whether these children would benefit from GH treatment depends on the etiology of the growth disturbance. The heterogeneity of the clinical responses to GH treatment in current clinical trials is not surprising, given the likelihood that various etiologies are responsible for the short stature within the study populations.

Received August 5, 1997.

Revised December 5, 1997.

Accepted December 17, 1997.

References

  1. Rudman D, Kutner M, Blackston D, Cushman R, Bain R, Patterson J. 1981 Children with normal-variant short stature: treatment with human growth hormone for six months. N Engl J Med. 305:123–130.[Abstract]
  2. Van Vliet G, Styne D, Kaplan S, Grumbach M. 1983 Growth hormone treatment for short stature. N Engl J Med. 309:1016–1022.[Abstract]
  3. Blethen SL, Gaines S, Weldon V. 1984 Comparison of predicted and adult heights in short boys: effect of androgen therapy. Pediatr Res. 467–469.
  4. Ranke MB, Aronson AS. 1989 Adult height in children with constitutional short stature. Acta Paediatr Suppl. 362:27–31.
  5. Crowne EC, Shalet SM, Wallace WHB, Eminson DM, Price DA. 1990 Final height in boys with untreated constitutional delay of growth and puberty. Arch Dis Child. 65:1109–1112.[Abstract]
  6. Crowne EC, Shalet SM, Wallace WHB, Eminson DM, Price DA. 1990 Final height in girls with untreated constitutional delay of growth and puberty. Eur J Pediatr. 150:708–712.
  7. Bramswig JH, Fasse M, Holthoff ML, Von Lengerke HJ, Petrykowski W, Schellong G. 1990 Adult height in boys and girls with untreated short stature and constitutional delay of growth and puberty: accuracy of five different methods of height prediction. J Pediatr. 117:886–891.[CrossRef][Medline]
  8. LaFranchi S, Hanna C, Mandel S. 1991 Constitutional delay of growth: expected vs. final adult height. Pediatrics. 87:82–86.[Abstract/Free Full Text]
  9. Albanese A, Stanhope R. 1993 Does constitutional delayed puberty cause segmented disproportion and short stature. Eur J Pediatr. 152:293–296.[CrossRef][Medline]
  10. Albanese A, Stanhope R. 1995 Predictive factors in the determination of final height in boys with constitutional delay of growth and puberty. J Pediatr. 126:545–550.[CrossRef][Medline]
  11. Zadik Z, Chalew S, Zung A, et al. 1994 Effect of long term growth hormone therapy on bone age and pubertal maturation in boys with and without classic growth hormone deficiency. J Pediatr. 125:189–195.[Medline]
  12. Sperlich M, Butonandt O, Schwarz HP. 1995 Final height and predicted height in boys with untreated constitutional growth delay. Eur J Pediatr. 154:627–632.[CrossRef][Medline]
  13. Wit JM, Boersma B, Keizor-Schrama SM, et al. 1995 Long term results of growth hormone therapy in children with short stature, subnormal growth rate and normal growth hormone response to secretagogues. Clin Endocrinol (Oxf). 42:365–372.[Medline]
  14. Wit JM, Kamp GA, Rikken B. 1996 Spontaneous growth and response to growth hormone treatment in children with growth hormone deficiency and idiopathic short stature. Pediatr Res. 39:295–302.[Medline]
  15. Spiliotis BE, August GP, Hung W, Sonis W, Mendelson W, Bercu BB. 1984 Growth hormone neurosecretory dysfunction. JAMA. 251:2223–2230.[Abstract]
  16. Cara JF, Johanson AJ. 1990 Growth hormone for short stature not due to classic growth hormone deficiency. Pediatric Clin North Am. 37:1229–1254.
  17. Hintz RL, on behalf of the Genentech Study Group. 1996 Increase in near-final height in short non-Growth Hormone deficient children treated with growth hormone. Clin Pediatr Endocrinol. [Suppl 7] 5:19–25.
  18. Bierich JR, Nolte K, Drews K, Brugmann G. 1992 Constitutional delay of growth and adolescence. Result of short-term and long-term treatment with growth hormone. Acta Endocrinol (Copenh). 127:392–396.[Medline]
  19. Zadik Z, Mira U, Landau H. 1992 Final height after growth hormone therapy for peripubertal boys with a subnormal integrated concentration of growth hormone. Horm Res. 37:150–155.[Medline]
  20. Loche S, Cambiaso P, Setzu S, et al. 1994 Final height after growth hormone in non-growth hormone deficient children with short stature. J Pediatr. 125:196–200.[CrossRef][Medline]
  21. Guyda HJ. 1996 Growth hormone treatment of non-growth hormone deficient subjects: the international task force report. Clin Pediatr Endocrinol. [Suppl 7] 5:11–18.
  22. Lantos J, Siegler M, Cuttler L. 1989 Ethical issues in growth hormone therapy. JAMA. 461:1020–1024.
  23. Cutler L, Silvers JB, Singh J, et al. 1996 Short stature and growth hormone therapy. JAMA. 276:531–537.[Abstract]
  24. Bayley N, Pinneau SR. 1952 Tables for predicting adult height from skeletal age: revised for use with the Greulich-Pyle hand standards. J Pediatr. 40:423–441.[CrossRef][Medline]
  25. Hamill PV, Drizd TA, Johnson CL, Reed RB, Roche AF, Moore WM. 1979 Physical growth: National Center for Health Statistics percentiles. Am J Clin Nutr. 32:607–629.[Abstract/Free Full Text]
  26. Blethen SL, Baptista J, Kuntze J, Foley T, LaFranchi S, Johnson A. 1997 Adult height in growth hormone (GH) deficient children treated with biosynthetic GH. J Clin Endocrinol Metab. 82:418–420.[Abstract/Free Full Text]
  27. MacGillivray MH, Clopper R, Sandberg DE, Buchlis JG, Irizarry L. 1997 Final height outcomes of hypopituitary children after growth hormone (GH) treatment during the pituitary GH (pGH) and recombinant GH (rGH) eras. Pediatr Res. 41:69A.
  28. Price DA, Ranke MB. 1994 Final height following growth hormone treatment. In: Ranke MB, Gunnarson R, eds. Progress in growth hormone - 5 years of KIGS. Mannheim, Germany: J & J Verlag; 129–144.
  29. Takahashi Y, Kaji H, Okimura Y, Goji K, Abe H, Chichara K. 1996 Brief report: short stature caused by a mutant growth hormone. N Engl J Med. 334:432–465.[Free Full Text]
  30. Laron Z. 1995 Prismatic cases: Laron syndrome (primary growth hormone resistance) from patient to laboratory to patient. J Clin Endocrinol Metab. 80:1526–1531.[Abstract/Free Full Text]
  31. Hintz RL, Attie KM, Johnson AJ, et al. Growth hormone treatment of idiopathic short stature increases mean final height. N Engl J Med. In press.



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Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals