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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 9 3262-3265
Copyright © 2000 by The Endocrine Society

Original Studies

Linear Growth and Final Height after Treatment for Cushing’s Disease in Childhood

Marie-Christine Lebrethon1, Ashley B. Grossman, Farhad Afshar, P. Nicholas Plowman, G. Michael Besser and Martin O. Savage

Pediatric Endocrinology Section (M.C.L., M.O.S.), Departments of Endocrinology (A.B.G., G.M.B.), Neurosurgery (F.A.), and Radiotherapy (P.N.P.), St. Bartholomew’s Hospital, London, United Kingdom EC1A 7BE

Address all correspondence and requests for reprints to: Prof. Martin O. Savage, Pediatric Endocrinology Section, Department of Endocrinology, St. Bartholomew’s Hospital, West Smithfield, London, United Kingdom EC1A 7BE. E-mail: m.o.savage{at}mds.qmw.ac.uk


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Cushing’s disease is associated with growth failure in childhood and adolescence. Growth and final height were analyzed in 10 patients who were cured or in remission after treatment of Cushing’s disease. Seven males and 3 females, aged 6.8–17.6 yr (bone age, 3.3- 15.4 yr), had transsphenoidal surgery, which was combined with pituitary irradiation (4500 cGy in 25 fractions) in 5 patients. At presentation, 5 patients were prepubertal (males), and 5 were pubertal (2 males and 3 females). The mean height SD score was -2.15 ± 1.26 (range, -0.21 to -4.32) compared with mean target height SD score of -0.43 ± 0.58. Height velocity in 6 patients was subnormal (0.9–3.8 cm/yr). After treatment, short-term height velocity, over a mean interval of 0.57 yr, in 8 patients not receiving human GH (hGH) therapy, was variable (range, 0.8–7.6 cm/yr). GH stimulation tests (insulin tolerance test/glucagon) in 9 subjects showed peak GH levels of 0.5–20.9 mU/L. Eight were treated with hGH (14 IU/m2·wk), combined in 2 girls and 1 boy with a GnRH analog. After 1 yr of hGH, the mean height SD score had increased from -2.45 ± 1.0 at initiation of hGH to -2.07 ± 1.2 (P = 0.01). GH therapy was continued until final height or latest assessment. The mean final height SD score (n = 6) was -1.24 ± 1.38, and at the latest assessment the mean height SD score (n = 4) was -1.52 ± 1.33. Combining these 2 groups, the mean height SD score was -1.36 ± 1.29. The difference between final or latest height SD score and target height SD score was 0.93 ± 1.13, i.e. less (P = 0.005) than the difference between height and target height SD score of 1.72 ± 1.26 at presentation. In conclusion, catch-up and favorable long-term growth was seen after treatment for Cushing’s disease. Posttreatment GH deficiency was frequent, and early hGH replacement may have contributed to the encouraging outcome.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
GROWTH FAILURE and weight gain are frequently seen in children and adolescents with pituitary-dependent Cushing’s syndrome, Cushing’s disease (1, 2, 3, 4, 5). Virilization may lead to acceleration of bone age and further compromise growth potential (6). A decrease in free insulin-like growth factor I (IGF-I) and resistance to IGF-I and other growth factors (7) may contribute to growth failure. GH deficiency, both before and after transsphenoidal surgery for childhood Cushing’s disease, has also been described (7). However, as reported in important studies from the NIH (3, 8), a major factor causing growth retardation may be prolonged exposure to supraphysiological free circulating glucocorticoids, which in their patients was associated with inadequate posttreatment catch-up growth and compromised final adult height.

We have previously reported normal final height after pituitary irradiation for Cushing’s disease (9). We now describe the growth features in 10 children and adolescents with Cushing’s disease managed in a single center and contrast our findings particularly with those of the NIH study (8). Our results show that long-term catch-up growth and satisfactory final height can be achieved in these patients.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Ten patients (seven boys and three girls), aged 12.9 ± 3.4 yr (range, 6.8–17.4) at presentation with Cushing’s disease, were investigated and treated in the Departments of Endocrinology, Neurosurgery, and Radiotherapy at St, Bartholomew’s Hospital (London, UK).

Diagnosis of Cushing’s disease

The diagnosis of Cushing’s disease was based on the following criteria: hypercortisolemia, confirmed by loss of serum cortisol circadian rhythm, i.e. a sleeping midnight cortisol greater than 50 nmol/L, and failure of serum cortisol to suppress to less than 50 nmol/L on a low dose dexamethasone suppression test (10). The diagnosis of Cushing’s disease was supported by suppression of serum cortisol to less than 50% of basal values in a high dose dexamethasone suppression test (10) in all patients plus a serum cortisol increase of more than 20%, compared with baseline values, during a CRH test in 8 of 10 patients (4). Cushing’s disease was confirmed by histological evidence of a corticotroph adenoma or cure after transsphenoidal surgery (TSS) or direct pituitary irradiation.

Treatment of Cushing’s disease

All patients underwent TSS, performed by the same surgeon (F.A.), as first treatment (4, 5, 11). Postoperatively, three patients were defined as being cured by demonstration of undetectable (<50 nmol/L) serum cortisol levels (12), and two patients were in remission based on a mean postoperative serum cortisol levels of less than 300 nmol/L during a 6-sample day curve (12). The remaining five patients had continuing hypercortisolemia after TSS and proceeded to external beam pituitary irradiation with a dose of 4500 cGy (4). Four were cured of their Cushing’s disease (defined by normal mean serum cortisol, normal circadian rhythm, and suppression of serum cortisol in low dose dexamethasone suppression test) within 17–39 months after radiotherapy. One patient remains on ketoconazole therapy 9 months after completing radiotherapy.

Evaluation of growth parameters

Physical examination included measurements of weight, height, and pubertal staging (13, 14). Height was expressed as the SD score according to the standards of Tanner (15). Body mass index (BMI) was expressed as the SD score for sex and chronological age (16). Skeletal maturation was evaluated using the TW2 RUS method (17). Target height (in centimeters) was calculated using the formula (boys: [mother’s height + father’s height + 13]/2; girls: [mother’s height + father’s height - 13]/2) (18) and was expressed as the SD score.

GH secretion

A glucagon (15 µg/kg, im; n = 2) or insulin (0.15 U/kg, iv; n = 7) GH stimulation test was performed in nine subjects at 4.2 months (range, 1–9) after TSS or radiotherapy. Peak GH ranged from 0.5–20.9 mU/L (Table 2Go). Eight patients were treated with human GH (hGH; 14 IU/m2·wk), associated in three, who were in puberty, with goserelin, a GnRH analog (Zoladex, ICI Biomedicals, Inc., Costa Mesa, CA) continued for 1.0–3.4 yr. hGH therapy was continued until final height or latest assessment.


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  		Table 2. Growth evolution of patients receiving GH treatment

 
Statistical analysis

Data are expressed as the mean ± SD. Differences between two matched groups were examined with the nonparametric Wilcoxon signed rank test, with P < 0.05 being considered sufficient to reject the null hypothesis of no difference between groups.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Growth parameters at presentation

At presentation, 5 patients were prepubertal (males), and 5 were pubertal (2 males and 3 females; Table 1Go). The mean height SD score was -2.15 ± 1.26 (range, -0.21 to -4.32). In 4 of 10 patients height SD score was less than -2 SD, and in 7 of 10 it was less than -1.5 SD. Bone age was consistent with chronological age (chronological age ± 1 yr) in 5 and was delayed (chronological age - bone age > 1 yr) in 5 patients. Height velocity (HV) was determined in 6 patients and ranged from 0.9–3.2 cm/yr. The mean BMI SD score was +2.96 ± 1.77 (range, 0.47–6.55); the BMI was more than 2 SD in 8 of 10 patients.


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  		Table 1. Clinical details of patients with Cushing’s disease

 
Short-term growth after TSS or radiotherapy

Short-term growth evaluation to assess catch-up growth was performed in all 10 patients. In 8 patients, short-term HV was variable (mean, 5.0 ± 2.2 cm/yr; range, 1.8–7.6) for a mean period of 0.58 yr (range, 0.30–0.80) after TSS or completion of radiotherapy.

GH assessment

In 2 patients (patients 6 and 8), hGH therapy was started immediately after radiotherapy to maximize linear growth due to ages of 17.2 and 17.6 yr, respectively, and pubertal development. These subjects had peak GH responses before radiotherapy of less than 1.0 and 20.3 mU/L, respectively. In 7 patients (no. 1, 2, 3, 4, 7, 9, and 10), GH stimulation tests were performed within 4.8 months of TSS or radiotherapy and showed peak GH values from 0.5–20.9 mU/L (Table 2Go). hGH therapy was initiated in an additional 6 patients due to poor catch-up growth.

GH therapy and GnRH analog therapy

In the eight patients who received hGH (Table 2Go), the mean height SD score at the start of therapy was -2.45 ± 1.12 (range, -0.96 to -4.31), i.e. not significantly different from the height SD score before treatment (mean ± SD, -2.5 ± 1.12). In three of these patients (Table 2Go), GnRH analog therapy was given to suppress gonadotropin secretion and improve growth potential. Two patients were girls (patients 3 and 7) with breast development stages 3 and 4, respectively. The other was a boy (patient 9) who went into puberty rather early at age 9.8 yr, 2 yr after radiotherapy, with a testicular volume of 6 mL.

Response to hGH therapy

After 1 yr of hGH therapy in all eight patients, the mean height SD score was -2.07 ± 1.20 and significantly different (P = 0.017) from the height SD score before hGH treatment (Table 2Go). The mean HV before hGH therapy was 4.45 ± 2.08 cm/yr (range, 1.6–7.2) and after 1 yr of treatment had increased to 6.07 ± 2.32 cm/yr (range, 2.2–8.9; P = 0.03). The difference in SD score between the 1-yr treatment height SD score and the target height SD score was -1.64 ± 1.07, i.e. significantly less (P = 0.01) than that between pre-hGH treatment height SD score and target height SD score, which was -2.03 ± 1.06 (Fig. 1Go).



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  		Figure 1. Evaluation of growth [change ({Delta}) in height SD score] in eight patients during hGH treatment.

 
At final height or latest assessment (n = 8 patients), the mean height SD score was -1.56 ± 1.37 (range, -3.86 to -0.08) and greater (P = 0.014) than the height SD score at the start of hGH therapy (Table 2Go). The difference between the latest height SD score and the target height SD score was -1.14 ± 1.18, significantly reduced compared with the difference from the SD score at the start of hGH therapy (Fig. 1Go). Three patients were still receiving hGH therapy (patients 1, 3, and 10), with HV of 4.2, 4.9, and 5.8 cm/yr, respectively.

Final height or latest assessment compared to target height

The mean final height SD score (n = 6 patients) was -1.24 ± 1.38, and the latest height SD score (n = 4 patients) was -1.52 ± 1.33 (Table 3Go). Combining these two groups, the difference in SD score between final or latest height SD score (mean, -1.36 ± 1.29; range, -3.86 to -0.08) and target height SD score (mean, -0.43 ± 1.26) was -0.93 ± 1.13 (Fig. 2Go). This is significantly less (P = 0.005) than the difference in SD score between presentation height SD score and target height SD score, i.e. 1.72 ± 1.26 (Fig. 2Go), indicating catch-up growth.


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  		Table 3. Height before transsphenoidal surgery and at final height or latest assessment compared to target height

 


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  		Figure 2. Height at presentation and at final height or latest assessment compared to target height.

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Cushing’s disease is rare in childhood and adolescence, and few studies are available of growth and final height after successful treatment (5, 8). Our previous data reporting normal final height in two patients treated with pituitary irradiation suggested that favorable long-term growth was achievable (9). At clinical presentation, weight gain is the predominant feature, frequently associated with growth failure (3, 4, 8). These abnormalities are often not recognized by parents or family doctors. In our series, 9 of 10 patients presented with Cushing’s disease with a history equal to or greater than 2 yr, comparable to the findings in the large series from the University of California-San Francisco, i.e. a mean of 2.2 yr (5). It is likely that age of onset and duration of hypercortisolemia before cure are features that contribute to the severity of growth failure.

Height was less than -1.5 SD in 6 of 10 patients, and HV, documented in 6 patients, was subnormal. This growth retardation may be due to a decrease in free IGF-I or a target resistance to IGF-I and other growth factors as a consequence of hypercortisolemia (19). The group headed by Chrousos from the NIH has reported that spontaneous and stimulated GH levels are suppressed in patients with Cushing’s disease both before and after TSS (7). No study of the effect of hGH therapy on growth after successful treatment of childhood Cushing’s disease has previously been reported.

All of our patients underwent TSS, which was followed by pituitary radiotherapy in 5. In 9 of 10, cure or remission was achieved, and 1 patient is still receiving ketoconazole 9 months after completion of radiotherapy. Pituitary radiotherapy is an effective mode of therapy in childhood and adolescent Cushing’s disease (4, 9, 20, 21), being used in our unit as second-line therapy when TSS is not curative (11). However, GH deficiency appears to be an almost unavoidable complication and may occur early (4, 22). Five of our patients received pituitary radiotherapy because of persisting hypercortisolemia after TSS. In 3, GH provocation was performed between 6 and 9 months after pituitary irradiation, with peak GH values of less than 20 mU/L. In the 2 other irradiated patients, GH stimulation tests demonstrated GH deficiency before radiotherapy was complete, suggesting that this might have been a complication of the preceding surgery. GH deficiency was frequent after TSS in our patients, as reported by others (7, 23).

The study from the NIH suggested that inadequate posttreatment catch-up growth is the main cause of disappointing final height (8). After the diagnosis of GH deficiency in 8 of our 10 patients, hGH therapy was started early after TSS or radiotherapy, when immediate catch-up growth had not occurred, a feature also in the NIH patients. Evaluation after 1 yr of hGH therapy showed an improvement of height SD score compared with target height. The contribution of GnRH analog therapy to posttreatment growth potential cannot be specifically assessed. However, all 3 patients treated in this way have achieved latest or final heights close to their target heights. In the study from NIH (8) no exogenous hGH or GnRH analog therapy was used.

Compared to the NIH study, our series presents a broadly similar group of patients, but with some possibly significant differences. Firstly, our patients were younger at diagnosis, i.e. 12.92 ± 3.4 compared with 15.5 ± 2.3 yr, and more had delayed bone age, providing them with a longer period of time for catch-up growth. Secondly, they were shorter (mean height SD score, -2.2 compared with -1.7 in the NIH study). Thirdly, half of our patients received pituitary irradiation after unsuccessful TSS.

The significant difference we reported between height at presentation and final adult height or latest assessment indicates catch-up growth. We have also shown a greater difference between height SD at presentation (-2.2) and at final height (-1.6) compared with the NIH group, i.e. (-1.7) and (-1.3). With four of our patients still growing, it is likely that early hGH and GnRH analog treatment together with a longer remaining growth period have contributed to more favorable posttreatment growth than previously reported in the NIH study.

We believe that these data emphasize the importance of investigation of GH secretion and also confirm the frequency of GH deficiency after treatment of childhood Cushing’s disease, whether by TSS alone or in combination with pituitary irradiation. Early treatment with hGH would seem to be indicated in most patients and may have contributed to the encouraging pattern of posttreatment growth.


   Footnotes
 
1 Present address: Division of Pediatric and Adolescent Medicine, Centre Hospitalier Universitaire Sart Tilman, B35 Liège, Belgium. Supported by an European Society of Paediatric Endocrinology sabbatical grant. Back

Received December 8, 1999.

Revised June 1, 2000.

Accepted June 4, 2000.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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  6. Hayles AB, Hahn HB, Sprague RG, Bahn RC, Priestley JT. 1966 Hormone-secreting tumours of the adrenal cortex in children. Pediatrics. 37:19–25.[Abstract/Free Full Text]
  7. Magiakou MA, Mastorakos G, Gomez MT, Rose SR, Chrousos GP. 1994 Suppressed spontaneous and stimulated with Cushing’s disease before and after surgical cure. J Clin Endocrinol Metab. 78:131–137.[Abstract]
  8. Magiakou MA, Mastorakos G, Chrousos GP. 1994 Final stature in patients with endogenous Cushing’s syndrome. J Clin Endocrinol Metab. 79:1082–1085.[Abstract]
  9. Johnston LB, Grossman AB, Plowman PN, Besser GM, Savage MO. 1998 Normal final height and apparent cure after pituitary irradiation for Cushing’s disease in childhood: long-term follow-up of anterior pituitary function. Clin Endocrinol (Oxf). 48:663–667.[CrossRef][Medline]
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