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Failure of catch-up in linear growth was experienced by a girl after total adrenal ectomy for Cushing's syndrome. There is a possible correlation between this and failure of catch-up growth in the cortisone-treated rat. The degree of catch-up growth after hyperadrenocorticism may be related to intens¬ ity and duration of glucocorticoid exposure, age of the patient, and individual susceptibil¬ ity of growth mechanisms to damage by ex¬ posure to high levels of glucocorticoids.Compl ete catch-up in linear growth has been observed after growth arrest resulting from hyperadrenocorticism in the human.1·2 On the other hand, failure of catch-up growth has been observed in corti¬ sone-induced experimental growth retardation in the rat.' In this report we describe an instance of failure of compensatory growth in a patient fol¬ lowing prolonged Cushing's syndrome and discuss briefly the implications of this case in the light of current re¬ search on the effect of adrenal glucocorticoids on cartilage metabolism and structure. Report of a CaseThe patient is a white woman who first showed evidence of Cushing's syndrome at 8 years of age. Left adrenalectomy was performed at the age of 10% 2 years. The adrenal cortex was hyperplastic. Urinary 17-hydroxycorticosteroid excretion level returned to normal, but six months postop-

Male Long-Evans rats were fasted or given cortisone injections beginning at 37 days of age in order to produce growth retardation. They were then allowed to recover for periods of up to 28 days. GH concentration was measured in trunk blood plasma of rats decapitated after minimal stress. During the recovery period there was a significant increase in plasma GH in both experimental groups. Organ weight/body weight ratios for liver and heart, protein/tissue, DNA/tissue, and DNA/protein ratios of liver, heart, and skeletal muscle were found to remain normal or to return to normal values during the recovery periods in both experimental groups. DNA content was reduced in both liver and heart at 14 days. At later recovery periods no significant differences from controls were observed. The findings indicate that increased GH release is common to the growth recovery period after both fasting or cortisone treatment. GH concentration in plasma does not correlate with presence or absence of catch-up growth. The organ weight/body weight ratios correlate with previous findings showing prompt return to normal proportions of body weight to tail length in both the cortisone and fast models irrespective of presence or absence of catch-up growth. The results indicate that failure of catch-up growth after cortisone treatment is not the result of decreased pituitary GH secretion. It is probable that multiple factors working in concert are responsible for recovery after transient growth retardation.

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The uptake of sulfate by rib cartilage in vitro and in vivo and the serum somatomedin activity by bioassay were determined in male rats during and after cortisone-induced growth arrest. Experimental treatment consisted of subcutaneous injections of cortisone acetate in a dose of 2.5 mg/rat/day for 4 days, beginning at 29 to 30 days of age in Buffalo rats, or 5 mg/rat/day for 4 or 5 days, beginning at 39 to 41 days of age in Long-Evans rats. Groups of hypophysectomized rats were studied in parallel in one experiment. The sulfate uptake in the controls declined linearly with increasing age in both the in vitro and the in vivo studies. Hypophysectomy resulted in a constant low level of sulfate uptake in vitro. At the end of cortisone treatment, the in vitro sulfate uptake was approximately midway between that of the hypophysectomized rats and that of controls; at 7 days recovery, it was at the control level; at 14 days it showed an additional rise above the control value; from 14 days to 35 days it declined parallel with but above the sulfate uptake of controls. The in vivo sulfate uptake was depressed by cortisone treatment. During recovery it approximately control values at recovery day 21. In succeeding recovery periods in vivo sulfate uptake remained at control levels. Serum somatomedin activity was significantly reduced during cortisone treatment; it returned to the control level by 21 days of recovery. The incubation of the cartilage of controls and cortisone-treated rats at 14 days of recovery with and without the presence of normal rat serum, cortisone recovery serum, or hypophysectomy serum resulted in significantly higher sulfate uptake in the cortisone-treated rat cartilage in each medium. These sera did not differ significantly in their stimulation of sulfate uptake in either cortisone recovery cartilage or control cartilage. Both treated and control cartilage had greater sulfate uptake with larger doses of serum added to the medium. The dose-response curves were parallel during treatment and early recovery; but the slopes of the dose-response curves of the cartilage of cortisone-treated rats were greater than those of the controls during late recovery. It is concluded that the increased in vitro sulfation after 14 days of recovery in cortisone-treated rats signifies a persistent alteration in cartilage metabolism. Normal in vivo sulfate uptake during that time may be the result of humoral controls. A mechanism other than the impairment of somatomedin production is probably involved in the failure of catch-up growth after glucocorticoid treatment in the rat.

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