Failure of Catch-up Growth After Cushing's Syndrome in Childhood

Mosier, H. David

doi:10.1001/archpedi.1972.02110140101015

Cited by 18 publications

(18 citation statements)

References 13 publications

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“…Here we decided to focus on Dexa-induced growth retardation since the capacity for catch-up growth after glucocorticoid exposure is of great clinical relevance. Our ex vivo finding that catch-up growth occurs after short-term (7 and 12 days) but not long-term (19 days) Dexa exposure mimics what occurs in children known to display catch-up growth after previous short-term glucocorticoid exposure while prolonged exposure results in incomplete catch-up growth and compromised final height (Mosier et al 1972, Strickland et al 1972. Mechanistic studies, showed that upon cessation of Dexa treatment, the level of chondrocyte proliferation rose above control after short-term exposure (7 days) but not long-term (19 days) exposure, whereas differentiation was unchanged in both cases, suggesting that increased proliferation most likely is the primary local underlying mechanism for the phenomenon of catch-up growth.…”

Section: Discussionmentioning

confidence: 54%

Catch-up growth after dexamethasone withdrawal occurs in cultured postnatal rat metatarsal bones

Chagin¹,

Karimian²,

Sundström³

et al. 2009

Journal of Endocrinology

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Children exposed to systemic glucocorticoids often exhibit growth retardation and after the cessation of therapy catch-up growth occurs in many, but not all patients. The developmental regulation and underlying cellular mechanisms of catch-up growth are not fully understood. To clarify this issue, we established an in vitro model of catch-up growth. Here we present a protocol for the long-term culture (up to 160 days) of fetal (E20) as well as postnatal (P8) rat metatarsal bones which allowed us to characterize ex vivo the phenomenon of catch-up growth without any influence by systemic factors. The relevance of the model was confirmed by the demonstration that the growth of fetal and postnatal bones were stimulated by IGF1 (100 ng/ml) and inhibited by dexamethasone (Dexa; 1 mM). We found that the capacity to undergo catch-up growth was restricted to postnatal bones. Catch-up growth occurred after postnatal bones had been exposed to Dexa for 7 or 12 days but not after a more prolonged exposure (19 days). Incomplete catch-up growth resulted in compromised bone length when assessed at the end of the 4-month period of culture. While exposure to Dexa was associated with decreased chondrocyte proliferation and differentiation, catchup growth was only associated with increased cell proliferation. We conclude that the phenomenon of catch-up growth after Dexa treatment is intrinsic to the growth plate and primarily mediated by an upregulation of chondrocyte proliferation.

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Section: Discussionmentioning

confidence: 54%

Catch-up growth after dexamethasone withdrawal occurs in cultured postnatal rat metatarsal bones

Chagin¹,

Karimian²,

Sundström³

et al. 2009

Journal of Endocrinology

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“…It has been proposed that the changes in cartilage produced by growth suppressive levels of glucocorticoids in young animals and humans account for the failure of catch-up growth during recovery (2)(3)(4)(5). However, the results of the present experiments show that both soft tissues and skeletal tissues maintain the capability of supporting catch-up growth after cortisone-induced stunting.…”

Section: Width Of the Tibial Epiphyseal Growth Plate (Experiments I)contrasting

confidence: 50%

“…(Pediatr Res 25373-376, 1989) Abbreviations GH, growth hormone s.c., subcutaneously Treatment of young rats with injections of growth-suppressive doses of cortisone over a period of 4-8 d results in permanent stunting of body size (1). Permanently stunted growth has also been observed in the human after high-dose glucocorticoid treatment (2) or after Cushing's syndrome (3). The absence of catchup growth in the recovery period has been attributed to a failure of response of target tissues to growth factors (4).…”

mentioning

confidence: 99%

Rats Stunted by High-Dose Glucocorticoid Treatment Are Capable of Undergoing Catch-Up Growth after Fasting

Mosier¹,

Jansons²

1989

Pediatr Res

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ABSTRACT. Experiments were carried out to test the hypothesis that permanent growth retardation after glucocorticoid-induced growth suppression is due to an alteration of a central set point for target size rather than an inability of peripheral tissues to carry out catch-up growth. Hats were injected subcutaneously with saline, a s controls, or with cortisone acetate, 1 mg/25 g body wt/d, for 4 d, beginning a t 37 d of age. The treated animals were submitted to acute fasting for 48 h, beginning a t 47 d of age, after which they were allowed to feed a d libitum. Cortisone treatment significantly stunted body wt, tail length, and tibia length. During recovery after fasting, both the cortisone-treated and the saline-injected rats exhibited catchup growth in body wt and tibial length. In other rats killed a t different time intervals during recovery after cortisone treatment, only, there was no pattern of catch-up growth in tibia length. There was no difference in tibial epiphyseal width between fasted and nonfasted rats within the salineor cortisone-treated group. The findings demonstrate that rats that are permanently stunted by high-dose glucocorticoid treatment retain the capability for catch-up growth in both soft and skeletal tissues. The data support the hypothesis that catch-up growth is regulated by a central control with a mechanism (set point) for setting target size of the body. Stunting resulting from glucocorticoid treatment may be the result of a reset of the putative set point. (Pediatr Res 25373-376, 1989)

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“…Evidence support ing the existence of an organismic set point in the rat has been reported by Bernardis et al [19] and Mosier [20], However, quite different results have been observed under conditions of other types of transient growth arrest. For example there is no catch-up growth following growth inhibition induced by glucocorticoid treatment or hypothyroidism (21)(22)(23)(24). In addition, the absence of acute catch-up growth has been observed following GHRH-ab treatment [7,9,12], In these instances, normal or even elevated GH concentrations have been reported.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Failure of Compensatory Growth in Rats following Acute Neonatal Passive Immunization against Growth Hormone-Releasing Hormone

Wehrenberg

Voltz²,

Cella³

et al. 1992

Neuroendocrinology

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Interruption of hypothalamic growth hormone-releasing hormone (GHRH) secretion by administration of antiserum against GHRH (GHRH-ab) decreases growth hormone (GH) secretion and inhibits growth in rats. The present study was undertaken to investigate whether there is a period of accelerated or catch-up growth following a period of growth arrest induced by GHRH-ab treatment. Neonatal male and female rats were injected daily on days 1-14 of age. Animals received normal rabbit serum (NRS) or GHRH-ab subcutaneously at a dose of 5 µl/l0 g body weight. Body weight, serving as an index of somatic growth, was monitored over the next 3 months. The increase in absolute body weight and growth velocity of GHRH-ab-treated rats, regardless of gender, was lower than the increase of NRS-treated animals. Significant decreases were observed by day 13 of age in the female rats and day 17 in the male rats. The percent differences and absolute difference in weight between the two treatment groups clearly demonstrated that the GHRH-ab-treated rats did not demonstrate any period of catch-up growth. A second group of animals was treated in a similar fashion to evaluate serum GH concentrations at three months of age. Pulsatile GH secretion, as assessed by peak frequency and amplitude, was normal in all of the rats, suggesting that the failure of catch-up growth in the GHRH-ab-treated animals was not due to decreased GH secretion. The failure of cateh-up growth following transient growth arrest induced by GHRH deprivation suggests that a functional GHRH/GH neuroendocrine system is critical during the neonatal period to establish normal growth of the animal on a long-term basis.

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Failure of Catch-up Growth After Cushing's Syndrome in Childhood

Cited by 18 publications

References 13 publications

Catch-up growth after dexamethasone withdrawal occurs in cultured postnatal rat metatarsal bones

Catch-up growth after dexamethasone withdrawal occurs in cultured postnatal rat metatarsal bones

Rats Stunted by High-Dose Glucocorticoid Treatment Are Capable of Undergoing Catch-Up Growth after Fasting

Long-Term Failure of Compensatory Growth in Rats following Acute Neonatal Passive Immunization against Growth Hormone-Releasing Hormone

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