Growth and growth hormone in children during and after therapy for acute lymphoblastic leukaemia

Caruso-Nicoletti, Manuela; Mancuso, M.; Spadaro, Giorgio; Dibenedetto, S. P.; Dicataldo, A; Schilirò, Gino

doi:10.1007/bf01953986

Cited by 33 publications

(27 citation statements)

References 21 publications

(33 reference statements)

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“…Femur length does not contribute to the mouse length as conventionally measured. This could explain the lack of difference in length, weight, and BMI among all groups in our study, contrary to what was found by follow-up studies of adult childhood cancer survivors [Crofton et al 2000;Caruso-Nicoletti et al 1993].…”

Section: Discussioncontrasting

confidence: 99%

“…An argument could be made as to whether the impairment is a direct effect of CTX on bone development, a growth hormone deficiency from pituitary damage, or a combination of the two. However, a growth hormone deficiency would be reflected in a long-term deficiency in height and weight, which was not observed in this study or human studies [Caruso-Nicoletti et al 1993]. Femur length does not contribute to the mouse length as conventionally measured.…”

Section: Discussioncontrasting

confidence: 54%

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Somatic and reproductive outcomes in mice treated with cyclophosphamide in pre-pubertal age

Detti

Williams

et al. 2013

Systems Biology in Reproductive Medicine

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Disruption in the normal timing of female puberty, such as in pre-pubertal cancer treatments, can cause abnormal somatic development. We sought to evaluate the impact of cyclophosphamide (CTX) on the somatic, uterine, and ovarian, development of pre-pubertal mice. Pre-pubertal (day 18 of life) C57BL/ 6J female mice were randomized to receive placebo (group 1A and 1B), 200 mg/kg CTX (group 2A), or 120 mg/kg CTX (group 2B). Mice were euthanized on day 56 (A groups) or 95 (B groups) of life. Body weight and length, uterine and ovarian weight and right femur length and weight were measured, and ovarian insufficiency was assessed. Data were analyzed using ANOVA and t-test. Body weight and length did not differ among groups at time of euthanasia. The femur was shorter and weighed less in mice treated with CTX than in controls. Uterine weight was lower in group 2B than 1B (46.1 mg, 95% CI: 42.9-49.4, vs. 62.2 mg, 95% CI: 58.5-65.8, respectively; p = 0.005) and was lower in mice that developed ovarian insufficiency than in mice that did not ( p < 0.05). Ovarian weight was lower in mice treated with CTX, regardless of whether they developed ovarian insufficiency. Even with no observable effect on adult body length and weight, CTX treatment in prepubertal mice appears to negatively affect femur, uterine, and ovarian development. However, uterine development seems to be dependent on the hormonal status created by CTX more than on its direct effect.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 54%

Somatic and reproductive outcomes in mice treated with cyclophosphamide in pre-pubertal age

Detti

Williams

et al. 2013

Systems Biology in Reproductive Medicine

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“…Multiple high dose chemotherapy is now an important part of the standard treatment for childhood malignancies, and while this form of treatment has become more successful, adverse long term side effects on growing skeleton have been noted including growth arrest, osteoporosis and fracture. [2][3][4][5][6][7][8] The sensitivity of the immature skeleton to chemotherapy has also been documented in animal studies. [9][10][11][12][13][14] Future trend for treatment of childhood malignancies looks set to involve further intensified use of chemotherapy, and therefore further understanding and characterization of the mechanisms by which chemotherapy disrupts bone growth is important.…”

Section: Introductionmentioning

confidence: 99%

Effects of etoposide and cyclophosphamide acute chemotherapy on growth plate and metaphyseal bone in rats

Chen¹,

Cool²,

Gangelen³

et al. 2007

Cancer Biology & Therapy

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“…There have been many reports of poor growth in children with acute lymphoblastic leukemia (ALL), especially during periods of intensive chemotherapy, but growth may return to normal during less-intensive periods and may show evidence of further catch-up after completion of chemotherapy (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). Of greater concern are a number of retrospective crosssectional studies on survivors of ALL that describe reduced bone mineral density (BMD) at various sites (14 -16).…”

mentioning

confidence: 99%

Bone Turnover and Growth During and After Continuing Chemotherapy in Children with Acute Lymphoblastic Leukemia

et al. 2000

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Children treated for acute lymphoblastic leukemia may develop reduced bone mineral density during treatment, but there is little information on the mechanisms involved. In a prospective, longitudinal study on 15 children with ALL, we undertook serial measurements of markers of bone and collagen turnover, insulinlike growth factor (IGF)-I and its binding proteins (IGFBPs)-3 and -2 during the second year of continuing chemotherapy. In eight patients we also measured lower leg length by knemometry. Height SD scores, lower leg length velocity, IGF-I, and markers of bone collagen turnover did not differ significantly from healthy children. However, bone alkaline phosphatase, a marker of the differentiated osteoblast, was lower (mean SD score, Ϫ0.64; p Ͻ 0.0001), whereas procollagen type III N-terminal propeptide (P3NP, a marker of soft tissue collagen turnover; mean SD score, ϩ0.93, p Ͻ 0.05), IGFBP-3 (mean SD score, ϩ0.76; p Ͻ 0.01), and IGFBP-2 (mean SD score, ϩ1.24, p ϭ 0.01) were all higher than in healthy children. IGFBP-3 decreased during episodes of afebrile neutropenia (p Ͻ 0.05). Within 3 mo after completion of treatment, bone ALP increased in all eight patients, but collagen markers showed little change. IGFBP-2 returned to normal posttreatment, but P3NP and IG-FBP-3 remained significantly elevated compared with healthy children (mean SD scores, ϩ1.51 and ϩ1.36, respectively; p Ͻ 0.01). We conclude that continuing chemotherapy was associated with normal growth and bone collagen turnover but enhanced soft tissue collagen turnover. Bone bone alkaline phosphatase was low throughout treatment, which suggests impaired osteoblast differentiation resulting from a direct effect of chemotherapy on bone. Although the effect was reversible, the long-term implications for bone health in survivors remain uncertain. There have been many reports of poor growth in children with acute lymphoblastic leukemia (ALL), especially during periods of intensive chemotherapy, but growth may return to normal during less-intensive periods and may show evidence of further catch-up after completion of chemotherapy (1-13). Of greater concern are a number of retrospective crosssectional studies on survivors of ALL that describe reduced bone mineral density (BMD) at various sites (14 -16). This may be associated with increased fracture risk, reduced peak bone mass, and a theoretical risk of osteoporosis in adult life. However, these previous studies reflect the outcome of earlier treatment protocols, most of which included cranial irradiation and are now obsolete. Current protocols generally use more intensive chemotherapy regimens but avoid cranial irradiation in all but a few high-risk cases. Recently, a number of prospective longitudinal studies have reported that the prevalence of radiologic osteopenia and fracture in children with ALL increases and that BMD decreases during chemotherapy, in the absence of cranial irradiation (17)(18)(19). However, the mechanisms responsible for these observations remain to be elucidated.There are a num...

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Growth and growth hormone in children during and after therapy for acute lymphoblastic leukaemia

Cited by 33 publications

References 21 publications

Somatic and reproductive outcomes in mice treated with cyclophosphamide in pre-pubertal age

Somatic and reproductive outcomes in mice treated with cyclophosphamide in pre-pubertal age

Effects of etoposide and cyclophosphamide acute chemotherapy on growth plate and metaphyseal bone in rats

Bone Turnover and Growth During and After Continuing Chemotherapy in Children with Acute Lymphoblastic Leukemia

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