Growth and growth hormone secretion in children with cancer treated with chemotherapy.

OBJECTIVE: To evaluate the effect of chemotherapy on growth and growth hormone (GH) secretion. METHODS: We analyzed growth and GH secretion in 60 children in complete remission after treatment by chemotherapy and surgery for malignant solid tumors. None of them received cranial radiotherapy. Growth hormone reserve was assessed by at least two stimulation tests (clonidine, L-dopa, growth hormone-releasing hormone). In 12 children the reserve of GH pretreatment was also evaluated. RESULTS: Growth hormone deficiency (GHD) was observed in 27 of 60 patients (45%). At diagnosis, mean standing height was +0.23 +/- 0.11 standard deviation score (SDS) in the GHD group and +0.16 +/- 0.10 SDS in the non-GHD group. After chemotherapy, mean standing height in the GHD group was -0.28 +/- 0.15 SDS and -0.14 +/- 0.11 in the non-GHD group (p < 0.05), and the growth rate was +0.13 +/- 0.07 SDS in the GHD group and +0.22 +/- 0.18 SDS in the non-GHD group. For a mean follow-up of 30 months, the mean standing height was -0.46 +/- 0.29 SDS in the GHD group and -0.24 +/- 0.16 SDS for the non-GHD group (p < 0.05), and the growth rate was -0.27 +/- 0.19 SDS in the GHD group and -0.16 +/- 0.12 SDS in the non-GHD group (p < 0.05). The GH response to clonidine was significantly less than that found with the other stimuli. There was correlation between the dose intensity of some drugs and the subsequent GH response to stimulation tests. The GHD group was found to have received significantly higher doses of actinomycin D than the non-GHD group (p < 0.05). Growth impairment and GHD were not found to be correlated with duration of treatment and follow-up, tumor type, sex, or age. CONCLUSIONS: Chemotherapy as the sole form of treatment in children with cancer interferes with growth. The observed impairment of growth depends, at least in part, on a GHD related to chemotherapy. The growth rate in conjunction with the GH response to clonidine provides a sensitive measure of GHD associated with chemotherapy.

Chemotherapy-induced growth hormone deficiency in children with cancer.

BACKGROUND: Chemotherapy (CT) may produce growth impairment, however, the pathogenesis is still unclear. METHODS: A series of 25 patients mean age 13.3 years (6.3-19.8), previously treated for malignant solid tumours with only CT and surgery were studied. Growth hormone (GH) reserve was assessed by two different provocative stimuli (Clonidine and L-Dopa). Mean time between completion of treatment and GH evaluation was 18.5 months (2-74 months). At that time, all patients were in complete remission. RESULTS: GH deficiency (GHD), defined by an impaired GH response to both provocative tests was observed in 11 out of 25 patients (44%). At diagnosis, mean standing height was +0.23 +/- 1.42 SDS in the GHD group (GHD-g) and +0.18 +/- 1.23 SDS in the non-GHD group (n-GHD-g). At the end of therapy, the mean standing height in the GHD-g was -0.31 +/- 1.22 SDS and -0.17 +/- 1.41 in the n-GHD-g, differing from the former group (P = 0.05). For a mean follow-up of 30 months from the end of treatment, the mean standing height was -0.48 +/- 1.23 SDS in the GHD-g and -0.24 +/- 1.51 SDS for the n-GHD-g (P = 0.03). Growth rate at the end of treatment was +0.13 +/- 1.54 in the GHD-g and +0.21 +/- 1.75 in the n-GHD-g. For a mean follow-up of 30 months from the end of treatment, the growth rate was different between GHD-g and n-GHD-g (-0.31 +/- 2.72 vs. -0.21 +/- 1.93, P < 0.05). CONCLUSIONS: 1) Growth impairment in children treated because of malignant diseases has a multifactorial etiology, but CT-induced GH deficiency is one potential adverse factor. 2) An endocrine follow-up should be introduced in order to detect and treat hormonal deficiencies as early as possible.

[The pediatric heart transplant. Its evolution and early postoperative complications]. / Trasplante cardíaco pediátrico. Evolución y complicaciones postoperatorias tempranas.

BACKGROUND: Cardiac transplantation is an acceptable therapeutic alternative for cardiac diseases refractory to other forms of management in adults as well as in infants and children. METHODS: Between 1987-1992 7 children (4 girls and 3 boys) underwent cardiac transplantation: four with dilated cardiomyopathy, one with cardiac fibroma and two with hypertrophic cardiomyopathy. Age at transplantation ranged from 2 months to 13 years and 5 months, with a follow-up ranging from 15 months to 5 years and 9 months. Prophylaxis of acute rejection consisted of cyclosporine, azathioprine and glucocorticoids. RESULTS: Two patients presented acute rejection three weeks after cardiac transplantation, with a good response to high dose glucocorticoids. Two patients developed severe infection (sepsis by Staphylococcus aureus) with successful outcome after antibiotic treatment. One patient died in the early postoperative period and other after 4 years 11 months postransplantation because myelodysplastic syndrome. At present only one case is receiving glucocorticoids in immunoprophylaxis. The status is asymptomatic in the other 5 patients with a normal height-weight development. CONCLUSIONS: Heart transplantation provides durable therapy for congenital and myopathic heart disease in infants and children with an excellent quality of life.

[Sneddon's syndrome vasculopathy with antiphospholipid antibodies in a child]. / Vasculopatía asociada a anticuerpos antifosfolípido. Síndrome de Sneddon en la niñez.

We studied a ten-year old girl with livedo reticularis and multiple central nervous system ischemic attacks beginning when she was five. Blood tests were positive for cryoglobulins and antiphospholipid antibodies; superior limb angiography showed occlusion and irregularities of the vessel walls and temporal artery biopsy revealed concentric thickening of the vessel wall due to fibrotic subendothelial proliferation. Sneddon's syndrome was diagnosed. Onset of this syndrome during early childhood has not been previously reported.