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Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth hormone (G.H.) or a G.H.-dependent somatomedin may be involved in the process of acute lymphoblastic leukaemia (A.L.L.). Growth hormone has a trophic effect on lymphoid tissue and also specific receptors on lymphocytes, most probably T cells. Hypophycess. Resting concentrations of G.H. and somatomedin activity are raised in some children with A.L.L. and may be reduced after remission is achieved. It is suggested that control of G.H. and/or somatomedin concentrations may be necessary for adequate treatment of some cases of A.L.L. in children.
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PMID:Possible effects of growth hormone on development of acute lymphoblastic leukaemia. 7 Jun 47

In 22 children who were in complete remission after acute lymphoblastic leukaemia endocrinological investigations were performed 5-12 weeks after cessation of therapy. The children had received central nervous system irradiation (tele-Co60, 850-1800 rad), and long term, aggressive cytostatic drug therapy during 21 to 36 months. Growth hormone, TSH, thyroxine, LH, FSH, cortisol secretion, and urinary concentrating capacity were found to be normal, with a few exceptions where borderline results were obtained.
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PMID:Endocrine function after antineoplastic therapy in 22 children with acute lymphoblastic leukaemia. 26 43

Growth hormone (GH) secretion was studied in 15 children at various times after treatment for acute lymphatic leukaemia. Impaired GH responses both to hypoglycaemia and to Bovril were found in 4 children. 13 of the children had been given prophylactic cranial irradiation of either 2500 rads in 10 fractions or 2400 rads in 20 fractions. The reduction in GH responses in those given the former dose was highly significant compared with the reduction in those given the latter dose. However, other differences between the two groups included the length of time since cranial irradiation and the chemotherapy used. The main cause of the GH deficiency is not yet clear, but we conclude that it may occur in children treated successfully for acute lymphatic leukaemia.
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PMID:Growth hormone deficiency after treatment of acute leukaemia in children. 106 58

Growth hormone was given to 13 children (nine boys, four girls) with acute leukaemia who had undergone treatment with cyclophosphamide and total body irradiation before bone marrow transplantation. Mean age at total body irradiation and bone marrow transplantation was 9.0 years (range 3.7-15.8). Endocrinological investigation was carried out at a mean of 2.0 years (range 0.4-4.0) after bone marrow transplantation. Peak serum growth hormone responses to hypoglycaemia were less than 10.0 micrograms/l (less than 20.0 mU/l) in 10, 10.5 micrograms/l (21.0 mU/l) in one, greater than 16.0 micrograms/l (greater than 32.0 mU/l) in two patients. Mean age of the patients at the start of growth hormone treatment was 12.2 years (range 5.8-18.2). The mean time between total body irradiation and bone marrow transplantation and the start of growth hormone treatment was 3.2 years (range, 1.1-5.0). Height velocity SD score (SD) increased from a mean pretreatment value of -1.27 (0.65) to + 0.22 (0.81) in the first year, +0.16 (1.11) in the second year, and +0.42 (0.71) in the third year of treatment. Height SD score (SD) changed only slightly from -1.52 (0.42) to -1.50 (0.47) in the first year, to -1.50 (0.46) in the second year, and -1.74 (0.92) in the third year. Measurement of segmental proportions showed no significant increase in subischial leg length from -0.87 (0.67) to -0.63 (0.65) in the first year, to -0.58 (0.70) in the second year, and -0.80 (1.14) in the third year of treatment. Our data indicate that children who have undergone total body irradiation and bone marrow transplantation respond to treatment with growth hormone in either of two dose regimens, with an increase in height velocity that is adequate to restore a normal growth rate but not to 'catch up', and that total body irradiation impairs not only spinal but also leg growth, possibly by a direct effect of irradiation on the epiphyses and soft tissues.
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PMID:Growth hormone treatment of growth failure secondary to total body irradiation and bone marrow transplantation. 205 88

Twenty-three patients (13 females, 10 males) with panmyelopathy (N = 9), chronic leukemia (N = 5), and acute leukemias (N = 9) were studied 1 to 6 years following allogenic bone marrow transplantation. All patients had received conditioning treatment with cyclophosphamide prior to aBMT, and 2 of the patients with bone marrow aplasia and all of the leukemia patients had been given radiotherapy. An endocrine assessment was performed by means of TRH, GnRH, oCRF and GHRH tests and estimation of thyroid and gonadal hormones. Whereas pituitary-adrenal function appeared to remain stable, there was a 17.4% incidence of subclinical hypothyroidism (25% of the irradiated patients). Growth hormone reserve was diminished, and ovarian failure occurred in all female patients after radiotherapy, whereas in the men, only a moderate elevation of gonadotropins was observed. Our results warrant observation of thyroid and gonadal function, and in children of growth hormone secretion, after allogenic bone marrow transplantation. They also show that replacement therapy may be needed in some patients.
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PMID:Allogenic bone marrow transplantation in adults: endocrine sequelae after 1-6 years. 253 5

Late effects of central nervous system (CNS) prophylaxis with cranial radiation (CR) and intrathecal chemotherapy encompass a broad spectrum of phenomena, ranging from fatal leukoencephalopathy to subclinical dysfunctions. Therefore, we studied 55 asymptomatic children with leukemia or solid tumors by means of visual-evoked potentials (VEP) in order to detect subclinical demyelination of the optic pathway after CNS prophylaxis. Ten of the 11 patients showed increased VEP latency after CR with 1,800 cGy, as compared with previous values. One third of our 34 children treated months to years before the study, with 2,400 cGy CR also showed increased VEP latency which was normal in children treated with intrathecal methotrexate only. Growth hormone secretion was investigated using sequential arginine (ARG) and insulin (INS) tolerance tests in 7 leukemic children treated with 1,800 cGy CR. At diagnosis all patients were responsive to both tests; after CNS prophylaxis, 2 patients were still responsive to ARG and INS, whereas the other 5 were responsive to ARG test only. These results are at variance with our previous experience in a series of 22 children treated with 2,400 cGy CR where 2 patients responded to ARG only and 5 did not respond to either stimulus. These data indicate that, even after a reduction of the CR dose, CNS prophylaxis is still associated with subclinical dysfunctions.
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PMID:Some aspects of neurotoxicity associated with central nervous system prophylaxis in childhood leukemia. 312 37

A summary is given of some activities of the Hungarian Study Group for Childhood Leukaemia. Coordinated efforts within the Study Group led to improved therapeutic results. The median survival of patients diagnosed in 1971 was 12 months. For a comparison, out of the 57 patients diagnosed in 1978, 34 are still in their first remission. Experimental work designed to approach the pathomechanism of the disease provided the following main points of interest. 1. Children diagnosed to have L1 type ALL according to the FAB categories fare better than those with L2. 2. ADA activity was essentially normal in patients being in remission and their parents. 3. Steroid receptor determinations can be of value in the planning of therapy. 4. Very low as well as very high initial WBC count indicates a bad prognosis. 5. Children who possess the DR 5 histocompatibility antigen have a better outlook for long complete remissions and cure. 6. Growth hormone secretion and, accordingly, growth rate was normal in the long surviving patients. 7. There was a slight impairment in the performance IQ of children who were under 6 years of age at the time of diagnosis. 8. Emotional disturbances were universal in all patients, but could be much alleviated by regular psychological care and play activity. 9. So far we observed one patient with a second malignancy: his AML manifested 4 years after the successful removal and chemo-radiotherapy of his brain tumour. 10. Children in long, continuous remission-thought to be cured of their disease-possess normal remission lymphocytes with a significantly shorter cell cycle than controls.
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PMID:Childhood leukaemia: therapeutic and experimental approach. 702 82

A 12 year-old girl developed a late relapse of acute lymphoblastic leukaemia (ALL) 10 years from first presentation. Initial chemotherapy included vincristine, methotrexate, prednisolone, and L-asparaginase with cranial radiotherapy (18 Gy) for central nervous system prophylaxis. Documented growth failure led to recombinant human growth hormone (rhGH) replacement therapy being instituted in May 1989, 6 years from end of therapy and 2 years prior to relapse. Three independent experiments demonstrated no increased cell proliferation in vitro when the patient's thawed cryopreserved fresh leukemic cells were incubated with rhGH. However, a pre-T ALL cell line (PER-255) consistently demonstrated enhanced proliferation when incubated with rhGH (132.1 +/- 13.4%, P < 0.01). Growth hormone has been associated with an increased incidence of leukemia and may be implicated in the late relapse of this child. The use of growth hormone in children with a past history of ALL needs to be examined critically in the light of the potential risk of inducing leukemic relapse.
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PMID:Late leukemic relapse 10 years from diagnosis in a child on recombinant human growth hormone. 844 49

Reciprocal communication between the neuroendocrine and immune systems is critical to the establishment of host homeostatic and defence mechanisms. The production and utilisation of common ligands and their receptors by cells of the immune and neuroendocrine systems constitutes a biochemical information circuit between and within the immune and neuroendocrine systems. Although the structures of the various signalling components appear to be similar in both systems, the regulation of their synthesis may be different. Growth hormone and prolactin have similar and marked influences on the function/activity of each of the major immune cell types, both in vitro and in vivo. The underlying molecular mechanisms are just beginning to be unravelled, and it is anticipated that further work in this rapidly developing field will establish abnormal pituitary and/or lymphocyte growth hormone and prolactin synthesis and function as a contributory factor to a number of pathologic situations, including leukaemia and autoimmunity.
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PMID:Immunoregulatory properties of growth hormone and prolactin. 878 73

Osteopenia has been reported in children surviving acute lymphoblastic leukaemia, apparently as a consequence of therapy. It has been suggested that cranial irradiation may play a crucial role in this disorder. To explore that possibility, survivors of brain tumours in childhood, all of whom had received radiotherapy, were examined for evidence of bone mineral loss. 19 children were assessed, on average at 7 years after treatment. Measurements of growth velocities, plain radiography of the skeleton, bone densitometry, health-related quality of life and physical activity were undertaken. Growth hormone (GH) deficiency had been detected in 6 children and 5 had received GH replacement, for a minimum of more than 3 years. 9 children were radiographically osteopenic (including the 5 who had received GH). Z scores for bone mineral density (BMD) were negative in the majority of children. Health-related quality of life was less and pain more frequent in those with low BMD scores. Pain was correlated negatively with both free-time activity and seasonal activity (P < 0.01). Osteopenia is a common sequel of therapy in children with brain tumours. Those with osteopenia have more pain and more compromised, health-related quality of life than those who are not osteopenic, and pain significantly limits physical activity. The pathogenesis of osteopenia in these children is still uncertain, but is likely to be multifactorial.
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PMID:Osteopenia in children surviving brain tumours. 979 85


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