Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients in the Kabi International Growth Study (KIGS) up to 1st January 1990 who had organic growth hormone deficiency (OGHD) were identified. They accounted for 21% of all patients with growth hormone deficiency (GHD). Diagnostic categories within the OGHD group included septo-optic dysplasia, postnatal trauma, craniopharyngioma, other cranial tumours, and following acute leukaemia. Features at presentation and during the first year of hGH treatment were compared with those of children with idiopathic growth hormone deficiency (IGHD). Ninety prepubertal children with OGHD were selected for comparison of observed first-year height velocity (HV) with predicted values based on those observed in 257 children with IGHD. Those with septo-optic dysplasia, postnatal trauma and craniopharyngioma responded as predicted, whereas those with other cranial tumours appeared to grow less well than predicted. Glucocorticoid treatment did not affect response, but previous cranial or craniospinal irradiation was found to be associated with an observed HV which was significantly less than predicted.
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PMID:Growth response in the first year of growth hormone treatment in prepubertal children with organic growth hormone deficiency: a comparison with idiopathic growth hormone deficiency. The Executive Scientific Committee of the Kabi International Growth Study. 226 Apr 51

External cranial radiation for the treatment of malignant diseases has become a frequent cause of growth hormone deficiency (GHD). The timing of occurrence and the frequency of GHD were related to the hypothalamic-pituitary radiation dose. Frequency varied from 50% in leukemia (2400 cGy) to 75% in face and neck tumors or medulloblastoma (2500-4500 cGy) and up to 100% in optic glioma (greater than 4500 cGy). The significantly more severe growth deficit in patients with GHD given higher radiation doses suggests different levels of residual GH secretion according to radiation dosage. The minimum harmful radiation dose is probably close to 1800-2000 cGy. Our data show that stimulation tests remain a useful means of defining GHD and predicting growth. A fair agreement between GH secretion and growth was found in most cases, regardless of the radiation dose. The only exception was a group of leukemic children (2400 cGy) who achieved normal prepubertal growth despite a low GH response. The 24-h spontaneous plasma GH profiles and IGF-I measurements may add information if growth is retarded despite a normal GH response. We showed that growth retardation occurring after some schedules of total body irradiation was not due to GH deficiency but rather to radiation-induced skeletal lesions. Early or true precocious puberty, generally associated with GHD, was another cause of height loss. As the role of GH deficiency in the final height reduction was demonstrated in all groups of patients after cranial radiation, we suggest that hGH therapy should be considered in any child with proven GH deficiency and significant growth retardation after such radiation.
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PMID:Growth and endocrine disorders secondary to cranial irradiation. 266 28

Ten children who underwent allogeneic (n = 5) or autologous (n = 5) bone marrow transplantation (BMT) for chronic myelogenous leukaemia (n = 2), acute lymphoblastic leukaemia (n = 1), acute myelogenous leukaemia (n = 2), severe aplastic anaemia (n = 2), malignant histiocytosis (n = 1), neuroblastoma (n = 1) and teratoma (n = 1) were assessed for endocrinological function. Transplant preparative regimens consisted of high-dose cyclophosphamide, high-dose cyclophosphamide in combination with high-dose busulphan, high-dose melphalan as well as BACT (BCNU, cytarabine, cyclophosphamide and 6-thioguanine) chemotherapy. None of the patients received total body irradiation (TBI). Median survival following BMT was 37 months (range 7-115). Growth hormone deficiency was present in only one patient; none of the patients had abnormal thyroid or adrenocortical function. This is in contrast to previous reports in which growth hormone deficiency and abnormal thyroid and adrenocortical function occurred in a much higher percentage of patients after BMT conditioned with TBI.
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PMID:Endocrine function after bone marrow transplantation without the use of preparative total body irradiation. 304 94

Between 1970 and 1979 acute lymphoblastic leukaemia was diagnosed in 378 children at this hospital. The outcome for the 181 survivors was examined six or more years after diagnosis to assess morbidity in an unselected group of long term survivors. One hundred and thirty seven of the survivors were in first remission and probably cured (group I). Forty four (group II) had had one or more relapses, some of whom, who had isolated extramedullary relapses, also have a good chance of cure. In group I 136 patients had prophylactic cranial or craniospinal irradiation, while patients in group II, in addition to having that treatment, received local testicular (17) or craniospinal radiation (seven) for testicular or central nervous system relapse. Eight had additional prophylactic cranial radiotherapy after bone marrow relapse, and six had total body irradiation before bone marrow transplantation. The incidence of clinically important growth and endocrine morbidity was 20% in group I and 68% in group II. The morbidity in patients in group I was mainly attributable to early pubertal maturation. In group II 30 patients had growth failure, of whom 19 had gonadal failure from testicular or total body irradiation, 14 had growth hormone deficiency after doses of cranial irradiation of over 2400 cGy, and 10 had spinal growth impairment after craniospinal irradiation. Two also had early pubertal maturation. Five out of six patients who received total body irradiation had multiple endocrine deficiency. Neuropsychological sequelae of treatment were seen in 40 (42%) of 96 schoolchildren in group I and in 12 (38%) of 32 schoolchildren in group II. Postinfective sequelae of treatment were found in patients in both groups. These results show that the survivors who were in their first remission had a 42% residual morbidity related to treatment compared with an 82% morbidity in the survivors of one or more relapses who had multiple treatments.
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PMID:Medical cost of curing childhood acute lymphoblastic leukaemia. 312 82

Seventeen children (11 M, 6 F) with acute leukaemia and myeloproliferative disorders were investigated for growth and endocrine dysfunction. All had undergone bone marrow transplantation prepared with cyclophosphamide and single fraction total body irradiation (900-1000 cGy) between 1.5 and 3.8 (mean 2.2) years previously. The majority of children exhibited growth failure, which was of multiple aetiology. Ten patients, of whom eight had had previous prophylactic cranial irradiation, had evidence of growth hormone deficiency based on the reduced growth hormone response to insulin induced hypoglycaemia. Three patients had evidence of hypothalamic damage as shown by their growth hormone response to 200 micrograms GHRH (1-29) NH2 intravenously. Gonadal failure was common, assessed clinically, and biochemically by basal gonadotrophin and sex steroid concentrations. All four girls of adolescent age (10.6-14.1 years) had ovarian failure requiring sex steroid replacement. Of the eight boys of adolescent age (12.3-18.3 years), two had testicular failure requiring sex steroid supplements. Both of these had had previous testicular irradiation. Five others had compensated gonadal failure, and one had normal Leydig cell function. Abnormalities of the TSH response to TRH occurred in 10 patients but only three had overt hypothyroidism. Unlike growth hormone deficiency, gonadal and thyroid dysfunction showed no correlation with previous cranial radiotherapy.
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PMID:The effect of total body irradiation and bone marrow transplantation during childhood and adolescence on growth and endocrine function. 332 61

The IGF regulatory system has been shown to mediate mitogenic effects during normal growth and tumor proliferation. The bioavailability of both IGF-I and IGF-II is regulated by at least six specific IGF binding proteins (IGFBPs). Whereas IGFBP-3 is the main IGFBP postnatally, IGFBP-2 is the predominant IGFBP during fetal life. In addition, IGFBP-2 is expressed in a range of tumor cell lines. In order to investigate the IGF regulatory pathway in malignancies we analyzed by RIA serum samples of 49 children with leukemia, Non-Hodgkins' Lymphoma (NHL) or solid tumors at the time of diagnosis. Serum concentrations of IGF-I (mean/range: -2.4/0.3 to -9.9 SDS), IGF-II (-2.5/0.2 to -5.6 SDS) and IGFBP-3 (-1.3/2.2 to -6.8 SDS) were significantly decreased, but IGFBP-2 (3.2/-0.9 to 8.6 SDS) was elevated. Both absolute as well as SDS values of IGF-I, -II and the sum of IGF-I and IGF-II (r = -0.49, p < 0.01) were inversely correlated with IGFBP-2. Serum levels of the growth factors IGF-I and IGF-II were significantly decreased in different types of malignancies to concentrations usually seen only in patients with growth hormone deficiency or during starvation. However, the elevated levels of IGFBP-2 in 70% of our patients exceeded by far those in growth hormone deficiency. Furthermore, in this study we could demonstrate that serum levels of IGF-I and IGF-II were inversely correlated to IGFBP-2 independent on the type of malignancy, indicating a common regulatory mechanism of the IGF signaling pathway in these diseases.
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PMID:[Serum concentrations of insulin-like growth factors (IGF)-I and IGF-II and IGF binding proteins (IGFBP)-2 and IGFBP-3 in 49 children with ALL, NHL or solid tumors]. 756 58

We describe a case of a 15 year old boy who developed acute megakaryoblastic leukemia (AMKL) while receiving treatment with human growth hormone (hGH) for idiopathic growth hormone deficiency (GHD). He was diagnosed as having idiopathic GHD and given hGH from December 1991. The examination of his peripheral blood showed mild pancytopenia 2 months before the start of the hGH therapy. Since January 1992, paleness of the skin, general fatigue and fervescence progressed gradually. In February 1992, because of the occurrence of acute leukemia, administration of hGH was discontinued. Judging from the results of surface marker analysis of the blast cells, the patient was diagnosed as having AMKL. He was treated with chemotherapy for acute non-lymphoblastic leukemia from March 1992. A complete remission was obtained after 4 weeks of treatment. The chemotherapy was completed in July 1993. He remains in complete remission 26 months after diagnosis. This case suggests the importance of hematological examination and, when there is any abnormality which is not caused by GHD, such as pancytopenia, more detailed medical examinations (for example bone marrow examination) are necessary.
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PMID:Occurrence of acute megakaryoblastic leukemia in a patient with idiopathic growth hormone deficiency. 779 61

Having noted symptomatic osteoporotic vertebral collapse in young adult survivors of childhood malignancy, bone mineral density (BMD) was examined at three sites by dual-energy X-ray absorptiometry in 64 patients treated in childhood for intracranial malignancy (group 1; n = 21) or acute leukaemia (group 2; n = 43). Patients in group 1 were selected for growth hormone deficiency (GHD) by auxological and biochemical criteria before the end of puberty (Tanner stage V). Seven patients (six men; mean (+/- SEM) age at study, 28.0 +/- 2.9 years; mean age at diagnosis, 8.7 +/- 1.5 years) in this group had been treated with human pituitary growth hormone (GH) for 1-12 years; and 14 patients (nine men; mean age at study, 26.8 +/- 1.0 years; mean age at diagnosis, 10.7 +/- 1.4 years) had not received GH. Bone densities in group 1 were normal in the GH-treated patients at the femoral neck (98.4 +/- 3.8% of control), lumbar spine (100.4 +/- 6.1% of control) and Ward's triangle (101.0 +/- 6.1% of control) but markedly reduced in the untreated group (femoral neck, 81.2 +/- 2.6% of control (p = 0.002); lumbar spine, 79.1 +/- 4.1% of control (p = 0.04); Ward's triangle, 80.1 +/- 3.6% of control (p = 0.01)). The majority of patients in group 2 had been treated for acute lymphoblastic leukaemia (ALL) and were in three subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone mineralization after treatment of growth hormone deficiency in survivors of childhood malignancy. 794 25

The aim of this study was to ascertain the frequency of adverse events occuring during GH therapy in Australia and New Zealand since 1988. Data for children receiving GH has been collected prospectively on a national database, OZGROW, after informed consent has been given. Adverse events were coded by clinicians and have been analysed in relation to the nature of the event and the underlying diagnosis. There were 2922 subjects analysed, representing 9004 years of GH therapy. 151 subjects reported a total of 210 adverse events giving an overall frequency of 2.3% adverse events/patient treated year. Events that were probably related to GH therapy included peripheral oedema, injection site problems and increased frequency of kyphoscoliosis and slipped epiphysis in some groups. Adverse events were more frequent in growth hormone deficient children who had previously been treated for leukaemia, 8.1%, and in children previously treated for craniopharyngioma, 5.6%. A lower frequency was found for those with a diagnosis of idiopathic short stature, 1.6%, and familial short stature, 0.9%. Kyphoscoliosis was more frequently seen in Turner's syndrome, and slipped epiphyses in adolescent individuals with growth hormone deficiency, especially following treatment for leukaemia. There were no de novo tumours reported but the frequencies of recurrence/patient year for leukaemia, solid cranial tumours and craniopharyngioma were 1.1%, 2.2% and 3.8% respectively. A low frequency of adverse events has been reported on the OZGROW database but subsets of patients may be at increased risk of musculoskeletal abnormalities during GH therapy. The frequency of tumour recurrence during therapy is not different from known rates of recurrence in individuals not treated with GH.
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PMID:Adverse events during growth hormone therapy. 882

Nine patients developed osteochondromata, a mean of 6 years after total body irradiation (TBI) given before bone marrow transplantation for childhood leukaemia. This represents 23% of patients receiving TBI during the period from 1981 to 1989 surviving > or =5 years after bone marrow transplantation. The patients were followed up for a mean of 12.5 years from diagnosis of leukaemia and a mean of 2.5 years from diagnosis of osteochondromata. No osteochondroma, including three lesions removed surgically, showed evidence of malignant change. Six patients received growth hormone for irradiation-induced growth hormone deficiency, but this did not appear to influence the natural history of the osteochondromata. Radiation-induced osteochondromata (RIO) are often multiple and are indistinguishable from the more common idiopathic type. The incidence of RIO after TBI was higher than that reported after local irradiation.
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PMID:Total body irradiation-induced osteochondromata. 960 May 63


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