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)

The growth of 95 children with malignant disease was studied over a 3- or 4-year period, and compared with the growth of normal children matched for age and sex by calculation of the standard deviation score. The mean standard deviation score of the children with leukaemia fell in the first year of treatment, and thereafter showed little change, remaining below the normal. This effect was related to cranial and craniospinal irradiation, but not to age or duration of chemotherapy. The loss in eventual height attained was small and does not suggest any long-term interference with growth hormone production.
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PMID:Effect of treatment of malignant disease on growth in children. 677 6

The effect of cytotoxic therapy (including cytosine-arabinoside and thioguanine) on the adrenal response to insulin-induced hypoglycemia has been investigated in 15 newly diagnosed patients with an acute form of leukemia. Hypoglycemia was induced with crystalline insulin (0.15 U kg-1). Cortisol, growth hormone and prolactin were determined by radioimmunoassay at 0, 30, 60, 90 and 120 min during the insulin-tolerance test and also before and after the completion of the therapy. There was a significant impairment of a cortisol response after the completion of the cytotoxic therapy, while no significant changes could be detected in growth hormone and prolactin response. It is concluded that either cortisol synthesis or release mechanism was compromised by the cytotoxic therapy and/or metabolic derangements brought about therewith.
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PMID:Effects of cytotoxic therapy on hypothalamic-pituitary-adrenal axis response to insulin-induced hypoglycemia in patients with a variety of acute leukemias. 704 70

Fourteen children who relapsed after initial remission of leukaemia were studied. Six received a second course of cranial radiotherapy, while the remaining eight children were given total body irradiation before bone marrow transplantation. The postirradiation somnolence syndrome was common after cranial radiotherapy. All children had mild/soft neurological signs, mostly of coordination. None had a major motor disability. All but the youngest child had cataracts; two children required an operation for these. All children were growth hormone deficient. Verbal IQ, attention, and concentration were selectively reduced (with respect to normative levels). The time between the two treatments, age at relapse, and higher doses of radiotherapy all correlated with cognitive outcome, with girls showing greater impairments than boys. Only two children were performing at age appropriate levels on measures of academic achievement. It is concluded that neurological and neuropsychological morbidity is significantly increased by the current treatments prescribed after the relapse of leukaemia.
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PMID:Neuropsychological and neurological outcome after relapse of lymphoblastic leukaemia. 751 91

To determine whether obesity complicated the treatment of childhood acute lymphoblastic leukemia, we studied the body mass index (BMI) of 63 female when and 51 male patients from the time of diagnosis of acute lymphoblastic leukemia to the time when final height was attained. The BMI z score was calculated for each patient at diagnosis, at end of treatment, and at attainment of final height. Obesity at attainment of final height was defined as a BMI greater than the 85th percentile of the normal reference population. At final height 23 of 51 male (45%) and 30 of 63 female patients (47%) were obese. Girls became obese between diagnosis and the end of chemotherapy (p = 0.02), after which they had no further increase, indicating that chemotherapy may have played a role in their obesity. Boys had a progressive and gradual increase in BMI z score through to attainment of final height. Obesity did not appear to be associated with growth hormone insufficiency, disproportionate growth, or abnormal timing of puberty. We conclude that approximately half the survivors of leukemia in childhood become obese young adults. Many of those treated with the more recent regimens studied are still only in their mid or preteen years and should be advised regarding a more active lifestyle and a healthy diet in an attempt to reduce the incidence of obesity.
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PMID:High incidence of obesity in young adults after treatment of acute lymphoblastic leukemia in childhood. 760 13

A few years ago it was reported that some growth-hormone-deficient children had developed leukemia following therapy with human growth hormone. This raised concern that this therapy may stimulate tumor development. Since it is known that the tendency to develop cancer is closely related to chromosome breakage, we decided to investigate whether recombinant human growth hormone (rhGH) therapy can increase chromosome fragility. Ten short normal children were studied during their first year of treatment. Lymphocytes were collected at 0, 6 and 12 months of rhGH therapy, and we assessed the rate of spontaneous chromosome aberrations, the frequency of sister chromatid exchanges, the proliferative rate indices, the expression of common fragile sites induced by aphidicolin, and the sensitivity towards the radiomimetic action of bleomycin. At 6 months of therapy, there was a significant increase in bleomycin-induced chromosome aberrations, which remained unchanged after 1 year of treatment. An increase in spontaneous chromosome rearrangements at 6 and 12 months of therapy was also observed. These findings are further supported by data obtained from the analysis of 16 short normal children already on rhGH therapy.
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PMID:Increased chromosome fragility in lymphocytes of short normal children treated with recombinant human growth hormone. 768 29

The use of growth hormone (GH) has been implicated as a possible risk factor for leukemia. We present data from six patients that support a working hypothesis that an increased risk of leukemia may exist in patients with GH deficiency not related to exogenous use of GH.
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PMID:Relationship of growth hormone deficiency and leukemia. 775 2

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

The improved treatment of childhood leukemia is a major achievement. The late effects of the treatment need further investigation. Growth inhibition has been demonstrated in earlier studies. Growth and the timing of puberty were studied in 179 girls who had been treated for acute lymphoblastic leukemia (ALL) in Denmark, Finland, Norway, and Sweden. The patients were divided into two groups according to mode of CNS prophylaxis: with or without cerebral irradiation. Longitudinal analysis of 103 patients showed no difference in prepubertal growth in irradiated and nonirradiated girls. Growth during puberty was normal in girls without irradiation and below normal in irradiated girls. There was no difference in growth between girls after 24 Gy or 20 Gy of cerebral irradiation. Irradiated girls had a final height which was one SD less than expected before puberty and menarche occurred one year earlier than in the nonirradiated girls. Prophylactic cerebral irradiation is the most important factor for subnormal growth after treatment for ALL. There is no short-term influence on growth but the effects of irradiation become apparent several years after therapy when girls enter puberty somewhat early and have a subnormal pubertal growth. Growth and growth hormone (GH) levels should be evaluated several years after CNS irradiation, and treatment with GH and/or luteinizing hormone releasing hormone (LHRH) analogues may be considered.
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PMID:Cerebral irradiation causes blunted pubertal growth in girls treated for acute leukemia. 815 98

Growth impairment and growth hormone (GH) deficiency have been reported in children treated for acute lymphoblastic leukaemia (ALL). We have studied growth and GH secretion in a group of 50 patients, affected by ALL, during a 2- to 5-year period after diagnosis, and in 12 "long-term-survivors". We observed a significant decrease in growth velocity during the 1st year (in particular during the first 6 months) of therapy and a catch-up growth after the end of therapy. "Long-term survivors" did not exhibit a significant reduction of height standard deviation score (SDS), as compared to height SDS at diagnosis. None of the patients showed GH deficiency. Our data indicate that chemotherapy significantly affects growth of patients treated for ALL, whereas radiotherapy-at the doses used in this study-does not induce GH deficiency, at least not within 9 years after diagnosis.
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PMID:Growth and growth hormone in children during and after therapy for acute lymphoblastic leukaemia. 822 2

Corn oil administered by oral gavage decreases the spontaneous incidence of mononuclear cell leukemia (MNCL) in male Fischer rats used as vehicle controls in long-term carcinogenesis experiments. We used an MNCL transplant model, an in situ MNCL cell proliferation assay and immune competence assays to explore mechanism(s) underlying the effects of corn oil gavage on MNCL development in male rats. Relative to non-gavaged or water-gavaged rats, corn oil-gavaged rats had approximately 25% lower MNCL incidence as well as longer MNCL latency and increased survival. There were no differences in body weight or caloric intake between treatment groups, as corn oil-gavaged rats compensated for calories supplied by the gavaged oil by consuming less food. These data indicate that transplanted MNCL cells grew slower in corn oil-gavaged rats than in non-gavaged or water-gavaged rats and suggest that corn oil gavage may exert its effects through a decrease in protein or other nutrients. Five-day proliferation rates of cultured MNCL cells in diffusion chambers implanted in male corn oil-gavaged rats were 40% less than in water-gavaged rats, suggesting nutrition-sensitive endogenous factors mediate the suppression of MNCL cell proliferation in corn oil-gavaged rats. Corn oil-gavaged rats had 54% lower serum growth hormone (GH) levels, and replacement of GH into corn oil-gavaged rats by osmotic minipump infusion increased in situ MNCL cell proliferation to rates observed in water-gavaged animals. Corn oil-gavaged rats also showed enhanced cellular immune competence as measured by mitogen stimulation, natural cytotoxicity and immunofluorescence assays. Taken together, these findings suggest corn oil administered by oral gavage may decrease MNCL development by slowing MNCL cell proliferation, mediated at least in part by altered levels of diffusible factors such as GH, and/or by enhancing immune competence.
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PMID:Inhibition of rat mononuclear cell leukemia by corn oil gavage: in vivo, in situ and immune competence studies. 831 8


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