Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in body composition, in particular the onset of obesity, may result from reductions in total daily energy expenditure (TDEE) as a consequence of relative physical inactivity. Children previously treated for acute lymphoblastic leukemia (ALL) become obese, yet the mechanism remains undefined. TDEE and physical activity levels [PAL = TDEE/basal metabolic rate (BMR)] were measured in 34 long-term survivors of ALL and compared with results from 21 survivors of other malignancies and 32 healthy sibling control subjects using the flex-heart rate technique. Body composition was measured by dual energy x-ray absorptiometry. The median TDEE was reduced in the ALL group (150 kJ x kg d(-1)) compared with other malignancies and controls (207 and 185 kJ x kg d(-1), respectively, p < 0.01). This reduction was accounted for mainly by a relative decrease in the PAL of the ALL group (1.24) compared with both other malignancies and controls (1.58 and 1.47, respectively, p < 0.01). TDEE and PAL were correlated with percentage body fat (r = -0.39, p < 0.001 and r = -0.24, p < 0.05, respectively). Obesity in survivors of ALL may, in part, be explained by a reduction in TDEE as a consequence of reduced PAL. The cause of such reduction is uncertain.
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PMID:Daily energy expenditure and physical activity in survivors of childhood malignancy. 958 6

The aim of this study was to investigate growth and final height in young adults after therapy for malignant diseases. Final height and weight was studied in 50 long-term survivors (LTS) of childhood cancer (aged 17-31 years; 30 men, 20 women) 3-18 years after treatment for malignant diseases (7 acute lymphoblastic leukemia, 20 lymphoma, 8 sarcoma, 15 malignant central nervous system [CNS] tumours). None of the LTS had been treated with growth hormone (GH). A decrease in final height SDS (Standard deviation score) occurred in both LTS of malignant CNS tumours (median height SDS at diagnosis, 0.3; range, -0.9 to 2.2; median final height SDS, -1.3; range, -3.9 to 1.9; p < 0.01) and LTS of lymphoma (p < 0.05) or leukemia (p < 0.05). However, only LTS who received cranial (p < 0.05) or craniospinal (p < 0.001) irradiation (XRT) exhibited reduced final heights. LTS who had received XRT not involving the CNS or had received no XRT at all presented no reduction in final height. LTS of CNS tumours treated with high craniospinal XRT doses (24 to 56 Gy) reached lower (p < 0.01) final heights when compared with LTS of leukemia who received lower cranial XRT doses (18 to 24 Gy). Final height SDS correlated with chronological age at initiation of therapy (p < 0.05). No correlation was found between the cumulative doses of applied chemotherapeutic agents and the final height of LTS. During follow-up LTS developed an increase in weight for height index (WFH) which occurred independent of XRT. In conclusion, cranial and craniospinal XRT especially in young children with malignancies resulted in a decrease in final height SDS. As 6 of 15 LTS of malignant CNS tumours exhibited a final height SDS below -2 SD, analysis of pituitary function and substitution of GH after diagnosis of GH deficiency should be considered for these patients at a young age. Others factors not directly related to XRT are responsible for the increased risk for obesity in LTS of childhood cancer.
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PMID:Final height and weight of long-term survivors of childhood malignancies. 962 45

Severely malnourished children afflicted by acute lymphoblastic leukemia (ALL), particularly in developing countries, have reduced tolerance to chemotherapy and a compromised prospect for survival. We investigated the prevalence and severity of alterations in growth and nutritional status in children with ALL from population-based referral areas in Canada. All children were treated with Dana-Farber Cancer Institute ALL Consortium protocols. First, the relative impact of cranial irradiation (CI) and chemotherapy on growth was studied in 116 children at diagnosis and at 6-month intervals during treatment. We observed a decline in height standard deviation (SD) score in the first year in all children, and a further decline in height SD score during the second year only in the children who received CI. Weight reduction occurred in the first year, but during the second year there was a disproportionate increase in weight compared with height, suggesting that children treated with ALL have a tendency toward obesity. Both chemotherapy and CI contribute to the altered growth observed in children treated for ALL. Second, intestinal functional integrity was assessed in 16 children during post-induction chemotherapy. Nutrient intake was adequate and there was minimal evidence of malabsorption: fat malabsorption occurred in only 1 child (after treatment-related pancreatitis), abnormal D-xylose absorption occurred in 2 children at 6 months of therapy (returning to normal 6 months later) and abnormal lactose absorption occurred in 4 children. Third, weight, height, whole body lean and fat mass measured by dual-energy X-ray absorptiometry and serum albumin were determined at diagnosis and at 6-month intervals throughout therapy in 19 children with ALL. Height SD scores decreased significantly during treatment. Serum albumin was abnormally low in 6/19 at diagnosis and 14/18 during intensive consolidation therapy. The mean change in the ratio of lean mass to total body weight showed a 5% reduction by 6 months of therapy. Body fat increased from a mean of 22% at diagnosis to 28% at completion of therapy. The majority of children treated for ALL thus have significant changes in nutritional status manifested by reductions in growth, alterations in lean and fat body mass and abnormally low serum proteins during intensive therapy.
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PMID:Growth and body composition in response to chemotherapy in children with acute lymphoblastic leukemia. 987 86

The receptor for the gene product of the obesity gene, leptin, was recently reported to be expressed on murine and human hematopoietic progenitor cells. Therefore, we studied the expression of the leptin receptor, OB-R, in normal myeloid precursors, human leukemia cell lines, and primary leukemic cells using reverse-transcriptase polymerase chain reaction. In normal hematopoiesis, OB-R was expressed in CD34(+) cells. Normal promyelocytes (CD34(-)33(+) and CD34(-)13(+)) expressed only very low levels of the short, presumably nonsignaling isoform. Both the long and short isoforms of OB-R were expressed in 10 of 22 samples from patients with newly diagnosed primary or secondary acute myeloid leukemia (AML), with a higher incidence of the long isoform in primary AML (87.6% v 28.6%; P =.01). The incidence of OB-R expression was higher in recurrent than in newly diagnosed AML (P <.001), and samples from four patients with refractory AML showed strong expression of both isoforms. Both OB-R isoforms were also expressed in newly diagnosed and recurrent acute promyelocytic leukemia cells but were essentially absent in samples of chronic or acute lymphocytic leukemia. In vitro growth of myeloid leukemic cell lines and of blasts from 14 primary AMLs demonstrated that recombinant human leptin alone induced low level proliferation, significantly (P <.05) increased proliferation induced by recombinant human granulocyte colony-stimulating factor, interleukin 3, and stem cell factor in a subset of AML and increased colony formation (P <.005). Also, leptin reduced apoptosis induced by cytokine withdrawal in MO7E and TF-1 cells. Serum leptin levels correlated only with body mass index (P <. 001) and gender (P =.03). Results confirm the reported expression of leptin receptor in normal CD34(+) cells and demonstrate the frequent expression of leptin receptors in AML blasts. While normal promyelocytes lack receptor expression, leukemic promyelocytes express both isoforms. We also demonstrate proliferative effects of leptin alone and in combination with other physiologic cytokines, and anti-apoptotic properties of leptin. These findings could have implications for the pathophysiology of AML.
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PMID:Expression and function of leptin receptor isoforms in myeloid leukemia and myelodysplastic syndromes: proliferative and anti-apoptotic activities. 1002 96

A high prevalence of obesity in survivors of acute lymphoblastic leukemia (ALL) has been described, but genetic and social influence in obesity has not been analyzed in this group of patients. The authors studied a population of 33 long-term (25 females, 8 males) in first remission who had reached their final height. All patients received cranial irradiation as part of their central nervous system (CNS)-directed therapy and no patient received growth hormone. The body mass index (BMI: weight/height2) of patients and their biological parents was calculated and submitted to statistical analysis. Obesity was defined as BMI greater than the 85th centile. No excessive obesity was found among the males at final height. Fifty-six percent of the females were obese. In this group of 14 obese female survivors 59% had obese mother, but only 14% had obese fathers. The results indicate a significant maternal predisposition to obesity.
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PMID:Obesity in leukemia survivors: the familial contribution. 1077 89

Alstrom syndrome is a rare autosomal recessive disease; less than 60 cases have been reported. No Chinese patient with this disease has been reported previously in the literature. Here, we describe an 11-year-old Chinese boy with this condition. His elder sister also had Alstrom syndrome, and his father had non-insulin-dependent diabetes mellitus. Both siblings had degenerative retinopathy, obesity, mental retardation, perceptive hearing loss, short stature, non-insulin-dependent diabetes mellitus, nephropathy, hyperlipidemia, acanthosis nigricans, and hepatic dysfunction. The boy also developed acute lymphoblastic leukemia, which was confirmed by cytochemistry and immunophenotyping findings. He received chemotherapy and radiotherapy for the malignancy. The present case suggests that acute lymphoblastic leukemia may be coincident with or may be a previously undescribed systemic manifestation of Alstrom syndrome.
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PMID:Acute lymphoblastic leukemia in one of two siblings with Alstrom syndrome. 1106 Oct 78

Primary care physicians will be providing longitudinal health care for long-term survivors of childhood acute lymphoblastic leukemia (ALL) with increasing frequency. Late effects (sequelae) secondary to treatment with radiation or chemotherapeutic agents are frequent and may be serious. Depending on treatment exposures, this at-risk population may experience life-threatening late effects, such as cirrhosis secondary to hepatitis C or late-onset anthracycline-induced cardiomyopathy, or life-changing late effects, such as cognitive dysfunction. Many survivors of childhood ALL will develop problems such as obesity and osteopenia at a young age, which will significantly affect their risk for serious health outcomes as they grow older. The goal of our review is to assist primary care physicians in providing longitudinal health care for long-term survivors of childhood ALL. We also highlight areas needing further investigation, including the prevalence of different late effects, determination of risk factors associated with a late effect, a better understanding of the potential impact of late effects on the premature development of common adult health problems, and the value and timing of different tests for screening asymptomatic survivors.
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PMID:Providing primary care for long-term survivors of childhood acute lymphoblastic leukemia. 1113 63

Insulin-like growth factor (IGF)-binding protein-2 (IGFBP-2) is altered in different diseases and might be used as an indication of its severity. The aims of our study were to investigate: (1) the developmental pattern of the serum IGFBP-2 concentration at birth and during childhood and adolescence; (2) whether the serum IGFBP-2 level could be a marker for the diagnosis and evolution of diseases where the growth hormone (GH)-IGF axis is altered, and (3) whether this binding protein shows a relationship with IGF-I, its free fraction, IGFBP-1 and -3. We report reference values for 55 normal full-term newborns and 221 normal children who were divided into 5 groups according to their Tanner stage. Serum levels were higher in newborns when compared with Tanner stages I-V (p < 0.001, ANOVA), with no further changes throughout development. Furthermore, we studied IGFBP-2 levels in 24 children with congenital GH deficiency (GHD), 26 with acute lymphoblastic leukemia (ALL), 75 obese children, and 60 girls with anorexia nervosa (AN) at diagnosis and during a follow-up period. IGFBP-2 at diagnosis was increased in GHD, ALL and AN, and decreased in obesity (p < 0.05, ANOVA). During the follow-up, IGFBP-2 concentrations tended to normalize. IGFBP-2 correlated positively with IGFBP-1 and negatively with IGF-I and IGFBP-3 in normal subjects and at diagnosis of the pathologies studied. Although IGFBP-2 functions are not well understood, these results suggest a possible role for this protein in diseases where the GH-IGF axis is altered.
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PMID:Insulin-like growth factor-binding protein-2 levels in pediatric patients with growth hormone deficiency, eating disorders and acute lymphoblastic leukemia. 1115 Aug 83

The adiposity rebound (AR), when body mass index begins to increase after its nadir in childhood, is a critical period for the regulation of energy balance and adult obesity risk. The aim of the present study was to test whether children treated for acute lymphoblastic leukemia (ALL) experience premature AR. This might, in part, explain their tendency to develop obesity. Timing of AR was assessed by visual inspection of body mass index plots in 68 patients treated for ALL in first remission. This sample comprised all eligible patients treated in Scotland between 1991 and 1998, age 30 months or less at the time of diagnosis. Timing of AR in patients was compared against a cohort of 889 healthy British children studied during the 1990s using the same method. AR occurred significantly earlier in the patients treated for ALL (chi(2) test, P < 0.001). The AR had occurred in 43% (29 of 68) of the patients and 4% (40 of 889) of the comparison group by age 37 months. At 49 months AR had occurred in 81% (55 of 68) of the patients and 21% (190 of 889) of the comparison group. Treatment of ALL is associated with a significantly advanced AR. This might, in part, explain the extremely high prevalence of obesity in long-term survivors. Clinical management should focus on minimizing excess weight gain during therapy to reduce long-term obesity risk.
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PMID:Premature adiposity rebound in children treated for acute lymphoblastic leukemia. 1139 86

Despite a widespread belief that glucocorticoid therapy is associated with positive energy balance and excess weight gain there is a dearth of quantitative evidence about its effects and the underlying mechanisms of any effects. The primary aim of the present study was to quantify the effect of dexamethasone and prednisone treatment on energy intake in children treated for childhood acute lymphoblastic leukemia. A secondary aim was to test for differences in excess weight gain between patients treated using the 2 glucocorticoids. We measured energy intake in 26 patients (mean +/- SD age, 6.3 +/- 2.3 yr) during a 5-d period "on" steroids and again in the week before steroid treatment. Changes in body mass index from diagnosis to 1 and 2 yr postdiagnosis were expressed as SD scores. Steroid treatment was associated with a significant increase in energy intake of approximately 20% (mean paired difference, 1.7 MJ/d; SD, 2.8; 95% confidence interval, 0.7-2.8 MJ/d), with no significant difference between the 2 steroids. The mean change in body mass index SD score was +0.38 (SD, 1.10; P < 0.05) to 1 yr and +0.68 (SD, 1.38; P < 0.05) to 2 yr, with no significant difference between the 2 groups of patients. Glucocorticoid treatment in childhood acute lymphoblastic leukemia increases energy intake markedly, and this effect contributes to the excess weight gain and obesity characteristic of patients being treated for acute lymphoblastic leukemia.
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PMID:Effect of glucocorticoid therapy on energy intake in children treated for acute lymphoblastic leukemia. 1150 5


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