摘要 :
We read with interest the tumour lysis syndrome (TLS) guidelines published by Cairo et al (2010), which updated earlier publications (Cairo & Bishop, 2004; Coiffier et al, 2008). We were particularly struck by the guidelines regarding TLS manag...
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We read with interest the tumour lysis syndrome (TLS) guidelines published by Cairo et al (2010), which updated earlier publications (Cairo & Bishop, 2004; Coiffier et al, 2008). We were particularly struck by the guidelines regarding TLS management for patients with acute lymphoblastic leukaemia (ALL) or acute myeloid leukaemia (AML) and a diagnostic white blood cell count (WBC) < 100 x 109/l. The new guidelines are risk stratified by lactate dehydrogenase (LDH) and recommend prophylactic rasburicase in all ALL patients with LDH level >2x upper limit of normal (ULN). In addition, AML patients with laboratory TLS are to receive rasburicase, regardless of the presenting WBC and clinical findings. The guidelines for the prophylactic use of rasburicase also potentially include patients with hyperkalaemia and/or hyper-phosphataemia without concomitant hypemricaemia (Fig 4 and text, Cairo et al, 2010). And lastly, the recommendation for prophylactic rasburicase in the defined high-risk subgroup is stated to be a grade A recommendation, yet no systematic review is identified (Cairo et al, 2010).
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Accumulating evidence suggests that childhood acute lymphoblastic leukemia (ALL) may be initiated in utero or early in the postnatal period. High birth weight (or rapid fetal growth) is associated with risk of ALL, but the mechani...
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Accumulating evidence suggests that childhood acute lymphoblastic leukemia (ALL) may be initiated in utero or early in the postnatal period. High birth weight (or rapid fetal growth) is associated with risk of ALL, but the mechanisms are not understood. In a population-based epidemiologic study of childhood ALL, we utilized a haplotype-based approach to assess the role of eight genes involved in fetal growth and body size regulation in 377 childhood ALL cases and 448 controls. We found significant haplotype associations with risk of childhood ALL for IGF1 among non-Hispanics and Hispanics together (p = 0.002), for IGF2 among Hispanics (p = 0.040), and for IGF2R among Hispanics and non-Hispanics (p = 0.051 and 0.009, respectively). No haplotype associations were observed for IGF1R or the studied genes involved in body size regulation, including LEP, LEPR, GHRL, and NPY. Our study is the first to identify an association between the genes involved in the IGF axis and risk of childhood ALL. These findings for childhood ALL emphasize the importance of fetal growth, when lymphoid progenitor cells are not yet fully differentiated and therefore more susceptible to malignant transformation. Additional studies are needed to confirm these findings and identify specific causal variants.
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Background: Nutritional deficiencies in children with cancer at time of diagnosis and during treatment may negatively affect disease outcome and increase treatment-related toxicity. Yet zinc, an essential nutrient important for su...
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Background: Nutritional deficiencies in children with cancer at time of diagnosis and during treatment may negatively affect disease outcome and increase treatment-related toxicity. Yet zinc, an essential nutrient important for supporting immune function and known for reducing diarrheal episodes, is rarely assessed in these children. Procedures: Fifty children (1 month to 18 years) with recently diagnosed cancer were enrolled in this study. An age and gender matched control group (n = 50) was also recruited. Plasma and urinary zinc, plasma copper, and C-reactive protein (CRP) levels were measured at baseline, 3, and 6 months following diagnosis. A retrospective review of the toxicity profile was performed in the cohort of children with cancer for the first 4 years after initial diagnosis. Results: CRP and plasma copper (both acute-phase reactants) were elevated in patients with cancer compared to controls at baseline, both p < .03. Plasma zinc levels were not significantly different from controls at baseline, but decreased by 11% in the cancer group over 6 months of treatment, 83.2 ± 15.6 to 74.3 ± 14.8 μg/dl, p = .01. Plasma zinc dropped to deficient levels in 35% of cases over the initial 6 months. Zinc deficiency at 6 months was related to an increased incidence of severe diarrhea during 4 years of follow-up, p < .001. Conclusions: Zinc deficiency is an underrecognized problem among patients undergoing treatment for cancer and is associated with severe diarrhea. Further studies are needed to evaluate causes for zinc deficiency, related effects, and a possible role for zinc supplementation.
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