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固定剂量重组尿酸氧化酶治疗儿科肿瘤细胞溶解综合征:区域癌症中心的经验。

Fixed-Dose Recombinant Urate Oxidase in the Treatment of Paediatric Tumour Lysis Syndrome: A Regional Cancer Centre Experience.

机构信息

Department of Paediatric Oncology, Kidwai Memorial Institute of Oncology, Bangalore, India.

出版信息

Asian Pac J Cancer Prev. 2021 Dec 1;22(12):3897-3901. doi: 10.31557/APJCP.2021.22.12.3897.

DOI:10.31557/APJCP.2021.22.12.3897
PMID:34967569
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9080352/
Abstract

BACKGROUND

Tumor lysis syndrome (TLS) is an oncologic emergency commonly seen in children with hemato-lymphoid malignancies. Recombinant urate oxidase (RUO) is used in both the prophylaxis and treatment of TLS. However, in resource-constrained countries, its role is mostly limited to the treatment of established TLS and data regarding the use of RUO and its outcome is sparse.

OBJECTIVE

To describe the outcome of Pediatric TLS following the use of a fixed - dose of RUO.

METHODS

A retrospective chart review of all children <15 years of age admitted in the Department of Paediatric Oncology, Kidwai Cancer Institute from April 2017 to July 2018 with TLS and treated with a single, fixed - dose (1.5 mg) RUO was undertaken.

RESULTS

During the study period, 255 children with hemato-lymphoid malignancies were diagnosed to be at risk of developing TLS. Of these, only 22 (8.6%) children developed TLS and received RUO. Among those with TLS, 15 (68.2%) had Acute Lymphoblastic Leukemia (ALL) while 7 (31.8%) had Non - Hodgkin lymphoma (NHL). 91% (20/22) children had spontaneous TLS and the remainder developed therapy-related TLS. Median age at presentation was 8 years (IQR 5.25,1.75) with 4.5:1 male: female ratio. The mean urate level at admission was 19.12 mg/dl (+/- 8mg/dl) (Range: 10.7-34.5). 91% (20/22) children received RUO at less than 0.15 mg/kg and the median dose of RUO was 0.05 mg/kg (IQR 0.038-0.08). Of the 22 children with TLS, 2 children failed to achieve normal serum urate levels at 24 hours in response to a single fixed-dose of RUO and hence received an extra dose of RUO. Serum urate levels remarkably declined following RUO administration from 19.12 mg/dl (+/-8) to 8.2 mg/dl (+/-3.9), 3.99 mg/dl (+/-1.6) and 2.84 mg/dl (+/-1.3) at 12h, 24h and 48h respectively. AKI was present in 15 (68.2%) children. The median eGFR of the group at diagnosis was 49 ml/min/1.73m2 (IQR 26.3, 70). None of the children required hemodialysis. No significant adverse events occurred.

CONCLUSION

Fixed-dose RUO can achieve rapid, adequate and sustained drop in serum urate levels in Paediatric TLS. It is a useful strategy for managing TLS in resource-constrained settings.

摘要

背景

肿瘤溶解综合征(TLS)是儿童血液淋巴系统恶性肿瘤中常见的肿瘤急症。重组尿酸氧化酶(RUO)既用于 TLS 的预防,也用于治疗。然而,在资源有限的国家,其作用主要限于治疗已确诊的 TLS,关于 RUO 的使用及其结果的数据很少。

目的

描述使用固定剂量 RUO 后儿科 TLS 的结果。

方法

对 2017 年 4 月至 2018 年 7 月在 Kidwai 癌症研究所儿科肿瘤科住院的所有<15 岁、有发生 TLS 风险的血液淋巴系统恶性肿瘤儿童的病历进行回顾性图表审查,并对这些儿童使用单一、固定剂量(1.5mg)的 RUO 进行治疗。

结果

在研究期间,有 255 名血液淋巴系统恶性肿瘤患儿被诊断为有发生 TLS 的风险。其中只有 22 名(8.6%)患儿发生了 TLS 并接受了 RUO 治疗。在有 TLS 的患儿中,15 名(68.2%)患有急性淋巴细胞白血病(ALL),7 名(31.8%)患有非霍奇金淋巴瘤(NHL)。91%(20/22)的患儿为自发性 TLS,其余患儿为治疗相关性 TLS。发病时的中位年龄为 8 岁(IQR 5.25,1.75),男女比例为 4.5:1。入院时尿酸平均水平为 19.12mg/dl(+/-8mg/dl)(范围:10.7-34.5)。91%(20/22)的患儿接受的 RUO 剂量低于 0.15mg/kg,中位数 RUO 剂量为 0.05mg/kg(IQR 0.038-0.08)。在 22 例有 TLS 的患儿中,有 2 例患儿在接受单一固定剂量 RUO 后 24 小时内未能使血清尿酸水平恢复正常,因此接受了额外剂量的 RUO。接受 RUO 治疗后,血清尿酸水平显著下降,12 小时、24 小时和 48 小时分别降至 8.2mg/dl(+/-3.9)、3.99mg/dl(+/-1.6)和 2.84mg/dl(+/-1.3)。15 名(68.2%)患儿存在 AKI。该组患儿在诊断时的中位 eGFR 为 49ml/min/1.73m2(IQR 26.3,70)。无患儿需要血液透析。未发生明显不良事件。

结论

固定剂量 RUO 可使儿科 TLS 患者的血清尿酸水平迅速、充分和持续下降。在资源有限的环境中,它是治疗 TLS 的一种有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c611/9080352/6f5f42e07941/APJCP-22-3897-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c611/9080352/39573a0a5c69/APJCP-22-3897-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c611/9080352/a7c3f368fa18/APJCP-22-3897-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c611/9080352/6f5f42e07941/APJCP-22-3897-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c611/9080352/39573a0a5c69/APJCP-22-3897-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c611/9080352/a7c3f368fa18/APJCP-22-3897-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c611/9080352/6f5f42e07941/APJCP-22-3897-g003.jpg

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