ライフサイエンスコーパス: tumor lysis syndrome

1 e aminotransferase, febrile neutropenia, and tumor lysis syndrome.

2 f management in diseases other than gout and tumor lysis syndrome.

3 d glucuronide metabolite AUC correlated with tumor lysis syndrome.

4 ity using this novel schedule was hyperacute tumor lysis syndrome.

5 Three patients had laboratory evidence of tumor lysis syndrome.

6 One patient developed grade 4 tumor lysis syndrome.

7 oproliferation, and urate nephropathy due to tumor lysis syndrome.

8 luded neutropenia (38%), mucositis (9%), and tumor lysis syndrome (7%).

9 ssociated with thrombocytopenia and, rarely, tumor lysis syndrome and cytokine release reactions; the

10 l monitoring and aggressive intervention for tumor lysis syndrome and hyperkalemia is necessary for s

11 s the use of urate oxidase for prevention of tumor lysis syndrome and the associated uric acid nephro

12 vel in vivo, with delayed development of the tumor lysis syndrome and with complete remission.

13 self, but complications such as leukostasis, tumor lysis syndrome, and disseminated intravascular coa

14 ti-CD19-CAR T cells, another CLL patient had tumor lysis syndrome as his leukemia dramatically regres

15 The tumor lysis syndrome developed in 1 patient; no treatmen

16 ts to the dose-escalation schedule, clinical tumor lysis syndrome did not occur in any of the 60 pati

17 on and kidney size, but a moderate degree of tumor lysis syndrome ensued.

18 zyme capable of treating gout and preventing tumor lysis syndrome in human patients.

19 of initial management include prevention of tumor lysis syndrome in patients at high risk and minimi

20 l death with regard to antitumor immunity or tumor lysis syndrome in patients.

21 ient were pneumonia (in five [29% patients); tumor lysis syndrome (in three [18%] patients); and seps

22 Acute tumor lysis syndrome necessitates intravenous hydration,

23 Clinical tumor lysis syndrome occurred in 3 of 56 patients in the

24 for 1 acute kidney failure, grade 3, due to tumor lysis syndrome, overall nephro- and hepatotoxicity

25 Dose-limiting toxicity was acute tumor lysis syndrome resulting in fatal hyperkalemia.

26 debulking, 36 of 40 patients (90%) with high tumor lysis syndrome risk at baseline shifted to medium

27 me risk at baseline shifted to medium or low tumor lysis syndrome risk categories.

28 Apart from the tumor lysis syndrome, the only other grade 3/4 toxic eff

29 ccur in four patients, as a result of severe tumor lysis syndrome; three of these patients required h

30 malignancy and were in danger of developing tumor lysis syndrome (TLS) and subsequent acute uric aci

31 Acute tumor lysis syndrome (TLS) is characterized by the triad

32 The pathophysiology of AKI during tumor lysis syndrome (TLS) is not well understood due to

33 onths to reduce the tumor burden and related tumor lysis syndrome (TLS) risk.

34 s were in the high tumor burden category for tumor lysis syndrome (TLS) risk; after ibrutinib lead-in

35 c malignancies at risk for hyperuricemia and tumor lysis syndrome (TLS) were randomly assigned to ras

36 s and prostate cancer, and the occurrence of tumor lysis syndrome (TLS) with (177)Lu-labeled peptides

37 Safety, including incidence of tumor lysis syndrome (TLS), did not differ between sched

38 yndrome was not observed, whereas laboratory tumor lysis syndrome was documented in three patients.

39 Clinical tumor lysis syndrome was not observed, whereas laborator

40 No tumor lysis syndrome was observed.

41 A single case of biochemical tumor lysis syndrome was observed.

42 e neutropenia occurred in 16% of cycles, and tumor lysis syndrome was rare.

43 Tumor lysis syndrome was the dose-limiting toxicity (DLT

44 No patients experienced tumor lysis syndrome with daily venetoclax ramp-up.