scholarly journals Tumor lysis syndrome during radiotherapy for prostate cancer with bone and bone marrow metastases without visceral metastasis

2012 ◽  
Vol 32 (3) ◽  
pp. 306-308 ◽  
Author(s):  
Muhammet Ali Kaplan ◽  
Mehmet Kucukoner ◽  
Gulistan Alpagat ◽  
Abdurrahman Isikdogan
2013 ◽  
Vol 2 (4) ◽  
pp. 319
Author(s):  
ManishKumar Singh ◽  
MadhuMati Goel ◽  
US Singh ◽  
Diwakar Dalela ◽  
SN Shankhwar ◽  
...  

1997 ◽  
Vol 157 (2) ◽  
pp. 569-574 ◽  
Author(s):  
Timothy J. McDonnel ◽  
Nora M. Navone ◽  
Patricia Troncoso ◽  
Louis L. Pisters ◽  
Claudio Conti ◽  
...  

2017 ◽  
Vol 24 (2) ◽  
pp. 153-155 ◽  
Author(s):  
Sharonlin Bhardwaj ◽  
Seema Varma

Tumor lysis syndrome is a serious and sometimes lethal complication of cancer treatment that is comprised of a set of metabolic disturbances along with clinical manifestations. Initiating chemotherapy in bulky, rapidly proliferating tumors causes rapid cell turnover that in turn releases metabolites into circulation that give rise to metabolic derangements that can be dangerous. This syndrome is usually seen in high-grade hematological malignancies. Less commonly, tumor lysis syndrome can present in solid tumors and even rarely in genitourinary tumors. In this report, the authors describe a specific case of tumor lysis syndrome in a patient with metastatic prostate cancer following treatment with docetaxel.


2019 ◽  
Vol 17 (1) ◽  
pp. e61-e64 ◽  
Author(s):  
Aline Bobato Lara Gongora ◽  
Felipe Sales Nogueira Amorim Canedo ◽  
André Luis Alves de Melo ◽  
Regis Otaviano Franca Bezerra ◽  
Paula Fontes Asprino ◽  
...  

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2165-2165 ◽  
Author(s):  
Marc Earl ◽  
Alex Fu ◽  
Matt Kalaycio ◽  
Anjali Advani ◽  
Yogen Saunthararajah ◽  
...  

Abstract Abstract 2165 Background: Few AML studies report data on AML patients (pts) with extramedullary hematopoiesis. While AML pts diagnosed with an isolated myeloid sarcoma (MS) purportedly have a better outcome than those with AML without MS, it is unknown whether these outcomes differed for pts diagnosed with MS with or without bone marrow involvement compared to AML without MS. We compared these groups, and also evaluated whether or not the diagnosis of MS increased the rate of tumor lysis syndrome (TLS), due to greater tumor volume. Methods: We reviewed all AML pts newly diagnosed between 1994 and 2009 and treated with a cytarabine-based induction regimen. Pts with a diagnosis of MS with BM involvement (≥5% blasts) or without BM involvement (<5% blasts) were then identified and validated using the pathology database. A 1:2 case-control matching analysis was conducted, in which AML pts with MS with or without BM involvement were defined as cases, while AML pts without MS functioned as controls. Matching was based on age (± 5 years), induction regimen, WBC (± 1 log), AML etiology, diagnosis year (± 5 years), and cytogenetics (risk defined by CALGB 8461). Regression analyses further controlled for age, gender, presenting white blood cell count (WBC), and year of diagnosis. The rate of TLS was compared in univariate analyses. Results: Of the 477 AML pts treated with a cytarabine-based induction regimen, 19 (4%) had MS, either with (n=12, 2.5%) or without (n=7, 1.5%) BM involvement. The mean age (+/−SD) of the entire cohort was 57.5 (14.5) years, and 58 years (24-80) for MS pts; within the entire cohort, 47% were female, 64% had de novo AML, mean WBC was 31k/ml, and 52% had good/intermediate risk cytogenetics, while for MS pts, 32% were female, 74% had de novo AML, mean WBC was 31k/ml, and 74% had good/intermediate cytogenetics. Comparing all MS cases to matched controls, baseline characteristics were similar, as expected. Outcomes were similar for the pooled case and control groups for CR rates (63.2% vs. 65.7%, p=.85) and median OS (0.7 vs. 0.8 years, p=.95). Incidence of tumor lysis syndrome was low in both groups (case 5%, control 3%, p=1.0). Focusing on comparing MS with BM involvement to matched controls, outcomes remained similar for CR rates (58% vs. 71%, p=.44), OS (.53 vs. 1.12 years, p=.4), and TLS (8% vs. 5%, p=1.0), both in univariate and regression analyses. Comparing MS pts without BM involvement to controls, however, CR rates were higher for MS patients (71% vs. 57%, OR 15.5, p=.15), as was median OS (1.14 vs. .64 years, HR .15, p=.027) in univariate and regression analyses. There were no cases of tumor lysis syndrome in either group. Conclusions: AML pts diagnosed with MS without BM involvement and treated with cytarabine-based induction regimen have a superior overall survival to patients with usual presentation of AML treated with a similar regimen. There was no difference in outcome for AML pts with MS with BM involvement, compared to AML pts without MS. Patients with MS were not at significantly higher risk of TLS. Cox model survival curve MS without BM involvement=dotted line AML=continuous line HR=.15, p=.027 Disclosures: No relevant conflicts of interest to declare.


2021 ◽  
Vol 28 (1) ◽  
pp. 440-444
Author(s):  
Sidra Javed

Prostate cancer can masquerade as just normocytic anemia and thrombocytopenia, thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or tumor lysis syndrome (TLS). We are reporting an intriguing case of metastatic prostate cancer which remained undiagnosed until the patient showed signs of tumor lysis syndrome (TLS), leading to urate nephropathy requiring urgent hemodialysis. Tumor lysis syndrome is an oncological emergency but an exceedingly rare complication in non-hematological malignancies, including prostate cancer. It is challenging to recognize features of TLS in a case such as this with an unknown diagnosis. In the case of an established diagnosis of malignancy, however, checking baseline renal function, uric acid, lactate dehydrogenase (LDH), potassium, and phosphate to monitor for TLS as well as considering urate lowering therapy can help prevent adverse outcomes.


1997 ◽  
pp. 569-574 ◽  
Author(s):  
Timothy J. McDonnel ◽  
Nora M. Navone ◽  
Patricia Troncoso ◽  
Louis L. Pisters ◽  
Claudio Conti ◽  
...  

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4578-4578
Author(s):  
William Blum ◽  
Rebecca B. Klisovic ◽  
Cheryl Kefauver ◽  
Amy Johnson ◽  
Mitch Phelps ◽  
...  

Abstract Flavopiridol is a cyclin-dependent kinase inhibitor that induces apoptosis in acute leukemia cell lines. In earlier studies with flavopiridol in several malignancies, plasma concentrations of flavopiridol were not reached or maintained at sufficient levels to induce apoptosis due to unexpectedly high levels of bound drug in human serum relative to fetal calf serum used in preclinical studies. PK modeling in chronic lymphocytic leukemia (CLL) cells cultured in human plasma in vitro indicated that administering flavopiridol by 30 minute intravenous (IV) bolus followed by 4 hour continuous IV infusion (CIVI) would achieve sustained in vivo plasma drug concentration and time exposure similar to that necessary to induce apoptosis. We designed a phase I dose escalation trial in acute leukemias of single agent flavopiridol given as a 30 minute bolus followed by a 4 hour CIVI on days 1–3 with the ability to repeat cycles every 21 days; 16 patients (pts) have been enrolled to date. Dose escalation was as follows (bolus dose/4 hr CIVI dose in mg/m2): 20/30 (n=3), 30/35 (n=7), 30/50 (n=3), and 40/60 (n=3). Based on prior experience with flavopiridol at our institution in CLL, aggressive measures for the prevention and management of hyperacute tumor lysis syndrome (TLS) were employed. Pts had relapsed/refractory AML (N=12) and ALL (N=4), and were 25–78 yrs old (median age 64 yrs). Average plasma levels were 1.0–2.5 μM at the first three dose levels during the infusion (N=13) and declined with terminal half-lives comparable to previously reported 72 hr and more recent 4.5 hr infusions. Clinically significant TLS occurred in 2/16 pts with chemical evidence of lysis in 4 additional pts. A dose-limiting toxicity (renal failure) occurred at dose level 4 (40 mg/m2 bolus/60 mg/m2 CIVI), and the level is currently being expanded. Treatment was otherwise well tolerated. Downregulation of Mcl-1 protein by standard immunoblotting at 4 and/or 24 hrs was demonstrated in blood and/or bone marrow cells of 6/10 patients Anti-leukemic activity including transient reductions in WBCs/circulating blasts (n=7), bone marrow blasts (n=2), and platelet transfusion independence (n=1) was observed. Two received a second course of therapy, but no pt experienced an objective response by standard criteria. The current dose level exceeds that previously given in ongoing CLL studies; dose escalation to identify the maximum tolerated dose using this pharmacokinetically derived schedule in acute leukemia continues. Given the activity of this drug as a single agent, combination studies with conventional chemotherapy or other novel agents in acute leukemias should be considered.


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