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Cisplatin-induced nephrotoxicity in children: what is the best protective strategy?
Ruggiero, A, Ariano, A, Triarico, S, Capozza, MA, Romano, A, Maurizi, P, Mastrangelo, S, Attinà, G
Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners. 2021;(1):180-186
Abstract
INTRODUCTION Platinum compounds, which are considerably effective for the treatment of childhood malignancies, have significantly contributed to the increase in long-term survival of children with cancer. Unfortunately, children receiving cisplatin-based chemotherapy have been known to be at risk for severe disabling adverse effects, such as nephrotoxicity. METHODS A literature research of the MEDLINE PubMed database was conducted to identify articles published between 1980 and 2019 reviewing "Cisplatin AND mannitol." RESULTS The primary pharmacodynamics and clinical characteristics of cisplatin were described, focusing on its renal toxic effects and potential preventive strategies, in order to improve clinical outcomes among children with cancer aged 1 to 14 years. Currently, selecting either hydration alone or hydration plus mannitol for preventing nephrotoxicity has been controversial considering the lack of guidelines to provide treatment recommendations both among adults and children. CONCLUSIONS Appropriate knowledge regarding the pharmacokinetics and toxicological profile of cisplatin may help physicians prevent renal toxicity. Unfortunately, published data regarding the nephroprotective utility of adding mannitol appear to be inconclusive. As such, appropriate hydration remains the main fundamental strategy for reducing the risk of cisplatin-induced nephrotoxicity. Considering the increasing number of children safely cured of their tumours, it is imperative that those treated with cisplatin receive the most appropriate nephroprotective strategy for reducing the negative impact of platinum compounds on quality of life.
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Interventions for cisplatin-induced hearing loss in children and adolescents with cancer.
Freyer, DR, Brock, P, Knight, K, Reaman, G, Cabral, S, Robinson, PD, Sung, L
The Lancet. Child & adolescent health. 2019;(8):578-584
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Abstract
The identification of preventive interventions that are safe and effective for cisplatin-induced ototoxicity is important, especially in children because hearing loss can impair speech-language acquisition development. Previous randomised trials assessed systemic drugs such as amifostine, sodium diethyldithiocarbamate or disulfiram, and sodium thiosulfate. Amifostine, sodium diethyldithiocarbamate, and disulfiram did not show hearing preservation. Paediatric trials assessing sodium thiosulfate showed efficacy in terms of hearing protection. The SIOPEL 6 trial consisted solely of patients with localised hepatoblastoma and no effects on survival were shown. In the ACCL0431 trial, which included heterogeneous patients, a post-hoc analysis showed significantly worse overall survival among patients who had disseminated disease receiving sodium thiosulfate than among controls, but not among those with localised disease. Intratympanically administered drugs have mainly been assessed in adults and include N-acetylcysteine and dexamethasone. Inconsistent effects of these drugs were identified but these studies were limited by design, small sample size, and statistical approach. Future studies of systemic drugs will need to consider the measurement of disease outcomes through study design and sample size, and ototoxicity endpoints should be harmonised to enhance comparability between trials.
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Which neoadjuvant chemotherapy regimen should be recommended for patients with advanced nasopharyngeal carcinoma?: A network meta-analysis.
Yuan, C, Xu, XH, Luo, SW, Wang, L, Sun, M, Ni, LH, Xu, L, Wang, XL, Zeng, G
Medicine. 2018;(34):e11978
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Abstract
BACKGROUND The clinical application has widespread disagreement on the different regimens of neoadjuvant chemotherapy (NCT) in the treatment of locoregionally advanced nasopharyngeal carcinoma (NPC). We conducted a network meta-analysis (NMA) to evaluate the efficacy of the different NCT regimens in the treatment of NPC. METHODS A systematic literature search was performed using PubMed, Embase, and Cochran Library. Totally, 31 randomized controlled trials (RCTs) (n = 4062) met study selection criteria and were incorporated in this NMA study. RESULTS Our study showed that certain NCT regimens improved the prognosis of patients, and found out the relative best solution for each endpoint, such as paclitaxel, carboplatin, and gemcitabine for 1-year overall survival (OS) rate, cisplatin, calcium folinate, and 5-fluorouracil for 2-year OS rate, vinorelbine and cisplatin (NP) for 3-year OS rate, cyclophosphamide, cisplatin, and 5-fluorouracil for 5-year OS rate, NP for complete remission rate, cisplatin and gemcitabine for overall remission rate of the primary tumor. In addition, for certain grade 3 and above toxicity, the results of the NMA reflected certain NCT regimens can reduce toxicity of chemoradiotherapy (CRT) to a minimum, such as NP for anemia, mucositis, and thrombocytopenia, paclitaxel, epirubicin, and cisplatin for neutropenia and skin toxicity. CONCLUSION Our NMA showed that certain cisplatin-based NCT regimens improved the prognosis of patients with NPC and reduced the toxicity of CRT. However, in view of survival rate and response rate, the best NCT regimen is not entirely consistent. Therefore, which NCT regimen will benefit most patients will need further explored.
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Renal toxicity and chemotherapy in children with cancer.
Ruggiero, A, Ferrara, P, Attinà, G, Rizzo, D, Riccardi, R
British journal of clinical pharmacology. 2017;(12):2605-2614
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Abstract
The clinical use of antineoplastic drugs can be limited by different drug-induced toxicities. Of these, renal dysfunction may be one of the most troublesome in that it can be cumulative and in general is only partially reversible with the discontinuation of the treatment. Renal toxicity may be manifested as a reduction of the glomerular filtration rate, electrolyte imbalances, or acute renal failure. Careful assessment of renal function has to be performed taking into account that the impairment of renal function is initially silent and only later may be clinically dramatic. When clinically indicated, the reduction or, in cases of severe nephrotoxicity, the suspension of chemotherapy should be considered to avoid the progressive deterioration of the compromised glomerular and/or tubular function.
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[Severe Hyponatremia after Cisplatin-Based Chemotherapy : Two Case Reports].
Ohtaka, M, Hattori, Y, Kumano, Y, Maeda, Y, Kondo, T, Mochizuki, T, Kawahara, T, Teranishi, J, Miyoshi, Y, Yumura, Y, et al
Hinyokika kiyo. Acta urologica Japonica. 2016;(7):361-6
Abstract
Hyponatremia is one of the common electrolyte disorders associated with cisplatin (CDDP) administration. We report here two cases of hyponatremia associated with CDDP. Case 1 : A 75-year-old man with urothelial carcinoma of bladder (cT3N1M0) underwent neoadjuvant chemotherapy with CDDP and gemcitabine. He lost consciousness on the eighth day after the chemotherapy. Blood tests showed severe hyponatremia (Na 113 mEq/l), low plasma osmolality and high level of plasma vasopressin. Urine tests showed low osmolality. These findings were consistent with the syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH). His consciousness level was improved after saline infusion and fluid restriction. Case 2 : A 54-year-old man with penile cancer (cT3N2M0) underwent neoadjuvant chemotherapy with CDDP, paclitaxel and fluorouracil. He lost consciousness on the seventh day after the chemotherapy. Blood tests showed hyponatremia(Na 121 mEq/l) with renal dysfunction. We concluded that the hyponatremia is due to the renal salt wasting syndrome (RSWS) based on renal dysfunction and high urinary sodium excretion. His consciousness level was improved after saline infusion. Although it is difficult to distinguish between SIADH and RSWS, correct evaluation is necessary for appropriate management of hyponatremia after CDDP administration.
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Pharmacogenomics of cisplatin sensitivity in non-small cell lung cancer.
Rose, MC, Kostyanovskaya, E, Huang, RS
Genomics, proteomics & bioinformatics. 2014;(5):198-209
Abstract
Cisplatin, a platinum-based chemotherapeutic drug, has been used for over 30 years in a wide variety of cancers with varying degrees of success. In particular, cisplatin has been used to treat late stage non-small cell lung cancer (NSCLC) as the standard of care. However, therapeutic outcomes vary from patient to patient. Considerable efforts have been invested to identify biomarkers that can be used to predict cisplatin sensitivity in NSCLC. Here we reviewed current evidence for cisplatin sensitivity biomarkers in NSCLC. We focused on several key pathways, including nucleotide excision repair, drug transport and metabolism. Both expression and germline DNA variation were evaluated in these key pathways. Current evidence suggests that cisplatin-based treatment could be improved by the use of these biomarkers.
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Cisplatin Properties in a Nanobiotechnological Approach to Cancer: A Mini-Review.
Marcato, PD, Fávaro, WJ, Durán, N
Current cancer drug targets. 2014;(5):458-76
Abstract
For many years, cisplatin has been used to treat many types of cancer, including urogenital, skin and lung cancers. Unfortunately, treatment with this drug causes serious side effects, such as severe toxicity; including nephrotoxicity, neurotoxicity, gastrointestinal toxicity, peripheral neuropathy, ototoxicity, asthenia and hematological toxicity.Therefore, the clinical use of cisplatin has been hampered.The incidence of nephrotoxicity frequently prevents the use of high enough doses to maximize the antineoplastic effects, and strict attention must be given to the hydration of cisplatin-treated patients to minimize kidney damage.Nanobiotechnology, or nanomedicine, was developed to mitigate, or even eliminate,the toxic effects of pharmaceutical compounds; for example, drug-targeting systems were developed to enable site specificity and to control the delivery drug. Therefore, biomedical nanotechnology researchers attempted to develop nanostructures not only to deliver chemotherapeutics to the desired treatment site but also to control when and how quickly the compounds are released. To achieve these ends, a drug can either be encapsulated in a matrix or attached to a particle surface. Studies concerning the encapsulation of cisplatin in liposomes, polymeric nanoparticles, solid lipid nanoparticles and carbon nanotubes, as well as the immobilization of cisplatin on metallic nanoparticles, have already been published. The association of cancer treatment, particularly chemotherapeutics, with nanotechnology is currently one of the most exciting areas of research. In this mini-review, cisplatin will be discussed in terms of its efficacy against many cancers, including bladder cancer. Additionally, established nanostructure-based drug delivery systems for cisplatin and their efficacy against different types of cancer will be reviewed. Because cisplatin is a standard treatment with good performance statistics and with an effective renal function-glomerular filtration rate, we expect that this review will be helpful for future research.
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Cisplatin plus etoposide versus other platin-based regimens for patients with extensive small-cell lung cancer: a systematic review and meta-analysis of randomised, controlled trials.
Jiang, L, Yang, KH, Guan, QL, Mi, DH, Wang, J
Internal medicine journal. 2012;(12):1297-309
Abstract
AIM: To determine whether the cisplatin plus etoposide (EP) combination was more efficacious and less toxic than other platinum-based regimens for patients with extensive-stage small-cell lung cancer. METHODS We performed an extensive literature search (from their inception to July 2010). Two reviewers independently assessed search results and methodological quality of included studies. Pooled hazard ratios (HRs) and relative risks (RRs) were calculated according to a random-effects model. RESULTS Twelve randomised, controlled trials involving seven different platinum-based chemotherapy regimens were included into this meta-analysis. The meta-analysis showed that compared with EP regimen, irinotecan plus cisplatin (IP) might decrease the risk of death (HR = 0.87, 95% confidence interval (CI) 0.78-0.97, P = 0.01) (five trials), unlike the sensitivity analysis (HR = 0.91, 95% CI 0.81-1.02, P = 0.12), progression-free survival (HR = 0.95, 95% CI 0.86-1.05, P = 0.28) and overall response rate (RR 1.08, 95% CI 0.93-1.24) that were not superior for IP. IP regimen produced more non-haematological toxicities and less haematological toxicities. One trial found that etoposide + cisplatin + epirubicin + cyclophosphamide and cisplatin + etoposide + ifosfamide regimen might prolong the overall survival respectively. Etoposide + cisplatin + epirubicin + cyclophosphamide regimen also might improve progression-free survival but with high rate of haematological toxicities. None of the other trials included in the study demonstrated a significant improvement in survival. CONCLUSIONS There is no strong evidence that any clinical advantage for extensive small-cell lung carcinoma patients requiring chemotherapy when comparing EP with other platin-based regimens, with exception of IP that might prolong overall survival. The decision to prescribe which chemotherapy should take into consideration both cost and treatment preference.
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Role of the human high-affinity copper transporter in copper homeostasis regulation and cisplatin sensitivity in cancer chemotherapy.
Kuo, MT, Fu, S, Savaraj, N, Chen, HH
Cancer research. 2012;(18):4616-21
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Abstract
The high-affinity copper transporter (Ctr1; SCLC31A1) plays an important role in regulating copper homeostasis because copper is an essential micronutrient and copper deficiency is detrimental to many important cellular functions, but excess copper is toxic. Recent research has revealed that human copper homeostasis is tightly controlled by interregulatory circuitry involving copper, Sp1, and human (hCtr1). This circuitry uses Sp1 transcription factor as a copper sensor in modulating hCtr1 expression, which in turn controls cellular copper and Sp1 levels in a 3-way mutual regulatory loop. Posttranslational regulation of hCtr1 expression by copper stresses has also been described in the literature. Because hCtr1 can also transport platinum drugs, this finding underscores the important role of hCtr1 in platinum-drug sensitivity in cancer chemotherapy. Consistent with this notion is the finding that elevated hCtr1 expression was associated with favorable treatment outcomes in cisplatin-based cancer chemotherapy. Moreover, cultured cell studies showed that elevated hCtr1 expression can be induced by depleting cellular copper levels, resulting in enhanced cisplatin uptake and its cell-killing activity. A phase I clinical trial using a combination of trientine (a copper chelator) and carboplatin has been carried out with encouraging results. This review discusses new insights into the role of hCtr1 in regulating copper homeostasis and explains how modulating cellular copper availability could influence treatment efficacy in platinum-based cancer chemotherapy through hCtr1 regulation.
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Mechanism of tumor resistance to cisplatin mediated by the copper transporter ATP7B.
Dmitriev, OY
Biochemistry and cell biology = Biochimie et biologie cellulaire. 2011;(2):138-47
Abstract
The Wilson disease protein (ATP7B) is a copper-transporting ATPase that is responsible for regulating copper homeostasis in human tissues. ATP7B is associated with cancer resistance to cisplatin, one of the most widely used anticancer drugs. This minireview discusses the possible mechanisms of tumor resistance to cisplatin mediated by ATP7B. Cisplatin binds to the N-terminal cytosolic domain of ATP7B, which contains multiple copper-binding sites. Active platinum efflux catalyzed by ATP7B is unlikely to significantly contribute to cisplatin resistance in vivo. Transient platinum sequestration in the metal-binding domain followed by transfer to an acceptor protein or a low molecular weight compound is proposed as an alternative mechanism of cisplatin detoxification in the cell.