氨磷汀减少鼻咽癌放射治疗中唾液腺损伤的临床研究

目的　观察氨磷汀 (am ifostine)的安全性及减少头颈部肿瘤放射治疗中的唾液腺损伤等副作用 ;观察氨磷汀与放射治疗联合应用时对头颈部肿瘤治疗效果的影响。方法　 31例鼻咽癌患者 ,随机分为两组 ,均予 6 MVX线照射 ,DT6 8- 72 Gy,在每日照射前 30分钟内予氨磷汀 A(试验组 )或 B(对照组 ) 2 0 0 mg/m2 ;观察两组患者放疗前后唾液量的变化 ,严重毒性反应发生率 ,两组患者放疗的有效率。结果　试验组的唾液量下降幅度较对照组小 ,试验组的平均唾液量明显多于对照组 ,均有统计学意义 ,P<0 .0 5。放射性粘膜炎试验组比对照组明显减少 ,有统计学差异。氨磷汀应用后 ,对血色素、白细胞、血小板及肝肾功能均无明显影响 ,但恶心、呕吐反应明显增加。结论　氨磷汀能保护鼻咽癌放疗患者的唾液腺 ,明显改善口干 ,同时并未降低近期肿瘤的消退率 ,对肿瘤无保护作用 ;但消化道反应有一定增加     

氨磷汀对同步放化疗所致肺癌细胞杀伤作用的影响

目的探讨氨磷汀在多西他赛(TXT)和同步放射治疗非小细胞肺癌过程中对肺癌组织细胞的保护作用。方法使用MTT方法评价在TXT和同步照射(10 Gy)体外培养的SPC-A1肺癌细胞过程中,氨磷汀对SPC-A1肺癌细胞的影响;以Lewis肺癌荷瘤鼠模型评价在TXT同步放射(10 Gy)在体Lewis肺癌过程中,氨磷汀对Lewis肺癌的影响。结果体外实验表明同步放化疗加氨磷汀组和同步放化疗组的吸光度分别相当于对照组的22.8%和24.4%,2组之间比较,经过t检验P>0.05。体内实验表明,同步放化疗加氨磷汀组和同步放化疗组在实验观察的20 d内,相同时间点2组动物的肿瘤体积没有统计学上的显著差异。结论在TXT和放疗同步治疗肺癌过程中,氨磷汀无论是对离体还是在体的肿瘤细胞没有保护作用,TXT和同步放射治疗肺癌的疗效不会因为使用氨磷汀而减弱。     

氨磷汀在同步放射治疗中对口腔黏膜的保护作用

目的观察氨磷汀在放射治疗中对口腔黏膜的保护作用。方法：将80例头颈部肿瘤的患者（其中鼻咽癌72例,舌癌9例）随机分成保护组和对照组,保护组40例和对照组40例均用6MVX线照射,外照射总量DT70Gy／7W,每周5次,每日一次,每次2Gy。保护组应用氨磷汀500mg静脉滴注15min,半小时内行放射治疗。结果保护组：黏膜反应1级5例、2级33例、3级2例;对照组：黏膜反应1级1例、2级18例、3级20例、4级1例;保护组出现3级以上急性口腔黏膜反应的例数明显少于对照组（P〈0．05）。结论氨磷汀对头颈部放射治疗过程的急性口腔黏膜反应有明显的保护作用。     

氨磷汀对细胞保护作用的研究现状

氨磷汀是一种细胞保护剂,能选择性地保护正常细胞免受放疗和化疗的毒害,而且不降低化疗和放疗的疗效.它通过稳定正常组织中的DNA分子、消除化疗和放疗产生的氧自由基等而发挥保护作用.本文总结了动物实验的药效学、药理学、药物动力学研究情况,临床药物动力学研究情况,并着重总结了氨磷汀的临床应用.目前,氨磷汀已批准的用途包括防止晚期卵巢癌患者使用顺铂和环磷酰胺时引起的中性粒细胞减少症、减轻非小细胞肺癌患者由于使用顺铂治疗引起的积蓄性肾毒性、减轻晚期非胚芽细胞实体瘤患者由于使用顺铂或含顺铂联合化疗引起的积蓄性肾毒性、用于头颈部癌症化疗时保护唾液腺和防止口干.广泛的临床研究结果表明,氨磷汀在防止放疗毒性、化疗毒性、放疗和化疗联合治疗时的不良反应及改善某些骨髓增生异常综合症患者的血细胞减少症等方面,均具有显著作用;并且,在使用推荐剂量的氨磷汀时,不良反应轻微,患者耐受性良好.随着今后研究的不断深入,氨磷汀有可能发展成为广谱的细胞保护剂.     

磷汀以细胞保护作用的研究现状

氨磷汀是一种细胞保护剂,能选择性地保护正常细胞免受放疗和化疗的毒害,而且不降低化疗和放疗的疗效,它通过稳定正常组织中的ＤＮＡ分子、消除化疗和放疗产生的氧基等而发挥保护作用,本文总结了动物实验的药效学、药理学、药物动力学研究情况,临床药物动力学研究情况,并着重总结了氨磷汀折临床应用,目前,氨磷汀已批准的胜任包括防止晚期卵巢癌患者使用顺铂和环磷酰胺时引起的中性粒细胞减少症,减轻非小细胞肺癌患者由于使用顺铂治疗引起的积蓄性肾毒 、减轻晚期非胚芽细胞实体瘤患者由于使用顺铂或含顺铂联合化疗引起的积蓄性肾毒性,用于头颈癌癌症化疗时保护唾液腺和防止口干、广泛的临床研究结果表明,氨磷汀在防止放疗毒性,化疗毒性,放疗和化疗联合治疗时的不良反应及改善某些骨髓增生异常综合症患者的血细胞减少症等方面,均具有显著作用,并且,在使用推荐剂量的氨磷汀捍,不良反应轻微、患者耐受良好,随着今后研究的不断深入,氨磷汀有可能发展成为广谱的细胞保护剂。     

氨磷汀对盆腔肿瘤患者放疗中肠道和膀胱黏膜的保护作用分析

目的将氨磷汀用于盆腔肿瘤患者放疗中,分析其对患者肠道、膀胱黏膜的保护作用。方法对我院收治的盆腔肿瘤放疗患者分组研究,参照组行单纯放疗治疗,研究组给予氨磷汀联合放疗治疗,对两组治疗结果进行观察。结果研究组放射性膀胱炎与放射性直肠炎总出现率为5.00%,均为Ⅰ级,参照组放射性膀胱炎、放射性直肠炎总出现率为25.00%,主要为Ⅱ级～Ⅳ级,两组放射性膀胱炎、直肠炎出现率相比,明显研究组更低(P<0.05);两组治疗前Apo2.7、Fas阳性表达率差异不明显(P>0.05),治疗后两组阳性表达率均显著上升,与治疗前相比明显更高(P<0.05),研究组治疗后Apo2.7阳性表达率与参照组相比,明显更低(P<0.05),两组治疗后Fas阳性表达率相比,无明显差异(P>0.05)。结论氨磷汀用于盆腔肿瘤患者放疗中效果显著,可对肠道黏膜细胞凋亡因子表达进行抑制,有效保护患者肠道与膀胱黏膜,值得临床应用。     

重组人表皮生长因子联合氨磷汀治疗鼻咽癌患者放射性口腔黏膜炎的临床观察

目的:观察重组人表皮生长因子外用溶液联合注射用氨磷汀治疗鼻咽癌患者放射性口腔黏膜炎的临床效果。方法:选取2013年8月-2014年8月在我院放疗科接受治疗的96例鼻咽癌患者为研究对象,按随机数字表法分为观察组和对照组各48例。对照组于每次放疗前15~30 min静脉滴注注射用氨磷汀,200 mg/m2,10 min内滴注完毕;观察组在对照组治疗基础上,加用重组人表皮生长因子外用溶液喷洒于口腔黏膜表面。比较两组患者放射性口腔黏膜炎程度、口腔黏膜疼痛程度、NRS2002营养风险评分及营养不良风险率的差异。结果:放疗期间,观察组患者放射性口腔黏膜炎及口腔黏膜疼痛程度均轻于对照组,差异具有统计学意义(P<0.05)。放疗结束后,观察组患者NRS2002营养风险评分及营养不良风险率均低于对照组,差异具有统计学意义(P<0.05)。结论:重组人表皮生长因子联合氨磷汀治疗鼻咽癌放疗患者,可有效降低放射性口腔黏膜炎发生率,减轻口腔黏膜疼痛,减少营养不良风险。     

氨磷汀对盆腔肿瘤放疗患者肠道和膀胱黏膜的保护作用

目的:考察氨磷汀对盆腔肿瘤患者放疗中肠道和膀胱黏膜的保护作用。方法:63例接受放疗的盆腔肿瘤患者按随机数字表法分为观察组(氨磷汀+放疗,32例)和对照组(单纯放疗,31例)。观察并记录两组患者放射性膀胱炎和放射性直肠炎发生情况,并测定放疗前后外周血淋巴细胞中细胞凋亡因子Fas和Apo2.7表达情况。结果:观察组和对照组中各出现2例和3例放射性膀胱炎。观察组出现放射性直肠炎6例(其中1级4例、2级1例、3级1例);对照组出现11例(其中1级1例、2级6例、3级4例),观察组2~3级放射性直肠炎发生率低于对照组,差异具有统计学意义(P<0.05)。放疗后,所有患者外周血淋巴细胞中凋亡因子Fas和Apo2.7表达均上调,但观察组Fas升高程度不如对照组明显,差异具有统计学意义(P<0.05)。结论:氨磷汀对盆腔肿瘤放疗患者的肠道具有保护作用,其机制可能与抑制肠道黏膜细胞凋亡因子Fas的表达相关。     

氨磷汀的临床应用概况

氨磷汀是一种广谱细胞保护剂,对放化疗患者有保护作用,对特发性血小板减少性紫癜、造血干细胞移植、骨髓增生异常综合征等方面均有应用。     

食管癌放疗患者配合氨磷汀的临床观察与护理

目的:探讨氨磷汀对食管癌放疗患者食管黏膜的保护作用及保证安全用药的护理。方法:氨磷汀400 mg加生理盐水50 mL,放疗前30 min静脉滴注,15 min滴完,观察患者情况。结果:32例中出现轻微恶心7例,一过性血压下降8例,头晕1例,16例经休息后症状缓解。结论:氨磷汀使用过程中,大部分患者有较好的耐受性,只要通过积极预防性处理与有效的护理干预和支持,大部分不良反应都可通过临床上的积极干预得以控制;氨磷汀对于放射性食管炎有一定的治疗效果。     

阿米福汀对鼻咽癌放射性口腔黏膜及涎腺损伤的保护作用

目的观察阿米福汀对鼻咽癌放射治疗后放射性口腔黏膜及涎腺损伤的保护作用。方法鼻咽癌患者在放疗期间,对照组予多贝氏漱口液,每天漱口4次;观察组在此基础上再予以注射阿米福汀;观察两组对放射性口腔黏膜及涎腺损伤的防治效果。结果阿米福汀可明显延缓或减轻放射性口腔黏膜反应及口干的发生,对照组0~2级口腔黏膜反应、口干发生率分别为30.8%(8/26)和34.6%(9/26),而阿米福汀观察组则为86.7%(26/30)和83.3%(25/30);同时对照组的3级以上口腔黏膜反应与口干发生率为69.2%和65.4%,观察组则为13.3%和16.7%,两组口腔黏膜反应与口干程度比较差异均具有显著意义(均P<0.05)。结论阿米福汀是一种安全有效的放疗反应保护剂,它可减缓和减轻放射性口腔黏膜反应与口干的程度。     

Amifostine: chemotherapeutic and radiotherapeutic protective effects

Amifostine (Ethyoltrade mark, Alza Pharmaceuticals) is an inorganic thiophosphate cytoprotective agent known chemically as ethanethiol, 2-[3- aminopropyl)amino]dihydrogen phosphate. It is a prodrug of free thiol (WR-1065) that may act as a scavenger of free radicals generated in tissues exposed to cytotoxic drugs and binds to reactive metabolites of such drugs. Amifostine was originally developed as a radioprotective agent in a classified nuclear warfare project. Following declassification of the project it was evaluated as a cytoprotective agent against toxicity of the alkylating drugs and cisplatin. Differences in the alkaline phosphatase concentration of normal versus tumour tissues can result in greater conversion of amifostine in normal tissues. Inside the cell, WR-1065 provides an alternative target to DNA and RNA for the reactive molecules of alkylating or platinum agents and acts as a potent scavenger of the oxygen free radicals induced by ionizing radiation and some chemotherapy agents. Preclinical animal studies have demonstrated that the administration of amifostine protects against a variety of chemotherapy-related toxicities including cisplatin-induced nephrotoxicity, cisplatin-induced neurotoxicity, cyclophosphamide- and bleomycin-induced pulmonary toxicity and the cytotoxicities (including cardiotoxicity) induced by doxorubicin and related chemotherapeutic agents. Amifostine has been shown to protect a variety of animal species from lethal doses of radiation. Amifostine gives haematological protection from cyclophosphamide, carboplatin, mitomycin C, fotemustine and radiotherapy; renal and peripheral nerve protection from cisplatin; mucosa, skin and salivary gland protection from radiotherapy. Multiple Phase I studies were carried out with amifostine in combination with chemotherapy for various neoplasms. Appropriate doses of amifostine were found to be 740 - 910 mg/m(2) in single-dose regimens and 340 mg/m(2) in multiple-dose regimens. In radioprotection, doses are generally 200 - 350 mg/m(2). For all these characteristics, amifostine has been recently approved and suggested in ASCO clinical practice guidelines as a radioprotector for head and neck cancer treatment and supportive agent during cisplatin-based chemotherapy, in lymphomas and solid tumours. Moreover, its spectrum of possible applications is enlarging. As data have been provided indicating that amifostine stimulates haematopoiesis, it has been employed with intriguing results in the treatment of myelodysplastic syndromes (MDS).     

Amifostine: chemotherapeutic and radiotherapeutic protective effects

Amifostine (Ethyol?, Alza Pharmaceuticals) is an inorganic thiophosphate cytoprotective agent known chemically as ethanethiol, 2-[3- aminopropyl)amino]dihydrogen phosphate. It is a prodrug of free thiol (WR-1065) that may act as a scavenger of free radicals generated in tissues exposed to cytotoxic drugs and binds to reactive metabolites of such drugs. Amifostine was originally developed as a radioprotective agent in a classified nuclear warfare project. Following declassification of the project it was evaluated as a cytoprotective agent against toxicity of the alkylating drugs and cisplatin. Differences in the alkaline phosphatase concentration of normal versus tumour tissues can result in greater conversion of amifostine in normal tissues. Inside the cell, WR-1065 provides an alternative target to DNA and RNA for the reactive molecules of alkylating or platinum agents and acts as a potent scavenger of the oxygen free radicals induced by ionizing radiation and some chemotherapy agents. Preclinical animal studies have demonstrated that the administration of amifostine protects against a variety of chemotherapy-related toxicities including cisplatin-induced nephrotoxicity, cisplatin-induced neurotoxicity, cyclophosphamide- and bleomycin-induced pulmonary toxicity and the cytotoxicities (including cardiotoxicity) induced by doxorubicin and related chemotherapeutic agents. Amifostine has been shown to protect a variety of animal species from lethal doses of radiation. Amifostine gives haematological protection from cyclophosphamide, carboplatin, mitomycin C, fotemustine and radiotherapy; renal and peripheral nerve protection from cisplatin; mucosa, skin and salivary gland protection from radiotherapy. Multiple Phase I studies were carried out with amifostine in combination with chemotherapy for various neoplasms. Appropriate doses of amifostine were found to be 740 - 910 mg/m² in single-dose regimens and 340 mg/m² in multiple-dose regimens. In radioprotection, doses are generally 200 - 350 mg/m². For all these characteristics, amifostine has been recently approved and suggested in ASCO clinical practice guidelines as a radioprotector for head and neck cancer treatment and supportive agent during cisplatin-based chemotherapy, in lymphomas and solid tumours. Moreover, its spectrum of possible applications is enlarging. As data have been provided indicating that amifostine stimulates haematopoiesis, it has been employed with intriguing results in the treatment of myelodysplastic syndromes (MDS).     

广谱细胞保护药——氨磷汀

氨磷汀是第一个被认可的广谱细胞保护药。本文概述了氨磷汀的药动学、作用机制以及在肿瘤的放、化疗中所显示的与器官特异性细胞保护药不同的高效、低毒、全面的正常细胞保护作用 ,不影响抗癌治疗效果。氨磷汀在各人群的安全性已得到临床证实。     

Amifostine: an update on its clinical status as a cytoprotectant in patients with cancer receiving chemotherapy or radiotherapy and its potential therapeutic application in myelodysplastic syndrome

Amifostine (WR-2721) is a cytoprotective agent that protects a broad range of normal tissues from the toxic effects of chemotherapy and radiotherapy without attenuating tumour response. This selective protection is due to the greater conversion and uptake of the active metabolite, WR- 1065, in normal versus neoplastic tissues. In a pivotal phase III trial, 242 patients with advanced ovarian cancer were randomised to receive treatment with cisplatin 100 mg/m2 and cyclophosphamide 1000 mg/m2 every 3 weeks with or without pretreatment with intravenous amifostine 910 mg/m2. Over 6 cycles of therapy, amifostine significantly reduced haematological, renal and neurological toxicities: treatment delays, treatment discontinuation and days in hospital related to these adverse events were also significantly reduced in patients receiving amifostine versus patients receiving chemotherapy alone. In another randomised phase III trial in 303 patients with head and neck cancer undergoing irradiation therapy (total dose 50 to 70Gy), pretreatment with intravenous amifostine 200 mg/m2 significantly reduced the incidence of acute and late grade > or =2 xerostomia. However, mucositis was not significantly reduced in amifostine recipients compared with patients receiving radiotherapy alone, although this has been shown in smaller randomised trials. Amifostine (340 mg/m2) also provided significant protection against pneumonitis and oesophagitis in patients with lung cancer receiving thoracic irradiation in a preliminary report from a phase III trial (n = 144). Other studies have demonstrated protective effects of amifostine in other tumour types and other chemotherapy, radiation and radiochemotherapy regimens; however, evidence is still limited in these indications. No evidence of tumour protection by amifostine has been demonstrated in any clinical trials. Amifostine has also been shown to stimulate haematopoietic stem cells and has been investigated as a therapy for patients with myelodysplastic syndrome in number of small preliminary studies. At the recommended dose and schedule, amifostine is generally well tolerated. Adverse effects are usually reversible and manageable and those most frequently experienced include nausea and vomiting, transient hypotension and somnolence and sneezing. CONCLUSION: The results of phase III trials have confirmed the safety and efficacy of amifostine as a cytoprotectant to ameliorate cisplatin-induced cumulative renal toxicity, for which it is the only agent proven to be effective, and neutropenia in patients with advanced ovarian cancer, and to reduce xerostomia in patients with head and neck cancer receiving irradiation therapy. Depending on the outcome of numerous ongoing clinical trials, amifostine may eventually find broader clinical applications, both as a cytoprotectant and as a potential therapy in myelodysplastic syndrome.     

Amifostine protects bone marrow from benzene-induced hematotoxicity in mice

Benzene is one of the most widely used industrial chemical agents. Long-term benzene exposure causes bone marrow aplasia and leads to a wide range of hematopoietic disorders including aplastic anaemia (AA). There are currently no effective approaches to protect people from benzene-induced hematotoxicity and AA. In addition, current treatments for AA have limitations with short- and long-term risks. Protective agents and new therapeutic approaches, therefore, are needed to prevent and treat the disease. Amifostine is a well-known cytoprotective agent and has been widely used in clinical for protecting normal tissues from the toxic effects of chemotherapy and radiotherapy. The authors utilized an established mouse model to determine the protective effect of amifostine on benzene-induced bone marrow hematotoxicity. Whole-blood cell count, morphological and histopathological alterations in the bone marrow and spleen, as well as the production of inducible toxic oxidative species were examined and compared among the mouse groups. Amifostine treatment in benzene-exposed mice significantly improved blood cell counts, and morphological and histopathological signs of hematotoxicity in the bone marrow as well as in the spleen. Moreover, amifostine prevented benzene-induced bone marrow and spleen cell apoptosis and rescinded the inhibition of cell proliferation induced by benzene exposure. Finally, amifostine significantly inhibited the levels of reactive oxidative species and lipid peroxidation induced by benzene exposure. These data suggest that amifostine appears to have substantial protective effect on benzene-induced bone marrow hematotoxicity.     

Life-threatening anaphylactoid reaction to amifostine used with concurrent chemoradiotherapy for nasopharyngeal cancer in a patient with dermatomyositis: a case report with literature review

Dermatomyositis is associated with malignancy in approximately 20-25% of cases. The most common associated cancers are ovarian, lung, pancreatic, stomach, colon and non-Hodgkin's lymphoma. Nasopharyngeal cancer is not common in the Caucasian population; however, there is a much higher incidence in Asian patients. Radiotherapy is the mainstay of treatment for early nasopharyngeal cancer, but combination chemoradiotherapy is becoming more common for patients with advanced disease since the Intergroup trial 0099 demonstrated improved progression-free survival and overall survival for chemoradiotherapy. Increasingly, the cytotoxic agent amifostine is being used prior to radiotherapy in an attempt to decrease associated morbidities. Amifostine has been found to significantly decrease acute and chronic xerostomia but not mucositis. It appears to be selectively protective to salivary glands and kidneys without being tumor protective. The most common side effects associated with amifostine are nausea, vomiting, hypotension, hypocalcemia and allergic reactions. We describe the case of a man with dermatomyositis and stage IV nasopharyngeal cancer treated with chemoradiotherapy and s.c. amifostine. The patient suffered a life-threatening anaphylactoid reaction to amifostine.     

小涎腺肿瘤的诊断与治疗

目的探讨小涎腺肿瘤的诊断与治疗。方法对本院1998～2003年收治的经病理检查确诊的60例小涎腺肿瘤患者的诊断与治疗进行了回顾性分析。结果60例口腔小涎腺肿瘤中,良性肿瘤26例占43.33%,恶性肿瘤34例占56.67%,良性肿瘤中的混合瘤多见,占良性肿瘤的69.23%,恶性肿瘤中以黏液表皮样癌为多,共14例,占恶性肿瘤的41.18%,手术 放疗者占恶性肿瘤的38.24%,5年生存率为34.48%。结论小涎腺肿瘤中恶性肿瘤多于良性肿瘤;术前X线检查和术中冰冻病理检查对诊断和治疗有指导意义;首次手术彻底性是防止复发的关键,术后辅助性放疗可降低恶性肿瘤复发率。     

The use of reduced doses of amifostine to ameliorate nephrotoxicity of cisplatin/ifosfamide-based chemotherapy in patients with solid tumors

This study evaluates the degree of kidney damage during cisplatin/ifosfamide-based combination chemotherapy and its possible prevention by amifostine. Thirty-one patients with solid tumors stratified according to pretreatment were randomized to receive cisplatin/ifosfamide-based chemotherapy with or without amifostine (1000 mg absolute) given as a short infusion prior to cisplatin. Chemotherapy consisted of cisplatin (50 mg/m2), ifosfamide (4 g/m2) and either etoposide (500 mg/m2) (VIP regimen) or paclitaxel (175 mg/m2) (TIP regimen) repeated at 3 weekly intervals. For all patients the glomerular filtration rate (GFR) measured by creatinine clearance, serum creatinine, electrolytes and differential urinary protein excretion were determined prior to, during and after each treatment cycle. A total of 62 cycles of chemotherapy were evaluable. In the amifostine arm the GFR was almost completely maintained after application of two cycles of chemotherapy (121 to 108 ml/min), whereas in the control group a 30% reduction of the GFR (105 to 80 ml/min) was observed. In both groups marked increases of glomerular and tubular marker profiles peaking at day 3 after chemotherapy were found with a nearly complete reversibility of these changes prior to the next chemotherapy cycle. Patients receiving amifostine had a lower degree of hypomagnesemia, as well as a lower urinary excretion of N-acetyl-glucosaminidase and albumin, indicating less tubular damage compared to the control patients. Treatment with 1000 mg amifostine resulted in an almost complete preservation of GFR. This corresponded to a slightly reduced excretion of tubular marker proteins and a lower incidence of hypomagnesemia during chemotherapy in amifostine patients compared to controls. This dose of amifostine may be sufficient for nephroprotection in patients without pre-existing risk factors for renal damage who undergo a restricted number of chemotherapy cycles.     

A risk-benefit assessment of amifostine in cytoprotection.

Recent advances in chemotherapy have focused on the benefit of high dose regimens, increasing the dose intensity of conventional chemotherapy and using intensified chemotherapy with or without autologous bone marrow rescue. Dose intensity usually increases objective response rates of antineoplastic drugs and might, in some circumstances, improves survival. However, unacceptable acute and/or cumulative toxicity often impairs the proper management of patients, leading to dose reduction or treatment delay, thus reducing the efficacy and potentially the quality of life of patients. Therefore, considerable efforts have been made to manage, to prevent, and to delay many acute and cumulative treatment-related toxicities. Amifostine (WR-2721 ) is a multiorgan cytoprotector which has demonstrated cytoprotective effects, in vitro and in vivo, against the most common cytotoxic drug-related toxicities and against radiation-induced adverse effects in healthy tissues. In vitro and in vivo, cytoprotection was observed in several organs including kidney, haematopoietic stem cells, myocardial cells, neural cells, and mucosa, without detectable protection of malignant cells. In addition, in preclinical studies, amifostine appeared to be able to reduce the risk of radiation-induced secondary neoplasms. Phase I studies showed that nausea/vomiting and hypotension are the dose-limiting toxicities of amifostine and these may be controlled by reducing the duration of injection of amifostine. Phase II and randomised studies have confirmed the efficacy of amifostine in protecting against radiotherapy-induced mucositis, cisplatin-induced nephrotoxicity, cyclophosphamide-induced neutropenia and carboplatin-induced thrombocytopenia. Importantly, the cytoprotection of healthy tissues occurred without any significant deleterious effect on response rate, time to progression, and survival of patients receiving amifostine. However, in addition to the potential quality of life benefit, the most important question of whether the use of a cytoprotective agent might translate into the possibility of maintaining the dose intensity of anticancer therapies has still to be answered. The real benefit of amifostine in the overall management of patients with cancer requires additional studies to determine whether this chemoprotective approach can be of benefit to patients by increasing response rate, time to progression, and long term survival in patients receiving the more recent combination therapies involving new drugs such as the taxanes and oxaliplatin.