急性肿瘤溶解综合征

急性肿瘤溶解综合征（ATLS）为肿瘤治疗过程中的一种严重并发症,主要表现为高尿酸血症、高钾血症和高磷血症,易并发低钙血症、酸中毒及肾功能衰竭,病死率较高。现综述急性肿瘤溶解综合征的病理生理机制、影响急性肿瘤溶解综合征的发生因素、临床表现以及预防、治疗和预后等方面的最新研究进展。     

急性肿瘤溶解综合征

急性肿瘤溶解综合征(ATLS)为肿瘤治疗过程中的一种严重并发症,主要表现为高尿酸血症、高钾血症和高磷血症,易并发低钙血症、酸中毒及肾功能衰竭,病死率较高。现综述急性肿瘤溶解综合征的病理生理机制、影响急性肿瘤溶解综合征的发生因素、临床表现以及预防、治疗和预后等方面的最新研究进展。     

血液肿瘤并发真菌血症23例

 目的　对恶性血液肿瘤并发真菌血症的临床及微生物学特征进行分析,为临床诊治提供参考。方法　对23例恶性血液肿瘤并发真菌血症的临床资料、危险因素、真菌菌群分类以及治疗及预后进行回顾性分析。结果　真菌血症患者病情危重,大多有2种或2种以上的危险因素;菌种分布显示白假丝酵母菌占47 ％;近平滑假丝酵母菌占17 ％;光滑假丝酵母菌占12 ％。23例患者中,13例治愈（56.5％）、8例死亡（34.7 %）;2例放弃（8.6 %）。结论　对有高危因素的恶性血液肿瘤患者应重视真菌血症的发生,积极治疗原发病,加强病原学检测和药敏试验,及时早期诊断并合理选用抗真菌药物可改善预后。     

肿瘤溶解综合征

恶性肿瘤患者由于某种原因引起大量的肿瘤细胞溶解破坏,使大量的代谢产物释放到血液中,导致高尿酸血症、高钾血症、高磷酸及低钙血症,甚至并发急性肾功能衰竭等一系列代谢紊乱综合征,临床上统称为肿瘤溶解综合征(tumorIysis syndrome,TLS).1 病因肿瘤溶解综合征偶可自发于恶性淋巴瘤及白血病患者,但多见于对抗癌药物比较敏感的肿瘤患者,在进行强烈化疗期间出现,如Burkitt淋巴瘤、非霍奇金淋巴瘤、急性淋巴细胞性白血病、急性粒细胞性白血病和慢性粒细胞性白血病加速期.还偶见于小细胞性肺癌、晚期乳腺癌及成神经管细胞瘤.此外,放射治疗、糖皮质激素、三苯氧胺及干扰素的应用也可诱发肿瘤溶解综合征的发生.目前认为,肿瘤溶解综合征的高危因素包括:①肿瘤细胞恶性程度高、增殖比率大;②肿瘤负荷较大的病人;③伴有高乳酸脱氢酶血症及有潜在肾功能不全者.     

胃肠道肿瘤腹膜转移治疗进展

胃肠道肿瘤通过腹腔局部播散和种植可导致腹膜转移癌(peritoneal carcinomatosis,PC),患者常会出现肠梗阻、恶性腹水、疼痛等并发症,为肿瘤终末期,预后较差.胃肠道肿瘤腹膜转移的治疗方法包括全身化疗、腹腔化疗、减瘤手术、减瘤手术联合腹腔热灌注化疗、分子靶向治疗等,这些治疗方法给患者的生存带来不同程度的获益,使腹膜转移癌的预后取得了较大的改善.本文将近年来消化道肿瘤的发病机制及其治疗方法做一回顾总结.     

肿瘤干细胞与肿瘤的诊断、转归和预后的关系

肿瘤干细胞(cancer stem cells,CSCs)是近年来干细胞研究和肿瘤研究的热点之一,它具有强大的自我更新和致瘤能力以及不断分化的潜能。目前研究发现肿瘤治疗后易复发、预后差、具有强耐药性与肿瘤中存在肿瘤干细胞有密切的关系。且肿瘤干细胞学说认为,肿瘤很可能是肿瘤干细胞产生的,并且已有学者和专家在造血系统肿瘤和多种实体瘤中分离并鉴定出肿瘤干细胞。对肿瘤干细胞、肿瘤干细胞与肿瘤的发生、发展、诊断、治疗及预后之间的关系作一综述。     

凝血和纤维蛋白溶解系统与实体瘤静脉血栓形成及转移的相关研究

 【摘要】　目的　探讨凝血和纤维蛋白溶解系统在实体瘤中的变化，对实体瘤易于并发血栓形成的机制以及实体瘤转移机制进行探讨。方法　ELISA 法检测实体瘤患者血浆组织因子（TF）和组织因子途径抑制物（TFPI）、组织型纤溶酶原活化剂（t-PA）、尿激酶型纤溶酶原活化剂（u-PA）及其抑制物PAI-1的浓度。同时发色底物法检测血浆蛋白C活性（PC：A）。结果　血浆TF、TFPI、u-PA、PAI-1 浓度实体瘤均高于正常对照；发生转移组高于无转移者。死亡组 u-PA、PAI-1高于存活组而TFPI降低。并发静脉血栓组t-PA明显增高而PC：A低于对照组。结论　实体瘤患者容易形成静脉血栓与其存在的凝血系统和纤维蛋白溶解系统紊乱有关；凝血和纤维蛋白溶解相关因子参与了肿瘤的转移和向周围组织的浸润；u-PA、PAI-1及TFPI与肿瘤预后有关。     

肿瘤干细胞与肿瘤的诊断、转归和预后的关系

肿瘤干细胞（cancerstemcells,CSCs）是近年来干细胞研究和肿瘤研究的热点之一,它具有强大的自我更新和致瘤能力以及不断分化的潜能。目前研究发现肿瘤治疗后易复发、预后差、具有强耐药性与肿瘤中存在肿瘤干细胞有密切的关系。且肿瘤干细胞学说认为,肿瘤很可能是肿瘤干细胞产生的,并且已有学者和专家在造血系统肿瘤和多种实体瘤中分离并鉴定出肿瘤干细胞。对肿瘤干细胞、肿瘤干细胞与肿瘤的发生、发展、诊断、治疗及预后之间的关系作一综述。     

急性肿瘤溶解综合征诊断与治疗

急性肿瘤溶解综合征(Acute tumor lysis syn-drome ATLS)是肿瘤治疗过程中出现的一种具有潜在性的致命的严重并发症.发病率为1.1%～6%[1,2],死亡率有时高达36%[3],尽管采取一些预防和治疗措施,仍有25%的患者在化疗期间发生急性肾功能衰竭[4].急性肿瘤溶解综合征虽然是一种危险的肿瘤急症,但可以逆转,关键是积极预防、早期诊断和有效的治疗,特别是对化疗患者予以足够的重视[5].     

1例化疗后致急性肿瘤溶解综合征的急救护理

急性肿瘤溶解综合征常发生于肿瘤增殖迅速及负荷较大而且对化疗较敏感的病人。由于肿瘤本身坏死或放疗化疗的应用引起肿瘤细胞崩解,大量细胞内代谢产物进入血液循环,从而形成高尿酸血症,高钾血症,高磷血症及低钙血症等一系列危急的综合征,如处理不及时,患者死亡率极高。这就要求医护人员除了迅速作出诊断外,还必须熟练地掌握各项抢救技能并采取相应有效的护理措施,     

Tumor lysis syndrome and metastatic melanoma

Tumor lysis syndrome (TLS) is a potential emergent complication of oncologic treatment. TLS is commonly reported in hematological malignancies with rapid cell turnover rates, but is relatively rare in solid tumors. TLS is most frequently a result of cancer treatment in combination with a large tumor burden, but has occasionally been reported to occur spontaneously, especially in cases of advanced or metastatic disease. In this article, we describe the case of a patient with newly diagnosed metastatic melanoma that developed TLS two days after initiation of corticosteroids. In addition, we present a brief literature review of melanoma-associated TLS and review the etiology, diagnosis, and management of TLS.     

Tumor lysis syndrome following docetaxel therapy for extensive metastatic prostate cancer

Tumor Lysis Syndrome (TLS) is characterized by biochemical changes due to rapid tumor lysis of malignant cells, usually after chemotherapy. Typically it is seen in patients with hematologic malignancies sensitive to chemotherapy within days of receiving chemotherapy. Recently Baeksgaard and Sorensen reviewed the small number of cases of TLS after treatment of nonhematologic malignancies reported between 1977 and 2002. After careful review of the literature, I describe what appears to be to the first reported case of TLS associated with chemotherapeutic treatment of metastatic prostate cancer.     

Tumor Lysis Syndrome in Chronic Lymphocytic Leukemia with Novel Targeted Agents

Tumor lysis syndrome (TLS) is an uncommon but potentially life‐threatening complication associated with the treatment of some cancers. If left untreated, TLS may result in acute renal failure, cardiac dysrhythmia, neurologic complications, seizures, or death. Tumor lysis syndrome is most commonly observed in patients with hematologic malignancies with a high proliferation rate undergoing treatment with very effective therapies. In chronic lymphocytic leukemia (CLL), historically, TLS has been observed less often, owing to a low proliferation rate and slow response to chemotherapy. New targeted therapies have recently been approved in the treatment of CLL, including the oral kinase inhibitors, idelalisib and ibrutinib, and the B‐cell lymphoma‐2 protein inhibitor, venetoclax. Several others are also under development, and combination strategies of these agents are being explored. This review examines the diagnosis, prevention, and management of TLS and summarizes the TLS experience in CLL clinical trials with newer targeted agents. Overall, the risk of TLS is small, but the consequences may be fatal; therefore, patients should be monitored carefully. Therapies capable of eliciting rapid response and combination regimens are increasingly being evaluated for treatment of CLL, which may pose a higher risk of TLS. For optimal management, patients at risk for TLS require prophylaxis and close monitoring with appropriate tests and appropriate management to correct laboratory abnormalities, which allows for safe and effective disease control.

Implications for Practice

Tumor lysis syndrome (TLS) is a potentially fatal condition observed with hematologic malignancies, caused by release of cellular components in the bloodstream from rapidly dying tumor cells. The frequency and severity of TLS is partly dependent upon the biology of the disease and type of therapy administered. Novel targeted agents highly effective at inducing rapid cell death in chronic lymphocytic leukemia (CLL) may pose a risk for TLS in patients with tumors characterized by rapid growth, high tumor burden, and/or high sensitivity to treatment. In this review, prevention strategies and management of patients with CLL who develop TLS are described.     

Spontaneous tumor lysis syndrome in a patient with cholangiocarcinoma

Tumor lysis syndrome (TLS) is a potentially deadly complication of tumors or their treatment. This syndrome consists of a constellation of laboratory parameters such as hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia and clinical complications such as seizures, acute renal insult, cardiac dysrhythmias and death. TLS is especially common in patients with hematological malignancies with rapid cellular turnover rates such as acute lymphocytic leukemia and Burkitt lymphoma, but is very rare in patients with solid tumors. However, it is essential to keep in mind that solid tumors can also lead to TLS. We present a case of a 66-year-old African American male with metastatic cholangiocarcinoma complicated by the development of spontaneous TLS. TLS has never been reported in a patient with cholangiocarcinoma.     

How we treat tumor lysis syndrome

Tumor lysis syndrome (TLS) is an oncology emergency that occurs as a result of rapid tumor cell breakdown and the consequent release of massive amounts of intracellular contents, including potassium, phosphate, and uric acid, into the systemic circulation. These metabolic disturbances lead to life-threatening conditions and may cause sudden death if not treated. TLS commonly occurs following initiation of cytotoxic treatment in patients with high-grade lymphomas or acute lymphoblastic leukemia. Spontaneous cases involving both solid and hematologic tumors have also been reported. Rarely, TLS occurs following treatment with irradiation, corticosteroids, hormonal therapy, or biologic therapy. It is necessary to identify patients at risk for TLS early in order to initiate preventive measures. In the event that preventive measures fail, the clinical parameters and signs of TLS must be understood and recognized so that treatment can begin as soon as possible, as this condition is a significant cause of morbidity and mortality.     

Incidence,medical resource utilisation and costs of hyperuricemia and tumour lysis syndrome in patients with acute leukaemia and non-Hodgkin's lymphoma in four European countries

Hyperuricemia (HU) and tumour lysis syndrome (TLS) are complications of acute leukaemia and non-Hodgkin lymphoma (NHL) leading to increased morbidity and mortality. The objective of this study was to define incidence and calculate health care cost associated with HU and TLS. 788 acute leukaemia and NHL patients from Belgium, The Netherlands, Spain and UK were screened retrospectively for HU and TLS. Resource use related to HU and TLS was recorded and costs were calculated applying local unit costs. Results showed that HU occurred in 18.9% of patients, and 27.8% of them fulfilled TLS criteria. The cost of HU without TLS was €672 (SE 181), the cost of TLS €7,342 (SE 1,412). TLS requiring dialysis incurred an average cost of €17,706. In conclusion, it is noted that the observed incidence rates were lower than earlier reports. In addition, some risk factors for HU and TLS (e.g. paediatric patients versus adults) were not associated with increased rates of HU or TLS as a consequence of higher rates of prevention. TLS cases incurred 11 times higher costs than HU cases in which TLS was absent. The main cost drivers in TLS are interventions requiring intensive care.     

Acute tumor lysis syndrome in solid tumors—a case report and review of the literature

PURPOSE: Tumor lysis syndrome (TLS) is a potential complication in cancer therapy. It may occur in highly sensitive tumors, especially in childhood cancers and acute leukemias, whereas it is rare in the treatment of adult solid tumors. TLS is characterized by hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia following massive lysis of malignant cells. Complications include acute renal failure and metabolic acidosis. We report the first case of TLS during chemotherapy in a patient with metastatic medulloblastoma, together with a review of the literature regarding the occurrence of TLS in patients with solid tumors. METHODS: Data regarding clinical and biochemical parameters were extracted from the actual patients' files. Reports of TLS in the English language literature up to 2002 were identified by searching Medline. RESULTS: A 23-year old male with metastatic medulloblastoma received chemotherapy with cisplatin and etoposide due to massive extracerebral manifestations including metastases to the liver, mediastinal lymph nodes and bone marrow metastases. The patient developed classical signs of TLS on the second day of chemotherapy, including acute renal failure. A 17-fold increase in plasma LDH up to 87608 U/l was observed together with a 4-fold increase in plasma creatinine. The patient was treated with aggressive hydration, allopurinol and repeated hemodialysis. During the following days the patient improved and the biochemical markers all returned to normal. REVIEW. Reviewing the literature, a total of 45 patients with solid tumors who developed TLS have been reported. Most of the patients presented with metastatic, therapy-sensitive disease. Although preventable in practically 100% of patients, TLS is a potentially fatal complication, and in this material the mortality rate was one in three. Risk factors included increased LDH, hyperuricemia and pretreatment azotemia. CONCLUSIONS: TLS is only rarely associated with treatment of solid tumors. Precautions should be taken to avoid this potentially fatal complication in (chemo)therapy of solid tumors, especially in therapy-sensitive tumors presenting with bulky, metastatic disease and preexisting risk factors, including azotemia, elevated LDH and hyperuricemia. Prophylactic treatment to avoid TLS includes allopurinol, hydration prior to treatment and alkalization of the urine. Urate oxidase (rasburicase) is now beginning to replace allopurinol as a more effective way of reducing hyperuricemia and thereby the risk of TLS.     

Tumour lysis syndrome in children: experience of last decade

The strategy against tumour lysis syndrome (TLS) had been hyperhydration, urine alkalinization, and allopurinol. Recently, rasburicase was added to the armament against this life-threatening condition. In Korea, rasburicase is used as a rescue therapy for cases with allopurinol-resistant hyperuricemia, because of the restriction by the National Health Insurance. We reviewed our experiences to re-assess the risk factors of TLS and the efficacy of rasburicase. Medical records were retrospectively reviewed for 396 children who were diagnosed as positive with acute leukemia and non-Hodgkin lymphoma between the years 2000 and 2009. The risk factors for TLS were analyzed statistically, and those before and after the availability of rasburicase were compared. Sixty eight patients (17.2%) had TLS. Multivariate analysis showed that pre-chemotherapy hypophosphatemia was a risk factor for TLS, in addition to the known risk factors of hyperuricemia and high lactate dehydrogenase concentration. The availability of rasburicase as a rescue therapy did not negate the importance of uric acid as a risk factor of TLS. Rasburicase as a second line treatment for intractable hyperuricemia was not effective in reducing the incidence of TLS. Pre-chemotherapy hypophosphatemia was a significant independent risk factor for TLS.     

Single-Dose Rasburicase Might Be Adequate To Overcome Tumor Lysis Syndrome In Hematological Malignancies

IntroductionTumor lysis syndrome (TLS) is a commonly observed oncological emergency that requires prompt diagnosis and treatment. Rasburicase is a recombinant urate oxidase endorsed in TLS for the treatment of hyperuricemia. The effect of single-dose 7.5 mg rasburicase at longer follow-ups was not widely investigated.Patients and MethodsEighty-two patients included in the study with clinical TLS and laboratory TLS. The primary endpoint was the normalization of uric acid (<6mg/dL) within 24 hours of rasburicase administration, which was described as treatment success. The secondary endpoint was defined as having sustained response at the first week. The third endpoint was defined as the reaching the baseline renal function before TLS.ResultsWe found that the use of a 7.5 mg dose of rasburicase controlled uric acid in 74 of 82 (90,2%) patients at the 24th hour. In the first week, uric acid remained at normal levels in 69 of 82 (84,1%) patients. At 24 hours, the TLS risk group was the only predictor for failing uric acid normalization; at the end of the first week, no predictive factor was identified for failing uric acid normalization.ConclusionRasburicase at 7.5 mg dose is an important agent for controlling laboratory and clinical TLS at 24 hours and extending its effect to the first week.     

Acute tumor lysis syndrome in a hemodialysis patient with diffuse large B cell lymphoma

Acute tumor lysis syndrome (TLS) is a life-threatening complication of cancer therapy requiring prompt recognition and aggressive management. It occurs particularly in patients with lymphoproliferative disease during potent myelosuppressive therapy. To our knowledge, acute TLS in end-stage renal disease (ESRD) patients with malignancy is extremely rare and has never been reported in English literature. We report the first case of acute TLS in an ESRD woman with diffuse large B cell lymphoma after chemotherapy. Aggressive treatments with daily hemodialysis and allopurinol rather than hydration benefit the patient. There is neither optimal therapy in treating ESRD patients with TLS nor adequate guidelines for how to adjust the chemotherapy drug in hemodialysis patients. This case provides our experience to clinician how to treat acute TLS in ESRD patients.