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C L I N I C A L F E AT U R E S
Tumor Lysis Syndrome: A Systematic Review of Case Series and Case Reports
Belal M. Firwana, MD 1 Rim Hasan, MD 1 Nour Hasan, MD 2 Fares Alahdab, MD 2 Iyad Alnahhas, MD 2 Seba Hasan, MD 2 Joseph Varon, MD, FACP, FCCP, FCCM 3
1 Department of Internal Medicine, University of Missouri, Columbia, MO; 2University of Damascus, Faculty of Medicine, Damascus, Syria; 3The University of Texas Health Science Center at Houston, Houston, TX
Abstract: Tumor lysis syndrome (TLS) is a clinical condition that is caused by a massive lysis of tumor cells that accumulate very rapidly and disturb hemodynamics. This oncologic emergency requires immediate intervention. Tumor lysis syndrome was ﬁrst described in the 19th century. Since then, it has become a well-known disease with improved management measures. Tumor lysis syndrome can occur after any type of neoplasm. It is highly associated with rapidly proliferating tumors compared with those that are well demarcated, such as acute lymphoblastic leukemia and high-grade non-Hodgkin lymphoma. Initiation of chemotherapy, radiotherapy, or steroid treatment may trigger TLS, or it may develop spontaneously. The release of massive quantities of intracellular contents may produce hyperkalemia, hyperphosphatemia, secondary hypocalcemia, hyperuricemia, and acute renal failure. Prevention and treatment measures include intravenous hydration, use of allopurinol and rasburicase, management of TLS-associated electrolyte abnormalities, and renal replacement therapy; the use of urine alkalinization remains controversial. In this article, we summarize the ﬁndings of case series and case reports published over the past 6 years in an effort to help familiarize clinicians better recognize and manage TLS. Keywords: tumor lysis syndrome; neoplasm; kidney failure; rasburicase; allopurinol; uric acid; hyperphosphatemia; hyperkalemia
Tumor lysis syndrome (TLS) is an oncologic emergency that requires immediate interventional action.1 It is caused by a massive lysis of tumor cells that accumulate very rapidly, or, more commonly, by the destruction of tumor cells by cytotoxic agents.2–4 Tumor lysis syndrome is considered an emergency because it disturbs hemodynamics. Because a large amount of cells are being destroyed, massive amounts of potassium, phosphate, and uric acid are released from these cells.5 Uric acid accumulates and precipitates in the kidney tubules, leading to acute kidney injury.6 The increase in serum phosphate and calcium phosphate lead to deposition of these salts in the tubules, leading to renal failure.7 Being a critical and emergent syndrome, many physicians try to avoid TLS through several preventive measures. Many studies have addressed various ways to prevent and manage TLS, which basically affect the kidney to prevent disposition of salts in its tubules, thus preventing the occurrence of renal failure.8 Some of these measures include aggressive intravenous hydration, urine alkalinization, or agents that decrease the concentration of uric acid in the serum in order to decrease its deposition in renal tubules, such as allopurinol and rasburicase.3
Correspondence: Joseph Varon, MD, FACP, FCCP, FCCM, The University of Texas Health Science Center at Houston, The University of Texas Medical Branch at Galveston, 2219 Dorrington St., Houston, TX 77030. Tel: 713-669-1670 E-mail: email@example.com
© Postgraduate Medicine, Volume 124, Issue 2, March 2012, ISSN – 0032-5481, e-ISSN – 1941-9260 ResearchShareTM: http://www.research-share.com/GetIt • Copyright Clearance Center: http://www.copyright.com
bibliographic references of identified articles were reviewed to find case reports and series not identified by the electronic searches. type of underlying neoplasm. © Postgraduate Medicine. ISSN – 0032-5481. we calculated numbers and percentages for dichotomous data and means and standard deviations for continuous data.com/GetIt • Copyright Clearance Center: http://www. and chronic lymphocytic leukemia (10%).copyright. Among patients who presented with a primary neoplasm and developed TLS. acute myelogenous leukemia (19%).4 5. Hematologic Malignancies Among hematologic malignancies. Two authors identified articles eligible for further review by screening abstracts and titles.Tumor Lysis Syndrome Methodology The primary aim of this systematic review was to describe cumulative TLS presentations of individual patients in case reports and case series. chronic lymphocytic leukemia. Results Description of Patients and Neoplasms A total of 91 individual case reports or case series were identiﬁed from the search. chronic myelogenous leukemia. This information is presented in order to enhance and encourage further clinical trials. Type of Neoplasms Preceding TLS Neoplasm Preceding TLS Hematologic malignancies Leukemia ALL AML CLL CML Non-Hodgkin lymphoma B-cell lymphoma T-cell lymphoma Multiple myeloma Hodgkin lymphoma Solid tumors Gastrointestinal cancers Hepatocellular Other gastrointestinal Lung cancers Castleman disease Melanoma Ovarian Others Neuroblastoma Prostatic Kidney Breast Testicular Thymoma Uterine Pelvic 13 8 5 5 4 3 3 11 2 2 2 1 1 1 1 1 12.8 3.0 31 13 6 3 9 25 22 4 7 1 29. Study Identification The data sources were searched for possible studies limited to publication dates between September 2004 and September 2010.9 1. a cutaneous Table 1.com . their underlying neoplasms. Statistical Analysis From the abstracted data. including patient demographics and baseline characteristics. March 2011. followed by chronic myelogenous leukemia (29%). the article was obtained and reviewed.” “lysis.9 8.9 1. the cause/trigger of TLS development. this article summarizes the etiologies. acute myelogenous leukemia. while solid tumors accounted only for 38% (Table 1). regardless of treatment or disease course.0 3.8 2.research-share.8 21.0 1. 49 ± 22 years) and 30 (29%) were women (mean age.7 1. TLS development triggers. Non-Hodgkin lymphoma represented 25% of hematologic malignancies. of which B-cell lymphoma constituted of 88%. CML. acute lymphocytic leukemia.6 4. We used SPSS statistical software (SPSS version 17. Volume 124. Only 1 (1%) patient had mycosis fungoides. and treatment modalities used. 73 (70%) were men (mean age.9 1. The final search identified 91 original articles that fulfilled the inclusion criteria.” and “chemotherapy” in the abstract or title. AML. from which a total of 105 patients with different neoplasms were reported.0 1. In addition. e-ISSN – 1941-9260 93 ResearchShareTM: http://www.0 N % Information Sources and Search Methods A comprehensive literature search was conducted using the Medline database for abstracts using various combinations of the terms “tumor. and outcomes that have been reported in previously published case series and individual case reports on TLS. The search was limited to Englishlanguage articles. the most common malignancy was leukemia (30%). Individual case reports or case series involving patients who had similar conditions were articles of interest. 41 ± 23 years).9–98 Of these.5 1. Acute lymphocytic leukemia was the most frequent presentation (42%).0) for data management and statistical analysis. TLS.9 10. and what treatments were used. treatments. hematologic malignancies accounted for 62% of those neoplasms.0 1.5 12. tumor lysis syndrome. CLL.8 4.9 2. Abbreviations: ALL.0 1. which could eventually lead to better evidence-based management.4 7. If a study was deemed relevant.8 6. Issue 2. Data Collection and Extraction The prespecified data elements were extracted from each trial. Because there are not many randomized clinical trials addressing these aspects. presentations.6 24.7 2.
N 60 27 7 3 7 2 1 1 1 1 1 % 57. testicular seminoma (1%). was used in 40% of patients (Table 3).3 35. tumor lysis syndrome. March 2012. TLS Treatment Modalitiesa TLS Triggers Hydration and IV fluids Allopurinol Urate oxidase (ie. or can occur spontaneously. glucose plus insulin. rasburicase and uric oxidase were used in 35% of patients. including both hemodialysis and peritoneal dialysis. e-ISSN – 1941-9260 ResearchShareTM: http://www. and 2 patients after surgical procedures. Some patients were given calcium carbonate. such as loop diuretics for increased levels of electrolytes. Three of the gastrointestinal tumors were colorectal cancers. breast cancer (2%). The rest of the cases were neuroblastoma (2%). 1 was a stomach neuroendocrine carcinoma. In 1929. 1 patient after splenic ar ter y emboliza tion. Some patients had their blood products replaced with fresh frozen plasma. tumor lysis syndrome. 1 was a small cell lung cancer.com .research-share. thymoma (1%). and 1 was a stage IV squamous cell carcinoma of the lung (Table 1). different gastrointestinal cancers were the most common presentation (12. Interestingly. The rest of the cohort had unusual presentations of TLS.0 1.2 40. which were used in 11% of patients. 26% of cases developed TLS spontaneously.copyright. Many patients were placed on mechanical ventilatory.5%). and ovarian cancer (3%). Abbreviation: IV.com/GetIt • Copyright Clearance Center: http://www.9 1.0 1. 94 Discussion and Literature Review History Tumor lysis syndrome was ﬁrst introduced in the medical literature during the early 20th century. TLS. or steroid therapy (Table 2).7 6. Bedrna and Polcàk99 described the effect of x-ray irradiation treatment Table 3. but developed TLS after reducing dosages of these regimens (Table 2). Seven percent of the cases were triggered by the initiation of glucocorticoid treatment and 3% occurred after radiotherapy. prostatic carcinoma (2%). cardiopulmonary. Castleman disease (4%).9 6. Some reports described other modalities for treating TLS and its complications. and inotropic support. Issue 2. Table 2. © Postgraduate Medicine. either hepatocellular carcinomas (8%) or other gastrointestinal neoplasms (5%). Two cases of lung cancer were adenocarcinomas.0 a Each case may be treated with 1 treatment modality. In most cases. without use of any chemotherapy. ISSN – 0032-5481. hydration with intravenous ﬂuids was used in 37% of patients.1 25. Burkitt’s lymphoma occurred in 5 patients. cumulative percentage does not equal 100%.7 2. or radiotherapy. TLS Triggering Factors TLS Triggers Chemotherapy Spontaneous Glucocorticoids Radiotherapy Others Anesthesia-induced After treatment of pneumonia After splenic artery embolization After staging laparotomy After a surgery (not specified) After dose reduction of immunosuppression Abbreviation: TLS. intravenous.0 1. TLS was triggered after initiation of chemotherapy for treatment of an existing neoplasm (57%). either with chemotherapy.2 36.0 Solid Tumors Among solid tumors.0 1.1 54. Volume 124. urine alkalization agents were used in 36% of patients. followed by lung cancers (5%). stage IV endometrial cancer. 1 patient after pneumonia treatment with an antibiotic. these chemotherapies vary in their mechanisms of action and in the target organelles that they affect. TLS Development Although almost all patients who developed TLS presented with a neoplasm prior to its development. and aluminum hydroxide for hyperphosphatemia and hydroxyurea. 7 patients presented with multiple myelomas. and the other patient was on immunosuppression therapy with azathioprine and tacrolimus prior to surgery. and sodium polystyrene sulfonate for hyperkalemia.Firwana et al T-cell lymphoma. and 1 patient developed TLS after having a Hodgkin-type lymphoma (1%) (Table 1). Allopurinol was used in 54% of patients. and renal replacement therapy. melanoma (3%). and others underwent autologous peripheral blood progenitor cell transplantation. kidney neoplasms (2%). Treatment Modalities Used for TLS A variety of treatment modalities are reported for treating TLS. Most patients developed TLS after the initiation of a treatment. glucocorticoid. rasburicase) Alkalization of urine Renal replacement therapy N 61 57 37 38 42 % 58. The f irst patient who developed TLS after surgery had a staging laparotomy. and pelvic neuroectodermal tumor (1%).7 1. radiotherapy. and 1 was a gastrointestinal stromal tumor. TLS can be triggered by different factors. Two patients developed TLS after initiation of anesthesia.
Measures used for the prevention and treatment of TLS include intravenous hydration. thymoma.118 steroid therapy. in select cases. TLS is a known consequence of various tumors after their treatment with chemotherapy and radiotherapy.136 © Postgraduate Medicine. TLS occurrence associated with these tumors is somewhat rare. and hyperuricemia (Figure 1).115. use of hypouricemic agents. 3 patients died shortly after the administration of x-ray therapy and had uremia. respectively.128 Hyperkalemia will result in several consequences.103 The different incidences of TLS in hematological and solid tumors are mainly due to the differences in sensitivities to anti-neoplastic treatment.105.com . 104. regardless of whether patients are treated with chemotherapy or radiotherapy. as uric acid does. at 35%. hyperuricemia and uricosuria were noted as complications of leukemia by Rudolph Virchow. are the most commonly associated with TLS among rapidly proliferative tumors. phosphate. which accumulates in the renal tubules and results in damage to the kidney and acute renal failure. e-ISSN – 1941-9260 95 ResearchShareTM: http://www. and hepatoblastoma. 113 Prevention and Treatment Patients at risk for developing TLS should have their risk stratiﬁed as low.74. renal replacement therapy.134 Risk stratiﬁcation is based on a 3-step risk attribution that considers: 1) laboratory-conﬁrmed TLS (increased uric acid. secondary hypocalcemia. management of TLS-associated electrolyte abnormalities.114 Tumor lysis syndrome can occur after small cell carcinoma of the lung. 4 the occurrence of TLS in patients with ALL and non-Hodgkin lymphoma is 47% and 22%. urine alkalinization.132 Epidemiology and Etiology Tumor lysis syndrome is observed after different types of cancers. or phosphate). Merrill100 noted that from 1927 to 1939.copyright.135. they affect heart automaticity by causing cardiac arrhythmias. 72. Merrill100 reported the occurrence of hyperuricemia following irradiation therapy. The metabolic consequences include hyperkalemia.134 The cornerstone of TLS management is using preventive measures.114 Pathophysiology In the presence of a tumor in the body with a high proliferative rate and/or a high sensitivity to treatment. and as a compound. intermediate. Years later.106–108 According to Coiff ier et al.110 although in a large series of patients. 104 Tumor lysis syndrome is highly associated with rapidly proliferating tumors compared with those that are well demarcated. 113.116 The mortality rate of patients with TLS reported in solid tumors is high. hyperphosphatemia. including abnormal heart rhythm and bradydysrhythmia with peaked T waves.Tumor Lysis Syndrome on patients with chronic leukemia. including potassium.127 An increase in blood phosphorus will lead to a decrease in blood calcium by binding each other.133.122. potassium. 112 Although solid tumors show a high percentage among tumor incidences.123 This releases massive quantities of intracellular contents. 105 Both acute lymphoblastic leukemia (ALL) and high-grade nonHodgkin lymphoma. The incidence of TLS among patients undergoing remission-induction chemotherapy is 10%. or high so that they may undergo the appropriate prevention and treatment modalities. particularly Burkitt’s lymphoma. Prior to these reports in the 19th century. These conditions started to be described in the literature more frequently after World Wars I and II. March 2011. As early as 1851.109.research-share. as solid tumors do not respond to those treatments as effectively as hematologic tumors.124–126 Nucleic acid is converted to hypoxanthine and xanthine. and. Currently. 133.120 can result in TLS. which can be metabolized to uric acid into the systemic circulation.130 and generalized muscle weakness (Figure 1). 2) disease type (hematological vs solid neoplasms).101 In 1870. 111 The mortality rate related to TLS complications has been reported to be as high as 1. breast carcinoma. Hypoxanthine and xanthine are then converted to uric acid.98.129 cardiac arrest. Volume 124.111. and 3) renal function/involvement. Issue 2.121 Tumor lysis syndrome can also occur spontaneously. Salkowski102 described a patient with “splenic leukemia” who had increased uric acid output in the urine. hyperuricemia and hyperuricosuria were described in patients with leukemia. Crush injury syndrome and rhabdomyolysis share the same pathophysiology of cell body injury and substance release as TLS. A model for TLS risk classiﬁcation has been recently proposed by an expert TLS panel consensus. respectively.119 or radiation therapy73. Acute myelogenous leukemia is reported to develop TLS less frequently than other neoplasms. both allopurinol and rasburicase. Phosphorus and calcium are deposited into renal tubules and cause renal failure. 17% of patients with AML developed TLS. and nucleic acids.14. by the enzyme xanthine oxidase.131.117 initiation of cytotoxic chemotherapy. and how they developed hyperuricemia and acute kidney failure afterward.com/GetIt • Copyright Clearance Center: http://www. germ-cell tumors.9% in patients with acute leukemia and non-Hodgkin lymphoma. ISSN – 0032-5481. among 12 patients who died of hematologic malignancies.
urinary alkalinization is no longer routinely used. preventing uric acid crystals from precipitating in renal tubules. glomerular ﬁltration rate.141 For these reasons. Volume 124. the only available experimental study using a rat model concluded that hydration with saline alone is as effective as alkalinization in the prevention of uric acid precipitation. e-ISSN – 1941-9260 ResearchShareTM: http://www. which is usually associated with TLS in malignant disease.com .copyright.134 Some data suggested that urine alkalinization has effectiveness similar to that of intravenous hydration in minimizing uric acid precipitation. Issue 2.138 This mechanism decreases the concentration of uric acid in renal tubules. enhancing renal blood ﬂow.com/GetIt • Copyright Clearance Center: http://www. ISSN – 0032-5481.137.Firwana et al Figure 1.research-share. making the precipitation of uric acid less likely. which catalyzes the conversion of xanthine and hypoxanthine to uric acid. March 2012. 135. and urine volume. The 2010 International Expert Panel guidelines recommended that the use of sodium bicarbonate only be indicated in patients with severe metabolic acidosis. heart. It works by increasing intravascular volume and thus decreasing serum solute concentration.8 The International Expert Panel guidelines published in 2010 recommended that patients with TLS receive intravenous ﬂuid initially at the rate of 2 to 3 L/m2 per day. Pathophysiology of tumor lysis syndrome. which may lead to xanthinuria. Use of either acetazolamide and/or sodium bicarbonate to alkalinize the urine has the potential beneﬁt of converting uric acid to the more soluble urate salt.134 form.118 In addition. and therefore bears the risk of xanthine nephropathy or xanthine stone © Postgraduate Medicine. Hypersensitive Neoplastic cells Chemotherapy Antibodies Radiation CH2 CH3 H HO H H H O Potassium Phosphorus Nucleic acids Normal cells Steroids K P Ca Ca-P K Extracellular space Myocyte Na + K + XO Uric acid Peaked T waves Dysrhythmia Acute renal failure Muscle weakness Intravenous Hydration Aggressive intravenous hydration is the cornerstone of preventing TLS. Urine output should be maintained within a range of 80 to 100 mL/m2 per hour. which in turn protects the kidney from obstructive uropathy. and other organs in patients with hyperphosphatemia.138 The problem with allopurinol use is that it increases serum levels of xanthine. and plays a minor preventive role.4.141 Urinary Alkalinization The role of urinary alkalinization in TLS remains controversial.139 Disadvantages of urine alkalinization include promotion of calcium phosphate deposition in the kidney. thereby promoting the urinary excretion of urate and diminishing the likelihood of uric acid precipitation in the tubules.140 Another drawback to systemic alkalinization is that it exacerbates hypocalcemia by shifting ionized calcium to its nonionized 96 Allopurinol Allopurinol is a purine that competitively inhibits xanthine oxidase. Inhibition of xanthine oxidase eventually leads to a decrease in uric acid formation and thus a decrease in blood and urine urate levels.
PhD. prevents the formation of uric acid.146 treatment fails for hyperphosphatemia. hydration. a xanthine oxidase inhibitor. JBFM. The best modality used for prophylaxis of TLS is aggressive intravenous hydration. Kingdom of Saudi Arabia. Aggressive intravenous hydration is recommended for all patients at high or intermediate risk for TLS.152 A recent systematic review showed that although urate oxidase might be effective in reducing serum uric acid. peritoneal dialysis. and when compared with allopurinol. 133 Conclusion Tumor lysis syndrome is an oncologic emergency that requires early detection and needs immediate interventional action. Rasburicase is recommended for the initial management of patients at high risk for TLS. were more effective and had an earlier onset of action. it is effective in preventing and treating hyperuricemia and TLS. 156 The 2011 guidelines for the management of TLS recommend renal replacement therapy whenever Acknowledgments The authors thank Mazen Ferwana. ISSN – 0032-5481. such as ALL and high-g rade non-Hodgkin lymphoma. rather than rasburicase.135.4. which is 5 to 10 times more soluble in urine than uric acid. It disturbs hemodynamics by releasing cell contents into the plasma current.2 mg/kg) and repeating the dose if necessary.153 Rasburicase is recommended to be initiated in adult and pediatric patients who are at high risk for TLS. if uric acid levels are not elevated prior to the treatment. as it is efficient in removing uric acid. hyperkalemia. Tumor lysis syndrome may occur spontaneously. ABFM. in addition to hydration and close monitoring.com . Early initiation of renal replacement therapy improves prognosis.research-share. Allopurinol may be considered prior to induction of chemotherapy and can be administered orally or intravenously.134. As allopurinol. 85. Rasburicase Rasburicase is a urate oxidase that converts uric acid to allantoin. and continuous arterial-venous hemodialysis) has been used as the last treatment option in some cases to maintain normal kidney function. 21% of children with advanced Burkitt’s lymphoma required hemodialysis during induction chemotherapy. serum uric acid and phosphate concentrations will decrease rapidly. from King Saud bin Abdualziz University for Health Sciences. e-ISSN – 1941-9260 97 ResearchShareTM: http://www. Allopurinol is recommended for the initial management in patients at intermediate risk for TLS.148–152 Randomized controlled trials conducted on pediatric patients showed that different doses of rasburicase were effective and well tolerated for the management of hyperuricemia. Tumor lysis syndrome is observed most frequently in patients with rapidly proliferating tumors. © Postgraduate Medicine. MD. hemodialysis. particularly Burkitt’s lymphoma. On the other hand. Rasburicase has been shown to decrease levels of plasma uric acid more rapidly in patients at high risk for TLS compared with allopurinol.156 Diminished urine flow responds quickly to hemodialysis. it is still unclear whether this translates into a reduction in mortality or renal failure. for help with outlining and designing the article. Volume 124. or may follow the initiation of treatment with chemotherapy or radiation therapy.142–145 Allopurinol should be initiated in patients with intermediate risk for TLS (100–300 mg orally every 8 hours) in addition to hydration and continuous monitoring for TLS and TLS complications. correct electrolyte abnormalities. a urate oxidase. 105. rasburicase.135. Riyadh. Renal replacement therapy is used as a last resort to improve kidney function and persistent electrolyte abnormalities.134.135 Renal Replacement Therapy Renal replacement therapy (eg. The aim of this article is to help clinicians to better recognize and manage TLS. or by destruction of tumor cells by cytotoxic agents.Tumor Lysis Syndrome formation. 155 When dialysis is initiated early. makes uric acid more soluble in urine and causes a rapid reduction in uric acid levels. 135. despite being treated with allopurinol.4. It decreases the concentration of uric acid in the urine. and improve patient outcomes. it prevents urate crystals from precipitating.154 In an oncologic pediatric population. It is a condition caused by a massive lysis of the tumor cells accumulating very rapidly. March 2011. serum uric acid levels decrease by about 50% with each 6-hour treatment. starting with 1 dose (0. Issue 2.com/GetIt • Copyright Clearance Center: http://www. precipitation of uric acid becomes less likely to occur in renal tubules. and it will lead to a complete recovery of renal function. and though.147 For this reason.4 Early initiation of dialysis improves prognosis. and therefore causes a rapid reduction in uric acid levels. and urinary alkalinization.copyright. rather than allopurinol. or renal dysfunction. Urinary alkalinization use is still controversial and is only indicated in patients with severe metabolic acidosis. uremia.1–0.
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