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Tumor lysis syndrome

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54: 516:) should receive appropriate intravenous hydration in order to improve blood flow to the kidneys, maximize urine output, and ultimately prevent precipitation of uric acid crystals that can lead to acute kidney injury. A diuretic may also be indicated to further increase urine output in addition to intravenous hydration. Another approach to prevent damage to the kidneys is to prevent the buildup of uric acid during TLS, and this can be accomplished with use of 331:. This entity is associated with acute kidney failure due to uric acid nephropathy prior to the institution of chemotherapy and is largely associated with lymphoma and leukemia. The important distinction between this syndrome and the post-chemotherapy syndrome is that spontaneous TLS is not associated with hyperphosphatemia. One suggestion for the reason of this is that the high cell turnover rate leads to high uric acid levels through 293:. Massive cell death and nuclear breakdown generates large quantities of nucleic acids. Of these, the purines (adenine and guanine) are converted to uric acid via the purine degradation pathway and excreted in the urine. However, at the high concentrations of uric acid generated by tumor lysis, uric acid is apt to precipitate as 417:
TLS should be suspected in patients with large tumor burden who develop acute kidney failure along with hyperuricemia (> 15 mg/dL) or hyperphosphatemia (> 8 mg/dL). (Most other acute kidney failure occurs with uric acid < 12 mg/dL and phosphate < 6 mg/dL). Acute uric
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Monitoring potassium levels in the blood frequently and cardiac monitoring (given the risk of cardiac arrhythmias) are important components in the prevention of adverse consequences in TLS. Other strategies, such as limiting oral intake of potassium, and excreting potassium through the
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Two or more electrolyte laboratory abnormalities must be present simultaneously to be considered related to TLS. In fact, some patients may present with one abnormality, but later another one may develop that is unrelated to the TLS (e.g., hypocalcemia associated with
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Chemo-sensitive tumors, such as lymphomas, carry a higher risk for the development of tumor lysis syndrome. Those tumors that are more responsive to a chemotherapy agent carry a higher TLS risk. Usually, the precipitating medication regimen includes combination
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It is important to prevent life-threatening manifestations associated with TLS which include acute kidney injury, hyperkalemia (which may cause cardiac arrhythmias), and or hypocalcemia (which may cause cardiac arrhythmias and neuromuscular irritability).
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Tumors with a high cell turnover rate, rapid growth rate, and high tumor bulk tend to be more associated with the development of tumor lysis syndrome. The most common tumors associated with this syndrome are poorly differentiated lymphomas (such as
304:(AUAN) due to hyperuricosuria has been a dominant cause of acute kidney failure, but with the advent of effective treatments for hyperuricosuria, AUAN has become a less common cause than hyperphosphatemia. Two common conditions related to excess 647:
The rate of mortality from tumor lysis syndrome may vary widely depending on the type of underlying malignancy. However, the occurrence of acute kidney injury is concerning given the high mortality that is generally associated with it.
1155:... result in severe metabolic derangements (e.g., hyperuricemia, hypocalcemia, lactic acidosis, and the acute tumor lysis syndrome) which require expeditious management. Hyperuricemia Uric acid is the end product of purine catabolism. 422:
may show uric acid crystals or amorphous urates. The hypersecretion of uric acid can be detected with a high urine uric acid - creatinine ratio > 1.0, compared to a value of 0.6–0.7 for most other causes of acute kidney failure.
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may also be indicated to maintain appropriate production of urine by the kidneys. Further treatment is targeted towards the specific metabolic abnormalities present in patients with TLS (see "main articles" linked above). Mild
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turnover but the tumor reuses the released phosphate for growth of new tumor cells. In post-chemotherapy TLS, tumor cells are destroyed and no new tumor cells are being synthesized. TLS is most common during
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Hyperphosphatemia is a common finding in TLS, and high phosphorus levels can in turn contribute to hypocalcemia. Therefore, phosphate binders may be beneficial in preventing this form of hypocalcemia.
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therapy or from cancers with high cell turnover and tumor proliferation rates. The metabolic abnormalities seen in tumor lysis syndrome can ultimately result in serious complications such as
1359:"Guidelines for the management of tumour lysis syndrome in adults and children with haematological malignancies on behalf of the British Committee for Standards in Haematology" 118:
and should receive preventive measures and treatments as necessary. TLS can also occur on its own (while not being treated with chemotherapy) although this is less common.
198:. High turnover of tumor cells leads to spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 6.5 mmol/L) and they include 489:
A 25% change from baseline should not be considered a criterion since such increases are rarely clinically important unless the value is already outside the normal range.
785:"Recommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensus" 851:
Coiffier B, Altman A, Pui CH, Younes A, Cairo MS (June 2008). "Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review".
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Davidson MB, Thakkar S, Hix JK, Bhandarkar ND, Wong A, Schreiber MJ (April 2004). "Pathophysiology, clinical consequences, and treatment of tumor lysis syndrome".
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Risk factors for tumor lysis syndrome depend on several different characteristics of the patient, the type of cancer, and the type of chemotherapy used.
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may be given in cases of severe hyperkalemia. Concerning symptoms related to hypocalcemia (e.g. seizures) in TLS patients can be treated with
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Certain patient-related factors can affect the development of clinical tumor lysis syndrome. These factors include elevated baseline serum
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Patients at risk for developing TLS (e.g. patients about to receive chemotherapy for a cancer with a high cell turnover rate, especially
1215:"Spontaneous Tumor Lysis Syndrome: A Case Report and Critical Evaluation of Current Diagnostic Criteria and Optimal Treatment Regimens" 409:
treatment alone, and sometimes without any treatmentβ€”in this case the condition is referred to as "spontaneous tumor lysis syndrome".
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is precipitated to form calcium phosphate, leading to hypocalcemia. Symptoms of hypocalcemia include (but are not limited to):
114:. This is a potentially fatal complication and patients at increased risk for TLS should be closely monitored while receiving 1127: 998: 17: 532:
inhibitor, which inhibits uric acid production) works by preventing the formation of uric acid following tumor cell lysis.
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are a result of the release of cellular contents of dying cells into the bloodstream. In this respect, TLS is analogous to
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Schafer AL, Shoback DM (2000), Feingold KR, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, et al. (eds.),
1141: 153:, with comparable mechanism and blood chemistry effects but with different cause. In TLS, the breakdown occurs after 438:: abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy. 1702: 1133: 481:
In 2011, Howard proposed a refinement of the standard Cairo-Bishop definition of TLS accounting for 2 limitations:
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A grading scale (0–5) is used depending on the presence of lab TLS, serum creatinine, arrhythmias, or seizures.
1525:"In-Hospital Outcomes of Tumor Lysis Syndrome: A Population-Based Study Using the National Inpatient Sample" 540:
enzyme and acts by degrading uric acid. It is not recommended to alkalinize urine in the management of TLS.
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and hydration are the mainstays of treatment in patients with clinical evidence of tumor lysis syndrome. A
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can also be used as options to remove potassium from the bloodstream when hyperkalemia is present.
559:) can also be used, but are temporary interventions, and potassium is not excreted from the body. 53: 547:
gastrointestinal tract using agents such as oral sodium polystyrene sulfonate, can be beneficial.
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Tosi P, Barosi G, Lazzaro C, Liso V, Marchetti M, Morra E, et al. (December 2008).
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Coiffier B, Riouffol C (February 2007). "Management of tumor lysis syndrome in adults".
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In 2004, Cairo and Bishop defined a classification system for tumor lysis syndrome.
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Niederhuber JE, Armitage JO, Doroshow JH, Kastan MB, Tepper JE (2014).
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Moreover, any symptomatic hypocalcemia should constitute clinical TLS.
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acid nephropathy is associated with little or no urine output. The
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Treatment is first targeted at the specific metabolic disorder.
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therapy (in conjunction with glucose administration) as well as
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are also predominantly intracellular. Hyperphosphatemia causes
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Tumor lysis syndrome is characterized by high blood potassium (
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Darmon M, Malak S, Guichard I, Schlemmer B (September 2008).
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sudden changes in mental status, including emotional lability
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increased serum creatinine (1.5 times upper limit of normal)
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Jones GL, Will A, Jackson GH, Webb NJ, Rule S (June 2015).
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Journal of Investigative Medicine High Impact Case Reports
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conduction abnormalities, and arrhythmias (can be fatal)
90:) from the treatment, releasing their contents into the 850: 1405: 1463: 783:
Cairo MS, Coiffier B, Reiter A, Younes A (May 2010).
1573: 1356: 1169:"Acute tumor lysis syndrome: a comprehensive review" 1125: 1077:
Rampello E, Fricia T, Malaguarnera M (August 2006).
1016:"Potassium Disorders: Hypokalemia and Hyperkalemia" 993:(Fifth ed.). Philadelphia: Elsevier Saunders. 635:. Tumor lysis patients may ultimately also require 94:. This occurs most commonly after the treatment of 937:Cheuk DK, Chiang AK, Chan GC, Ha SY (March 2017). 885: 226:in tumor lysis syndrome, because of deposition of 936: 623:, while a temporizing agent such as rapid acting 405:, but TLS can be triggered in cancer patients by 1679: 1264: 1044: 728: 447:phosphate > 4.5 mg/dL or 25% increase 329:Pretreatment spontaneous tumor lysis syndrome 1522: 1399: 1301: 1070: 316:, are not features of tumor lysis syndrome. 1406:Cammalleri L, Malaguarnera M (March 2007). 1307: 1212: 943:The Cochrane Database of Systematic Reviews 658: 639:such as through hemodialysis if indicated. 441:uric acid > 8 mg/dL or 25% increase 1523:Durani U, Shah ND, Go RS (December 2017). 1126:Moossa AR, Schimpff SC, Robson MC (1991). 1053:, South Dartmouth (MA): MDText.com, Inc., 426: 52: 1548: 1491: 1481: 1431: 1412:International Journal of Medical Sciences 1374: 1325: 1238: 1184: 1094: 1013: 962: 913: 903: 800: 754: 450:calcium < 7 mg/dL or 25% decrease 1208: 1206: 1204: 1079:"The management of tumor lysis syndrome" 729:Howard SC, Jones DP, Pui CH (May 2011). 1173:Revista Brasileira de Terapia Intensiva 1047:"Hypocalcemia: Diagnosis and Treatment" 615:without symptoms can be treated with a 14: 1680: 1213:Weeks AC, Kimple ME (26 August 2015). 444:potassium > 6 meq/L or 25% increase 1459: 1457: 1455: 1453: 1451: 1260: 1258: 1201: 886:Belay Y, Yirdaw K, Enawgaw B (2017). 724: 722: 720: 718: 716: 176: 984: 982: 846: 844: 842: 840: 838: 836: 834: 832: 830: 828: 778: 776: 774: 714: 712: 710: 708: 706: 704: 702: 700: 698: 696: 476: 242:. Because of the hyperphosphatemia, 1308:Cairo MS, Bishop M (October 2004). 1267:Expert Review of Anticancer Therapy 1014:Viera AJ, Wouk N (September 2015). 735:The New England Journal of Medicine 24: 1698:Conditions of the subcutaneous fat 1448: 1255: 1129:Comprehensive textbook of oncology 1083:Nature Clinical Practice. Oncology 464:cardiac arrhythmia or sudden death 25: 1719: 1569: 1134:Lippincott Williams & Wilkins 979: 930: 825: 771: 693: 1327:10.1111/j.1365-2141.2004.05094.x 802:10.1111/j.1365-2141.2010.08143.x 667:The American Journal of Medicine 102:and in particular when treating 1541:10.1634/theoncologist.2017-0147 1516: 1350: 1186:10.1590/S0103-507X2008000300011 1160: 1119: 436:Laboratory tumor lysis syndrome 376:(AML). Other cancers (such as 348: 1363:British Journal of Haematology 1314:British Journal of Haematology 1038: 1007: 955:10.1002/14651858.CD006945.pub4 879: 789:British Journal of Haematology 13: 1: 651: 496: 456:Clinical tumor lysis syndrome 398:Chemotherapy characteristics: 991:Aebeloff's Clinical Oncology 853:Journal of Clinical Oncology 679:10.1016/j.amjmed.2003.09.045 642: 576: 412: 370:acute lymphoblastic leukemia 208:muscle weakness or paralysis 112:acute lymphoblastic leukemia 7: 302:Acute uric acid nephropathy 159:acute uric acid nephropathy 10: 1724: 731:"The tumor lysis syndrome" 580: 141:). These changes in blood 1651: 1577: 1020:American Family Physician 637:renal replacement therapy 314:uric acid nephrolithiasis 295:monosodium urate crystals 133:), high blood uric acid ( 125:), high blood phosphate ( 82:, where large amounts of 37: 32: 1279:10.1586/14737140.7.2.233 1231:10.1177/2324709615603199 865:10.1200/JCO.2007.15.0177 384:Patient characteristics: 1703:Oncological emergencies 1225:(3): 2324709615603199. 427:Cairo-Bishop definition 230:crystals in the kidney 72:metabolic abnormalities 1483:10.3324/haematol.13290 553:beta-receptor agonists 374:acute myeloid leukemia 357:Tumor characteristics: 129:), low blood calcium ( 108:acute myeloid leukemia 86:cells are killed off ( 78:from the treatment of 747:10.1056/NEJMra0904569 621:polystyrene sulfonate 366:Non-Hodgkin Lymphomas 342:hematologic neoplasms 18:Tumour lysis syndrome 905:10.1155/2017/9684909 506:Acute kidney injury: 272:) movement disorders 163:acute kidney failure 104:non-Hodgkin lymphoma 74:that can occur as a 64:Tumor lysis syndrome 33:Tumor lysis syndrome 892:Journal of Oncology 338:cytotoxic treatment 224:acute kidney injury 171:cardiac arrhythmias 1652:External resources 1096:10.1038/ncponc0581 362:Burkitt's lymphoma 218:. Like potassium, 177:Signs and symptoms 1675: 1674: 1535:(12): 1506–1509. 1476:(12): 1877–1885. 1424:10.7150/ijms.4.83 1376:10.1111/bjh.13403 1000:978-1-4557-2865-7 859:(16): 2767–2778. 741:(19): 1844–1854. 633:calcium gluconate 629:calcium carbonate 587:hyperphosphatemia 477:Howard definition 228:calcium phosphate 215:Hyperphosphatemia 127:hyperphosphatemia 61: 60: 27:Medical condition 16:(Redirected from 1715: 1575: 1574: 1563: 1562: 1552: 1520: 1514: 1513: 1495: 1485: 1461: 1446: 1445: 1435: 1403: 1397: 1396: 1378: 1354: 1348: 1347: 1329: 1305: 1299: 1298: 1262: 1253: 1252: 1242: 1210: 1199: 1198: 1188: 1164: 1158: 1157: 1152: 1150: 1123: 1117: 1116: 1098: 1074: 1068: 1067: 1066: 1065: 1042: 1036: 1035: 1011: 1005: 1004: 986: 977: 976: 966: 934: 928: 927: 917: 907: 883: 877: 876: 848: 823: 822: 804: 780: 769: 768: 758: 726: 691: 690: 662: 530:xanthine oxidase 70:) is a group of 57: 56: 30: 29: 21: 1723: 1722: 1718: 1717: 1716: 1714: 1713: 1712: 1693:Blood disorders 1678: 1677: 1676: 1671: 1670: 1647: 1646: 1586: 1572: 1567: 1566: 1521: 1517: 1462: 1449: 1404: 1400: 1355: 1351: 1306: 1302: 1263: 1256: 1211: 1202: 1165: 1161: 1148: 1146: 1144: 1132:. 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Index

Tumour lysis syndrome
Specialty
Oncology
hematology
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metabolic abnormalities
complication
cancer
tumor
lysed
bloodstream
lymphomas
leukemias
non-Hodgkin lymphoma
acute myeloid leukemia
acute lymphoblastic leukemia
chemotherapy
hyperkalemia
hyperphosphatemia
hypocalcemia
hyperuricemia
BUN
electrolytes
metabolites
rhabdomyolysis
cytotoxic
acute uric acid nephropathy
acute kidney failure
seizures
cardiac arrhythmias

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