br Conclusions br Conflict of interest br

Conclusions
Conflict of interest
Acknowledgments This study was based in part on data from the National Health Insurance Research Database provided by the Bureau of National Health Insurance, Department of Health and managed by the National Health Research Institutes (registration number 101115). The interpretation and conclusions contained herein do not represent those of the Bureau of National Health Insurance, Department of Health, or the National Health Research Institutes.
Introduction Tumor lysis syndrome is frequently observed in hematologic cancer or in rapidly growing and bulky tumors. The symptoms of this condition include decreased urine output, hyperkalemia, hyperphosphatemia, hypocalcemia and hyperuricemia and may be accompanied by metabolic acidosis, arrhythmia or even seizure. Tumor lysis syndrome rarely occurs in solid tumors but it can frequently be observed in sensitive bulky solid tumors post-treatment with chemotherapy or radiotherapy. Treatment for acute tumor lysis includes renal replacement therapy in patients with severe oliguria or anuria, persistent hyperkalemia, hyperphosphatemia and with a calcium-phosphate product ≧70 mg2/dL.2
Case report Results from computerized tomography showed tumor recurrence in the pelvic region with fistula formation from the urinary bladder, extending into the presacral space (Figs. 1–4). Thereafter, chemotherapy with FOLFOX (leucovorin, fluorouracil, oxaliplatin) regimen (first oleuropein chemotherapy after noted recurrent) was initiated. Upon completion of chemotherapy (exact chemotherapy regimen with: oxaliplatin 160 mg (85 mg/m2), 5-FU 2800 mg (1500 mg/m2) for 1 day and leucovorin 200 mg), the patient complained of chest tightness followed by alternating periods of consciousness and ventricular tachycardia requiring cardiopulmonary-cerebral resuscitation and defibrillation. Following his initial resuscitation, the patient was admitted to the intensive care unit and laboratory data showed hyperkalemia, acute kidney injury and oliguria. After 1 day, laboratory data showed persistent hyperammonemia (ammonia 304 ug/dL), which elevated our suspicion that there was complicit drug toxicity due to 5-FU. However, the patient\'s high potassium levels persisted, along with ventricular arrhythmia, after which he received defibrillation. Follow-up data on day 4 showed the following: hyperuricemia uric acid: 15.9 mg/Dl (normal range: 4.8–8.7 mg/dL) and hypocalcemia Ionized Ca: 1.01 mmol/L (normal range:1.09–1.30 mmol/L) and serum creatinine increased from 2.14 to 3.14 mg/dL from day 4 to day 5 with normal serum phosphorus level. The patient\'s condition was stable before the initiation of chemotherapy. Given the fact that our patient suffered from 5-FU toxicity first which was complicated with tumor lysis syndrome as evidenced by hyperkalemia with ventricular fibrillation twice, hypocalcemia, hypruricemia, and poor renal function, the typical electrolyte changes may not be as “typical” as suggested. The dose of chemotherapy (FOLFOX) had been adjusted before the initiation of treatment. Subsequently, the patient was successfully extubated on day 11. By that point, the final creatinine level was back to 1.41 mg/dL. After this episode, we had shifted chemotherapy to capecitabine 1000 mg–1500 mg daily, to maintain an antitumor effect and diminish poor activity. The patient received another course of chemotherapy Irinotecan 300 mg (180 mg/m2), leucovorin 600 mg (400 mg/m2), 5-FU 2000 mg (1500 mg/m2), after which this treatment scenario concluded. To date, no additional tumor lysis has occurred and the patient is doing well. Our facility did not performed any follow-up imaging arising from the fact that the patient had just received two courses (with one incomplete) of chemotherapy.
Discussion Tumor lysis syndrome can be classified in terms of both clinical and laboratory parameters, according to the Cairo and Bishop grading system. First, at least two or more metabolic abnormalities must be noted simultaneously. Second, a 25% change in the baseline laboratory data should not be considered as a criterion. Third, any symptomatic hypocalcemia should constitute the symptoms of clinical tumor lysis syndrome. Our patient met the criteria of both clinical and laboratory parameters for tumor lysis syndrome (clinically: cardiac dysrhythmia, disturbance in consciousness, and increased serum creatinine level; laboratory: hyperuricemia, hypocalcemia, and hyperkalemia). Tumor lysis syndrome is most frequently observed during treatment of hematologic malignancies, usually leukemia and lymphoma. Most of the hematologic tumors associated with tumor lysis syndrome are poorly differentiated lymphomas, such as Burkitt\'s lymphoma, and leukemias such as acute lymphoblastic leukemia and acute myeloid leukemia. Tumor lysis syndrome is rare in solid tumors and more frequently found in bulky tumors and chemotherapy sensitive cancers such as small cell lung cancer, and widespread gastrointestinal tract adenocarcinoma or breast cancer. Several studies have reported the occurrence of tumor lysis syndrome in solid tumors post-radiotherapy or even target therapy, such as metastatic gestational trophoblastic neoplasia, renal cell carcinoma, and metastatic transitional cell carcinoma. The prognosis of tumor lysis syndrome is poor in the case of solid tumors compared to hematology malignancy, which may be due to the frequent lack of early recognition and prevention. One study mentioned tumor lysis syndrome occurring in solid tumor patients typically manifests a later onset than in hematological malignancies, which may be related to the more synchronous kinetics of lymphomyeloproliferative disorders cells than solid tumor cells. The patient had suffered from chemotherapy-associated hyperammonia complicated with tumor lysis syndrome, as indicated by ventricular fibrillation caused by hyperkalemia and hyperuricemia. We do not refer to this scenario as “late onset tumor lysis syndrome”. In fact, we believe the tumor lysis probably occurred after the chemotherapy but was masked by the hyperammonia that might be caused by 5-FU. In the very beginning, we did not contemplate the possibility of tumor lysis since it is rare - especially for the FOLFOX regimen. Not until the patient had twice suffered ventricular fibrillations with hyperkalemia did we think the possibility of tumor lysis.