Tumor lysis syndrome after induction chemotherapy in small-cell lung carcinoma

Small-cell lung cancer (SCLC) is responsive to combination chemotherapy. Response rates of 50-80% can be achieved depending on whether the cancer is limited or extensive. Rarely, patients with SCLC respond so rapidly to induction chemotherapy that they develop a tumor lysis syndrome. This syndrome may lead to azotemia and renal failure if not recognized early and treated appropriately. This complication of therapy is important to recognize as the treatment of SCLC is sometimes administered on an outpatient basis. In addition, certain chemotherapeutic agents used in SCLC, such as cis-platin, are nephrotoxic and could potentially aggravate the azotemia secondary to the tumor lysis syndrome.     

Tumor lysis syndrome in a patient with metastatic Merkel cell carcinoma

A first course of combination chemotherapy for large volume metastatic disease in a patient with Merkel cell carcinoma resulted in a tumor lysis syndrome. After this course a nearly complete response was documented. This case report extends further the chemosensitivity of Merkel cell carcinoma and demonstrates the need for tumor lysis syndrome prophylaxis in patients with bulky disease or fast-growing tumors.     

Tumor lysis syndrome in small cell lung cancer

Tumor lysis syndrome, resulting from the abrupt release of intracellular ions into the blood stream due to sudden tumor cell death, is a serious complication of chemotherapy treatment. This syndrome occurs more frequently in hematologic malignancies and lymphomas. Its incidence in solid tumors is rare, but has a high mortality rate owing to the lack of prophylactic therapy to prevent this complication. We report a case of tumor lysis syndrome accompanied by death in a patient with extensive stage small cell lung cancer who was treated with cisplatin and etoposide, and review the risk factors associated with the syndrome in solid tumor patients who are likely to respond to chemotherapy.     

Tumor lysis associated with sudden onset of syndrome of inappropriate antidiuretic hormone secretion

Syndrome of inappropriate antidiuretic hormone secretion is frequent in small-cell lung carcinomas. We report on a case of syndrome of inappropriate antidiuretic hormone secretion after each of the first 2 cycles of chemotherapy for small-cell lung cancer. The association with chemotherapy-induced tumor lysis is proposed, particularly based on the course of antidiuretic hormone levels, and a review of the literature is presented. Syndrome of inappropriate antidiuretic hormone secretion can occur during tumor lysis syndrome.     

Severe spontaneous acute tumor lysis syndrome and hypoglycemia in patient with germ cell tumor

Tumor lysis syndrome has been observed in patients with bulky, treatment-sensitive tumors, in particular hematological malignancies, especially after medical treatment (chemotherapy, corticosteroids, radiation, hormonal agents, and biological response modifiers). Tumor lysis syndrome has been observed also in solid malignancies and it very rarely occurs spontaneously. Tumor lysis syndrome-associated metabolic abnormalities include hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia and uremia. Severe hypoglycemia is another rare metabolic disorder, uncommonly associated with solid malignancies. The case described here is peculiar for the abrupt onset of these two rare conditions in a patient with a metastatic germ cell tumor.     

Acute Tumor Lysis Syndrome Following Intrathecal Methotrexate

We report a 17-year-old boy with meningeal involvement of lymphoblastic lymphoma who experienced acute tumor lysis syndrome following intrathecal administration of methotrexate. Intrathecally injected methotrexate provides a slow- release reservoir of methotrexate into the bloodstream with prolonged cy totoxic levels. To the best of our knowledge, this is the second case of tumor lysis syndrome to be described after intrathecal methotrexate injection. The pathogenesis of this unusual complication of intrathecal chemotherapy is discussed.     

Rapid tumor lysis syndrome in a patient with metastatic colon cancer as a complication of treatment with 5-fluorouracil/leucoverin and irinotecan

Tumor lysis syndrome is a potentially fatal complication of anti-cancer therapy that is usually seen in patients with bulky, rapidly proliferating, treatment-sensitive tumors such as hematological malignancies, but it rarely occurs in a variety of solid tumors such as colorectal carcinoma. Combination chemotherapy with infusional 5-fluorouracil/leucoverin and irinotecan has been recently accepted as the first treatment option for metastatic colorectal cancer. We present a case of tumor lysis syndrome in a patient with metastatic colon carcinoma that occurred 72 hrs after the initial course of a combination chemotherapy with irinotecan and 5-fluorouracil/leucoverin. Despite the immediate treatment with aggressive hydration by a sodium bicarbonate infusion, followed by forced diuresis and uricolytic therapy, he died of a sudden cardiac arrest complicated by acute renal failure. Our case indicates that administration of 5-fluorouracil/leucoverin and irinotecan for bulky tumors of colorectal origin with a rapid doubling time may induce an acute tumor lysis syndrome, which necessitates frequent laboratory monitoring and a close follow-up of the patient as well as prompt initiation of appropriate therapeutic measures.     

Fatal acute tumor lysis syndrome with metastatic breast carcinoma

A 53-year-old woman presented with an extensively metastatic and rapidly growing breast adenocarcinoma, markedly elevated lactate dehydrogenase, and mildly elevated blood urea nitrogen. She received 5-fluorouracil, doxorubicin, and cyclophosphamide. Eighteen hours after chemotherapy she was noted to have hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and acute renal failure. She experienced cardiac arrest and died 72 hours after receiving chemotherapy. A postmortem liver biopsy revealed adenocarcinoma undergoing necrosis. This case represented the acute tumor lysis syndrome that occurred after chemotherapy of breast carcinoma. Patients with metastatic breast carcinoma and similar presentations should be considered for prophylactic therapy with allopurinol and hydration before chemotherapy.     

Tumour Lysis Following Hydrocortisone Prior to a Blood Product Transfusion in T-Cell Acute Lymphoblastic Leukaemia

The acute tumour lysis syndrome is a well recognised complication of chemotherapy for lymphoid malignancies. There are few reports, however, of this complication after corticosteroid therapy alone. We report a case of T-cell acute lymphoblastic leukaemia who developed the biochemical picture of tumour lysis after two doses of hydrocortisone given prior to platelet transfusion. Prophylactic corticosteroids prior to blood product infusion should be reserved for patients who have experienced febrile or allergic reactions in the past and it is suggested that they should only be administered to patients with active lymphoid malignancies with due caution.     

Tumour lysis following hydrocortisone prior to a blood product transfusion in T-cell acute lymphoblastic leukaemia.

The acute tumour lysis syndrome is a well recognised complication of chemotherapy for lymphoid malignancies. There are few reports, however, of this complication after corticosteroid therapy alone. We report a case of T-cell acute lymphoblastic leukaemia who developed the biochemical picture of tumour lysis after two doses of hydrocortisone given prior to platelet transfusion. Prophylactic corticosteroids prior to blood product infusion should be reserved for patients who have experienced febrile or allergic reactions in the past and it is suggested that they should only be administered to patients with active lymphoid malignancies with due caution.     

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.     

Increasing recognition of corticosteroid-induced tumor lysis syndrome in non-Hodgkin's lymphoma

The acute tumor lysis syndrome has been reported in patients with aggressive non-Hodgkin's lymphoma, acute lymphoblastic leukemia, and rarely in other malignancies in association with the administration of cytotoxic chemotherapy. We report a case of a young man with a large cell lymphoma in whom the acute tumor lysis syndrome developed in association with the administration of corticosteroids. Two similar cases have been reported recently. Clinicians who treat patients with neoplastic diseases should be aware that corticosteroids alone may produce this potentially life threatening complication.     

Acute tumor lysis syndrome and treatment response in patients treated for refractory chronic lymphocytic leukemia with short-course, high-dose cytosine arabinoside, cisplatin, and etoposide

Acute tumor lysis syndrome resulting from rapid neoplastic cell lysis after chemotherapy is an unusual event, generally seen in histological aggressive lymphatic tumors. The authors saw four patients who developed acute tumor lysis syndrome when treated for advanced-stage, refractory chronic lymphocytic leukemia (CLL) with an initial cycle of cytosine arabinoside (Ara-C) 2 g/m2 every 12 hours x 4, cisplatin 35 mg/m2 every 24 hours x 2, and etoposide 100 mg/m2 every 24 hours x 2 (ACE). With aggressive hydration, urine alkalinization, forced diuresis, and high-dose allopurinol, acute tumor lysis syndrome was not seen in three subsequent cases of CLL treated with ACE. Of a total of eight patients treated, seven patients had marked reductions in lymphocyte counts after the first course of ACE. Of the eight patients, three are alive: one in a complete remission greater than 2 years, one in partial remission after three cycles of ACE, and one in Richter's transformation to large cell lymphoma. The remaining patients died after one cycle of ACE chemotherapy, one as a direct complication of acute tumor lysis and pancytopenia, and four others from complications of severe pancytopenia and general debilitation. Therefore, ACE appears to cause a rapid dissolution of tumor cells in CLL, and with appropriate aggressive management of the tumor lysis and infectious complications may have a favorable impact on survival in advanced CLL.     

肿瘤溶解综合征11例报告

目的：探讨肿瘤溶解综合征发生的危险因素及其治疗。方法：对11例化疗早期发生肿瘤溶解综合征的肿瘤患者临床特点及化疗前后各项实验生化指标进行分析。结果：初次治疗、男性、年轻、肿瘤负荷高、化疗前有肾功能不全、血尿酸水平高、血乳酸脱氢酶高、存在脱水和酸性尿等为发生肿瘤溶解综合征的危险因素。结论：对存在发生肿瘤溶解综合征的危险因素的患者，必须高度重视和早期采取发适当治疗措施。     

急性淋巴细胞白血病并发肿瘤溶解综合征7例

目的 :探讨急性淋巴细胞白血病 (AL L )患者化疗后发生肿瘤溶解综合征 (TL S)的临床特征。方法 :对 7例化疗发生 TL S的 AL L患者进行各项生化指标的分析。结果 :TL S患者表现为高尿酸血症、高血钾、高血磷、低血钙 ,并有不同程度的肾功能损伤 ,其中 1例发生了急性肾功能不全。用别嘌呤醇及静脉碱化利尿后 ,6例短期内血生化指标恢复正常。1例死于心衰。结论 :早期诊断并及时给予别嘌呤醇及静脉碱化利尿是治疗 TL S的关键     

Hyperuricemia in Patients with Cancer

Hyperuricemia is a common early complication in patients with hematological malignancies treated with intensive chemotherapy. It results from the breakdown of nuclear proteins leading to increased blood levels of hypoxanthine and xanthine. These compounds are degraded into uric acid by the enzyme xanthine oxidase. Because the mechanisms of excretion of uric acid are limited in humans and blood levels are near saturation level, a common complication of hyperuricemia is renal failure resulting from the deposition of uric acid in renal tubules. When renal insufficiency occurs in conjunction with other metabolic aberrations, such as hyperkalemia, hyperphosphatemia, and hypocalcemia, this process is termed tumor lysis syndrome. Patients with acute lymphoblastic leukemia and non-Hodgkin’s lymphoma, particularly Burkitt’s lymphoma, are at greatest risk because of the high sensitivity of the cells to chemotherapy. Other factors associated with increased risk of hyperuricemia and tumor lysis syndrome include hyperleukocytosis, massive organomegaly, renal enlargement, extrinsic compression of the genitourinary tract, and elevated serum lactate dehydrogenase activity. Conventionally, patients at risk of developing hyperuricemia receive alkalinized fluids and allopurinol, an inhibitor of the enzyme xanthine oxidase. These measures have been effective in reducing mortality associated with metabolic complications during tumor lysis in the majority of the cases. However, as many as 25% of patients at high-risk of developing tumor lysis syndrome require dialysis, and some of them have the treatment course altered because of these complications. Recently, a synthetic recombinant form of the enzyme urate oxidase, rasburicase has become available in the US. This enzyme acts directly on urate and degrades it to allantoin, a much more soluble compound.     

Acute tumor lysis syndrome triggered by zoledronic acid in a patient with metastatic lung adenocarcinoma

We report the case of a 52-yr-old man with metastatic lung adenocarcinoma who developed tumor lysis syndrome after administration of zoledronic acid. Tumor lysis syndrome in solid tumors and the antitumor effect of the zolendronic acid are discussed in light of the pertinent literature.     

Acute lysis pneumopathy after chemotherapy for acute myelomonocytic leukemia with abnormal marrow eosinophils.

Acute respiratory failure developed in two patients with hyperleukocytic acute myelomonocytic leukemia with abnormal marrow eosinophils within 1 to 3 days after the beginning of high-dose induction chemotherapy. The presence of moderate pulmonary leukostasis before chemotherapy initiation, the simultaneous occurrence of an acute tumor lysis syndrome, the lack of evidence of any other cause of respiratory distress, and the clinical evolution lead the authors to attribute pulmonary injury to lysis of resident leukemic cells. The responsibility of eosinophilic cellular constituents for the diffuse alveolar damage is discussed.     

Burkitt's acute lymphocytic leukemia (L3ALL) in adults

Burkitt's acute lymphocytic leukemia is a rare type of adult ALL, probably difficult to distinguish from disseminated Burkitt's lymphoma involving the bone marrow. This tumor is highly proliferative and tends to involve the CNS at diagnosis or early during the disease course. It shows rapid chemosensitivity, initially leading to the risk of severe acute tumor lysis syndrome. Principles of its treatment, by comparison with the other types of ALL, include: 1. A low-dose chemotherapy prephase to prevent acute tumor lysis syndrome. 2. Multiagent chemotherapy using high-dose cyclophosphamide, an anthracycline, high-dose MTX, high-dose ara-C, and probably VP16. A short and intensive treatment (6 to 8 months) without maintenance is indicated. 3. Early intensive CNS treatment, with multiple triple intrathecal injections, high-dose MTX, and high-dose ara-C, and possibly cranial irradiation. Autologous or allogeneic stem cell transplantation do not seem to be useful in first CR. Using such approaches, recent results suggest that about two thirds of L3ALL in adults can be cured, more than in any other type of adult ALL.     

Posterior leukoencephalopathy in association with the tumour lysis syndrome in acute lymphoblastic leukaemia--a case with clinicopathological correlation

We report a case and autopsy findings of posterior leukoencephalopathy (PL) developing during induction chemotherapy for B-cell acute lymphoblastic leukaemia (B-ALL) complicated by tumour lysis syndrome. PL may present with seizures, headache, altered mental status and occipital blindness, associated with transient parieto-occipital abnormalities on neuro-imaging studies. Precipitants include immunosuppressive agents, renal insufficiency, hypertension and fluid retention. It has also been reported in association with pre-eclamptic and eclamptic states, nephrotic syndrome and following liver and bone marrow transplantation. Only rare cases of PL developing during treatment for haematological malignancy have been reported and to our knowledge it has not been previously reported in association with tumour lysis syndrome. Since the condition is generally regarded as being fully reversible few autopsy findings have been reported.