Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor lysis syndrome (TLS) refers to the constellation of deranged metabolic state, characterized by hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia, and/or azotemia, secondary to rapid breakdown of tumor cells. It is a life threatening emergency that typically follows administration of chemotherapy or may be spontaneous. Malignancies which have a large tumor burden, rapid turnover, as well as speedy breakdown following chemotherapy are susceptible. Acute lymphoblastic leukemia and non-Hodgkins lymphoma (particularly Burkitt's lymphoma) are typically predisposed. TLS is best managed by early anticipation and preventive measures than the complicated task of treating an established TLS. Vigorous intravenous hydration is the cornerstone of prevention as well as treatment. Rasburicase has revolutionized the management. It is available in India for past 1 1/2 y, although the cost is a limiting factor. Children with acute leukemia in developing countries may reach health facility late, with severe anemia and hyperleukocytosis. Exchange transfusion may have to be restored to in such patients to simultaneously correct anemia and hyperleukocytosis and enable safe administration of fluids. Dialysis may be required when the metabolic 'trash' overwhelms the renal excretion, resulting in renal failure. Chemotherapeutic drugs are often administered in a phased manner in susceptible patients, in an attempt to prevent precipitous lysis of tumor cells. Presentation and management of TLS in relevance to the pediatric emergency room is outlined.
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PMID:Tumor lysis syndrome. 2369 52

Tumor lysis syndrome(TLS)induced by chemotherapy for solid tumors is rare. We report a case of a 59-year-old woman with breast cancer who developed TLS. She underwent surgery to treat breast cancer in 1992. 19 years after surgery, however, she was diagnosed with multiple bone metastases(disease free interval, 13 years and 3 months). In March 2011, gemcitabine regimen was initiated(1,250mg/m2, 14 days followed by a 7-day rest period)because of worsening of multiple bone metastases. The patient was immediately admitted and treated for suspected TLS when she presented at our hospital with symptoms such as depressed level of consciousness, serious anemia, hypercalcemia, hyperuricemia, and liver/renal dysfunction on day 16 of the first line of regimen. Rasburicase was found to be effective for hyperuricemia.
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PMID:[Gemcitabine-induced tumor lysis syndrome caused by recurrent breast cancer in a patient without hemodialysis]. 2423 8

Rasburicase is a recombinant urate-oxidase enzyme and is a very important medication for tumor lysis syndrome. Methemoglobinemia and hemolysis are known side effects of rasburicase that result from oxidative stress caused by hydrogen peroxide, a byproduct generated during the breakdown of uric acid to allantoin. Patients with G6PD deficiency have a decreased tolerance to oxidative stress and are therefore at a greater risk of hemolysis and methemoglobinemia with rasburicase. Our patient is a 56-year-old Caucasian male with a recent diagnosis of grade 2-3a non-Hodgkin's lymphoma who presented to our emergency department with shortness of breath and dark discoloration of urine. Patient was discharged 36 hours ago from our hospital after he was given a first course of R-CHOP regimen and a dose of rasburicase. On further evaluation, patient was found to have severe anemia with hemolytic picture, hyperkalemia and acute kidney injury. He also had a discrepancy of the transcutaneous saturation (75%) and the saturation in an arterial blood gas value (99%). His methemoglobin level was found to be 11.9%. We were aware that methylene blue is a contraindication in patients with G6PD deficiency but considering patient being Caucasian and low risk for it and his deteriorating respiratory condition, it was decided to offer the treatment and patient received 1 dose of methylene blue which failed to improve his methemoglobinemia. He was also given vitamin C and 8 units of packed red blood cell throughout his stay in the hospital. Patient's hospital course was complicated by ARDS needed to be on mechanical ventilation support for 4 days and acute renal failure secondary to pigment nephropathy and acute tubular necrosis which required a hemodialysis support. Even if rasburicase induced methemoglobinemia and hemolysis are not very common complications, clinicians who prescribe and follow patients should detect this serious complication early and manage it accordingly. Our case can be used as a reminder that patients should be followed closely and given the right instructions on discharge to treat these complications which are associated with severe consequences. It is also vital to assume a diagnosis of G6PD deficiency until proven otherwise in a patient who presents with rasburicase induced hemolysis and avoid administration of methylene blue even if the patient is from a low risk ethnicity for G6PD as in our patient.
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PMID:Rasburicase induced severe hemolysis and methemoglobinemia in a Caucasian patient complicated by acute renal failure and ARDS. 3060 5