Abstract

Being diagnosed with cancer comes with numerous challenges and tumor lysis syndrome (TLS) is just one of many complications a cancer patient may be faced with while undergoing treatment. This is considered an oncologic emergency that occurs when large amounts of tumor cells rapidly break down and release phosphate, potassium, lactate dehydrogenase, and nucleic acids into the bloodstream. The majority of cases are associated with treatment in acute lymphoblastic leukemia and high-grade lymphoma, although it can occur in other instances of cancer with a large tumor burden, high proliferative rate, and even rarer, may occur spontaneously in the absence of those features. A 55-year-old male with a past medical history of COPD, coronary artery disease status post CABG, heart failure with reduced ejection fraction, type 2 diabetes mellitus, hypothyroidism, and multiple myeloma was transferred to our facility for further workup of acute encephalopathy and severe hypercalcemia. He was initially taken to an outside hospital by family members after they noticed he became disoriented and lethargic over the course of a couple of days. His family also noticed he was gradually becoming weaker and experienced a 30-pound unintentional weight loss over the course of the month and a half following his discharge from the hospital after undergoing CABG. Labs were drawn upon admission and were significant for a critical calcium level of 16.4 mg/dL, PTH 6.7 pg/mL, creatinine 2.49 mg/dL, and ammonia 105.0 uMOL/L. Myeloma labs showed M spike of 4.7 g/dL, IgA of 6147 mg/dL with Kappa light chains of 1086 mg/L with a ratio of 221. When asked about his multiple myeloma diagnosis and treatment he was unable to provide much information, but our local oncology team was able to contact his home oncologist who informed us he had been diagnosed 2 years prior to this admission. He underwent a bone marrow transplant but chose to forgo any further treatment and was not following up regularly with his oncologist. The hypercalcemia was attributed to his malignancy and treated on arrival to the hospital with IV fluids, zoledronic acid, and calcitonin with a favorable response. He was continued on calcitonin until resolution of severe, symptomatic hypercalcemia. A uric acid level ordered the following morning came back at a critical value of 16.2 mg/dL. At that time, he was diagnosed with spontaneous tumor lysis syndrome and was immediately treated with 6 mg rasburicase followed by daily 300 mg allopurinol. Chemotherapy was initiated while inpatient and he received two rounds of bortezomib/cyclophosphamide therapy prior to discharge. He remained hospitalized for nine days with significant clinical improvement and on the day of discharge labs showed a calcium level of 6.6 mg/dL, improvement in renal function with creatinine down to 2.09 mg/dL, and uric acid level 4.5 mg/dL. He was set up with close outpatient follow-up with his home oncologist and plans to continue this chemotherapy regimen. Although not uncommon, in more recent years there has been a trend downward in the incidence of tumor lysis syndrome thanks in part to better prevention methods and early recognition. For multiple myeloma specifically, the risk of tumor lysis syndrome is actually less than one percent and the risk of spontaneous TLS is likely even rarer. The actual incidence of developing spontaneous TLS, in general, is difficult to predict and in multiple myeloma other than a few case reports, it has not been widely documented. The goal of sharing this case is to contribute to the information already known about this condition and hopefully encourage others to share similar cases to improve recognition for earlier treatment and lower morbidity and mortality associated with spontaneous TLS in the future.

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