Abstract: FR-PO688
Severe Hypophosphatemia in a Patient with a Relapsing Lymphoma
Session Information
- Electrolytes and Cancer Trainee Case Reports
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1500 Onco-Nephrology
Authors
- Deng, Xiaoying, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, United States
- Guzman-Suarez, Edgar, Jefferson Hospital, Philadelphia, Pennsylvania, United States
- Yadav, Anju, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, United States
- Gulati, Rakesh, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, United States
Introduction
Hypophosphatemia in cancer patients is commonly ascribed to chemotherapy, renal wasting or malnutrition from anorexia and poor oral intake. We report a case of hypophosphatemia caused by rapid cancer cell proliferation.
Case Description
Hypophosphatemia was observed in a 61-year-old woman with history of marginal zone lymphoma diagnosed in 2017 presenting with fatigue and undetectable phosphate (phos) levels. Her symptoms started 5 days prior with reported decreased oral intake, but no other gastrointestinal symptoms. Blood work showed phos <1 mg/dl; iPTH level was 17. Her medications included Acyclovir 400mg daily and Allopurinol 100mg daily. Her phos further dropped to <0.3 mg/dl on admission. This severe hypophosphatemia required aggressive intravenous phos treatment and simultaneous oral phos supplementation thereafter. 24 hr urinary fraction excretion of phos was only 1.8%, ruling out renal loss of phos, including acyclovir induced phos wasting. Initial white blood count (WBC) was 41 B/L, phos was <0.3 mg/dl, compared to phos of 3.3 mg/dl with WBC of 0.9 B/L a week prior to this admission. She then developed hyperphosphatemia upon re-initiation of chemotherapy, after repeated computerized tomograhy scan and flow cytometry confirmed lymphoma relapse. She received 4 days of Dexamethasone where the hypophosphatemia converted to hyperphosphatemia, likely from tumor lysis, then further worsened by chemotherapy. Her phos peaked at 14.8 mg/dl. Acyclovir was resumed and it did not cause recurrent hypophosphatemia. A similar hypophosphatemia-hyperphosphatemia pattern was also observed in her previous hospitalization, and correlated with her WBC (Figure 1).
Discussion
The hypophosphatemia correlated with hyperproliferation of cancerous cells. Therefore, hypophosphatemia might be a surrogate biomarker of recurrence of rapidly proliferating hematological malignancy. Phos levels can serve as an excellent adjuvant, widely available, non-invasive and cost-effective biomarker.