SAT221 A Case Of Severe Hypocalcemia After Treatment Of Plasma Cell Leukemia
Authors: Tabassum Humera , Goettemoeller Travis , Jason Epstein Eric , Cooper Dennis 
Published: October 2023

Disclosure: H. Tabassum: None. T. Goettemoeller: None. E.J. Epstein: None. D. Cooper: None.

Background: Hypocalcemia has been well described in cancer patients receiving skeletal protecting medications (denosumab and to a lesser extent zoledronic acid) and in patients with osteoblastic metastasis (prostate or breast cancer). A rare cause of hypocalcemia in malignancy has been described following treatment of a multiple myeloma (MM) patient with a high volume of metastatic lytic lesions, with a mechanism thought to be secondary to rapid bone remineralization. Here we report a case of severe and protracted hypocalcemia resulting in a seizure occurring after treatment of plasma cell leukemia. Clinical Case: A 58-year-old male with plasma cell leukemia IgG kappa type and innumerable osteolytic lesions underwent chemotherapy treatment with cyclophosphamide-bortezomib-dexamethasone followed by lenalidomide and carfilzomib-daratumumab-dexamethasone. Prior to treatment initiation, calcium, phosphorus, and magnesium levels were within normal range. No denosumab or bisphosphonates were given. The patient became hypocalcemic within three weeks of initiation of chemotherapy, and he was started on calcium supplementation without improvement. The patient presented to the ED after an episode of seizure, and was found to have severe hypocalcemia with calcium 5.6 mg/dL (N: 8.5 - 10.5 mg/dL), ionized calcium 0.78 mmol/L (N: 1.10 - 1.35 mmol/L), albumin 3.5 g/dL (3.5 - 5.0 g/dL), magnesium &lt;1.0 mg/dL (N: 1.7 - 2.8 mg/dL), phosphate 3.7 mg/dL (N: 2.5 - 4.5 mg/dL), 25-hydroxy Vitamin D 21.5 ng/mL (N 30.0 - 60.0 ng/mL), and PTH 292.7 pg/mL (N: 20.0 - 80.0 pg/mL). IgG levels had declined from 3,417 mg/dL (N: 700 - 1600 mg/dL) prior to chemotherapy to 870 mg/dL, consistent with a good response to treatment. The patient’s seizure prior to admission was thought to be secondary to severe hypocalcemia and hypomagnesemia. Treatment was initiated with an IV calcium gluconate drip, IV magnesium, calcium carbonate 1,000 mg three times a day orally, and calcitriol 0.25 mg twice a day with improvement in corrected calcium to 8.4 mg/dL, magnesium 1.9 mg/dL and PTH level of 145.7 pg/mL. The patient had no further seizures. He was discharged with calcium carbonate 1,500 mg three times a day, calcitriol 0.25 mg twice daily, and magnesium oxide 400 mg daily. Conclusion: Rapid remineralization of bone in a patient with MM and high volume of lytic lesions causing severe hypocalcemia has been previously described in a patient with undetectable PTH. In our case, the cause of hypocalcemia was thought to be multifactorial; low magnesium and Vitamin D may be implicated, but a rapid uptake of calcium and magnesium into bone, with a profound release of ineffective PTH seems a likely reason for the dramatic protracted and severe course of hypocalcemia. This case offers insights into an extremely rare presentation of hypocalcemia with a mechanism not too dissimilar to hungry bone syndrome.

Presentation: Saturday, June 17, 2023