SAT254 Elevated Vitamin D 1,25-Dioh Leading To The Diagnosis Of Diffuse Large B-cell Lymphoma With Excessive Vitamin D Intake Confounding The Clinical Picture

Disclosure: R. Barai: None. C. Hurtado: None. We present a patient with acute-onset hypercalcemia in the setting of excessive vitamin D intake, found to have elevated vitamin D 1,25-DiOH and PTHrP, eventually resulting in a diagnosis of diffuse large B-cell lymphoma. 76-year-old man with PMH of idiopathic pulmonary fibrosis s/p left lung transplant, CKD secondary to calcineurin inhibitor toxicity, hypothyroidism, HTN, type 2 DM, and OSA presented with progressively worsening fatigue for four weeks, found to be hypercalcemic to 15.3 mg/dL on presentation with low-normal intact PTH, 14 pg/mL. Three weeks prior to admission, patient had normal calcium, 9.9 mg/dL, with sudden increase to 12.8 mg/dL one week prior to admission, which was not treated. Patient reported taking 5,000 IU of vitamin D PO daily for 5 years, which confounded the clinical picture as the etiology was initially thought to be secondary to excessive vitamin D intake in the setting of frankly elevated vitamin D 25(OH)D of 160 ng/mL. Further work-up revealed elevated 1,25-DiOH of 339 pg/mL with elevated PTHrP of 5 pmol/L and low ACE level of <10 U/L, which was inconsistent with vitamin D intoxication and was concerning for malignancy as the etiology of the hypercalcemia. Patient was treated with 4 doses of calcitonin, fluids and 2 low-doses of pamidronate in the setting of AKI on CKD with only modest improvement in hypercalcemia during the hospitalization. Patient was discharged with calcium 11.4 mg/dL. On CT chest, patient was found to have an enlarged R epicardiac lymph node, prompting PET/CT that demonstrated extensive intensely FDG avid nodular thickening of the right pleura and peritoneum with FDG avid thoracic and abdominopelvic lymphadenopathy and two FDG avid liver masses. US-guided biopsy of a peritoneal nodule was consistent with diffuse large B-cell lymphoma (DLBCL). Colonoscopy demonstrated 5 cm cecal mass with DLBCL, and transverse colonic mass with adenocarcinoma. Liver biopsy flow cytometry was consistent with DLBCL. Patient’s calcium has since normalized with further treatments of denosumab, calcitonin, zoledronic acid and treatment of DLBCL with rituximab, high-dose prednisone, and cyclophosphamide with plan for surgical resection of colon adenocarcinoma. It is important to highlight that elevated 1,25-DiOH would not be typical of hypervitaminosis D as the activity of 1-alpha-hydroxylase (the enzyme that converts the inactive form of vitamin D, 25(OH)D, to the bioactive form, 1,25-DiOH) would be low with hypercalcemia. With the elevated 1,25-DiOH and PTHrP, we were concerned for granulomatous disease or malignancy as the etiology, and we recommended investigation for causes of hypercalcemia other than excessive vitamin D intake. The diagnosis of lymphoma was made due to the incongruity of the history of excessive vitamin D intake and the elevated 1,25-DiOH. Hypercalcemia, in our patient’s case, was due to lymphoma-induced vitamin D activation. Presentation: Saturday, June 17, 2023