SUN-801 Hypercalcemia Associated Posterior Reversible Encephalopathy Syndrome: A Rare Presentation of Lung Malignancy

Abstract Disclosure: V. Leong Shi Ying: None. L.S. Fen: None. H. Liew: None. Posterior reversible encephalopathy syndrome (PRES) is characterized by acute neurological presentation such as encephalopathy, seizures, visual disturbances, headache and distinctive neuroimaging findings of symmetrical distribution of parieto-occipital vasogenic edema. We describe a rare case of PRES in a patient presented with severe hypercalcemia as the first manifestation of presumed metastatic lung malignancy.A 62-year-old Chinese man with no past history of hypertension, presented with slurred speech and generalized weakness. His calcium level was markedly elevated at 3.82 mmol/L [2.15 - 2.50 mmol/L] with normal parathyroid hormone level of 1.3pmol/L [0.8 - 6.8 pmol/L]. Non contrast brain magnetic resonance imaging (MRI)revealed scattered subcortical T2 hyperintensities in the supra and infratentorial brain and multiple skull vault lesions suspicious for metastases. Computed tomography of the thorax, abdomen and pelvis showed left hilar pulmonary mass with widespread abdominal and bone metastases. Initial treatment included aggressive intravenous hydration, subcutaneous calcitonin and intravenous zoledronic acid (ZA). On day 2, he developed left gaze deviation, nystagmus, and leftward head version, suggestive of non-convulsive seizure. MRI brain with contrast demonstrated T2/FLAIR hyperintensities in the bilateral parieto-occipital, right temporal lobes, bilateral thalami, pons and cerebellar likely due to PRES. Electroencephalogram showed severe encephalopathy and seizure. Further workup showed a normal PTH-related peptide level of 1.4 pmol/L [< 4.2pmol/L], a low 1,25-dihydroxy vitamin D level of 10 pg/mL[18-72pg/ml] and myeloma panel was negative. His serum calcium corrected to 2.35mmol/L four days after ZA administration. Due to the rapid downward trajectory in calcium levels, prophylactic treatment with cholecalciferol, calcium carbonate, and calcitriol were initiated. The nadir serum calcium was 2.09mmol/L at ten days since ZA administration, normalizing to 2.24mmol/L the next day and subsequently stabilised. Interval brain imaging showed partial resolution of the PRES changes. His mentation improved and no further seizure activity was observed. Ultimately, the patient’s family declined bronchoscopy for histological confirmation. He was transitioned to hospice care and passed away. Hypercalcemia, a rare cause of PRES, may induce brain edema through vasospasm and proinflammatory-cytokine-mediated disruption of the blood-brain barrier. This case highlights the importance of early recognition of PRES in the setting of hypercalcemia and early onset of bisphosphonate-induced hypocalcemia when correcting malignant hypercalcemia in patient with concomitant vitamin D insufficiency and acute kidney injury. Presentation: Sunday, July 13, 2025