SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Hyponatremia can be associated with clinically significant disease and often portends worse outcomes, significant hospital morbidity, increased length of stay and hospital cost.[1] Pseudohyponatremia, may be a culprit in overusing hospital resources and unnecessary workup. Here we present a case of altered mental status (AMS) thought initially to be due to hyponatremia. CASE PRESENTATION: A 58 year-old Caucasian male with a history of glioblastoma multiforme (GBM) treated with resection, radiation and temozolomide, on chronic tube feeds (TF) through gastrostomy tube presented with two weeks of AMS. The spouse reported maintenance of TF but was unsure of how much free water she was actually giving. The patient’s exam was significant for blood pressure of 89/60 mmHg, tachycardia at 101 beats per minute, he had lethargy with response to painful stimuli, significant scleral icterus, dry mucous membranes with no gross motor deficits and unremarkable lung and cardiac exams. His workup was significant for sodium of 120 mmol/L, blood urea nitrogen of 48 mg/dL, creatinine of 1.5 mg/dL, direct hyperbilirubinemia of 47 mg/dL (thought to be due to hepatic injury from temozolomide), aspartate aminotransferase of 1,025 U/L, alanine aminotransferase of 595 U/L, alkaline phosphatase of >1,200 U/L, undetectable ammonia level and a negative drug screen. He was started on intravenous fluids and lactulose without any clinical improvement and minimal change in sodium levels. Further workup showed a serum osmolality of 315 mOs/kg (which pointed towards a pseudohyponatremia picture), triglycerides of 343 mg/dL, cholesterol of 1,652 mg/dL, LDL of 24 mg/dL. Full lipoprotein profile and lipid electrophoresis identified lipoprotein X (LpX) which accounted for the observed pseudohyponatremia. MRI head showed possible recurrent GBM without intracranial shift, thought to be the culprit behind his AMS. DISCUSSION: LpX appears in the serum secondary to cholestasis. It is a result of reflux of bile acid into the serum that combines with albumin to form LpX. It is also composed of small amounts of triglycerides, free cholesterol and apolipoprotein C.[2] Interestingly, LpX was not found to be associated with ischemic heart disease. This is thought to be due to a particle size of 18-25 nm, which prevents it from incorporating into the endothelium. It may even be protective against LDL induced atherosclerosis as it decreases LDL oxidation.[3] Thus, lipid lowering medication may not be needed. It is important to note that LpX may cause a hyperviscosity syndrome and could require lipopheresis. CONCLUSIONS: Our case highlights LpX as a rare cause of pseudohyponatremia and the importance of differentiating between true hyponatremia and pseudohyponatremia to avoid unnecessary workup and therapy that may increase morbidity and length of hospital stay. Physicians should be aware of this entity and include it in future practice. Reference #1: Corona G, Giuliani C, Parenti G, et al. The Economic Burden of Hyponatremia: Systematic Review and Meta-Analysis. Am J Med. 2016;129(8):823-835.e4. doi:10.1016/j.amjmed.2016.03.007 Reference #2: Fellin R, Manzato E. Lipoprotein-X fifty years after its original discovery. Nutr Metab Cardiovasc Dis. 2019;29(1):4-8. doi:10.1016/j.numecd.2018.09.006 Reference #3: Chang PY, Lu SC, Su TC, et al. Lipoprotein-X reduces LDL atherogenicity in primary biliary cirrhosis by preventing LDL oxidation. J Lipid Res. 2004;45(11):2116-2122. doi:10.1194/jlr.M400229-JLR200 DISCLOSURES: No relevant relationships by Youssef Abouleish, source=Web Response Speaker/Speaker's Bureau relationship with Genentech Please note: $5001 - $20000 Added 04/01/2020 by Joshua Sill, source=Web Response, value=Honoraria
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