FRI358 A Rare Cause Of SIADH: Leptomeningeal Deposits Metastatic From T-cell Proliferative Disorder

Abstract

Abstract Disclosure: S. Bendaram: None. R. Zielinski: None. V. Kantorovich: None. Introduction: Atypical causes of SIADH, though rare, are important to identify and diagnose in order to optimize timely treatment. Case: Patient is a 51-year-old male with history of obesity and pre-diabetes who presented to the ED with symptoms of generalized weakness and severe fatigue with no antecedent events such as nausea, vomiting, diarrhea, fever or recent illness. He denied lightheadedness or a syncopal episode. History was significant for the use of prednisone for a skin rash in the recent past. Labs were significant for mild hyponatremia with sodium level of 130 mmol/L [136-141] with a low serum osmolality at 273 mOsm/kg and a urine osmolality of 287 mOsm/kg. Further evaluation revealed a low cortisol level of 1.9 ug/dL [6.2 - 19.4]. Repeat cortisol was also low at 1.1 ug/dl. Cosyntropin stimulation test resulted in insufficient response, and iatrogenic adrenal insufficiency was suspected due to prior steroid use. Steroid replacement therapy was initiated with Hydrocortisone. The patient’s ACTH was found to be inappropriately normal at 17pg/ml (6-50). For further evaluation, he underwent MRI Pituitary which revealed leptomeningeal lesions concerning for an infectious, inflammatory, or malignant metastatic process. At this time, he was still hyponatremic with sodium of 130 mmol/L and continued to complain of weakness and not feeling well overall, however denied any neurological symptoms. Repeat labs for hyponatremia showed serum osmolality of 283 mOsm/kg and urine osmolality of 573 mOsm/kg while urine sodium was 100 mmol/L, concerning for mild SIADH. This was managed with fluid restriction initially and then with addition of salt tablets. He underwent lumbar puncture with Cerebrospinal fluid analysis, which did not reveal an infectious etiology. A rheumatological work up for inflammatory cause was negative. Imaging of his chest and abdomen in a search for primary malignancy revealed soft tissue lesions in the abdominal subcutaneous fat. Biopsy of the soft tissue lesions were concerning for a T-cell lymphoproliferative disorder with the absence of typical histological features. Repeat biopsy, flow cytometry and cytogenetic studies were inconclusive, which was suspected to be secondary to the patient receiving steroids prior to the biopsy. Conclusion: This case represents SIADH likely caused by a T-cell lymphoproliferative disorder. Although the biopsies have been inclusive, if the patient has Non-Hodgkin’s T cell lymphoma (NHL), leptomeningeal spread is a known complication of this disorder. The underlying mechanism that we propose behind SIADH in our patient is the leptomeningeal lesion located near the hypothalamus enhancing ADH release. Presentation: Friday, June 16, 2023