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Abstract: SA-PO468

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) Secondary to Untreated Parkinson Disease

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical

Authors

  • Yaseen, Najjar, Albany Medical Center, Albany, New York, United States
  • Awad, Mina, Albany Medical Center, Albany, New York, United States
  • Faddoul, Geovani, Albany Medical Center, Albany, New York, United States
Introduction

Hyponatremia is the most common electrolyte disorder associated with neurological conditions and is mediated by excess release of antidiuretic hormone. The etiology can range from a straightforward SIADH to the poorly understood mechanism of cerebral salt wasting. Whereas acute intracranial process such as acute stroke, intracranial bleeding or tumor are typical etiologies of SIADH, neurodegenerative diseases such as Parkinson’s disease or ALS have not been known to be associated SIADH. However, SIADH has been reported as a side effect of anti-Parkinson medication e.g. Levodopa/Carpidopa. Parkinson’s disease per se has not been known to be associated by SIADH and hyponatremia. We present a case of hyponatremia due of SIADH in the setting of untreated Parkinson.

Case Description

A 71-yo male patient with DM II and hypothyroidism presented to the hospital with progressive confusion, slow speech and severe fatigue over las few days accompanied with sluggish body movements for few months. On exam, he appeared to be euvolemic. Neurological exam revealed mild arm rigidity, bradykinesia, resting tremors, and stiff gait. Initial blood work showed hypo-osmolar hyponatremia (sodium 122 mEq/L, serum osmolarity 275 mOsm/Kg, uric acid 2.3 mg/L, TSH 3.5 UIU/mL, AM cortisol 24 UG/dL). Urine studies showed (urine sodium: 92 mEq/L, osmolarity 672 mOsm/Kg). A Brain MRI did not show any structural abnormality. CT chest showed localized infiltrate. Initially SIADH was thought to be due to pulmonary process. After starting him on fluid restriction of 1.5L/day and urea 15 mg BID, sodium improved gradually to 133 mEq/L on discharge. Urine osmolality continued to ranges 700-800 mOsm/Kg. Active pulmonary process was ruled out by pulmonologist. Parkinsonism was confirmed by outpatient neurology who started Carbidopa/Levodopa. As extrapyramidal symptoms improved with Carbidopa/Levodopa, urine osmolality improved to 400 mOsm/Kg. Successfully, sodium level was maintained between 135-137 while being off urea and fluid restriction. He was diagnosed with new-onset SIADH and extrapyramidal symptom.

Discussion

This case demonstrated an association of SIADH and untreated Parkinson’s disease. In contrary to literature, SIADH resolved with anti-Parkinson treatment which supports Parkinson’s disease as a causal mechanism. As dose increased of anti-Parkinson’s agent, urine osmolality improved and extrapyramidal symptoms resolved.