SUN-375 Graves’ Disease Complicating Gitelman Syndrome

Abstract Disclosure: T. Hinshaw: None. H. Woomer: None. A. Haider: None. Background: Thyrotoxic periodic paralysis (TTP) is an acquired painless paralysis characterized by high thyroid hormone levels and hypokalemia. Gitelman syndrome (GS) is an autosomal recessive disorder that causes hypokalemia, hypomagnesemia, and metabolic alkalosis. We present a case of worsening hypokalemia from new onset hyperthyroidism in a patient with well compensated GS. Clinical Case: An 18-year-old white female with history of GS (biallelic mutation of SLC12A3) and recently diagnosed Graves’ disease presented with three-week history of bilateral lower extremity weakness that acutely worsened her ability to ambulate the morning of presentation. On exam, she was unable to move her lower extremities against resistance. She was found to be hypokalemic (K 2.0 mmol/L) with hypomagnesemia (Mg 1.3 mg/dL) despite adherence to home medications of potassium chloride 140mEq total daily and magnesium oxide 2800mg total daily. She was admitted for IV electrolyte replacement. Patient had been admitted two months prior for similar concerns; one month ago, she had been diagnosed with Graves’ disease (TSH <0.0008 ulU/mL, free T4 2.72 ng/dL, and TRAb 22.65 IU/L) and started on methimazole 15mg daily and propranolol 20mg TID. Upon admission, her thyroid levels remained uncontrolled (TSH <0.0008 ulU/mL, free T4 2.32 ng/dL), prompting endocrinology consultation. Given patient had previously been stable on electrolyte replacement for many years, patient’s worsening hypokalemia and lower extremity weakness was likely due to hyperthyroidism. Methimazole was increased to 30mg daily. Two days later, the patient’s lower extremity weakness improved, and patient was able to ambulate independently prior to discharged. Free T4 decreased to 2.17 ng/dL and potassium and magnesium levels were within normal limits. She was continued on new methimazole dose of 30mg daily; no changes to home electrolyte replacement regimen were made. At outpatient follow up one week later, patient’s weakness had not recurred, and electrolyte levels remained within normal limits.Clinical Lesson: The incidence of concurrent thyroid dysfunction in GS is higher than the general population. The exact reason is not defined, however SLC12A3 gene is not associated pathogenesis of thyroid dysfunction. Electrolyte abnormality, including severe magnesium deficiency, is associated with the recurrence of thyroid dysfunction. TTP is thought to cause hypokalemia due to the rapid shift of potassium into cells due to thyroxine-induced activation of Na+/K+-ATPase channels. GS interferes with NaCl reabsorption in the distal convoluted tubule, leading to hypokalemic metabolic acidosis. Despite a previously stable home electrolyte regimen for patient’s GS, her potassium levels became uncontrolled shortly after she was diagnosed with Graves’ disease and did not normalize until treatment of her thyroid disease was optimized. Presentation: Sunday, July 13, 2025