8612 Thyrotoxic Periodic Paralysis in Marine-Lenhart Syndrome

Abstract Disclosure: I.A. Guatemala Funes: None. A. Tasnim: None. Y. El-Soufi: None. T. Zahedi: None. F. Zhang: None. Introduction: Thyrotoxic periodic paralysis (TPP) is a form of periodic muscle weakness that can be present in any form of hyperthyroidism. Patients present with progressive muscle paralysis as a result of acute hypokalemia. It is commonly seen in the Asian population, males more than females. We report a rare case of an Afro-American patient with TPP who also has a suspected coexistence of Graves' disease and functioning thyroid nodule, known as Marine-Lenhart syndrome. Case Report: The patient is a 31-year-old African American man with no past medical history, who presented with progressive generalized weakness predominantly in the extremities with grade 1 muscle strength after a meal high in carbohydrates. CT head, CT angiogram head neck, and MRI spine were unremarkable. Labs revealed hypokalemia 1.8 mmol/L, suppressed TSH < 0.015 uIU/mL, elevated Free T4 2.36 ng/dL, T3 13.5 pg/mL, thyroid stimulating immunoglobulin (TSI) 2.43 IU/L, thyrotropin receptor autoantibodies (TRAb) 2.03 IU/L, and thyroid peroxidase antibodies (TPO) 323 IU/mL. Thyroid ultrasound showed a markedly heterogeneous thyroid gland with bilateral multiple solid nodules, which confirmed the coexistent nodular goiter in Graves' disease. His symptoms improved after receiving Methimazole and electrolytes replacement. However, patient did not take Methimazole after discharge due to abnormal liver function. Five months later, he was readmitted with the similar presentation of progressive weakness and unable to stand up. Labs revealed hypokalemia 2.3 mmol/L, TSH 0.000 uIU/mL, and elevated Free T4 2.41 ng/dL, which suggested TPP. His paralysis resolved with treatment and patient was discharged with a radioactive iodine (RAI) uptake test scheduled to define the diagnosis but he was lost to follow-up. Discussion: The underlying mechanism of TPP is not completely understood. The overstimulation of the NA+/K+ ATPase pumps due to a hyperadrenergic state and elevated insulin level has been described as one of the major reasons along with a decrease in the outward potassium channels. A high carbohydrate intake and demanding exercise are some of the factors that can trigger the episode. The mainstay of therapy for TPP is controlling the hyperthyroidism and potassium replacement which usually resolve the paralysis. Proper differential diagnosis of hyperthyroidism such as Marine-Lenhart syndrome will benefit patients to identify the optimum long-term therapy with thioamides, surgery, or RAI ablation. Presentation: 6/1/2024