Thyroid
Bhavreet Singh, MD (he/him/his)
Resident
Department of Medicine, New York Medical College - Metropolitan Hospital, New York-NY, 10029
New York, New York, United States
Thyrotoxic periodic paralysis (TPP) is an uncommon and potentially life-threatening condition manifesting with hypokalemia and muscle weakness. The degree of hypokalemia is variable, with extremely low values more frequently reported. However, two cases of thyrotoxic normokalemic periodic paralysis (TNPP) have been described. Early treatment initiation during paralysis is important to prevent cardiopulmonary manifestations such as tachyarrhythmias. We present the third case of TNPP, with neurological symptoms resolving after potassium supplementation independent of its serum levels.
Case(s) Description :
A 24-year-old male with a history of Graves’ disease presented to the ED with an episode of quadriparesis and palpitations. Further history revealed previous admissions for similar symptomatology and was found to be hypokalemic and in a thyrotoxic state. During this last presentation, his symptomatology was worse, involving all limbs. Interestingly, laboratories showed low-normal potassium of 3.6 mEq/L (3.5-5.1 mEq/L) in addition to suppressed TSH of 0.01 ulU/ml (0.27-4.20 uIU/mL) and low-normal free of T4 0.7 ng/dl (0.9-1.8 ng/dL). Compared to previous admissions, treatment was driven by symptomatology rather than potassium levels. He received 10 mEq IV potassium chloride, leading to immediate resolution of neurologic symptoms. The dose of methimazole was adjusted, and propranolol was continued at discharge.
Discussion :
TNPP presents as abrupt attacks of weakness and hypokalemia in the setting of hyperthyroidism. The exact mechanism is not yet well understood. However, it has been proposed that around 33% of cases are related to a transient intracellular shift of potassium due to a loss-of-function mutation of two different inward rectifier K channels, Kir2.1 encoded by KCNJ2 gene and Kir2.6 encoded by JCNJ18 gene. The genes are expressed in skeletal muscle but also have an upstream response on the thyroid gland. Some of the documented triggers that can precipitate an attack include a high carbohydrate diet, strenuous exercise, emotional stress, and corticosteroids. Treatment includes four stages: emergency therapy, prevention of recurrence, determination of the cause, and definitive therapy. Supplementing potassium is the first and most crucial step. As in our case, it can be of such benefit in patients with low-normal levels. Another important consideration is that thyroid hormone levels do not directly correlate with the episodes of paralysis, although euthyroid state can lead to resolution of these episodes and should be targeted.