Endocr Pract. 2020 Feb;26(2):197-206. doi: 10.4158/EP-2019-0374. Epub 2019 Oct 25.
Hypothyroidism is not commonly considered a cause of hyperkalemia. We previously reported that hyperkalemia was observed mainly in elderly patients treated with renin-angiotensin-aldosterone system (RAS) inhibitors when levothyroxine treatment was withdrawn for the thyroidectomized patients with thyroid carcinoma to undergo radioactive iodine treatment. Here, we investigated whether acute hypothyroidism causes hyperkalemia in patients who were not treated with RAS inhibitors. We also investigated factors influencing potassium metabolism in hypothyroid patients. We conducted a single-center, prospective cohort study of 46 Japanese patients with thyroid carcinoma undergoing levothyroxine withdrawal prior to radioiodine therapy. All patients were normokalemic before levothyroxine withdrawal. Blood samples were analyzed 3 times: before, and at 3 and 4 weeks after levothyroxine withdrawal. We investigated factors that may be associated with the elevation of serum potassium levels from a euthyroid state to a hypothyroid state. None of the patients developed symptomatic hyperkalemia. The mean serum potassium level was significantly higher at 4 weeks after levothyroxine withdrawal compared to baseline. The serum sodium levels, the estimated glomerular filtration rate (eGFR), and the plasma renin activity (PRA) decreased significantly as hypothyroidism advanced. In contrast, the plasma levels of adrenocorticotropic hormone, cortisol, aldosterone, and antidiuretic hormone were not changed, while serum thyroid hormone decreased. At 4 weeks after their levothyroxine withdrawal, the patients' serum potassium values were significantly correlated with the eGFR and the PRA. Acute hypothyroidism can cause a significant increase in the serum potassium level, which may be associated with a decreased eGFR and decreased circulating RAS. = adrenocorticotropic hormone; = antidiuretic hormone; = adenosine triphosphatase; = estimated glomerular filtration rate; = glycated hemoglobin; = potassium; = sodium; = plasma renin activity; = renin-angiotensin-aldosterone system; = thyroxine; = thyroid-stimulating hormone.
甲状腺功能减退症通常不被认为是高钾血症的原因。我们之前报道过,当甲状腺癌患者在接受放射性碘治疗前进行甲状腺切除术时,停用左甲状腺素治疗后,主要观察到老年患者出现高钾血症。在这里,我们研究了未接受肾素-血管紧张素-醛固酮系统(RAS)抑制剂治疗的患者中,急性甲状腺功能减退症是否会导致高钾血症。我们还研究了影响甲状腺功能减退症患者钾代谢的因素。
我们进行了一项单中心前瞻性队列研究,纳入了 46 名日本甲状腺癌患者,这些患者在接受放射性碘治疗前停用了左甲状腺素。所有患者在停用左甲状腺素前血钾正常。采集了 3 次血样:停用左甲状腺素前、停用左甲状腺素后 3 周和 4 周。我们研究了从甲状腺功能正常状态到甲状腺功能减退状态时,可能与血清钾水平升高相关的因素。
无患者出现症状性高钾血症。与基线相比,停用左甲状腺素后 4 周时血清钾水平显著升高。随着甲状腺功能减退的进展,血清钠水平、估算肾小球滤过率(eGFR)和血浆肾素活性(PRA)显著降低。相反,促肾上腺皮质激素、皮质醇、醛固酮和抗利尿激素的血浆水平没有变化,而血清甲状腺激素水平降低。在停用左甲状腺素后 4 周时,患者的血清钾值与 eGFR 和 PRA 显著相关。
急性甲状腺功能减退症可导致血清钾水平显著升高,这可能与 eGFR 降低和循环 RAS 减少有关。