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Amiodarone-Induced Hypothyroidism Initially Presenting as Decompensated Heart Failure and Hyponatremia

Introduction: Amiodarone is an effective antiarrhythmic, but it is associated with altering thyroid function, ranging from thyrotoxicosis to hypothyroidism. In this study, we discuss amiodarone-induced hypothyroidism (AIH) presenting with hyponatremia and myxedema. Case Presentation: A 75-year-old C...

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Detalles Bibliográficos
Autores principales: Ayesh, Hazem, Burmeister, Cameron, Beran, Azizullah, Akpunonu, Basil
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8265919/
http://dx.doi.org/10.1210/jendso/bvab048.1880
Descripción
Sumario:Introduction: Amiodarone is an effective antiarrhythmic, but it is associated with altering thyroid function, ranging from thyrotoxicosis to hypothyroidism. In this study, we discuss amiodarone-induced hypothyroidism (AIH) presenting with hyponatremia and myxedema. Case Presentation: A 75-year-old Caucasian man with a history of ischemic heart disease with an ejection fraction of 55-60% was seen in the ED with complaints of worsening lower limb edema and shortness of breath. Associated symptoms of constipation, generalized weakness, daytime sleepiness, and increased urinary frequency were noted. He was recently diagnosed with atrial fibrillation with a CHA₂DS₂-Vasc score of 5 and started on amiodarone nine months ago. He weighed 235 lbs with a BMI of 33.85 and vital signs are as follows: blood pressure 90/64, heart rate 64, respiration rate 13, and a temperature of 36.6 °C. Physical examination revealed a well-developed man in mild distress and slightly lethargic, with a palpable thyroid gland, heart sounds revealed an irregularly irregular heart rate, elevated JVD, bilateral rales, and bilateral pitting edema. Labs showed mildly low HB of 11.7, low Na of 125 mmol/L, elevated creatinine at 1.67 mg/dl, low urine osmolality at 270 mOsm/kg, and BNP of 24 with negative troponin. Chest x-ray showed cardiomegaly. TSH was elevated at 93 uIU/mL and low free T4 at less than 0.25 ng/dL with a negative anti-TPO. A diagnosis of amiodarone-induced hypothyroidism was made, and the patient was started on increased furosemide and levothyroxine 25 mcg daily. Significant improvement was noted in mental status, sodium level, and volume status within three days; and the patient was discharged home on 50mcg of levothyroxine. Discussion: This case illustrates the need to constantly investigate the etiology of decompensated heart failure, especially when new medications with potential culprit side effects are noted or suspected. Amiodarone which is helpful in the management of atrial fibrillation has been known to cause thyroid dysfunction as hypo or hyperthyroidism. What is not widely known is that these endocrine dysfunctions can occur just a few weeks after therapy initiation. Conclusion: We recommend that patients who started on amiodarone be monitored for thyroid dysfunction; especially when they present with deterioration in the cardiac function or show symptoms of endocrinopathy.