Pitting edema was noted in the lower extremities, and mounding phenomena were observed in his arms and legs. Thyroid enlargement was not clearly observable. His voice was still hoarse, and his eyebrows were thin. Therefore, we suspected clinical hypothyroidism.Ī physical examination revealed a body temperature of 36.2☌, blood pressure of 126/87 mmHg, pulse rate of 81 beats/min, and respiration rate of 18 breaths/min. A blood test was performed at a different hospital, showing a serum thyroid-stimulating hormone (TSH) level of 93.06 μIU/mL. In addition, his voice had become hoarse. Moreover, it was noticed that he asked the same questions repeatedly and could not choose clothes according to the weather 2 months before admission. He also experienced abnormal sensations in his fingers and plantar surfaces.
Six months before his admission, the patient had noticed himself wandering while walking, accompanied by swelling of his face and legs. Subsequently, 600 mg/day gabapentin was started at 2 years after the accident.
Conventional cranioctomy had been performed at the time of the accident, and he was also prescribed 200 mg/day phenytoin at this time. He had a traumatic and acute subdural hematoma following an accident and developed post-traumatic seizures approximately 10 years before his admission. 2 Case presentationĪ 75-year-old man was admitted to our hospital because of memory impairment and lethargy. Our case suggests that administration of gabapentin and/or phenytoin can lead to symptomatic hypothyroidism. Here, we report a patient who developed neurologic and systemic symptoms because of hypothyroidism induced by AEDs. Indeed, clinically significant thyroid disorders are reported to occur very rarely following AED use, including after phenytoin or gabapentin administration. However, in most cases, patients treated with AEDs present with subclinical hypothyroidism. Thyroid abnormalities have been reported in one-third of patients on AEDs. Various drugs, including amiodarone, lithium, tyrosine kinase inhibitors, interferon-alpha, thalidomide, monoclonal antibodies, and antiepileptic drugs (AEDs), are known to be associated with the development of hypothyroidism. Therefore, clinicians should be aware of the association between anticonvulsants and symptomatic hypothyroidism. AEDs can not only cause asymptomatic thyroid hormone abnormalities but also clinically observable hypothyroidism. In this case, the patient's hypothyroidism was assumed to result from different mechanisms of the 2 AEDs leading to thyroid hormone reduction. His symptoms markedly and promptly improved alongside continued antiepileptic therapy. The patient was treated with replacement therapy (levothyroxine 25 μg/day). Phenytoin and/or gabapentin were strongly suspected as causing his hypothyroidism. Negative thyroid-related autoantibody tests and the lack of goiter excluded the possibility of Hashimoto disease.
#Hypothyroidism medication free
The patient had low free T4 (0.21 ng/dL) and high TSH (113.2 μIU/mL), which indicated hypothyroidism. He had been administered phenytoin and gabapentin for the treatment of symptomatic traumatic epilepsy 8 years before.
Patient concerns:Ī 75-year-old man experienced neurologic symptoms including memory impairment, ataxic gait, sensory polyneuropathy and myopathy, lethargy, and edema of the face and lower extremities.
Severe symptomatic hypothyroidism following AEDs is rarely reported in the literature. In most cases, AED-induced hypothyroidism is subclinical and indicated only by abnormalities of free thyroxine (T4) and/or thyroid-stimulating hormone (TSH) levels. Īntiepileptic drugs (AEDs) are one of the causative drugs of drug-induced hypothyroidism. The work cannot be changed in any way or used commercially without permission from the journal.
#Hypothyroidism medication license
This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The authors report no conflicts of interest. ∗Correspondence: Kazuhiro Ishii, Department of Neurology, Division of Clinical Medicine, Faculty of Medicine, University of Tsukuba, Tennodai 1-1-1, Tsukuba, Ibaraki305-8575, Japan (e-mail: ).Ībbreviations: AED = antiepileptic drug, CK = creatine kinase, CYP = cytochrome P450, GABA = gamma-aminobutyric acid, MMSE = mini-mental state examination, MRI = Magnetic resonance imaging, T3 = triiodothyronine, T4 = thyroxine, Tg = thyroglobulin, TPO = thyroid peroxidase, TRH = thyrotropin-releasing hormone, TSH = thyroid-stimulating hormone, UGT = uridine diphosphate glucuronosyltransferase, VPA = valproic acid. Department of Neurology, Division of Clinical Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
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