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Table of Contents
LETTER TO THE EDITOR
Year : 2019  |  Volume : 33  |  Issue : 4  |  Page : 222-224

A levothyroxine-related paresthesia in a middle-aged female patient after receiving hemithyroidectomy


Department of Psychiatry, Ministry of Health and Welfare Hengchun Tourism Hospital, Pingtung, Taiwan

Date of Submission09-May-2019
Date of Decision01-Jul-2019
Date of Acceptance28-Sep-2019
Date of Web Publication23-Dec-2019

Correspondence Address:
Horng-Maw Chen
No. 188, Hengnan Road, Hengchun Township, Pingtung County 946
Taiwan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/TPSY.TPSY_41_19

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How to cite this article:
Chen HM. A levothyroxine-related paresthesia in a middle-aged female patient after receiving hemithyroidectomy. Taiwan J Psychiatry 2019;33:222-4

How to cite this URL:
Chen HM. A levothyroxine-related paresthesia in a middle-aged female patient after receiving hemithyroidectomy. Taiwan J Psychiatry [serial online] 2019 [cited 2020 Jan 25];33:222-4. Available from: http://www.e-tjp.org/text.asp?2019/33/4/222/273862



Paresthesia is a neuropathic pain, that is reported as pins-and-needle or tingling sensation, and may arise from an abnormality in the somatosensory system and other pain-processing brain regions [1]. Here, I present the case of a patient who had paresthesia during levothyroxine treatment.


  Case Report Top


The patient was a 57-year-old female nurse. When she was 49 years old, she had a neck mass found accidentally in her routine clinic visits for type 2 diabetes mellitus. She did not have any symptom before and after the neck mass was noted. In ultrasonography, this mass was found to be 2.95 cm × 2.33 cm in size, located in the largest section in the lower pole of the right side of the thyroid gland, with a well-defined margin. The diagnosis was a nontoxic thyroid nodule after a pathological examination.

Seven years later, the size of the patient's nodule did not cause any discomfort, but she decided to have it removed. Before the surgical removal, she was in euthyroid state confirmed in February 2017, with the serum levels of triiodothyronine (T3, normal reference: 0.8–2 ng/mL), thyroxine (T4, normal reference: 5.1–14.1 μg/dL), and thyroid-stimulating hormone (TSH, normal reference: 0.27–4.2 μIU/mL) being 1.24 ng/mL, 9.1 μg/dL, and 0.865 μIU/mL, respectively. Besides, the serum level of thyroglobulin antibody was lower than 20 IU/mL (normal reference: < 40 IU/mL), and the serum level of the microsomal antibody was lower than 10 IU/mL (normal reference: < 35 IU/mL). The result of antinuclear antibody test was 1: 40 (normal reference: 1: 40) in March 2017. The autoimmune thyroid diseases were not favored for the diagnosis. An otorhinolaryngologist did the right side hemithyroidectomy with dissections of lymph nodes, and parathyroidectomy, as well as with parathyroid autotransplantation on July 14, 2017. Then, she started to take levothyroxine 0.1 mg/day to prevent hypothyroidism. But she got paresthesia over four limbs after taking levothyroxine in the same day. She continued regular levothyroxine treatment in spite of her persisting paresthesia.

The patient's paresthesia was presented itself everyday as tingling, persisting all day to cause huge distress. The pain score in visual analog scale (VAS, maximum score: 10) reached 7–9. Three weeks later, her paresthesia was still persisting. The result of the laboratory examination showed hyperthyroidism on August 4, 2017, with TSH and free T4 (fT4, normal reference: 0.93–1.7 ng/dL) being 0.018 μIU/mL and 2.03 ng/dL, respectively, and the glycated hemoglobin was 5.8%. This was the first time to check thyroid state in laboratory tests of serum level after the hemithyroidectomy. The otorhinolaryngologist titrated down levothyroxine to 0.05 mg/day, and the VAS was decreased to 5–6. But she still could not tolerate the all-day tingling. She visited a neurological clinic in September 2017. The neurological examination revealed nonspecific finding except for the paresthesia. She also received electrodiagnostic study, and it was normal in finding. Diabetic neuropathy and fibromyalgia were both ruled out. Then, she was suggested to take duloxetine 60 mg/day by the neurologist.

After patient's taking duloxetine, the pain became tolerable with VAS reducing to 1–2. Its pain frequency was reduced to less than three times per week, and it persisted about only 7 h/day at most. She was surprised at the effect and did not discontinue it. In January 2018, the laboratory tests revealed a euthyroid state, with TSH and fT4 being 1.99 μIU/mL and 1.39 ng/dL, respectively, but the paresthesia still existed.

Because of her relocation, the patient visited a psychiatric clinic for prescription of duloxetine. During the following 15 months, the psychiatrist did not find any solid diagnosis according to the DSM-5 criteria, while she was still regularly taking duloxetine 60 mg/day and levothyroxine 0.05 mg/day [Figure 1].
Figure 1. The course of paresthesia. Above the time axis is the paresthesia symptom course: the thickest line means the severest symptom, the median line means symptom decreasing in intensity, and the thinnest and dotted line means symptom even decreasing in intensity and frequency. Under the time axis is the levothyroxine treatment course: the linear box filled with black means dosage of 0.1 mg/day and the linear box with arrow filled with gray means dosage of 0.05 mg/day. Under the levothyroxine treatment course is the duloxetine treatment course: the dosage was fixed at 60 mg/day throughout the course. The patient continued with both two medications. The double oblique lines means that some time elapsed were omitted to focus on important events of this patient. T3, triiodothyronine; T4, thyroxine; fT4, free thyroxine;
TSH, thyroid-stimulating hormone; VAS, visual analog scale; y/o, years old.


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  Comment Top


The incidence of hypothyroidism is ranged from 5% to 49% with most between 15% and 30% after hemithyroidectomy [2]. But the patient did not have hypothyroidism. Levothyroxine can be used as a treatment or prophylaxis for hypothyroidism, but it has the potential to cause hyperthyroidism. But the prevalence levels of levothyroxine-related and hyperthyroidism-related paresthesia are both unknown [1],[3]. This case report is the first to describe the levothyroxine-related paresthesia and its treatment course.

The patient did not receive laboratory test for thyroid function after she started to take lower dose of levothyroxine on August 4, 2017, until January 2018, so the hyperthyroidism course was not checked to correlate with paresthesia course [Figure 1]. Nevertheless, the paresthesia still existed in a euthyroid state, so the levothyroxine is highly suspected to be related with her paresthesia. In addition, the levothyroxine-related paresthesia was dose dependent in this patient [Figure 1]. Besides, there is currently no report about duloxetine's effect to thyroid hormone change, so the effect of duloxetine to paresthesia may not be through the change of the thyroid state.

Among patients with hyperthyroidism, the motor system abnormality is more noticeable in published articles compared with sensory system abnormality [3],[4]. But Duyff et al. in a prospective cohort study indicated that there may be an underestimate of sensory abnormality among patients with hyperthyroidism in previous studies. Besides, they also reported that the sensory abnormality occurs soon after the occurrence of hyperthyroidism, but it is also reduced if hyperthyroidism has been subsided. The time course was compatible to that in the patient [Figure 1]. Her paresthesia arose within several hours after taking levothyroxine and improved in the same day of duloxetine treatment. According to the study done by Duyff et al., the electrodiagnostic studies have shown more neuropathic condition than the clinical complaints about sensory abnormality [3]. Contrarily, my patient had a normal electrodiagnostic study. This finding suggests that levothyroxine-related paresthesia might be attributed to an abnormality of central nervous system, rather than an abnormality of peripheral nerves.

Levothyroxine can increase T3 biological activity, and may further enhance neurogenesis in hippocampus, which is associated with pain processing. Levothyroxine might cause paresthesia directly through this pathway or indirectly because hippocampus can modulate the pain processing with circuit connecting to dorsolateral prefrontal cortex (DLPFC) [5],[6],[7],[8],[9]. The paresthesia is possibly improved due to the change of pain processing in the cortex by duloxetine through increased dopamine transmission in DLPFC [9],[10].

Further study is needed to clarify the time course, mechanism of levothyroxine-related paresthesia, as well as the relationship between it and hyperthyroidism-related paresthesia. Besides, more studies are also needed to confirm the treatment effect of duloxetine to this symptom and to figure out whether placebo effect can influence the effect of duloxetine. In my opinion, understanding of the levothyroxine-related paresthesia can help clinicians improve post-(hemi-)thyroidectomy care quality and the patients' quality of life. (This case study was approved by the institutional review board of Jianan Psychiatric Center for publication (protocol number = 19-013, approval date = March 25, 2019) with the requirement of obtaining signed informed consent from the patient.).


  Financial Support and Sponsorship Top


Nil.


  Conflicts of Interest Top


The author declares no potential conflicts of interest.



 
  References Top

1.
Roper AH, Samuel MA, Klein JP: Adams and Victor's Principles of Neurology. 10th ed. St. Louis, USA: McGraw-Hill Education, 2014: 128-67.  Back to cited text no. 1
    
2.
Lee J, Chung WY: Hypothyroidism after hemithyroidectomy: incidence, risk, factors, natural history and management. In: Springer D, (ed): Hypothyroidism: Influences and Treatments. Rijeka, Croatia: In-Tech, 2012: 35-50.  Back to cited text no. 2
    
3.
Duyff RF, Van den Bosch J, Laman DM, et al.: Neuromuscular findings in thyroid dysfunction: a prospective clinical and electrodiagnostic study. J Neurol Neurosurg Psychiatry 2000; 68: 750-5.  Back to cited text no. 3
    
4.
Chang LH: Thyrotoxicosis presenting as a movement disorder. Taiwan J Psychiatry 2007; 21: 225-9.  Back to cited text no. 4
    
5.
Mullur R, Liu YY, Brent GA: Thyroid hormone regulation of metabolism. Physiol Rev 2014; 94: 355-82.  Back to cited text no. 5
    
6.
Brent GA: Mechanisms of thyroid hormone action. J Clinic Invest 2012; 122: 3035-42.  Back to cited text no. 6
    
7.
Remaud S, Gothié JD, Morvan-Dubois G, et al.: Thyroid hormone signaling and adult neurogenesis in mammals. Front Endocrinol (Lausanne) 2014; 5: 62.  Back to cited text no. 7
    
8.
Liu MG, Chen J: Roles of the hippocampal formation in pain information processing. Neurosci Bull 2009; 25: 237-66.  Back to cited text no. 8
    
9.
Ong WY, Stohler CS, Herr DR: Role of the prefrontal cortex in pain processing. Mol Neurobiol 2019; 56: 1137-66.  Back to cited text no. 9
    
10.
Stahl SM: Stahl's Essential Psychopharmacology: Neuroscientific Basis and Practical Application. 4th ed. New York: Cambridge University Press, 2014: 284-443.  Back to cited text no. 10
    


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