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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 18  |  Issue : 1  |  Page : 44-46

Lithium-induced hyperthyroidism in a patient with bipolar type 1 affective disorder: A rare occurrence


Department of Psychiatry, Kasturba Medical College, Manipal, Karnataka, India

Date of Submission02-Jun-2020
Date of Acceptance15-Feb-2021
Date of Web Publication22-Mar-2021

Correspondence Address:
Shreya Singh
Kasturba Medical College, Manipal, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/am.am_46_20

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  Abstract 


A 46-year-old female, previously diagnosed with bipolar affective disorder on lithium therapy, presented to us with manic symptoms. The blood investigations revealed elevated thyroxine and reduced thyroid-stimulating hormone with technetium thyroid scintigraphy indicating lithium-induced thyroiditis.

Keywords: Bipolar affective disorder, lithium induced, thyroiditis


How to cite this article:
Singh U, Nayak MS, Singh S, Praharaj SK. Lithium-induced hyperthyroidism in a patient with bipolar type 1 affective disorder: A rare occurrence. Apollo Med 2021;18:44-6

How to cite this URL:
Singh U, Nayak MS, Singh S, Praharaj SK. Lithium-induced hyperthyroidism in a patient with bipolar type 1 affective disorder: A rare occurrence. Apollo Med [serial online] 2021 [cited 2021 Sep 24];18:44-6. Available from: https://www.apollomedicine.org/text.asp?2021/18/1/44/311629




  Introduction Top


The efficacy of lithium for treating mania was discovered in 1949, making it the first medication specifically developed to treat bipolar disorder.[1] Lithium remains a mainstay of treatment for manic-depressive illness, especially for acute mania and maintenance treatment. In addition, lithium has been shown to reduce the risk of suicide in patients with bipolar disorder.[2],[3],[4] Lithium is not metabolized and is excreted almost exclusively through the kidneys, thus its elimination and half-life depend on renal function.[5]

Its use has been associated with myriad of thyroid abnormalities. Among them, the association between lithium therapy and hypothyroidism is well documented, with the prevalence ranging between 6% and 52% in various studies.[6] However, the cases of lithium associated hyperthyroidism have rarely been reported in the literature. The following case presents thyroiditis where serum T4 was elevated with low thyroid-stimulating hormone (TSH) value.


  Case Report Top


A 46-year-old female with bipolar affective disorder of 25 years' duration presented to the outpatient clinic of our department with complaints of recent onset decreased need for sleep, excessive talking, and paranoid delusions. Her self-care and socio-occupational functioning had declined over the previous month. She had the several episodes of mania and depression over the years which were treated with sodium valproate, chlorpromazine, sertraline, and amitriptyline. There was a history of suicide attempt in the past by jumping into a well, and there was a family history of depression and suicidality. At the time of admission, she was receiving lithium 800 mg/day. Her thyroid function tests were normal at baseline before starting the medication.

After admission, detailed assessment was done. She was noted to have tremors in hands, excessive thirst, and weakness. On examination, she was clinically dehydrated and angular stomatitis and pallor was noted. On the mental status examination, she was disoriented, affect was irritable, and had pressured speech but no dysarthria. She had a fine tremor in her upper limbs and brisk-tendon reflexes but no ataxia. She had Grade 1 insight. The clinical features were suggestive of manic episode. Her complete blood count result showed lower hemoglobin levels (10.4 g%). Electrolytes, renal function, and urine analysis were within the normal limits. In addition, her serum lithium level was found to be within the therapeutic range of 1.2mEq/L. Her thyroid function, on admission, was consistent with hyperthyroidism with TSH of 0.093 uIU/mL and total T4 of 17ug/dL. Tc-99m Pertechnetate scan was suggestive of thyroiditis [Figure 1]. Ultrasound of the neck showed benign hypoechoic lesion in the left lobe of thyroid. Her score on the Naranjo scale[7] was 6, which was suggestive of probable lithium-associated thyroiditis.
Figure 1: Technetium-99 m pertechnetate scan showing faint radiotracer uptake in the thyroid gland and physiologic uptake in the salivary gland

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The dose of lithium was reduced to 600mg/day and aripiprazole (dose) 20 mg was added for control of manic symptoms. For the treatment of hyperthyroidism, propranolol 40 mg/day was added. At the time of discharge, 7 days later, the patient's mood symptoms had improved significantly. In the subsequent follow-up after 6 weeks, lithium levels were 0.6 mmol/L and thyroid function test showed TSH 10.21uIU/mL, free T4 0.83 ng/dL which were suggestive of a diagnosis of hypothyroidism (iatrogenic). She was started on oral levothyroxine 50 μg and propranolol was stopped by the endocrinology department. On follow-up after 8 weeks, she was euthyroid with TSH 3.4 uIU/mL and free T4 – 1.20 ng/dL. There were no complaints of mood symptoms [Figure 2].
Figure 2: Graph showing the trends of thyroid-stimulating hormone and thyroxine (T4) from initiation of lithium therapy to follow-up postthyroxine

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  Discussion Top


Lithium is concentrated in the thyroid gland 3–4 times more than plasma.[8] The main thyroidal action of lithium is to inhibit thyroid hormone synthesis and release. It exerts this effect by altering the tubulin polymerization and inhibiting the action of TSH on cAMP. Lithium also causes alteration of thyroglobulin structure leading to subsequent iodotyrosine coupling defects. Given its goitrogenic effect, lithium-induced thyrotoxicosis is an interesting phenomenon.

Lithium-induced hyperthyroidism is very infrequent with studies estimating a prevalence of thyrotoxicosis with lithium to range between 1.7% and 1%.[9] Etiologies of hyperthyroidism in lithium-treated patients include diffuse goiter, toxic multinodular goiter, and painless thyroiditis.[10] Our patient's blood investigations revealed elevated T4 levels with reduced TSH consistent with hyperthyroidism. In most cases, hyperthyroidism occurs after many years of treatment.[11],[12] In our patient, it developed within 2 years of initiation of lithium therapy.

Our patient underwent a Tc99m scan which showed features suggestive of thyroiditis, which is one of the common etiologies in patients with lithium-induced hyperthyroidism. She had no symptoms of pain, fever, and her erythrocyte sedimentation rate was normal which further suggests that she had painless thyroiditis. It directly damages thyroid cells, with consequent release of thyroglobulin and thyroid hormones into the circulation; therefore, thyrotoxicosis caused by silent thyroiditis might be associated with lithium use.[12] In 23 patients in one single center, transient thyrotoxicosis with painless thyroiditis was noted in nine patients (23%) where the median duration of lithium therapy was 6 years.[13]

Patients with confirmed thyroiditis must be managed conservatively with beta-blockers for symptomatic relief, anti-thyroid drugs, and radioiodine ablation must not be used as the hyperthyroidism is not due to excess hormone synthesis and uptake of radioiodine is low.[14] Most patients with thyroiditis eventually develop hypothyroidism as the initial surge in thyroid hormones released due to the damaged thyroid follicles is metabolized and need thyroxine supplementation. Our patient received beta-blocker for symptomatic relief until she had high levels of thyroid hormones. On follow-up, it was found that she had an elevated TSH, low free T4, and was diagnosed with hypothyroidism. She was started on thyroxine supplements.

This case substantiates that it is important to keep the association of lithium-induced hyperthyroidism in mind when caring for lithium-treated patients. Before initiating prophylaxis or treatment with lithium in bipolar affective disorders, the assessment of baseline thyroid function is recommended for all patients and subsequently should be repeated every year.

Learning points

  1. Lithium has profound effects on thyroid physiology, goiter, and hypothyroidism being the common manifestations
  2. Thyroid gland function should be tested before lithium therapy is commenced and monitored regularly during lithium therapy
  3. In case of lithium-induced thyroiditis, conservative management with supportive therapy and regular follow-up is indicated because most patients subsequently develop hypothyroidism.


Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Cade JF. Lithium salts in the treatment of psychotic excitement. Med J Aust 1949;2:349-52.  Back to cited text no. 1
    
2.
Malhi GS, Gessler D, Outhred T. The use of lithium for the treatment of bipolar disorder: Recommendations from clinical practice guidelines. J Affect Disord 2017;217:266-80.  Back to cited text no. 2
    
3.
Cipriani A, Hawton K, Stockton S, Geddes JR. Lithium in the prevention of suicide in mood disorders: (Updated systematic review and meta analysis. BMJ 2013;346:f3646).  Back to cited text no. 3
    
4.
Song J, Sjölander A, Joas E, Bergen SE, Runeson B, Larsson H, et al. Suicidal behavior during lithium and valproate treatment: A within-individual 8-Year prospective study of 50,000 patients with bipolar disorder. Am J Psychiatry 2017;174:795-802.  Back to cited text no. 4
    
5.
Kamali M, Krishnamurthy VB, Baweja R, Lithium. In: Schatzberg AF, Nemeroff CB, editors. The American Psychiatric Association Publishing Textbook of Psychopharmacology. 5th ed. Arlington, VA: American Psychiatric Association Publishing; 2017. p. 889.  Back to cited text no. 5
    
6.
Bocchetta A, Bernardi F, Pedditzi M, Loviselli A, Velluzzi F, Martino E, et al. Thyroid abnormalities during lithium treatment. Acta Psychiatr Scand 1991;83:193-8.  Back to cited text no. 6
    
7.
Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981;30:239-45.  Back to cited text no. 7
    
8.
Lazarus JH. Lithium and the Thyroid Gland Endocrine and Metabolic Effects of Lithium. New York and London: Plenum Medical Book Company; 1986. p. 99-124.  Back to cited text no. 8
    
9.
Yassa R, Saunders A, Natase C, Camille Y. Lithium-induced thyroid disorders: A prevalence study. J Clin Psychiatry 1988;49:14-6.  Back to cited text no. 9
    
10.
Miller KK, Daniels GH. Association between lithium use and thyrotoxicosis caused by silent thyroiditis. Clinic Endocrinol 2001;55:501-8.  Back to cited text no. 10
    
11.
Livingstone C, Rampes H. Lithium: A review of its metabolic adverse effects. J Psychopharmacol 2006;20:347-55.  Back to cited text no. 11
    
12.
Lazarus JH. Lithium and thyroid. Best Pract Res Clin Endocrinol Metab 2009;23:723-33.  Back to cited text no. 12
    
13.
Brownlie BE, Turner JG. Lithium associated thyrotoxicosis. Clin Endocrinol 2011;75:402-3.  Back to cited text no. 13
    
14.
Nikolai TF, Coombs GJ, McKenzie AK, Miller RW, Weir GJ Jr. Treatment of lymphocytic thyroiditis with spontaneously resolving hyperthyroidism (silent thyroiditis). Arch Intern Med 1982;142:2281-3.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2]


This article has been cited by
1 Editorial
Raju Vaishya,SatishKumar Agarwal
Apollo Medicine. 2021; 18(1): 1
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