Lithium-induced Thyroiditis in a Patient with Bipolar Affective Disorder: A Rare Presentation

Introduction

Lithium continues to be a primary treatment for manic-depressive illness, particularly for acute mania and maintenance therapy. Furthermore, studies have shown that lithium can lower the risk of suicide in patients with bipolar disorder.[1] The use of lithium has been linked to numerous thyroid abnormalities. The relationship between lithium therapy and hypothyroidism is well-documented, with prevalence rates ranging from 0% to 52% in different studies. However, cases of lithium-associated thyrotoxicosis are seldom reported. The following case involves thyroiditis, characterized by elevated serum T4 and a low thyroid-stimulating hormone (TSH) value.

Case Report

A 24-year-old male, diagnosed with bipolar affective disorder for 6 years, reported symptoms of diarrhea, weight loss, anxiety, and tremors for 2 months. He had no history of fever, pain, or tenderness in the neck region. He also had no family history of thyroid disease. His baseline thyroid function test was within the normal range before the commencement of lithium therapy. He has been taking lithium (900 mg/day) and sodium valproate (1000 mg/day) for 6 years.

Upon examination, he was found to be afebrile and tachycardic, with a heart rate of 102 beats/min. There was no palpable goiter or cervical lymphadenopathy. His current thyroid function was indicative of thyrotoxicosis, with TSH at <0.05 μIU/ml (0.34–5.5), total T3 at 2.88 ng/ml (0.7–2.04), and total T4 at 20.9 μg/dl (4.85–15.6). A Tc-99 m pertechnetate scan revealed severely reduced tracer uptake in both lobes of the thyroid gland, suggesting thyroiditis [Figure 1].

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Figure 1 Tc-99 m pertechnetate thyroid scan showing severely reduced tracer uptake in both lobes of the thyroid

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Discussion

Lithium is a cornerstone medication for bipolar disorders, displaying efficacy in managing acute manic and depressive episodes. Validated by extensive studies, it is a first-line choice for the long-term prevention of mood recurrences in bipolar disorders. The prophylactic effectiveness of lithium is well-substantiated by over 50 years of research. Lithium is associated with a reduced risk of rehospitalization in patients with severe recurrent depression, demonstrating its importance in maintaining patient stability. Its role in preventing suicidal behavior in mood disorders and modulating immune-endocrine components of bipolar disorder broadens the scope of lithium’s therapeutic applications. Thus, despite requiring careful monitoring, lithium’s diverse benefits make it an invaluable tool in psychiatric treatment.[23]

The thyroid gland absorbs lithium and can have four possible negative impacts on thyroid function: It can inhibit iodine uptake, interfere with iodotyrosine coupling, alter thyroglobulin structure, and inhibit the secretion of thyroxine.[4]

Goiter is the most common clinical observation among patients undergoing lithium therapy. Lithium inhibits thyroid hormone synthesis and release, increasing TSH concentrations and thyroid enlargement. Hypothyroidism and subclinical hypothyroidism, with or without concurrent goiter, are prevalent in patients on lithium therapy, with reported frequencies ranging from 0% to 52%. Thyrotoxicosis, characterized by transient and painless thyroiditis, has been noted in a few patients on long-term lithium therapy. This thyroiditis is thought to be caused by lithium’s direct toxic effect on the thyroid gland or due to autoimmunity and autoantibody production. In such cases, ablative radioiodine is not typically indicated due to poor uptake.[5]

In a study of 1562 patients on lithium therapy, 16 episodes of thyrotoxicosis corresponding to an incidence rate of 0.88 episodes per 1000 person-years were identified. Of the 16 episodes of hyperthyroidism, 6 (37.5%) concerned thyroiditis.[6] In a study by Kirov et al., the incidence rates of thyrotoxicosis per 1000 survivor-years during lithium treatment were 6.4 for women and 2.7 for men.[7] In India, only a few cases of thyroiditis among patients treated with lithium have been documented.[89] The typical scintigraphy pattern for Graves’ disease shows a uniform increase in radiotracer uptake across both thyroid lobes. In contrast, thyroiditis displays a diminished radiotracer distribution pattern, indicating disrupted follicles, suggesting iatrogenic thyroiditis that could be induced by lithium.[10]

Hence, before starting lithium prophylaxis for bipolar affective disorders, it is recommended that thyroid function be assessed in all patients. This assessment should include plasma levels of TSH and antithyroid antibodies. Once treatment with lithium salt begins, thyroid function tests should be repeated annually.

Conclusion

In an acute setting, thyrotoxicosis can complicate or mimic mania, leading to lithium toxicity. Differentiating a relapse of bipolar illness from thyroid dysfunction is crucial. This distinction guides the most effective treatment approach, and thyroid scintigraphy may significantly affect patient outcomes.