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Vol 16, No 2
Table of Contents

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<p class="frontmatter-fieldnotes disclaimernew" style="margin-bottom:15px;">This work may not be copied, distributed, displayed, published, reproduced, transmitted, modified, posted, sold, licensed, or used for commercial purposes. By downloading this file, you are agreeing to the publisher’s <a href="/pages/termsofuse.aspx" target="_blank">Terms & Conditions</a>.</p> <div id="x13l01604">
  <div class="story">
    <p class="ltrs-br-ltr-br-title"><span class="bold">Lithium-Induced Transient Euthyroid Hyperthyroxinemia: A Case Report</span></p>
    <p class="ltrs-br-ltr-br-body-text"><span class="semibold">To the Editor:</span> Sixty years after its introduction, lithium remains a first-line medication in the treatment of bipolar disorder.<span class="htm-cite"><a href="#ref1">1</a></span> While lithium treatment has been associated with a wide range of adverse effects,<span class="htm-cite"><a href="#ref2">2</a>,<a href="#ref3">3</a></span> thyroid-related abnormalities, especially hypothyroidism, are the most commonly reported ones.<span class="htm-cite"><a href="#ref4">4</a>,<a href="#ref5">5</a></span> Lithium-associated hyperthyroidism, however, is quite rare, and only a few sporadic case reports of thyrotoxicosis that developed after several years of lithium therapy or after stopping lithium<span class="htm-cite"><a href="#ref3">3</a>,<a href="#ref6">6</a></span> are described in the literature. Lithium-induced euthyroid hyperthyroxinemia, described as an elevation in serum thyroid hormone levels without clinical manifestations of thyrotoxicosis,<span class="htm-cite"><a href="#ref7">7</a></span> has not been reported to our knowledge. Stratakis and Chrousos<span class="htm-cite"><a href="#ref8">8</a></span> described a case of transient euthyroid hyperthyroxinemia associated with discontinuation of chronic lithium treatment. We report a patient who developed transient euthyroid hyperthyroxinemia within a few weeks of initiation of lithium therapy. </p>
    <p class="ltrs-br-ltr-br-body-text">&nbsp;</p>
    <p class="ltrs-br-ltr-br-body-text"><span class="semibold-ital">Case report.</span> Ms A, a 24-year-old African American woman with a 4-year history of schizoaffective disorder, bipolar type (<span class="italic">DSM-IV-TR</span>), was admitted to our hospital in December 2011 with signs and symptoms consistent with mania with psychosis. At admission, she presented with a labile mood with aggressive and violent behavior, insomnia, poor concentration, pressured speech with racing thoughts, and increased psychomotor activity. She was also very paranoid, reported auditory hallucinations, and was often found responding to internal stimuli. She had no acute medical findings, except for past history of gastroesophageal reflux/dyspepsia symptoms and urinary urgency. She had never been pregnant, and her family history was negative for thyroid abnormalities. Her admission laboratory workup, including thyroid function, was unremarkable except for elevated serum total creatine kinase level of 574 U/L (normal range, 26–140 U/L), which subsequently normalized. She was started on lithium carbonate titrated to 900 mg daily, risperidone, and clonazepam. Under this regimen, her mood and psychotic symptoms started to improve. Serum lithium, free T<span class="subscript">4</span>, and thyroid-stimulating hormone (TSH) levels were serially monitored over the course of her hospitalization (<span class="callout"><a href="#" onclick="createFigure('f1'); return false;">Figure 1</a></span>). </p>
    <div id="figure" class="right"> <a href="#" onclick="createFigure('f1'); return false;"><img src="13l01604F1.gif" alt="Figure 1" id="f1" border="0" /></a>
      <p class="click-to-enlarge">Click figure to enlarge</p>
    </div>
    <p class="ltrs-br-ltr-br-body-text">About 2.5 months after treatment initiation, we noticed an elevation in her free T<span class="subscript">4</span> levels with a slight decrease in TSH levels. During this period, she remained clinically euthyroid with no evidence of thyrotoxicosis. A full hyperthyroidism workup revealed the following: an elevated serum total thyroglobulin level over 180 ng/mL (normal range, 1.2–35 ng/mL), thyroid antibody levels within normal limits, no evidence of a thyroid nodule on ultrasonogram, a 0.9% I<span class="superscript">123</span> uptake at 4 hours (normal, 5%–15%) and a 0.3% uptake at 24 hours (normal, 5%–15%) on a thyroid uptake scan, and no evidence suggestive of an ectopic thyroid tissue. Lithium therapy was continued with careful monitoring for evidence of thyrotoxicosis. Elevation of free T<span class="subscript">4</span> and associated drop in TSH levels persisted for the next 2 months (<span class="callout"><a href="#" onclick="createFigure('f1'); return false;">Figure 1</a></span>). During the fourth month of treatment, free T<span class="subscript">4</span> levels returned to within normal limits.</p>
    <p class="ltrs-br-ltr-br-body-text">&nbsp;</p>
    <p class="ltrs-br-ltr-br-body-text">The incidence of transient euthyroid hyperthyroxinemia in acute psychiatric inpatients at admission has been reported to be at 9%–18%.<span class="htm-cite"><a href="#ref7">7</a></span> The subject in the present report had normal TSH and T<span class="subscript">4</span> levels at admission. To our knowledge, this is the first reported case of lithium-induced transient euthyroid hyperthyroxinemia. Although the role of lithium in thyroid hormone synthesis and release has been extensively investigated and reviewed,<span class="htm-cite"><a href="#ref9">9</a></span> how it may induce euthyroid hyperthyroxinemia is unclear. From a clinical perspective, if a clinician finds elevated thyroxine levels in the absence of overt thyrotoxicosis in a patient started on lithium therapy, it would seem prudent to carefully monitor clinically for development of thyrotoxic symptoms without immediately resorting to an extensive and expensive diagnostic workup.</p>
    <p class="ltrs-br-ltr-br-references-head"><span class="smallcaps">References</span></p>
    <p class="references-references-text-1-9"><a name="ref1"></a>1. American Psychiatric Association. Practice guideline for the treatment of patients with bipolar disorder (revision). <span class="italic">Am J Psychiatry</span>. 2002;159(4 suppl):1–50.<span class="pubmed-crossref"> <a href="http://www.ncbi.nlm.nih.gov/pubmed/11958165">PubMed</a></span></p>
    <p class="references-references-text-1-9"><a name="ref2"></a>2. McKnight RF, Adida M, Budge K, et al. Lithium toxicity profile: a systematic review and meta-analysis. <span class="italic">Lancet</span>. 2012;379(9817):721–728. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=22265699&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1016/S0140-6736(11)61516-X">doi:10.1016/S0140-6736(11)61516-X</a></span></p>
    <p class="references-references-text-1-9"><a name="ref3"></a>3. Livingstone C, Rampes H. Lithium: a review of its metabolic adverse effects. <span class="italic">J&nbsp;Psychopharmacol</span>. 2006;20(3):347–355. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16174674&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1177/0269881105057515">doi:10.1177/0269881105057515</a></span></p>
    <p class="references-references-text-1-9"><a name="ref4"></a>4. Kibirige D, Luzinda K, Ssekitoleko R. Spectrum of lithium induced thyroid abnormalities: a current perspective. <span class="italic">Thyroid Res</span>. 2013<span class="italic">;</span>6(1):3.</p>
    <p class="references-references-text-1-9"><a name="ref5"></a>5. Bocchetta A, Loviselli A. Lithium treatment and thyroid abnormalities. <span class="italic">Clin Pract Epidemiol Ment Health</span>. 2006;12;(2):23.<span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16968542">PubMed</a></span></p>
    <p class="references-references-text-1-9"><a name="ref6"></a>6. Bou Khalil R, Richa S. Thyroid adverse effects of psychotropic drugs: a review. <span class="italic">Clin Neuropharmacol</span>. 2011;34(6):248–255. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=21996646&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1097/WNF.0b013e31823429a7">doi:10.1097/WNF.0b013e31823429a7</a></span></p>
    <p class="references-references-text-1-9"><a name="ref7"></a>7. Borst GC, Eil C, Burman KD. Euthyroid hyperthyroxinemia. <span class="italic">Ann Intern Med</span>. 1983;98(3):366–378. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6187257&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.7326/0003-4819-98-3-366">doi:10.7326/0003-4819-98-3-366</a></span></p>
    <p class="references-references-text-1-9"><a name="ref8"></a>8. Stratakis CA, Chrousos GP. Transient elevation of serum thyroid hormone levels following lithium discontinuation. <span class="italic">Eur J Pediatr</span>. 1996;155(11):939–941. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8911893&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1007/BF02282883">doi:10.1007/BF02282883</a></span></p>
    <p class="references-references-text-1-9"><a name="ref9"></a>9. Lazarus JH. Lithium and thyroid. <span class="italic">Best Pract Res Clin Endocrinol Metab</span>. 2009;23(6):723–733. <span class="pubmed-crossref"><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=19942149&dopt=Abstract">PubMed</a> <a href="http://dx.doi.org/10.1016/j.beem.2009.06.002">doi:10.1016/j.beem.2009.06.002</a></span></p>
    <p class="ltrs-br-ltr-br-author" style="margin-top:15px;" ><span class="bold">Lakshminarayana Chekuri, MD, MPH</span></p>
    <p class="ltrs-br-ltr-br-author"><a href="Mailto:lchekuri@uams.edu" target="_blank">lchekuri@uams.edu</a></p>
    <p class="ltrs-br-ltr-br-author"><span class="bold">Jaquelyn R. Lange, MD</span></p>
    <p class="ltrs-br-ltr-br-author"><span class="bold">Purushottam B. Thapa, MD, MPH</span></p>
    <p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Author affiliations:</span> Department of Psychiatry, University of Arkansas for Medical Sciences, Little Rock.</p>
    <p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Potential conflicts of interest:</span> None reported.</p>
    <p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Funding/support:</span> None reported.</p>
    <p class="ltrs-br-ltr-br-endmatter-fieldnotes"><span class="semibold-ital">Published online: </span>April 24, 2014.</p>
    <p class="ltrs-br-ltr-br-copyright-doi"><span class="italic">Prim Care Companion CNS Disord 2014;16(2):</span><span class="doi">doi:10.4088/PCC.13l01604</span></p>
    <p class="ltrs-br-ltr-br-copyright-doi"><span class="italic">© Copyright 2014 Physicians Postgraduate Press, Inc.</span></p>
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