Acute Psychosis in a Patient with Hashimoto's Thyroiditis

Case Report Taiwanese Journal of Psychiatry Vol. 23 No. 4 2009 337 Acute Psychosis in a Patient with Hashimoto's Thyroiditis Zon-Yi Tsai, M.D., Hua-An Shuai, M.D., Chia-Chun Wang, M.D., Guang-Yang Tsai, M.D. 2 Objective: We report a patient with Hashimoto's thyroiditis (HT) who presented with hyperthyroidism and psychotic symptoms. Case report: A 43-yearold male patient had suffered from palpitations of the heart for one year. One week before admission, he had a sudden onset of delusion and hallucinations. Three days after admission, he developed delirium. The results of the laboratory examinations showed HT in hyperthyroid state with high level of anti-thyroid antibodies. After having received anti-thyroid drugs and antipsychotic drugs, he was observed to have complete recovery of the physical and psychotic symptoms. Based on the progressive nature of the course of this patient s disease and the response to treatment, we diagnosed the patient to have psychotic disorder due to HT. He had been well in the follow-up. Conclusion: This case report suggests that screening of serum anti-thyroid antibodies for any patient with atypical psychosis with thyroid dysfunction is needed, and that Hashimoto's disease should be considered in any patient with atypical psychosis, as prompt recognition and management can lead to an excellent treatment outcome. Key words: psychosis, Hashimoto's thyroiditis, hyperthyroidism, delirium (Taiwanese Journal of Psychiatry 2009;23:337-42) Introduction The clinical manifestations of many medical and surgical diseases are accompanied or even dominated by psychotic symptoms. Psychiatrists in the emergency department are often asked to evaluate patients with disturbances of mood, behavior, and cognition. The first and most crucial step in the evaluation process is to eliminate possible physical causes for a patient with psychiatric symptoms []. Patients with thyroid disorders, both due to excess and deficiency of the thyroid hormone, may present with psychiatric symptoms, even with acute psychosis [2]. Hashimoto's thyroiditis (HT) is the most common cause of hypothyroidism in the United States, and is an autoimmune of the chronic lymphocytic type of thyroiditis. Being named after the Japanese physician, Hakaru Department of Psychiatry, Armed Forces Taichung General Hospital 2 Department of Neurology, Armed Forces Taichung General Hospital Received: December 9, 2008; revised: February 6, 2009; accepted: March 23, 2009 Address correspondence to: Dr Zon-Yi Tsai, Department of Psychiatry, Armed Forces Taichung General Hospital, No.348, Section 2, Zhongshan Road, Taiping City, Taichung 4, Taiwan

338 Psychosis in Hashimoto s Thyroiditis Hashimoto, HT was first described in 92. Having high serum thyroid autoantibodies, HT is rare and occur at any age, but often in middle-aged women. In adults, it is estimated that the disease occurs in 3.5 out of every,000 women and 0.8 out of every,000 men every year [3]. A few patients with HT are found to undergo a hyperthyroid phase, called hashitoxicosis, before eventually becoming hypothyroid. This hyperthyroid period is generally short, and is followed by a period of time when the thyroid functions properly. However, this period of having normal thyroid function is short-lived. As scarring in the thyroid gland sets in, the patient finally develops hypothyroidism. Although HT is the most common cause of hypothyroidism, we report here a case of an HT patient who presented with hyperthyroidism and psychotic symptoms. Case Report A 43-year-old single male patient, the eldest of the three siblings, who was tender and responsible by nature, lived together with his family. After he graduated from senior high school, he worked in a restaurant. He maintained a harmonious relationship with his colleagues with good performance at work. He had had no special medical problem in the past until one year ago when he started to have palpitations of the heart, felt difficult to perform his work. Three months ago, he could no longer tolerate heat and increased sweating, making him difficult to stay in the kitchen for a long time. In the meantime, he also felt anxious, got angry easily and was distractive, resulting in getting disputed with other persons easily and showing bad work performance. As the living and working status becomes worse, he felt having greater pressure day after day. Later, those physical symptoms became even worse. Unfortunately, one week ago, he started to have psychotic disturbances. The chief problems were tactile hallucinations feeling things moving around in his nose and on his face and as well as somatic delusion believing to have something in his nose. Although the results of the physical examination performed by a physician was normal, he still believed that something strange was in his nose and he often dug his nose so much so that it bled. Sometimes he heard voices calling his name or commenting on his behaviors, and he also felt his being followed and monitored by pedestrians. Therefore, he was admitted to our psychiatry ward. According to information provided by his family and himself, he did not have any past personal or family history of psychiatric illness and he denied any psychoactive drug or alcohol abuse. The findings of the physical examination showed heart rate 0 beats per minute, and frequent bowel movements. He did not show any palpable nodules over neck and thyroid gland, or abnormal neurological sign. In mental state examination, he was conscious, cooperative, appropriate in attitude, relevant in speech, oriented to place/time/ person, but distracted, nervous, irritable, pressured in speech, having auditory and tactile hallucinations, delusion of reference, somatic delusion, and having poor sleep and appetite. Patient s complete blood count and biochemical studies showed no abnormality. He had normal findings in urine sediment and chest X-ray films. The result of his electrocardiogram showed sinus tachycardia. Due to his sensation something in his nose, otolaryngologist was consulted but the patient did not have any abnormality. Patient s initial impression was psychotic disorder, not otherwise specified. He started to receive treatments with risperidone (2 mg/d) and

Tsai ZY, Shuai HA, Wang CC, et al. 339 propranolol (40 mg/d). After his being hospitalized, he also complained of tremors and headache. Three days later, he had fluctuation of disorientation and conscious disturbance. He fainted the day after that he was sent to the intense care unit for treatment. The results of T4 serum levels were increased (>60 μg/dl; normal range: 4.5 2μg/dL), and the serum levels of TSH were also decreased (0.08 miu/ ml; normal range: 0.3 5.0 miu/ml). He also had high levels of anti-thyroglobulin antibodies (60 IU/ ml; normal range <75 IU/mL), and anti-microsomal antibodies (400 IU/mL; normal range <20 IU/mL). The electrocardiogrphic finding showed arterial fibrillation with rapid ventricular response (00/min). The ultrasonography of thyroid showed diffusely heterogeneous and hypoechoic pattern. But he did not show nodular lesion. The result of fine-needle aspiration cytology showed follicular cell infiltration by lymphoid cells and fibrosis, but no evidence of malignancy. The results of his hemogram, ionogram, liver and renal function, glucose, bacteriology, serological studies for HIV and syphilis, were unremarkable. According to the results of laboratory examinations, he was diagnosed to have hyperthyroid phase of HT and received propylthiouracil 300 mg /day. He recovered to have normal consciousness and cognition recovered seven days later. His heat intolerance, excessive sweating and tremors disappeared 4 days later while delusion and hallucinations disappeared 8 days later. He had been maintained with risperidone for another 2 days. His propylthiouracil was withdrawn after his having achieved a euthyroid state 24 days later, and he was discharged well 30 days later with the discharged diagnosis of psychotic disorder due to HT. He had received regular follow up for his thyroid function, showing his good general mental condition. Four months after the discharge, the patient s thyroid function tests showed the findings of hypothyroidism (T4: 3.0μg/dL: TSH: 20 miu/ml). Under the treatment with levothyroxine, the patient had been free from mental problem during near two-year follow-up. Discussion Psychosis or cognitive disorder is rare in psychiatric setting as symptoms of thyroid disorder but either or both may be the presentation of an untreated hyperthyroidism. The first and the most important step in the assessing a patient with psychiatric symptoms is to rule out and to eliminate the physical causes []. The diagnosis of HT is simply diagnosed by two blood tests. First, the routine thyroid function tests are needed to confirm whether a patient has an underactive thyroid gland. Second, the thyroid antibody (anti-microsomal or anti-thyroglobulin) tests are required to pinpoint HT as the cause of the hypothyroidism [3]. Although the above test findings are usually enough to permit a diagnosis, histological confirmation may be obtained by needle biopsy [4]. Of those two kinds of tests, the most important examination from the clinical standpoint, are the thyroid antibody tests [4]. In our case, thyroid function test showed the finding of hyperthyroidism initially. The most common cause of hyperthyroidism is Graves disease, followed by multinodular goiter and HT [5]. High titers of anti-microsomal antibodies also may be found in Graves disease [4]. The test of 24-hour radioactive iodine uptake or fine-needle aspiration cytology is useful to distinguish Graves disease from HT [4]. Based on the presence of thyroid autoantibodies and the cytological findings of lymphocytes infiltration, with biopsy specimen, we confirmed that our patient had HT, but no Graves disease.

340 Psychosis in Hashimoto s Thyroiditis Patients with thyroid disorders may present psychiatric symptoms, even including acute psychosis. Once acute psychotic disturbance is noted, the chief differential task is to distinguish between a secondary and a primary psychoses [6]. Primary psychotic disorder such as schizophrenia or brief psychotic disorder, may present with symptoms which are identical or similar to psychotic disorder due to a general medical condition [7]. But in primary disorders, no medical or substance cause is identifiable, despite of the physical examination and laboratory work-ups [7]. Patients with primary psychoses generally have gradual onset in adolescence or early adult years [6]. Unique characteristics may help differentiate primary from secondary psychoses. Most psychoses with nonauditory hallucinations are due to general medical conditions, the use of substances, or both, but psychosis with auditory hallucinations can be primary and secondary [7]. Diagnosis can be made by chronology of symptoms, response to removal of suspected substances, alleviation of medical illness, and toxicology results [,7]. Our middleaged male patient had no past personal or familial history of psychiatric disease, and he denied any psychoactive drug or alcohol abuse. He developed symptoms of hyperthyroidism (the palpitations of the heart, heat intolerance and increased sweating) first before he had delusions and hallucinations. With normalization of thyroid hormones with anti-thyroid treatment, he recovered in both mental and physical conditions. With continuous HT treatment, he did not have any relapse of psychotic symptoms. Considering the presence of HT combined with tactile hallucinations, and temporal relationship between thyroid dysfunction and the course of psychotic symptoms, we gave the diagnosis of psychotic disorder due to HT first. But we also need to rule out primary psychotic disorder, such as schizophrenia or brief psychotic disorder. Our patient had symptoms of hyperthyroidism first, then adding delusions and hallucinations. Three days after admission, he started to have fluctuation of conscious disturbance and disorientation. Thus, our patient s mental condition had two-stage representations: psychosis and delirium. Being characterized by confusion and loss of short-term memory, delirium may be accompanied by hallucinations and delusion. Delirium is immediately distinguished from psychotic disorder due to a general medical condition (also called secondary psychosis) by the presence of confusion or cognitive deficits such as disorientation [6]. Having a sudden onset (hours or days) and a brief and fluctuating course [8], delirium may be superimposed with a preexisting secondary psychosis when the underlying disease got worse or combined with other risk factors [6,8]. Both delirium and secondary psychosis are rapidly improved after the causative factor is identified and eliminated [6,8]. Based on medical history and results of laboratory examinations, we thought that our patient s delirium was due to his worsened thyroid function. After correcting his thyroid dysfunction, he got improved in consciousness and cognition. About 0% to 30% of medically ill hospitalized patients have delirium. Endocrinologic disorders are the common causes of delirium [8]. In autoimmune thyroid disease, changes of mood and cognitive function can be caused by thyroid dysfunction (hypo- or hyperthyroidism) or associated with the presence of anti-thyroid antibodies [3]. Even a small change in thyroid hormone serum concentration is associated with change of cognitive function [3]. Nearly all the hyperthyroid patients show minor psychiatric signs (insomnia, irritability and anxiety), and infrequently psychosis. Psychoses occurs in 0% to 20% of hyperthyroid patients, but in fewer than 5% of hypothyroid patients [2]. According to our literature review, while

Tsai ZY, Shuai HA, Wang CC, et al. 34 for some diseases with hyperthyroidism psychotic developments are well-known, for a rare autoimmune thyroiditis, HT, only one case of development of psychotic symptoms is reported [9]. That patient also presented psychotic symptoms in rare hyperthyroidism stage and recovered well in four weeks after being controlled for HT and treated with antipsychotic drugs and benzodiazepines [9]. Although hyperthyroidism is unusual in classical HT, we suggest that HT should be considered in the differential diagnosis of atypical psychosis, even in patients with hyperthyroidism. HT is not curable but treatment generally is focused on managing the level of thyroid hormone. If the level is low, as it is in most cases, thyroid hormone replacement therapy (levothyroxine) is needed. If the thyroid serum level is high, an anti-thyroid drug (propylthiouracil) needs to be prescribed to block thyroid hormone from working in the body. Rarely, surgery may be needed if the thyroid gland gets too big. Regular observation of thyroid hormone is needed to avoid the medicine causing hypothyroidism. Delirium is associated with an increased risk in mortality. Once the diagnosis of delirium is made, the underlying disorders should be treated. Antipsychotic agents may be necessary to control the psychotic symptoms associated with hyperthyroidism [0]. Most patients with psychiatric symptoms get remitted with treatment of the underlying thyroid dysfunction, but some patients have presented psychotic symptoms after receiving anti-thyroid treatment [0]. After having received anti-thyroid drugs and antipsychotic drugs, our patient showed complete recovery of cognition in seven days and the psychotic symptoms in 8 days. He could have his psychotropic medication discontinued 2 days later, and he remained well in the follow-up visits. In conclusion, our patient has shown the possibility of an association between Hashimoto disease and psychosis. We suggest that in case of acute psychosis anti-thyroid antibodies should be looked for in the differential diagnosis, because HT is the treatable cause. A patient with HT often requires to be monitored and treated for life. Periodic thyroid function tests are recommended to monitor the course of the disease. References. Lagomasino I, Daly R, Stoudemire A: Medical assessment of patients presenting with psychiatric symptoms in the emergency setting. Psychiatr Clin North Am 999;22:89-50. 2. Benvenga S, Lapa D, Trimarchi F: Don't forget the thyroid in the etiology of psychoses. Am J Med 2003;5:59-60. 3. Zarković M: Autoimmune thyroid disease and brain. Srp Arh Celok Lek 2005;33:88-9. 4. Jameson JL, Weetman AP: Disorder of the thyroid gland. In: Fauci AS, Braunwald E, Kasper DL et al. eds. Harrison's Principles of Internal Medicine, 7th ed. New York: McGraw-Hill, 2008:2224-47. 5. Moore DP, Jefferson JW: Handbook of Medical Psychiatry. 2nd ed. Philadelphia: Elsevier Mosby, 2004:386-7. 6. Moore DP, Jefferson JW: Handbook of Medical Psychiatry. 2nd ed. Philadelphia: Elsevier Mosby, 2004:28-9. 7. Sadock BJ, Sadock VA: Kaplan & Sadock's Synopsis of Psychiatry: Behavioral Sciences/ Clinical Psychiatry. 0th ed. Philadelphia: Lippincott Williams & Wilkins, 2007:352-3. 8. Sadock BJ, Sadock VA: Kaplan & Sadock's Synopsis of Psychiatry: Behavioral Sciences/ Clinical Psychiatry. 0th ed. Philadelphia: Lippincott Williams & Wilkins, 2007:322-9. 9. Teuber I, Volz HP: Acute schizophreniform disorder in Hashimoto disease. Psychiatr Prax 2003;30: S83-4. 0. Geffken GR, Ward HE, Staab JP, Carmichael SL, Evans DL: Psychiatric morbidity in endocrine disorders. Psychiatr Clin North Am 998;2:473-89.

342 台灣精神醫學第 23 卷第 4 期,2009 個案報告摘要 橋本氏甲狀腺炎引發之急性精神病 蔡宗益 帥華安 王家駿 2 蔡光洋 一橋本氏甲狀腺炎患者, 病程中呈現甲狀腺機能亢進並引發急性精神病 一位 43 歲男性, 一年前開始感到心悸, 住院前一週突然出現妄想及幻覺, 住院第三天呈現譫妄現象, 經檢查診斷橋本氏甲狀腺炎, 以抗精神病藥及抗甲狀腺藥物治療後精神及身體症狀消失 考量疾病病程發展, 身 心症狀 出現之時間關聯性以及對治療反應, 診斷為橋本氏甲狀腺炎引發急性精神病 在甲狀腺藥物治療下, 未再出現精神症狀 當個案出現急性精神症狀併甲狀腺功能異常, 宜檢驗自體抗體, 考慮橋本氏甲狀腺炎引發精神疾病可能性 關鍵詞 : 精神病, 橋本氏甲狀腺炎, 甲狀腺機能亢進, 譫妄 ( 台灣精神醫學 2009;23:337-42) 國軍台中總醫院精神科 2 國軍台中總醫院神經內科受理日期 :2008 年 2 月 9 日 ; 修正日期 :2009 年 2 月 6 日 ; 接受日期 :2009 年 3 月 23 日通信作者地址 : 蔡宗益, 4 台中縣太平市中山路二段 348 號國軍台中總醫院精神科