甲狀腺機能亢進患者常會有心理或精神方面的變化，一般其程度輕微，例如失眠、注意力不集中、焦應、情緒不穩定等，至於嚴重至昏迷者極為罕見，根據過去的文獻報告，多是在甲狀腺風暴(thyroid storm)時才會有如此嚴重的意識變化。所謂「甲狀腺風暴」是一種臨床診斷，常用以診斷的標準率是「高燒」、「極度心率加速」、「腸胃器官障礙」、及「中樞神經系統障礙」。另外，甲狀腺機能亢進會加速骨的再吸收，可能造成高血鈣，但很少造成症狀。我們報告一位中年男性先因噁心嘔吐的症狀求診，然後被發現有高血鈣，而後病情惡化至昏迷時才診斷出甲狀腺機能亢進。病人為33歲男性，初因噁心及嘔吐至某醫院求診，做胃鏡檢查發現消化性潰瘍，治療後沒有改善，再到另一家醫院求診發現高血鈣(12.4mg/dL)，血中副甲狀腺荷爾蒙(intact parathyroid hormone)的值是32pg/mL（正常範圍：10-60），他們以生理食鹽水及利尿劑降其血鈣而意識反而變不清醒。轉到本院時呈現昏迷，檢查發現嚴重心跳加速(140-150/min)、體溫36.9℃、而甲狀腺腫大可見，生化檢驗顯示輕微高血鈣(10.5mg/dL)及腎前性高血氮(BUN: 78mg/dL, creatinine: 1.8mg/dL)，甲狀腺功能檢驗顯示TSH:<0.03μU/mL（正常值: 0.35-5.5），T3:665.12ng/dL(80-190)，Free T4:9.8ng/dL
(0.7-1.8)。針對甲狀腺機能亢進給予口服propylthiouracil每6小時200毫克，propranolol每6小時先40後60毫克，稀釋之Lugol's solution 3毫升每天3次，靜脈注射hydrocortisone每6小時100毫克，及大量的液體補充治療。心跳速率逐漸下降，第三天檢驗的血鈣濃度正常，Lugol's solution及hydrocortisone使用四天後即停用，其他藥物的劑量亦逐漸減少，第七天檢驗的血鈣濃度亦正常，患者七日後才醒來但神智不清三天後才完全清醒，出院後追蹤無神經學後遺症。由藥物治療的反應我們認為其各種表現及高血鈣主要是因於「甲狀腺機能亢進」，此為一罕見的嚴重甲狀腺亢進造成昏迷的病例，已接近「甲狀腺風暴」，因為沒有發燒並不典型，故稱之為「甲狀腺毒性昏迷」。

Mental changes are common in patients with thyrotoxicosis. These changes are usually mild, such as insomnia, poor concentration, anxiety and emotional lability. Severe cases, such as coma, are rare and usually happen in "thyroid storm" according to previous literature. The diagnosis of "thyroid storm" is a clinical one, which the cardinal criteria are high fever, severe tachycardia, gastrointestinal dysfunction and central nervous system dysfunction. Besides, as a consequence of acceleration in bone resorption, hypercalcemia may occur in thyrotoxicosis. However, the patient is rarely symptomatic due to the hypercalcemia. Herein, we report a middle-aged male who visited doctor firstly due to nausea and vomiting. Later on, hypercalcemia was found. Hyperthyroidism was not diagnosed until his condition deteriorated to coma. This 33-year-old man visited some hospital firstly due to nausea and vomiting. The endoscopy disclosed peptic ulcer. His symptoms did not improve after treatment. He visited another hospital where hypercalemia (12.4 mg/dL) was found and intact parathyroid hormone level was 32 pg/mL (normal range: 10-60). Consciousness became unclear though the hypercalcemia was ameliorated by normal saline and diuretics. He was in status of coma while arriving at our hospital. Physical examination revealed severe tachycardia (140-150/min), body temperature 36.9 and visible diffuse goiter. Laboratory data revealed mild hypercalemia (10.5 mg/dl) and prerenal azotemia (BUN: 78 mg/dL, creatinine: 1.8 mg/dL). Thyroid function test revealed TSH: <0.03μU/mL (normal range 0.35-5.5); T3 665.12 ng/dL (80-190); and Free T4 9.8 ng/dL (0.7-1.8). We treated the thyrotoxicosis with oral propylthiouracil 200 mg Q6H, propranolol 40 then 60 mg Q6H, diluted Lugol's solution 3 c.c. TID, intravenous hydrocortisone 100 mg Q6H, and a lot of fluid. Heart rate slowed down gradually. The serum calcium level checked on the third day was normal. Lugol's solution and hydrocortisone was discontinued after 4 days of use. The dosage of other medicine was decreased gradually, too. The serum calcium level on the 7th day was normal, too. He recovered his consciousness after 7 days of coma, but was confused for another 3 days before completely clear. There was no neurological sequela while seen after discharge. By the response to treatments, we thought the manifestations and hypercalcemia were attributed to thyrotoxicosis. This is a rare case of coma resulting from severe thyrotoxicosis, which nearly reached "thyroid storm", that was atypical because there was no fever. So we name it "thyrotoxic coma".