Search

Background/Aims: The Korean Diabetes Association (KDA) guidelines recommend adults aged ≥ 40 years and adults aged ≥ 30 years with diabetes risk factors for diabetes screening. This study aimed to determine the age threshold for diabetes screening in Korean adults.Methods: This study was based on the analyses of Korean adults aged ≥ 20 years using the Korea National Health and Nutrition Examination Survey (KNHANES) and the National Health Insurance Service-National Sample Cohort (NHIS-NSC). To evaluate screening effectiveness, we calculated the number needed to screen (NNS).Results: NNS to detect diabetes decreased from 63 to 34 in the KNHANES and from 71 to 42 in the NHIS-NSC between the ages of 30–34 and 35–39. When universal screening was applied to adults aged ≥ 35, the NNS was similar to that of adults aged ≥ 40. Compared to the KDA guidelines, the rate of missed screening positive in adults aged ≥ 20 decreased from 4.0% to 0.2% when the newly suggested screening criteria were applied.Conclusions: Universal screening for adults aged ≥ 35 and selective screening for adults aged 20 to 34, considering diabetes risk factors, may be appropriate for detecting prediabetes and diabetes in South Korea.

A 59-year-old man was admitted with numbness, pain, and a tingling sensation in both lower legs. He was initially diagnosed with diabetic peripheral neuropathy based on a symptom questionnaire and a quantitative sensory test. Despite symptomatic treatment of diabetic neuropathy, he complained of worsening sensory symptoms and additional motor weakness in both lower extremities. As the motor weakness of both extremities became more aggravated over time, brain and spine imaging tests and a nerve conduction test were performed. The nerve conduction study revealed motor and sensory axonal neuropathy. In his cerebrospinal analysis, albumino-cytologic dissociation, which is compatible to the Gillian-Barre syndrome, was found. Cerebrospinal fluid analysis showed albumino-cytologic dissociation. He was treated with intravenous immunoglobulin and his neurologic deficits were gradually improved.

A 39-year-old woman presented to our clinic with incidentally detected hyperglycemia. Her medical history revealed no specific illness except for a previously diagnosed 2 cm sized thyroid nodule which was diagnosed benign nodular hyperplasia by ultrasound (US) guided fine-needle aspiration (FNA) biopsy for 3 years ago. Laboratory findings show hyperglycemia, hypercalcemia, hypophosphatemia, and increased parathyroid hormone (PTH) level. So, we perform neck US and 99mTc-sestamibi scintigraphy (Tc-MIBI) forprimary hyperparathyroidism(PHPT) evaluation. Neck US showed a 2 cm ill-defined isoechoic nodule in the left thyroid that had previously existed (Fig. 1A). Figure 1 (A) Neck ultrasonography: the 1.69 × 1.70 cm, ill-defined isoechoic thyroid nodule. (B) Preoperative 99mTc-sestamibi scintigraphy scan: it shows a single lesion with strong, hot uptake in the left thyroid gland. (C) Follicular carcinoma cells ... Tc-MIBI showed a single focus of hot uptake (Fig. 1B) and pathology of the left mass after lumpectomy revealed a minimally invasive follicular thyroid carcinoma and uncorrected hypercalcemia (Fig. 1C). Follow-up Tc-MIBI showed a new increased focal uptake below the lower pole of the right thyroid (Fig. 2) which was confirmed parathyroid adenoma by reoperation. The serum PTH and calcium levels were normalized. Figure 2 Postoperative 99mTc-sestamibi scintigraphy (Tc-MIBI) scan of the patient. Tc-MIBI shows a small lesion of hot uptake below the lower pole of the right thyroid gland, detected postoperatively. Yellow arrows indicate parathyroid adenoma. Although neck US is sensitive method for neck mass evaluation, false-negative rate for thyroid FNA is still high and parathyroid tumors may be difficult to distinguish from thyroid follicular lesions, particularly when the tumor is located in the thyroid gland. While Tc-MIBI remains the most useful method for preoperatively localization of parathyroid adenoma, differentiated thyroid cancers can take-up Tc-MIBI during parathyroid imaging, resulting in a false-positive parathyroid scan. This is an important distinction given the association between PHPT and nonmedullary thyroid cancer. However, little is known regarding the mechanistic relationship between PHPT and nonmedullary thyroid cancer, the overall incidence of thyroid malignancy with PHPT is 2% to 6%, proper diagnostic work-up with careful interpretation is essential for an accurate diagnosis in cases of coincidental presentation of a thyroid nodule and biochemical PHPT. When interpreting Tc-MIBI, the clinician should carefully consider parathyroid adenoma and thyroid cancer.

To the Editor, Hyperthyroidism is associated with increased plasma levels of procoagulants and antifibrinolytic clotting factors such as fibrinogen and plasminogen activator inhibitor-1 [1,2]. Similarly, thyrotoxicosis is associated with the occurrence of arterial thrombosis that is primarily due to atrial arrhythmias; the overall incidence of thromboembolism varies from 8% to 40% [3]. Thrombosis is often observed in patients with thyrotoxicosis but there are few reports of arterial thrombosis in conjunction with thyrotoxicosis that are independent of atrial arrhythmias. The present study is a case report of a patient with Graves' disease who presented with a renal infarction without atrial fibrillation. A 54-year-old man visited our emergency department due to the sudden onset of left flank pain for 30 minutes that was accompanied by dysuria in the absence of other symptoms of pyelonephritis in conjunction with neck enlargement and eyeball protrusion. The patient did not have a medical history of diabetes, hypertension, or cardiovascular disease but he had a 10 pack-per-year history of smoking. An electrocardiogram (ECG) revealed sinus tachycardia but his chest X-ray was unremarkable. His vital signs were as follows: blood pressure of 140/90 mmHg, heart rate of 108 beats per minute, respiration rate of 22 breaths per minute, and body temperature of 36.5℃. His laboratory findings were as follows: urinary analysis of 5 to 9 red blood cells per high power field, +1 proteinuria, a thyroid stimulating hormone (TSH) level of 0.01 µU/mL (normal range, 0.55 to 4.78), a free thyroxine level of 28.33 pmol/L (normal range, 11.5 to 22.7), and a TSH-binding inhibitory immunoglobulin level of 40.00 IU/L (normal level, 1.75 or less). Coagulation tests, including prothrombin time and activated partial thromboplastin time, were performed while the patient was in the emergency room and were within normal ranges. In addition, the patient's levels of Factor VIII, von Willebrand factor, antithrombin III, fibrinogen, and plasminogen activator inhibitor-1 were also assessed to screen for coagulation and fibrinolytic system disorders. All levels were within normal ranges and further tests for antiphospholipid antibodies, cytoplasmic antineutrophil cytoplasmic antibodies, and perinuclear antineutrophil cytoplasmic antibodies, which are associated with vasculitis, were negative. Initial Holter monitoring (24 hours) revealed sinus tachycardia but the patient's echocardiogram findings were normal. An enhanced abdominal computed tomography (CT) scan revealed a hypoechoic lesion with a clear wedge-shaped margin on the left kidney and a thrombus in the left renal artery (Fig. 1A). The renal infarction was diagnosed based on the symptoms of the patient and typical CT findings and he was treated with intravenous unfractionated heparin infusions. A thyroid ultrasonography revealed increases in the size and vascularity of both thyroid glands (Fig. 1B) and a technetium-99m thyroid scan was compatible with a diagnosis of Graves' disease (Fig. 1C). The patient was initially treated with methimazole and was switched to warfarin therapy after 5 days of heparin infusions. A second round of Holter monitoring (24 hours) after 1 week showed nonspecific findings and a subsequent ECG showed a normal sinus rhythm. Figure 1 (A) An enhanced abdomen computed tomography scan showing a left renal infarction in the transverse view (left) and the coronal view (right). (B) Thyroid ultrasonography revealing increases in the size and vascularity of both lobes. (C) A technetium-99m ... Hyperthyroidism is associated with a hypercoagulable state and is thought to increase the risk of venous thrombosis [2]. However, the relationship between thyroid function and the risk of venous thrombosis has yet to be fully explored. Thyrotoxicosis shifts the haemostatic balance of an individual towards a hypercoagulable and hypofibrinolytic state [2], but unlike venous thrombosis, the arterial embolisms that are associated with thyrotoxicosis typically result from atrial arrhythmias. Patients with hyperthyroidism frequently present with atrial fibrillation, and its incidence is approximately 10% to 25% for all patients with thyrotoxicosis [3]. The overall rate of systemic embolisms is 8% to 40% in patients with thyrotoxic atrial fibrillation [3], but as in the present case, the presence of arterial thromboembolism in thyrotoxic patients without cardiac arrhythmia is very rare and not fully characterized. Only seven cases of acute cerebrovascular ischemic disease have been reported [1] and in some of these instances, including the present case, paroxysmal atrial fibrillation or vasculitis that may contribute to embolic phenomena could not be entirely excluded. In the present case, the patient presented with a renal infarction during the course of thyrotoxicosis that was caused by hyperthyroidism induced by Graves' disease. Although the relationship that likely exists between arterial embolisms, particularly renal infarctions, and hyperthyroidism needs to be clarified, the present case suggests that uncontrolled thyrotoxicosis is associated with a risk of renal infarction.

To the Editor, Pancreatic adenocarcinoma is an aggressive cancer; the tumor is localized and potentially curable in fewer than 20% of patients at diagnosis. Thus, the overall 5-year survival rate of pancreatic cancer is less than 5%. Several studies have found an increased incidence of pancreatic cancer in patients with diabetes mellitus (DM); however, other studies have shown that pancreatic cancer may cause glucose intolerance. Diabetic ketoacidosis (DKA) is a lethal complication of DM characterized by severe hyperglycemia and metabolic ketoacidosis caused by absolute or relative insulin def iciency. However, DKA is rarely an initial presenting symptom of complicated pancreatic adenocarcinoma. Here we present a case of pancreatic adenocarcinoma that manifested as DKA and its diagnosis was delayed because of a coexisting pancreatic abscess; additionally, we review the relevant literature. A 36-year-old woman visited our emergency department complaining of dyspnea, fever, and abdominal discomfort. She had a history of gestational diabetes mellitus (GDM) during her second pregnancy (6 years ago) and had no familial history of DM or malignancies including pancreatic cancer. She had no history of smoking or alcohol consumption. On arrival, her vital signs were as follows: blood pressure 130/80 mmHg, heart rate 130 per minute, respiration rate 32 per minute, and body temperature 38.6℃. Physical examination showed a soft and non-tender abdomen and no abnormal findings. Laboratory f indings were as follows: urinalysis (glucose [+++], ketone [++++], protein [+]), random serum glucose 334 mg/dL, arterial blood gas analysis (pH 7.1, HCO3 4.5 mmol/L, anion gap 17.6), serum osmolality 285 mOsm/kg, white blood cell count 27.95 (4.8-10.8)×103/µL, high-sensitivity C-reactive protein 204.27 [-5] mg/L, aspartate aminotransferase 89 U/L, alanine aminotransferase 87 U/L, amylase 59 IU/L, lipase 109 U/L, glycated hemoglobin (HbA1c) 9.7%, insulin 6.8 (2.6-24.9) µIU/mL, C-peptide 1.13 (1.1-4.4) ng/mL, cancer antigen 19-9 30.36 (-37) U/mL. Based on the high HbA1c level, low but relatively preserved insulin secretion, and previous history of GDM, the patient was diagnosed as type 2 DM. However, the sudden onset of DKA is unusual in patients with type 2 DM, and high fever is not a sign of DKA [1]. Thus, we performed further diagnostic evaluations to determine the predisposing factors. An abdominal computed tomography (CT) scan revealed a massive retroperitoneal abscess originating from the pancreas (Fig. 1A). The abscess had multifocal air fluid levels and had invaded adjacent structures such as the small intestine and posterior surface of the stomach. In accordance with the examination results, our initial diagnosis was DKA precipitated by pancreatic abscess in a newly diagnosed type 2 DM. Fluid therapy and intravenous insulin infusion with empirical antibiotics were administered and ultrasound guided drainage was performed by percutaneous tube. The cytology finding was compatible with the presence of an abscess, and Klebsiella pneumoniae was identified in the abscess. The patient's condition did not improve following these interventions, and we made the decision to perform an exploratory laparotomy. During surgery we performed a partial resection of the pancreas with debridement of the necrotic tissue because the frozen biopsy showed nonspecific chronic inf lammation. The postoperative pathological diagnosis was chronic pancreatitis with fibrosis (Fig. 1B). After internal and external drainage, the patient was discharged and multiple insulin injections were continued for glucose control. At follow-up, the abdominal CT scan revealed that the abscess had increased in size (Fig. 2A), and her general condition had not improved. We reoperated on the pancreatic mass and confirmed the diagnosis of pancreatic adenocarcinoma complicated by a pancreas abscess (Fig. 2B and 2C). Following the surgery, the patient was treated with palliative chemotherapy and died 6 months after her first visit to our emergency department. Figure 1 (A) Abdominal computed tomography scan showing a massive, multifocal air filled abscess originating from the pancreas expanding into the retropancreatic space with invasion of adjacent structures such as the small intestine and posterior aspect of the ... Figure 2 (A) Abdominal computer tomography scan of the reoperative specimen. Although the air filled abscess lesion was drained, the mass continued to grow and expand into the adjunct structures. (B) Low power microscopic view of the reoperative specimen showing ... Among adult patients presenting with DKA, 47% had known type 1 DM, 26% had known type 2 DM, and 27% had newly diagnosed DM. Precipitating factors in the development of DKA are infections, intercurrent illnesses, psychological stress, and poor compliance with therapy. Infection is the most common precipitating factor for DKA, occurring in 30% to 50% of cases. Other acute conditions that may precipitate DKA include cerebrovascular accident, alcohol or drug abuse, pancreatitis, pulmonary embolism, myocardial infarction, and trauma. However, a significant overlap exists between the clinical presentation of acute pancreatitis and DKA, which may make the diagnosis of pancreatitis in DKA difficult and potentially overlooked [2]. Furthermore, acute pancreatitis is more likely to be associated with severe DKA with marked acidosis. Thus, it is likely that both DKA and the pancreatic abscess contributed to the development of metabolic acidosis in our patient. DKA has been documented as a presenting symptom of a pancreatic tumor only in endocrine tumors such as glucagon-secreting islet cell neoplasm or somatostatinomas, which are rare conditions. Furthermore, DKA associated with a pancreatic adenocarcinoma is very rare and only one case has been reported previously: the patient, who had a long-standing history of type 2 DM, presented with DKA and was found to have a pancreatic adenocarcinoma [3]. However, DKA as an initial presenting symptom of pancreatic adenocarcinoma in patients without DM is extremely rare. Approximately 80% of patients with pancreatic cancer have glucose intolerance or f lank diabetes; however, evidence for a cause and effect relationship between DM and pancreatic cancer is inconclusive. Although prolonged hyperinsulinemia has been suggested to stimulate pancreatic carcinogenesis [4], a meta-analysis that included 36 clinical trials of patients with type 2 DM showed that diabetes is a risk factor for pancreatic cancer [5]. Currently, considerable experimental and epidemiological evidence supports both arguments. Thus, further studies are necessary to clarify the relationship between DM and pancreatic cancer. In general, the classical presentation of an adenocarcinoma of the pancreas includes one or more of the following symptoms: obstructive jaundice, dark urine, weight loss, and deep-seated abdominal pain. However, the early symptoms of pancreatic cancer are nonspecific, and associated symptoms may occur later in the disease progression; thus, most pancreatic cancers are diagnosed in the advanced stage. Previous reports have documented that pancreatic carcinomas may coexist with complications such as acute pancreatitis, a pancreatic pseudocyst, and pancreatic abscess. Thus, a carcinoma may present as a septic complication of pancreatitis such as an infected pseudocyst, pancreatic abscess, or infected pancreatic necrosis, although this situation is exceedingly rare because the pancreatitis associated with pancreatic cancer is usually mild. Thus, the diagnosis of a complicated pancreatic adenocarcinoma is likely to be delayed unless the physician has a high index of suspicion. In summary, we report here a patient with undiagnosed type 2 DM presenting as DKA resulting from a massive pancreatic abscess. The initial operative biopsy revealed chronic inf lammatory cells associated with extensive inflammation and necrosis of pancreatic tissues. Although this clinical situation is unusual, physicians should not overlook the possibility of pancreatic cancer in newly detected type 2 DM presenting with DKA, particularly when obvious precipitating factors are not present. Furthermore, the fact that pancreatic cancer can coexist with complicated pancreatitis should be taken into consideration. Despite numerous investigations, the relationship between pancreatic cancer and DM is not clear, highlighting the need for further study.

To the Editor, Neuropathy is common in patients with diabetes mellitus (DM). The condition involves several neurological systems resulting in a variety of symptoms and diverse treatments [1]. Truncal neuropathy is among the spectrum of peripheral neuropathies associated with DM. It manifests as localized chest or abdominal pain, which may be confused with referred pain from the intrathoracic or intra-abdominal organs [2], and when treated as such it may lead to extensive and unnecessary clinical investigations. Although truncal neuropathy is generally managed using oral medication, we report here successful treatment of truncal neuropathy in a patient with type 2 DM using a topical agent and nerve block. We also present a review of the literature. A 50-year-old male presented at the emergency department of Chonbuk National University Hospital, South Korea, complaining of lower abdominal pain, such as burning and a lacerating pain, during the past 2 weeks. He complained of severe lancinating pain from the lower costal area to upper inguinal area, and his numeric rating scale (NRS) pain symptom score was 10. He had been diagnosed with type 2 DM 2 years previously and was prescribed premixed 70:30 insulin for 6 months. The patient was 168 cm tall, weighed 45 kg, and had smoked 20-pack years. On physical examination, the patient had no diarrhea, abdominal discomfort, fever, or skin lesions. During the previous 3 months, he experienced severe weight loss of 10 kg (20% of total body weight). Laboratory tests were as follows: complete blood count (white blood cell 6,240/µL, hemoglobin 12.8 g/dL, platelet 357 k), sodium 139 mmol/L, potassium 3.9 mmol/L, alanine transaminase 15 IU/L (normal range, 12 to 33), aspartate transaminase 18 IU/L (normal range, 5 to 35), erythrocyte sedimentation rate (ESR) 13 mm/hr (normal range, 0 to 9), highly sensitive C-reactive protein 0.2 mg/L (normal range, 0 to 5), hemoglobin A1c 95 mmol/mol (10.8%), fasting insulin 5.0 µU/mL (normal range, 2.6 to 24.9), C-peptide 1.17 ng/mL (normal range, 1.1 to 4.4), homeostasis model assessment for insulin resistance 2.5, and albumin to creatinine ratio 91.9 mg/g. He had nonproliferative diabetic retinopathy. Tumor marker and abdomen pelvic computed tomography were performed to screen for cancer. The scans revealed no evidence of cancer or intra-abdominal organ pathology. Furthermore, no abnormalities in rheumatic autoantibodies, such as rheumatoid factor or antinuclear antibodies, were found nor were there suspected symptoms of vasculitis or other connective diseases. Plain X-ray revealed no thoracolumbar spine abnormalities. The quantitative sensory test showed small and large fiber neuropathy at the upper and lower extremities. A nerve conduction study revealed sensorimotor polyneuropathy in the trunk. The patient was diagnosed with type 2 DM with triopathy involving truncal neuropathy. He was managed with pregabalin 300 mg/day, nortryptiline 50 mg/day, and α-lipoic acid 600 mg/day. After 2 weeks, his NRS symptom score improved to 3, and he was discharged. However, 3 months later, the patient complained of aggravation of the same abdominal wall. His neuropathic medications had not changed during this time. According to his self-monitored blood glucose values, fasting glucose was 80 to 110 mg/dL and postprandial glucose was 180 to 230 mg/dL using premixed insulin. He reported recently smoking and heavy alcohol consumption following a stressful situation. His pain symptom score increased to NRS 7. He complained of extreme aching, burning, and lancinating pain, which severely disrupted his daily activities. His current oral medication regime was not effective for reducing his pain, and the dose could not be increased because of side effects such as nausea and drowsiness. Thus, we prescribed topical capsaicin cream and a lidocaine patch. Furthermore, we performed an epidural nerve block at the 10 to 11 thoracic nerve using lidocaine, ropivacine, and triamcinolone. After 2 to 3 weeks of using this topical treatment, the patient's symptom score improved to NRS 2. He was maintained on topical capsaicin cream, lidocaine patch, and pregabalin and was able to decrease his dose of nortryptiline to 10 mg/day and discontinue α-lipoic acid. Peripheral neuropathy is a common microvascular complication of DM. It presents in various ways such as peripheral sensory neuropathy, motor neuropathy, and autonomic neuropathy. Factors commonly associated with peripheral neuropathy are being male, a smoker, long duration of DM, and poor glycemic control. Painful diabetic neuropathy is best managed by maintaining good control of glucose level and using medication to relieve painful symptoms [3]. Truncal neuropathy is a type of acute painful neuropathy. It presents as an acute onset pain in a dermatomal distribution over the thorax or the abdomen [2]. The acute asymmetrical pain may be associated with local bulging of the abdominal wall. Lauria et al. [4] compared symptomatic and non-symptomatic skin biopsies from three patients with truncal neuropathy to investigate the neuropathological features of truncal neuropathy. They found the loss of intraepideraml nerve fiber densities and the presence of degenerative changes in dermal nerve fibers associated with truncal neuropathy. Furthermore, the lesions were correlated with the subjective sensory symptoms. We did not assess nerve fiber changes before and after treatment using nerve biopsy; thus, the relationship between topical agents and neuropathy must be clarified in future studies. Several cases of truncal neuropathy in patients with DM have been reported previously (Table 1). Most patients have been male with a DM duration > 2 years, and the neuropathy has primarily been unilateral. Three cases have shown abdominal wall weakness similar to an abdominal hernia. About half of patients had used systemic oral pain medications to control pain, as in the present case. However, the present case is the only one to have used the topical medications capsaicin cream and lidocaine to control pain. Most previous patients have had a good prognosis, and the pain spon taneously remitted in two patients so they did not require further pain relief medication. Our patient improved following the administration of systemic oral medication, topical cream, and epidural nerve block. Table 1 Review of truncal neuropathy in patients with diabetes Diabetic peripheral neuropathy is typically managed by controlling blood glucose levels and administering tricyclic antidepressants, anticonvulsants, α-lipoic acid, opioids, and topical agents. Furthermore, truncal neuropathy may be managed using oral medications such as gabapentin, pregabalin, and duloxetin (Table 1). Truncal neuropathy pain generally improves completely 3 to 12 months following treatment. However, our patient experienced severe acute pain, which significantly disrupted his sleep and daily activities. Thus, we used systemic oral medications, topical agents, and an epidural nerve block to treat his pain, which was successfully relieved after 2 to 3 weeks. Epidural nerve block is generally used to control cancer pain and irreversible neuropathy pain [5]; however, our case indicates that epidural nerve block may be effective for patients with inadequate pain control after optimal use of systemic medications or intolerance to systemic analgesic side effects. It is important to manage the appropriate patient for nerve block because postprocedure neuritis or deafferentation neuralgia may develop in some patients. Epidural nerve block has not previously been used in patients with DM, possibly because some diabetic peripheral nerve damage may be reversible. However, as our patient demonstrates, topical epidural nerve block may be an effective treatment for patients who have severe truncal neuropathy that is not controlled by oral medications or for those who cannot tolerate their medications. Further studies on the efficacy of nerve block for the management of truncal neuropathy in patients with DM are warranted. To the best of our knowledge, our patient is the first case of truncal neuropathy successfully managed using topical cream and epidural nerve block.

We describe an unusual case of systemic lupus erythematosus with pulmonary manifestations presenting as hypoglycemia due to anti-insulin receptor antibodies. A 38-year-old female suffered an episode of unconsciousness and was admitted to hospital where her blood glucose was found to be 18 mg/dL. During the hypoglycemic episode, her serum insulin level was inappropriately high (2,207.1 pmol/L; normal range, 18 to 173) and C-peptide level was elevated (1.7 nmol/L; normal range, 0.37 to 1.47). Further blood tests revealed the presence of antinuclear antibodies, anti-double-stranded DNA antibodies, and anti-Ro/SSA, anti-La/SSB, anti-ribonucleoprotein, and anti-insulin receptor antibodies. A computed tomography scan of the abdomen, aimed at tumor localization, such as an insulinoma, instead revealed ground-glass opacities in both lower lungs, and no abnormal finding in the abdomen. For a definitive diagnosis of the lung lesion, video-associated thoracoscopic surgery was performed and histopathological findings showed a pattern of fibrotic non-specific interstitial pneumonia.

We describe herein an unusual case of subacute thyroiditis presenting as acute psychosis. An 18-year-old male presented at the emergency department due to abnormal behavior, psychomotor agitation, sexual hyperactivity, and a paranoid mental state. Laboratory findings included an erythrocyte sedimentation rate of 36 mm/hr (normal range, 0 to 9), free T4 of 100.0 pmol/L (normal range, 11.5 to 22.7), and thyroid stimulating hormone of 0.018 mU/L (normal range, 0.35 to 5.5). A technetium-99m pertechnetate scan revealed homogeneously reduced activity in the thyroid gland. These results were compatible with subacute thyroiditis, and symptomatic conservative management was initiated. The patient's behavioral abnormalities and painful neck swelling gradually resolved and his thyroid function steadily recovered. Although a primary psychotic disorder should be strongly considered in the differential diagnosis, patients with an abrupt and unusual onset of psychotic symptoms should be screened for thyroid abnormalities. Furthermore, transient thyroiditis should be considered a possible underlying etiology, along with primary hyperthyroidism.