Thyroid Antibody Tests Research Articles

Thyroid function and antibody testing in patients receiving pegylated-interferon therapy

Thyroid function and antibody testing in patients receiving pegylated-interferon therapy

Association between systemic lupus erythematosus and autoimmune thyroid dysfunction in pediatric population: a single center experience

BackgroundSystemic Lupus Erythematosus (SLE) patients are more likely than the general population to suffer from thyroid illness. The major goal was to assess the thyroid dysfunctions due to immunological factors in Egyptian SLE children and how they are related to the course and severity of the illness.MethodsFifty children and adolescents with SLE are included in this cross-sectional observational study. Every patient underwent a thorough physical examination and a comprehensive history taking. An enzyme-linked immunosorbent assay (ELISA) approach was used to evaluate the thyroid profile, anti-thyroglobulin (Anti-TG), and anti-thyroid peroxidase (anti-TPO) antibodies.ResultsOf the 50 patients, the female: male ratio (F: M = 7:1) was 44 females and 6 males (12%). They were between the ages of 5 and 17. Out of the patients, thirty-two (64%) had thyroid dysfunctions, 19 (38%) had euthyroid sick syndrome, ten (20%) had overt hypothyroidism, three (6%) had subclinical hypothyroidism, and none had hyperthyroidism. Of the 50 patients, one (2%) had increased anti-TPO, whereas all other patients had normal anti-TG levels. A statistically significant negative correlation (p-value 0.007) was seen between the disease duration and free thyroxine (FT4). Furthermore, a significant negative correlation (p-values 0.015 and 0.028) was found when comparing the disease duration with thyroid antibodies (anti-TG and anti-TPO).ConclusionIn Juvenile Systemic Lupus Erythematosus (JSLE), thyroid dysfunctions can be identified. The disease duration but not its activity was significantly correlated with thyroid antibodies. For children with JSLE, thyroid function testing should be done on a regular basis. It is preferable to carry out additional thyroid antibody tests when necessary.

FRI571 Maternal Graves’ Disease With Foetal Thyrotoxicosis And Goitre

Abstract Disclosure: D. Fennell: None. J. Walsh: None. M. Hatunic: None. Background: Graves’ disease (GD) is an uncommon condition affecting 0.2% of pregnancies. Foetal and neonatal thyrotoxicosis occurs in between 1-5% of pregnant patients with a history of GD, typically beyond 20 weeks gestation. Given its potential for serious morbidity and mortality, prompt recognition and treatment of the condition is essential. Clinical case: A 34-year-old female was referred at 21+2 weeks’ gestation from another hospital due to concerning cardiac findings noted on routine prenatal ultrasound (US). Her medical history was significant for GD (TRAb positive) with moderate ophthalmopathy and total thyroidectomy ten months prior, on L-thyroxine 150 mcg daily. Foetal tachycardia 170-180bpm was noted, with US showing with right ventricular hypertrophy, small pericardial effusion and a 1.9 x 2.7 x 2.8cm neck mass, suspicious for foetal goitre. Maternal laboratory studies showed TSH 2.38mIU/L (0.27-4.2), FT4 16.0pmol/L (12-22), TPO antibody negative <3.0IU/ml and TRAb markedly elevated >30IU/L (0-1.8). A diagnosis of foetal thyrotoxicosis secondary to placental passage of maternal TRAb was made. She was commenced on carbimazole 20mg twice daily at 21+6 weeks’ gestation as treatment, with the goal of normalising foetal heart rate. Careful, weekly follow-up with US scanning noted gradual improvement in the foetus’ condition, with resolution of pericardial effusion and foetal heart rate normalisation. Maternal TFTs were monitored weekly and she remained euthyroid on increased dose L-thyroxine (200 mcg daily). Multidisciplinary team consensus was to proceed with elective Caesarean section at 34 weeks’ gestation, to avoid risk of airway obstruction from foetal goitre. A healthy male infant was born with spontaneous breathing and normal heart rate at delivery. Apgar scores were 9 and 9 at 1 and 5 minutes. Maternal carbimazole was immediately discontinued post-delivery and L-thyroxine reduced to 150 mcg daily. She had an uncomplicated recovery post-Caesarean section. The infant was closely monitored in the neonatal ICU. On day five of life, he became unwell, developing a supraventricular tachycardia. Thyrotoxicosis was confirmed on laboratory studies (FT4 >100pmol/L). Carbimazole, propranolol and Lugol’s iodine were all used as treatment. Thyroid hormone levels normalised within days, with gradual clinical improvement. He was discharged home well four weeks after birth, remaining on propranolol 0.3mg four times daily and carbimazole 0.5mg twice daily, with close paediatric outpatient follow-up planned. Conclusion: Foetal thyrotoxicosis is a rare condition, but can cause serious morbidity, as demonstrated here. First trimester maternal thyroid antibody testing is recommended for all patients with a history of GD, to identify those at risk. Management of the condition is complex, requiring multidisciplinary specialist input for favourable outcome. Presentation: Friday, June 16, 2023

Changes in therapeutic response, ocular manifestations of Graves' orbitopathy and quality of life during the first year after orbital radiotherapy.

The aim of our study was to assess the changes in the therapeutic response, ocular manifestations of GO and quality of life during the first year after OR. The study involved 26 consecutive patients with active moderate-to-severe GO indicated for OR, 18 females, mean age 57 ± 12.5. At baseline, all patients underwent comprehensive ocular examination and thyroid hormone and antibody testing. Then, OR was performed with a total dose of 20Gy, divided into 10 sessions of 2Gy each with concomitant oral intake of low-dose glucocorticoids. Therapeutic response and individual ocular manifestations were evaluated 1, 3, 6 and 12months after OR, and QoL-at 3, 6 and 12months by a disease-specific questionnaire. One month after OR, 61.6% of patients had a therapeutic response (full or partial). During the follow-up, the proportion of full-responders gradually increased up to 57.5% at 12months, while that of non-responders gradually decreased, reaching 11.5% at 12months. All individual ocular manifestations improved significantly 1-3months after OR. QoL related to visual functioning increased significantly at 6months, whereas QoL related to appearance improved significantly at 12months. The vast majority of our patients with active moderate-to-severe GO exhibited full or partial therapeutic response after OR. The initial effect on the therapeutic response and individual ocular parameters was evident as soon as 1-3months after the procedure. OR also has a beneficial effect on patients' QoL. NCT05775185/07.03.2023, retrospectively registered.

Elevated Thyroid Autoantibodies Aggravate Stroke Severity in Euthyroidism with Acute Ischemic Stroke.

Introduction Studies have indicated that immune reactions contribute to endothelial dysfunction and atherosclerosis. It is unclear whether thyroid dysfunction or elevated thyroid autoantibodies are associated with atherosclerosis. Therefore, we investigated the influence of thyroid autoimmunity related to elevated thyroid autoantibodies on functional outcome in euthyroidism with acute ischemic stroke (AIS). Methods All patients with AIS underwent tests for thyroid function and thyroid antibodies (thyroid peroxidase antibody and thyroglobulin autoantibody). We divided the patients suffering from euthyroidism and AIS into positive thyroid autoantibody and negative thyroid autoantibody groups. Demographic profiles, risk factors, and functional outcomes were compared between the two groups. Results Out of the total 422 patients, 50 (11.8%) were included in the positive thyroid autoantibody group. The National Institutes of Health Stroke Scale (NIHSS) score at admission and discharge was higher in the positive thyroid autoantibody group than the negative thyroid autoantibody group (P < 0.05). In addition, there was significant difference in the mortality during hospitalizations between the two groups (P < 0.01). Conclusion This study showed that thyroid autoantibodies aggravate stroke severity in euthyroidism with AIS. We speculate that vascular damage related to thyroid autoimmunity may aggravate the increased risk of unfavorable outcomes, independent of thyroid function.

Effects of animal protein intake during pregnancy on autoimmune thyroiditis in pregnant women with mild iodine deficiency.

Iodine and animal protein may affect thyroid function. In the present study, we explored the association between animal protein intake and thyroid antibody status in pregnant women following universal salt iodisation. Pregnant women were enrolled using a multistage, stratified random sampling method in Shanghai. In total, 4646 eligible women were interviewed in person. We used a validated food frequency questionnaire and food composition tables to calculate the daily intakes of protein and iodine. We collected urine samples and performed thyroid antibody tests. Positive thyrotropin receptor antibody (TR-Ab) rates were different among animal protein intake groups (p < 0.05). Median urinary iodine concentration (UIC) was higher in the thyroid peroxidase antibody (TPO-Ab) positive group than in the negative group (p < 0.05). The median of total protein intake, animal protein intake and UIC was higher in the TR-Ab positive group than in the negative group (p < 0.05). The median of total protein intake and UIC was higher in the TPO-Ab/TG-Ab/TR-Ab positive group than in the negative group (p < 0.05). Multivariable logistic regression results showed that insufficient iodine had a negative correlation with positive TPO-Ab and positive TR-Ab (p < 0.05). The middle third and top third animal protein intakes served as protective factors for TR-Ab (coefficient = 0.559, 95% confidence interval [CI] = 0.415-0.752, p < 0.001; coefficient = 0.0.406, 95% CI = 0.266-0.621, p < 0.001) and positive TPO-Ab/TR-Ab/TG-Ab (coefficient = 0.817, 95% CI = 0.687-0.971, p = 0.022; coefficient = 0.805, 95% CI = 0.672-0.964, p = 0.018). Adequate animal protein intake protects against elevated anti-thyroid antibody levels in pregnant women with mild iodine deficiency.

Brain dysfunction and thyroid antibodies: autoimmune diagnosis and misdiagnosis.

Hashimoto encephalopathy, also known as steroid-responsive encephalopathy associated with autoimmune thyroiditis, has been defined by sub-acute onset encephalopathy, with elevated thyroid antibodies, and immunotherapy responsiveness, in the absence of specific neural autoantibodies. We aimed to retrospectively review 144 cases referred with suspected Hashimoto encephalopathy over a 13-year period, and to determine the clinical utility of thyroid antibodies in the course of evaluation of those patients. One hundred and forty-four patients (all thyroid antibody positive) were included; 72% were women. Median age of symptom onset was 44.5 years (range, 10–87). After evaluation of Mayo Clinic, 39 patients (27%) were diagnosed with an autoimmune CNS disorder [autoimmune encephalopathy (36), dementia (2) or epilepsy (1)]. Three of those 39 patients had neural-IgGs detected (high glutamic acid decarboxylase-65, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-receptor and neural-restricted unclassified antibody), and 36 were seronegative. Diagnoses among the remaining 105 patients (73%) were functional neurological disorder (n = 20), neurodegenerative disorder (n = 18), subjective cognitive complaints (n = 14), chronic pain syndrome (n = 12), primary psychiatric (n = 11), sleep disorder (n = 10), genetic/developmental (n = 8), non-autoimmune seizure disorders (n = 2) and other (n = 10). More patients with autoimmune CNS disorders presented with sub-acute symptom onset (P < 0.001), seizures (P = 0.008), stroke-like episodes (P = 0.007), aphasia (P = 0.04) and ataxia (P = 0.02), and had a prior autoimmune history (P = 0.04). Abnormal brain MRI (P = 0.003), abnormal EEG (P = 0.007) and CSF inflammatory findings (P = 0.002) were also more frequent in the autoimmune CNS patients. Patients with an alternative diagnosis had more depressive symptoms (P = 0.008), anxiety (P = 0.003) and chronic pain (P = 0.002). Thyoperoxidase antibody titre was not different between the groups (median, 312.7 versus 259.4 IU/ml; P = 0.44; normal range, <9 IU/ml). None of the non-autoimmune group and all but three of the CNS autoimmune group (two with insidious dementia presentation, one with seizures only) fulfilled the autoimmune encephalopathy criteria proposed by Graus et al. (A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol 2016; 15: 391–404.) (sensitivity, 92%; specificity, 100%). Among patients who received an immunotherapy trial at our institution and had objective post-treatment evaluations, the 16 responders with autoimmune CNS disorders more frequently had inflammatory CSF, compared to 12 non-responders, all eventually given an alternative diagnosis (P = 0.02). In total, 73% of the patients referred with suspected Hashimoto encephalopathy had an alternative non-immune-mediated diagnosis, and more than half had no evidence of a primary neurological disorder. Thyroid antibody prevalence is high in the general population, and does not support a diagnosis of autoimmune encephalopathy in the absence of objective neurological and CNS-specific immunological abnormalities. Thyroid antibody testing is of little value in the contemporary evaluation and diagnosis of autoimmune encephalopathies.

Reference Intervals for Thyroid-Associated Hormones and the Prevalence of Thyroid Diseases in the Chinese Population.

BackgroundThyroid diseases are highly prevalent worldwide, but their diagnosis remains a challenge. We established reference intervals (RIs) for thyroid-associated hormones and evaluated the prevalence of thyroid diseases in China.MethodsAfter excluding outliers based on the results of ultrasound screening, thyroid antibody tests, and the Tukey method, the medical records of 20,303 euthyroid adults, who visited the Department of Health Care at Peking Union Medical College Hospital from January 2014 to December 2018, were analyzed. Thyroid-associated hormones were measured by the Siemens Advia Centaur XP analyzer. The RIs for thyroid-associated hormones were calculated according to the CLSI C28-A3 guidelines, and were compared with the RIs provided by Siemens. The prevalence of thyroid diseases over the five years was evaluated and compared using the chi-square test.ResultsThe RIs for thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), total thyroxine (TT4), and total triiodothyronine (TT3) were 0.71–4.92 mIU/L, 12.2–20.1 pmol/L, 3.9–6.0 pmol/L, 65.6–135.1 nmol/L, and 1.2–2.2 nmol/L, respectively. The RIs of all hormones except TT4 differed significantly between males and females. The RIs of TSH increased with increasing age. The prevalence of overt hypothyroidism, overt hyperthyroidism, subclinical hypothyroidism, and subclinical hyperthyroidism was 0.5% and 0.8%, 0.2% and 0.6%, 3.8% and 6.1%, and 3.3% and 4.7% in males and females, respectively, which differed from those provided by Siemens.ConclusionsSex-specific RIs were established for thyroid-associated hormones, and the prevalence of thyroid diseases was determined in the Chinese population.

SAT-491 Transient Thyrotoxicosis with Immune Checkpoint Inhibitors Therapy: The Importance of Endocrine Evaluation

IntroductionThe immune checkpoint-blocking antibody nivolumab is recognized as having a crucial role in different malignancies by blocking programmed death-1 (PD-1) receptor immune cells. Besides its benefits, nivolumab may cause endocrine immuno-related adverse events (irAEs), including thyroid dysfunction (TD).Clinical caseA 71-year-old man, with an uneventful past medical history, was diagnosed with stage IIIB (T4N2M0), epithelial-growth-factor-receptor (EGFR) wild type, lung adenocarcinoma.The patient underwent 4 cycles of first line chemotherapy with cisplatin/vinorelbine and then radiotherapy, obtaining a partial response.After 4 months, tumor progression was identified, as assessed by whole-body 18-Fluorodeoxyglucose positron emission tomography (FDG-PET) scan, showing pleural and nodal metastasis. Nivolumab, 3 mg/kg every 2 weeks, was started at this point.While pre-nivolumab thyroid function was normal, 3 months after starting the therapy, a low serum TSH level of 0.04 mUI/mL (0.38-5.33) was found, associated with a normal level of FT4, of 10.8 pmol/L (7.9-14.4). Thyroid antibody (Ab) tests, including TSH-receptor Ab, were negative. At ultrasound examination, thyroid gland parenchyma was normo-echoic, demonstrating an isoechoic thyroid nodule in the right lobe, with regular margins, measuring 14mm diameter. Previous medical history was negative for thyroid disease.One week after the referred thyroid function tests, nivolumab was discontinued due to progressive disease as assessed by abdominal magnetic resonance, demonstrating right adrenal metastasis and patient started cisplatin/permetrexed chemotherapy. One month after nivolumab suspension, patient had already normalized thyroid tests, with TSH 2.27 mUI/mL and FT4 9.1 pmol/L. More recently (6 months after nivolumab discontinuation), thyroid function tests continued stable, with TSH 1.05 mUI/ml and T4L 9.4 mmol/l. At this point, patient was receiving permetrexed maintenance therapy.ConclusionsImmune checkpoint molecules as nivolumab, play a crucial role in anti-tumor immunity evasion. Besides its benefits, it may cause irAEs, including TD.We believe it’s essential to perform thyroid function tests at baseline and before the administration of each nivolumab dose, if possible. Additionally, large prospective studies are required in order to assess, the impact of autoimmunity on the development of TD induced by nivolumab, and its potential effect on overall survival and specific cancer survival data.

SAT-576 Possible Involvement of Thyroid Function in PCSK9 Inhibitor Therapy

INTRODUCTIONProprotein convertase subtilisin kexin type 9 (PCSK9) inhibition is an effective strategy for lowering plasma LDL-cholesterol and enhancing the LDL-cholesterol lowering ability of statins. PCSK9, a serine protease that binds to the LDL receptor promoting its degradation, is an important regulator of LDL metabolism. In addition, LDL-cholesterol is also controlled by TSH and thyroid hormones via PCSK9. TSH has received increasing attention as being closely associated with increased LDL-cholesterol level and higher atherosclerotic risks. In vitro study, the effects of TSH on hepatic PCSK9 expression in HepG2 cells were reported (1). I here report a case of transient hyperthyroidism secondary to PCSK9 inhibitor therapy. This case highlights the involvement of thyroid function in PCSK9 Inhibitor therapy.CLINICAL CASEA 65-year-old man had a weight loss of 6 kg (13 lbs.) in 4 months, accompanied with fatigue. He had a past history of myocardial infarction and his LDL was 83 mg/dL by 2.5mg of rosuvastatin and heart rate was controlled by 10mg of carvedilol. Six months ago, he started a PCSK9 Inhibitor therapy with 140mg of evolocumab every 2 weeks for 6 weeks. He had no preceding viral illness and denied anterior neck pain or tenderness. His height was 1.53 m, weight 52.6 kg (115 lbs.), and body mass index (BMI) 22.46 kg/m2. His thyroid was not enlarged and non-tender without clear palpable thyroid nodules or neck lymph nodes. Hyperthyroidism was suspected and confirmed by thyroid function tests: TSH was less than 0.0005 μIU/mL (normal 0.35–4.94), and free T4 1.830 ng/dL (0.70–1.48). Graves’ disease was considered, and thyroid antibody tests performed. Thyroid peroxidase (TPO) antibody titer was less than 9 IU/mL (<9), and TSI 141% (<120%). To confirm the diagnosis of this hyperthyroid patient, Technetium-99m uptake and scan was done which showed uptake of 0.8% (0.5–7%). After careful observation for 2 months with 5mg of carvedilol, he turned asymptomatic and free T4 lowered to 1.480 ng/dL and TSH remained less than 0.0005 μIU/mL.CLINICAL LESSONSI here report a case of transient hyperthyroidism secondary to PCSK9 inhibitor therapy. There has been no report of hyperthyroidism induced by PCSK9 inhibitors. Immunological influence of anti-PCSK9 therapy on thyroid is unknown. In this case, the decrease of TSH due to hyperthyroidism was considered to reduce hepatic PCSK9 expression, leading to additive effect to PCSK9 inhibitor. PCSK9 inhibitors may modify the effects of hyperlipidemia treatment by causing changes in thyroid function. When using PCSK9 inhibitors, follow-up of thyroid function should be considered. This case highlights the involvement of thyroid function in PCSK9 inhibitor therapy.Reference(1) Gong, Y., Ma, Y., et al. Thyroid stimulating hormone exhibits the impact on LDLR/LDL-c via up-regulating hepatic PCSK9 expression. Metabolism. 2017;76;32–41

Hyperthyroid Phase of Hashimoto's Thyroiditis

Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient areas of the world. This condition, however, can sometimes show hyperthyroidism. A 39-year-old femalewas admitted to hospital due to shortness of breath and tremor four hours before hospitalization. There were nausea, chestpain, cold chills, and palpitation. She was diagnosed with Hashimoto's thyroiditis and routinely received tyrosol,propranolol, and dexamethasone. Physical examination showed cervical mass, afebrile, blood pressure of 130/70 mmHg,pulse rate of 110 beats/minute and respiratory rate of 20 breaths/minute. Laboratory examinations showed WBC 7.53 x 109/L, Hb 11.0 g/dL and platelet count of 168 x 109/L. Chest X-Ray: negative for infiltrates. Several laboratory testswere performed, abnormal results were as follows: FT4 level of 2.96 ng/dL (increased), TSH level of 0.003 µIU/mL(decreased), anti-TPO (antithyroid microsomal antibody) level of 306 IU/ml (increased), and IgE level of 213.6 IU/mL(increased). Peripheral blood smear, coagulation test, serum electrolytes, liver function tests, renal function tests, urinalysis,CEA and Ca 125 were within normal limits. Thyroid ultrasound was performed and showed a benign lesion. Fine needleaspiration biopsy showed lymphocytic Hashimoto's thyroiditis. Echocardiography showed hyperthyroid heart disease. Dueto an increase of anti-TPO and FT4 levels, a decrease of TSH levels and lymphocytic thyroiditis from FNAB, this patient wasdiagnosed with a hyperthyroid phase of Hashimoto's thyroiditis. Thyroid function tests and thyroid antibody tests must bemonitored to distinguish between the hyperthyroid and hypothyroid phase of Hashimoto thyroiditis.

HASHIMOTO’S THYROIDITIS HYPERTHYROID STAGE

Preliminary: Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine- sufficient areas of the world, but can sometimes show hyperthyroidism. Case: A 39-year-old female was referred due to shortness of breath and tremor, four hours before hospitalization. There was nausea, chest pain, cold chills and palpitation. She was diagnosed with Hashimoto’s thyroiditis and routinely received tyrosol, propanolol and dexamethasone. Physical examination: cervical mass, afebrile, blood pressure 130/70 mmHg, pulse rate 110 x/minute and respiratory rate 20 x /minute. Laboratory examinations showed WBC 7.53 x 109/L, Hb 11.0 g/dL and platelet count 168 x 109/L. Chest X-Ray: negative for infiltrates. Several laboratory tests were performed, abnormal results were as follows: FT4 2.96 ng/dL (increased), TSH 0.003 uIU/mL (decreased), anti-TPO (antithyroid microsomal antibody) 306 IU/ml (increased), Ig E 213.6 IU/mL (increased). Peripheral blood smear, coagulation test, serum electrolytes, liver function tests, renal function tests, urinalysis, CEA and Ca 125 were within normal limits. A thyroid ultrasound resulted in a benign lesion. Fine Needle Aspiration Biopsy concluded in lymphocytic Hashimoto’s thyroiditis. Echocardiography showed hyperthyroid heart disease. Discussion: Due to an increase in anti-TPO and FT4, a decrease in TSH and lymphocytic thyroiditis from FNAB, this patient was diagnosed with Hashimoto’s Thyroiditis Hyperthyroid Stage. Conclusion: Thyroid function tests and thyroid antibody tests must be monitored to decide whether it is hyperthyroid or hypothyroid stage of Hashimoto thyroiditis.

Thyroid Autoimmunity and Autoimmunity in Chronic Spontaneous Urticaria Linked to Disease Severity, Therapeutic Response, and Time to Remission in Patients with Chronic Spontaneous Urticaria.

Background Chronic spontaneous urticaria (CSU) is autoimmune in nature and associated with thyroid autoimmunity (TA), but evidence on autoimmunity in relation to CSU progression and prognosis is limited. We evaluated whether TA and autoimmunity in CSU are correlated with disease severity, therapeutic response, and time to remission and establish an association between CSU characteristics linked to thyroid autoantibody. Methods Medical records of patients diagnosed with urticaria attending outpatient dermatology clinic at a university-based hospital from 2013 to 2017 were retrospectively reviewed. Data on the clinical characteristics, laboratory investigations particularly thyroid antibody titers, autologous serum skin test (ASST) and autologous plasma skin test (APST) results and their link to disease severity, treatments, and time to remission of CSU patients were analyzed. Results Of 1,096 patients with urticaria, 60.2% had CSU. Three-hundred patients fulfilled the inclusion criteria for CSU with complete thyroid antibody testing. Positive TA was significantly associated with female gender and age > 35 years (p = 0.008). Antithyroid peroxidase (anti-TPO)-positive patients suffered from CSU longer than 12 and 18 months compared to anti-TPO-negative patients (100.0% vs. 82.6%, p = 0.042, and 100.0% vs. 75.9% p = 0.020, respectively). The presence of urticarial attacks > 4 days/week was significantly seen in ASST and APST-positive patients compared to those without (84.6% vs. 61.3%, p = 0.011, and 85.3% vs. 61.8%, p = 0.006, respectively). Positive APST patients were more difficult to treat than those with negative results (61.2% vs. 37.8%, p = 0.017). Conclusions Antithyroid peroxidase is a predictor of time to remission, while autologous skin testing is linked to disease severity (ASST and APST) and therapeutic response (APST) in CSU patients.

Laboratory Evaluation of Vocal Fold Paralysis and Paresis

This study aimed to assess the value of comprehensive laboratory evaluation in patients with vocal fold paralysis or paresis. This is a retrospective chart review. Records of 231 patients with vocal fold paralysis or paresis were reviewed to determine whether there is a significant increase in the number of abnormal test results compared with rates of abnormal results for these tests in the general population and whether testing resulted in clinically important diagnosis. Laboratory data were collected from charts from initial visits from 2010 to 2014 and compared with national data. When controlled for age and sex, white blood cell count was found to have a significantly higher rate of abnormal test results (P < 0.001) in patients with vocal fold paralysis or paresis than the general population. Although hemoglobin, thyroid-stimulating hormone, and thyroid antibody tests were more likely to be abnormal in our patient population, the trend was not statistically significant. Further, the prevalence of syphilis and myasthenia gravis was found to be higher in these subjects than their respective national prevalences, and the incidence of Lyme disease was found to be higher than the national prevalence of Lyme disease. Several patients were diagnosed with medically important conditions such as diabetes, thyroid dysfunction, syphilis, myasthenia gravis, and Lyme disease based on these tests. This study suggests that comprehensive testing of patients with vocal fold movement disorders results in diagnoses that would be missed without a comprehensive evaluation, some of which are important medically, although their causal relationship to vocal fold paralysis or paresis was not investigated or established.

Moyamoya Disease Associated With Thyroid Carcinoma

Thyroid carcinoma associated with Moyamoya disease has not been reported in the literature. We first described a 46-year-old woman of Moyamoya disease after 10 years of thyroidectomy due to papillary adenocarcinoma of thyroid. During the 10-year medicine history, the patient was treated with levothyroxine (100 µg/d), and thyroid antibody tests demonstrated that elevated thyrotropin receptor antibody sustained for long time. After 10 years, the patient was diagnosed with Moyamoya disease according to digital subtraction angiography findings. The case suggested that thyroid autoimmune stimuli of papillary thyroid carcinoma with thyroid-stimulating hormone receptor antibody may be associated with pathogenic mechanism of Moyamoya disease.

Prevalence of thyroid dysfunction and thyroid antibodies in a private obstetrical practice in Sydney.

Hypothyroidism in pregnancy is associated with adverse obstetrical events and neurodevelopmental disorders in infants. The prevalence of thyroid dysfunction during pregnancy in Australia is not well documented, and universal screening remains questionable. To assess the prevalence of thyroid dysfunction and positive thyroid antibodies and review the indications for universal screening of thyroid function in pregnancy. The prospective observational study was undertaken between 2009 and 2014. Thyroid-stimulating hormone (TSH), free thyroxine (FT4) levels, thyroglobulin antibodies (TgAb) and thyroid peroxidase antibodies (TPOAb) were measured in 1069 women at booking-in. One hundred and three women, (9.6%), exhibited subclinical hypothyroidism, with TSH levels >2.5mIU/l. Eighty-seven women (8.1%) had TSH levels > 2.5 and ≤5 mIU/l. Of these, 41.4% (36 patients) were positive for TPOAb. Twelve women (1.5%) had a TSH >5 and ≤10 mIU/l with 66.7% (8 patients) positive for TPOAb. Four patients (0.4%) had a TSH level >10 mIU/l with 50% (2 patients) positive for TPOAb. Positive thyroid antibodies were detected in 258 patients (24.13%). Although statistically significant, the rank correlations between TSH and TPOAb (r = 0.08, P = 0.023) and TgAb (r = -0.081, P = 0.021) were weak. Similarly, weak rank correlations were observed between TSH and age (r = -0.095), parity (r = -0.081) and weight (r = 0.089). A high prevalence of subclinical hypothyroidism and positive thyroid antibodies exists in this cohort, as well as unsuspected chemical hypothyroidism, providing a strong case for universal screening with TSH and the consideration of thyroid antibody testing of all Australian pregnant women.

Iatrogenic thyrotoxicosis secondary to compounded liothyronine.

A 71-year-old woman presented with ST segment elevation myocardial infarction (STEMI) associated with hypotension (100/70 mm Hg) and dizziness. Her husband stated that she appeared confused and was experiencing visual hallucinations. Her medical history was significant for hypertension, pulmonary embolism, hypothyroidism, and gastroesophageal reflux disease. Preadmission medications were reported as amlodipine 2.5 mg daily and pantoprazole 40 mg daily. She denied any recreational drug use or history of mental illness (including hallucinations). She was living independently at home with her husband. The patient’s atypical cardiac symptoms prompted referral to the neurology service. However, neurogenic causes such as Hashimoto encephalitis and cerebrovascular accident were ruled out by negative results on thyroid antibody testing and computed tomography of the head. Incidentally, the laboratory panel for Hashimoto encephalitis included measurement of thyroid hormones, which showed that the level of free tri-iodothyronine was greater than 50 pmol/L (normal range 3–6.8 pmol/L). Thyroidstimulating hormone was 0.03 mIU/L (normal range 0.34–5.6 mIU/L) and free thyroxine was 15 pmol/L (normal range 10–23 pmol/L). The thyroid was not examined, and Grave disease was ruled out on the basis of the normal thyroxine level. In light of the laboratory results, a more detailed investigation for an exogenous iatrogenic cause was initiated. The only discrepancy between the patient’s in-hospital medications and her preadmission medications was a compounded product that she had been taking before the admission, specifically compounded liothyronine capsules (25 μg of liothyronine in hydroxypropyl methylcellulose [hypromellose] for once-daily dosing). The diagnosis was iatrogenic thyrotoxicosis secondary to a compounding error involving liothyronine. The patient’s symptoms, her history related to the current illness, and the supratherapeutic level of tri-iodothyronine were consistent with acute toxicity. She was given supportive care until her mental status and hemo dynamics returned to normal and was then discharged to home. The consequences of the poisoning included STEMI, acute renal injury secondary to hypotension (with serum creatinine twice her baseline value), and a 13-day hospital stay for delirium. Hospital staff contacted the patient’s outpatient pharmacy and alerted them to these findings.

Postpartum thyroid measures and depressive symptomology: a pilot study.

While correlations have been demonstrated between postpartum depression and psychosocial and circumstantial risk factors, some evidence exists for a similar relationship between postpartum depression and thyroid measures. To search at 4 weeks postpartum for correlations of numerical scores on a postnatal depression screening tool and thyroid measures. Subjects took the Edinburgh Postnatal Depression Scale (EPDS) prenatally and at 4 weeks postpartum. Participants were also given blood tests for thyroid-stimulating hormone (TSH), free thyroxine4, thyroid peroxidase, and thyroglobulin at the same testing intervals. Fifty-one subjects aged 18 years or older were recruited. Subjects with higher serum TSH at 4 weeks postpartum tended to have higher EPDS scores. Similarly, the 7 subjects (13.7%) with positive postnatal thyroid antibody tests were more likely than their counterparts to have higher EPDS scores. Presence of thyroid autoantibodies or higher TSH levels during the postpartum period may be related to depressive symptoms or dysphoric mood, even when clinical depression is not present. Either or both of these associations may contribute, along with other physiologic and psychosocial risk factors, to postpartum depression. (ClinicalTrials.gov number NCT00565032).

The Normal TSH Reference Range: What Has Changed in the Last Decade?

Serum TSH assessment is the most sensitive screening test for the diagnosis of thyroid dysfunction in the absence of pituitary or hypothalamic disease. This test has been used increasingly in the last decade to detect subclinical thyroid dysfunction (STD). Recent data suggest that STD is a common disorder that may be associated with important adverse events (1–5). The American Association of Clinical Endocrinologists (AACE) and American Thyroid Association (ATA) 2012 guidelines recommend treatment of subjects with persistent increased serum TSH levels 10 mIU/L and undetectable serum TSH ( 0.1 mIU/L) (6, 7). The treatment of mild thyroid hormone excess (TSH 0.1–0.4 mIU/L) ordeficiency (serumTSH 10mIU/L) is controversial (1,2). However, what is the normal TSH reference range? Obviously, this issue is critical in deciding whether or not to treat patients with mild STD and in identifying individuals with high-normal or low-normal serum TSH. It is also important in defining the TSH target level in patients receiving thyroid hormone replacement therapy. In 2002, the National Health and Nutrition Examination Survey (NHANES) III, a US population-based study, evaluated the normal TSH range in the “thyroid disease-free adult population” (8).Theauthors excludedsubjectswith risk factorsandafamilyhistoryofthyroiddysfunction,self-reported thyroid disease or goiter, and thyroid autoimmunity. The study suggested that 95% of the US disease-free population had a serum TSH concentration between 0.45 and 4.12 mIU/L (8). However, TSH values did not have a Gaussian distribution because the curve was skewed by individuals with occult autoimmune thyroid dysfunction despite negative thyroid peroxidase antibodies (9). In 2005, the National Academy of Clinical Biochemistry (NACB) recommended that thyroidultrasonographybeperformedineuthyroidsubjects to exclude the presence of occult thyroid autoimmunity in order to define the serum TSH reference interval more accurately (10). They suggested that the upper limit of the TSH reference range be lowered to 2.5 mIU/L (10). The upper and lower limits of the normal serum TSH concentration continue to be debated by expert clinical thyroidologists. In 2005, two back-to-back articles appeared in the JCEM: one article, by Wartofsky and Dickey (11), favored a narrower TSH reference range, but according to the other, by Surks et al (12), the TSH range should remain unchanged. It should be mentioned that the sensitivity and specificity of TSH assays can affect the evaluation of serum TSH because some assays may detect biologically inactive circulating TSH isoforms (1). The upper TSH reference limit has progressively declined over the last decade thanks to more sensitive TSH assays, more accurate thyroid antibody tests, and a more accurate selection of the reference population. Different TSH cut-off limits have been reported in population-based studies conducted in various countries (1). Subsequent findings confirmed that ethnicity, iodine intake, gender, age, and body mass index can influence the reference range of serum TSH. In fact, the normal TSH upper limit was lower in African Americans (3.6 mIU/L) than in Mexican Americans or Caucasians (4.2 mIU/L) (8). Reanalysis of these data 5 years later showed that the upper limit of normal serum TSH at the 97.5th percentile was 3.5 mIU/L in individuals 20–29 years old, 4.5 mIU/L in those 50–59 years old, and 7.5 mIU/L in those older than 80 years (13). Variations in thyroid function within the reference range have been associated with body weight in several cross-sectional and longitudinal studies (14). Moreover, serum TSH levels at the upper limit of the normal range have been found in obese adults and have been positively correlated with body mass index (14).

A case of Hashimoto’s encephalopathy misdiagnosed as viral encephalitis

Patient: Male, 61Final Diagnosis: Hashimoto’s encephalopathySymptoms: Neuropsychiatric or neurological manifestationsMedication: Steroids and immunoglobulinsClinical Procedure: Immunoglobulin combined with corticosteroid therapySpecialty: NeurologyObjective:Mistake in diagnosisBackground:Hashimoto’s encephalopathy is a rare autoimmune syndrome characterized by various neuropsychiatric or neurological manifestations and associated with Hashimoto’s thyroiditis, responsive to steroids. Until now, misdiagnosis and delay of treatment of Hashimoto’s encephalopathy are very common because of the diversity of the symptoms.Case Report:This recent case of a 61-year-old man presented with unconsciousness, spasms and a previous misdiagnosis as viral encephalitis. Response to anti-viral and steroid therapy was unsatisfactory, but treatment with immunoglobulin combined with corticosteroid therapy achieved rapid and complete recovery.Conclusions:Any patient presenting with acute or subacute unexplained encephalopathy should be considered Hashimoto’s encephalopathy, even if the thyroid function is normal. Thyroid antibody testing should be performed because this may be the most important clue to diagnosis. As soon as the diagnosis is made, steroid therapy is the first choice. If the steroid therapy does not lead to immediate improvement, IVIG is an effective alternative treatment.