scholarly journals SAT-477 Melanoma Treated with Pembrolizumab Leading to Thyroiditis and Subsequent Hypothyroidism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Heather Fishel
Keyword(s):  
Thyroid Function ◽  
T Cell Activation ◽  
Thyroid Dysfunction ◽  
Subsequent Development ◽  
Thyroid Function Tests ◽  
Free T4 ◽  
Specific Patient ◽  
Normal Thyroid ◽  
Free T3 ◽  
History Of

Abstract Background: Pembrolizumab (PD-1) is an immune checkpoint inhibitor used for treating melanoma and has been associated endocrine immune-related adverse events. Case Presentation: 76-year-old Caucasian male presented for evaluation of abnormal thyroid labs. Significant co-morbidities included recurrent melanoma, heart failure, atrial fibrillation, coronary artery disease, type 2 diabetes, hypertension. Patient’s melanoma was being treated with Pembrolizumab. Further history revealed no family/personal history of thyroid disease but a history of mouth cancer treated with radiation over 30 years ago. He denied any recent glucocorticoid or biotin use. Symptoms included worsening fatigue, weight loss, and diarrhea. He was afebrile and vitally stable. Physical exam was unremarkable. Prior to this year, patient had normal thyroid labs. Recent thyroid labs showed TSH of 0.01 uIU/mL (normal 0.34-4.94 uIU/mL), confirmed with repeat labs a week later (TSH: < 0.01, Free T4: 2.23 ng/dL, normal Free T4: 0.7-1.48 ng/dL). There was a high suspicion that these labs were related to Pembrolizumab, but other etiologies were evaluated. Completed thyroid uptake and scan showed no evidence of increased activity (4-hour uptake: 1.6%, 24-hour update: 1.2%). Repeat thyroid labs indicated recovering thyroid function with a TSH: 0.14 uIU/mL, Free T4: 0.49 ng/dL, Free T3: 1.5 pg/mL (normal Free T3 2.3-4.2 pg/mL), TSI: 96% (normal < 140%), TPO Ab: 111 IU/mL (normal TPO Ab < 9 IU/mL). One month later thyroid tests resulted as TSH: 72.81 uIU/mL, Free T4: < 0.40. He was started on levothyroxine, which was titrated over several weeks. Discussion: Pembrolizumab (PD-1) is an IgG4 programmed cell death 1-directed monoclonal antibody, whose mechanism of action is to inhibit cancer cells ability impede T-cell activation. However, because of this mechanism, some T-cells, will remain activated, leading to autoimmune diseases. PD-1 has been associated with thyroid dysfunction, with an incidence rate as high as 14-20%. The clinical presentation varies from isolated thyrotoxicosis to overt hypothyroidism. In our patient, he developed thyrotoxicosis with subsequent development of hypothyroidism. Generally, the timing of thyroid dysfunction after the initiation of PD-1 ranges from 3 to 40 weeks, with the median onset at week 6. Baseline TSH and free T4 should be obtained with rechecking of these labs monthly for the first 6 months. For patients who present with thyrotoxicosis, Grave’s disease should be ruled out, and initial treatment should include beta-blockers. Hypothyroidism should be treated with levothyroxine with titration to normal thyroid function tests. What remains to be determined is the mechanism in which PD-1 causes thyroid dysfunction and if specific patient characteristics, such as thyroid antibodies, can be used to risk stratify the likelihood of a patient developing thyroid dysfunction.

scholarly journals MON-478 Impaired Sensitivity to Thyroid Hormone - A Diagnostic and Therapeutic Challenge

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jorge Pedro ◽  
Vanessa Gorito ◽  
Cristina Ferreras ◽  
Ferreira João Silva Maria ◽  
Sofia Ferreira ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Thyroid Function Tests ◽  
Pediatric Endocrinology ◽  
Free T4 ◽  
Peripheral Tissues ◽  
Free T3 ◽  
Function Tests ◽  
Trh Stimulation ◽  
History Of

Abstract Background: Impaired sensitivity to thyroid hormone refers to any process that negatively affects its action, including defects in its transport, metabolism and action on the receptor. Resistance to thyroid hormone due to beta-receptor mutations (RTH-beta) is the most common form of this entity and is characterized by reduced response of peripheral tissues to the action of thyroid hormone. The genetic variability of cofactors involved in the action of thyroid hormone explains the heterogeneity of resistance among affected individuals. Generally, patients with this disorder, have increased levels of free T4 and free T3 in association with normal or high TSH. Clinical case: 11-year-old boy, with personal history of Attention-deficit/hyperactivity disorder (ADHD). A pediatric endocrinology consultation was requested to evaluate abnormalities in his thyroid function tests. A few months earlier, his father was referred to endocrinology consultation because of thyroid function tests abnormalities: TSH - 3.01 μIU / mL (N: 0.35 - 4.94); Free T4 1.7 ng / dL (N: 0.7-1.48); Free T3 4.77 pg / mL (N: 1.71-3.71). Initially, two diagnostic hypotheses were considered: central hyperthyroidism or impaired sensitivity to thyroid hormone. The adult underwent pituitary magnetic resonance, which raised the hypothesis of a pituitary microadenoma, and TRH stimulation test, whose result was strongly suggestive of the second diagnostic possibility. A genetic study was requested and the presence of the c700 G> A variant (p. Ala 324 trh) in the THRB gene was identified, which confirmed the most likely hypothesis. At the time of the pediatric endocrinology consultation, the 11-year-old boy had the results of his lab tests: TSH - 6.67 μIU / mL (N: 0.35 - 5); T4L 2.27 ng / dL (N: 0.88-1.58); T3L 7.79 pg / mL (N: 2-4.20). Given his perfect height and weight evolution and the absence of symptoms suggestive of hypo or hyperthyroidism, it was decided not to start any medication, keeping only periodic surveillance. Conclusion: This case exemplifies unusual thyroid function tests. This discordance between serum thyroid hormone and TSH concentrations should raise the possibility of impaired sensitivity to thyroid hormone. In this condition, patients may present with symptoms of hypo or hyperthyroidism and the etiology of thyroid function tests abnormalities are not easily recognized. This can lead to misdiagnosis and consequently unnecessary treatment.

scholarly journals MON-481 Remarkable Euthyroid Hyperthyroxinemia Mistaken for Thyrotoxicosis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Annavi Baghel ◽  
Joshua D Maier
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Clinical Status ◽  
Thyroid Function Tests ◽  
Thyroid Disorder ◽  
Diagnostic Challenge ◽  
Free T4 ◽  
Free T3 ◽  
History Of ◽  
Euthyroid Hyperthyroxinemia

Abstract CLINICAL CASE A 46 year old caucasian female with past medical history of menorrhagia was referred from primary care for evaluation of thyrotoxicosis. Thyroid function was assessed in the context of menometrorrhagia. She did not have any history of thyroid disorder or abnormal thyroid function tests. Per outside records, recent labs demonstrated TSH 0.88 uIU/mL (0.36-3.74), Free T4 > 8.00 ng/dL (0.76-1.46), Free T3 2.9 pg/mL (2.18-3.98). All other labs were within normal limits. Thyroid ultrasound revealed normal parenchyma and volume. She did not take any medications or supplements including biotin. She denied heat intolerance, anxiety, palpitations, dyspnea, tremors, hyperdefecation, or change in hair, skin, or mood. No epiphora, diplopia, or eye irritation was reported. Her father had been diagnosed with hyperthyroidism, mother with hypothyroidism. Repeat labs at our visit revealed normal TSH of 1.05 uIU/mL (0.358- 3.74), normal Free T3 2.58 pg/mL (2.18- 3.98), normal Total T3 136 ng/dL (80-200), elevated Free T4 >8.00 ng/dL (0.76-1.46) and elevated Total T4 11.6 ug/dL (4.5-10.5). These lab values were not consistent with patient’s euthyroid clinical status, prompting assessment of Free T4 by dialysis, normal at 1.5 ng/dL (0.9-2.2) and T3 uptake, high at 40% (24-39%). This picture was consistent with Familial Dysalbuminemic Hyperthyroxenemia (FDH). The decision was made not to treat the patient with anti-thyroid medications and to perform a confirmatory genetic testing to test for mutations in the ALB (albumin) gene. DISCUSSION The free T4 assay used by our institution is performed on the Siemens Dimension Vista platform using a two-step chemiluminescent immunoassay. While in theory two-step assays should not yield abnormal results in FDH, several two-step assays are known to yield falsely high results in patients with FDH (1, 2, 3). Other potential etiologies for discordant Free T4 levels include thyroid hormone autoantibodies, heterophile antibodies, biotin use, and anti-streptavidin antibodies (3). CONCLUSION Recognition of laboratory error in the workup of thyroid disease is essential. Clinicians must ensure thyroid function labs are consistent with each other and with the patient’s presentation. In such cases misdiagnosis of hyperthyroidism or thyroid hormone resistance may lead to unnecessary testing and inappropriate treatment (3). References 1. Cartwright D et al. Familial dysalbuminemic hyperthyroxinemia: a persistent diagnostic challenge. Clin Chem. 2009 May;55(5):1044-6 2. Ross HA et al. Spuriously high free thyroxine values in familial dysalbuminemic hyperthyroxinemia. Clin Chem. 2011 Mar;57(3):524-5 3. Favresse J et al. Interferences With Thyroid Function Immunoassays: Clinical Implications and Detection Algorithm. Endocr Rev. 2018 Oct 1;39(5):830-850.

scholarly journals Aspects of hormonal testing of thyroid function in patients with type 1 diabetes mellitus and chronic kidney disease

2021 ◽  
Vol 17 (1) ◽  
pp. 32-37
Author(s):  
A.G. Sazonova ◽  
T.V. Mokhort ◽  
N.V. Karalovich
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Thyroid Disorders ◽  
Free T4 ◽  
Free T3 ◽  
Peripheral Conversion

Background. Chronic kidney disease (CKD) is known to affect the thyroid axis, including thyroid hormone metabolism. It has been established that a decrease in renal function can be combined with changes in thyroid function. Thyroid dysfunction also has implications for renal blood flow, glomerular filtration rate (GFR), tubular transport, electrolyte homeostasis, and glomerular structure. The purpose of the study was to determine the features of thyroid function in patients with type 1 diabetes mellitus (T1DM) and CKD and develop recommendations for hormonal testing of thyroid pathology. Materials and methods. One hundred and twenty-one patients with T1DM with CKD were divided into 3 groups: group 1 — 78 individuals with GFR ≤ 60 ml/min/1.73 m2, group 2 — 20 people receiving renal replacement therapy (RRT), group 3 — 23 patients after renal transplantation (RT) with adequate graft function (the duration of the renal transplant is 3.62 (1.47; 4.28) years). Results. In T1DM and CKD group, the diagnostic value of thyroid-stimulating hormone is reduced due to the absence of differences in its values with a decrease in T4 and T3. Free T3 is the most sensitive marker of thyroid dysfunction in CKD. Thyroid disorders in T1D and CKD patients have a non-immune genesis. T1DM patients on RRT after hemodialysis (HD) procedure have an increase in total and free T4 and free T3, consequently, monitoring of thyroid disorders should be done immediately after the HD session. The restoration of normal values of peripheral conversion index and free T3 occurs within 1–2 years after TR, depending on the duration of RRT receiving. After more than 3 post-transplantation years, there is an increase in peripheral conversion index, which characterizes the imbalance of peripheral thyroid hormones towards a decrease in free T3 with relatively stable free T4. Conclusions. Thyroid dysfunctions are typical for all stages of the pathological process in CKD in patients with type 1 diabetes mellitus, including patients at the terminal stage and after successful kidney transplantation. The changes in thyroid hormones are associated with the RRT experience and can potentially affect the survival of patients.

scholarly journals STUDY OF INSULIN RESISTANCE AND THYROID PROFILE IN WOMEN WITH SPONTANEOUS ABORTIONS

2020 ◽  
pp. 1-3
Author(s):  
Annapoorani R ◽  
Nagasudha D
Keyword(s):  
Insulin Resistance ◽  
Thyroid Dysfunction ◽  
Previous History ◽  
Oral Glucose ◽  
Study Group ◽  
Thyroid Function Tests ◽  
Model Assessment ◽  
Spontaneous Abortions ◽  
Free T4 ◽  
Free T3

Thyroid dysfunction and insulin resistance are important endocrinological causes of spontaneous abortions. This study is resistancewith spontaneous abortions Thyroid dysfunction and Insulin resistance are common endocrinological causes of abortions.The present study is a case control study where 75 patients with spontaneous abortions below 20 weeks were taken as cases and 75 patients with normal on going pregnancy without previous history of miscarriage were taken as controls. Thyroid Function Tests (Free T3 ,Free T4,TSH) ,Oral Glucose Tolerance Test following 75 mg glucose load were done in cases and controls. Fasting glucose and insulin levels were measured and Insulin resistance was calculated using homeostatic model assessment method (HOMA- IR).Free T3 levels were signicantly lower and TSH levels were signicantly higher in study group indicating the presence of hypothyroidism in the abortus group. The HOMA-IR insulin resistance scores were apparently higher in the study group than in the controls, but it was not statistically signicant.

Thyroid dysfunction in chronic schizophrenia in albania

2011 ◽  
Vol 26 (S2) ◽  
pp. 1515-1515 ◽  
Author(s):  
Y. Themeli ◽  
I. Aliko ◽  
A. Hashorva
Keyword(s):  
Thyroid Hormones ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Chronic Schizophrenia ◽  
Hashimoto Thyroiditis ◽  
Diabetes Mellitus Type 1 ◽  
Thyroid Function Tests ◽  
Thyroid Antibodies ◽  
Normal Thyroid ◽  
Function Tests

BackgroundThyroid dysfunction is relatively common in patients with schizophrenia.This study seeks to determine the prevalence and pattern of thyroid dysfunction and thyroid antibodies presence in a group of adult psychiatric inpatients with chronic schizophrenia.MethodsThyroid function tests and thyroid antibodies measurement were performed on 88 patients hospitalized in Psichiatric Clinic of UHC “Mother Teresa” from december 2006 to december 2007.55 of them (62,5%) were females and 33 of them (37,5%) males. A median age of 43 years (range16 to 70 years) and a median duration of hospitalization of 10 years (range 1 to 30 years) was assessed.ResultsTAb were found in 22 patients (25%), of which 18 females and 4 males. 16% of them resulted with positive anticorps for Hashimoto Thyroiditis; 9% for Graves‘disease.According to thyroid function tests70% had normal test, 8% had elevated TSH: 3% of them with low thyroid hormones and 5% with normal thyroid hormones. 20% of cases had low TSH: 5% of them with high level of thyroid hormones, 15% with normal thyroid hormones. Hypothyroidism was more frequent in elderly patients ( > 60 years old), and in those treated with Risperidone. Most of cases (73%) with thyroid disorders resulted from endemic geographic areas. 37% of them mentioned familial history for thyroid pathology, and 23% for diabetes mellitus type 1.ConclusionThyroid abnormalities are common in patients with chronic schizophrenia.This fact call for caution in the use and interpretation of thyroid function tests in these patients.

scholarly journals Overt Hypothyroidism Induced by Prolonged Therapy With Imatinib

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A945-A946
Author(s):  
Ally W Wang ◽  
Emily V Nosova
Keyword(s):  
Tyrosine Kinase ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Case Reports ◽  
Myelogenous Leukemia ◽  
Prolonged Treatment ◽  
Overt Hypothyroidism ◽  
Imatinib Treatment ◽  
Thyroid Function Tests ◽  
History Of

Abstract Background: Imatinib, a tyrosine kinase inhibitor (TKI), is commonly used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors. TKI-induced thyroid dysfunction is recognized as an adverse class effect with most cases occurring between six to twelve months after treatment initiation. Clinical Case: 76-year-old man with hypertension and CML on Imatinib that had been started twenty months prior was admitted for confusion. The patient also reported constipation, cold intolerance, and weight gain despite no change in diet, appetite, or physical activity. On evaluation, his responses to questioning were noticeably delayed, however he was not lethargic. His vital signs were normal and he was otherwise euthyroid on physical exam. He had no known history of thyroid dysfunction. Labs showed a TSH of 94.7 (0.4 - 4.2 uIU/mL), Free T4 0.4 (0.8 - 1.5 ng/dL), and Total T3 30 (87 - 178 ng/dL). Thyroglobulin antibody was 1016 (0.0 - 4.1 U/mL) and TPO antibody was >2000 (0.0 - 5.6 IU/mL). A TSH checked two months before admission was 1.1. Antibody levels had not been checked previously. Thyroid ultrasound demonstrated a hyperemic and heterogeneous thyroid, consistent with thyroiditis. Levothyroxine at a dose of 50 mcg daily was advised, due to patient’s advanced age as well as history of arrhythmia. The patient’s confusion resolved on hospital day three. Repeat thyroid function tests will be checked four to six weeks after Levothyroxine initiation. Discussion: As a class, tyrosine kinase inhibitors are known to cause thyroid dysfunction with the most common medication being Sunitinib. Data related to the effects of thyroid function during Imatinib treatment are limited. Previous cases of Imatinib-induced thyroid dysfunction report only hypothyroidism in thyroidectomized patients and no clinically significant change in thyroid function among patients who were euthyroid prior to therapy initiation. Our case reports a patient with no prior thyroidectomy who developed overt hypothyroidism while on Imatinib for nearly two years. The mechanism for TKI-induced thyroid dysfunction has not been elucidated. Due to relatively acute onset and markedly positive TPO and thyroglobulin antibodies, we suspect that TKI may alter HLA recognition on thyroid follicular cells, thereby inducing autoimmunity. Our case showcases the need to maintain awareness and continuous surveillance for thyroid dysfunction when patients are on long term TKI as overt hypothyroidism may be induced by prolonged treatment.

Prevalence of thyroid dysfunction and effect of contrast medium on thyroid metabolism in cardiac patients undergoing coronary angiography

2013 ◽  
Vol 54 (1) ◽  
pp. 42-47 ◽  
Author(s):  
Paolo Marraccini ◽  
Massimiliano Bianchi ◽  
Antonio Bottoni ◽  
Alessandro Mazzarisi ◽  
Michele Coceani ◽  
...  
Keyword(s):  
Coronary Angiography ◽  
Contrast Medium ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Thyroid Stimulating Hormone ◽  
Low T3 Syndrome ◽  
Free T4 ◽  
Free T3 ◽  
Iodinated Contrast ◽  
Low T3

Background Iodinated contrast media (CM) may influence thyroid function. Precautions are generally taken in patients with hyperthyroidism, even if subclinical, whereas the risks in patients with hypothyroidism or low triiodothyronine (T3) syndrome are not considered as appreciable. Purpose To assess the presence and type of thyroid dysfunction in patients admitted for coronary angiography (CA), to assess the concentration of free-iodide in five non-ionic CM, and to evaluate changes in thyroid function after CA in patients with low T3 syndrome. Material and Methods We measured free T3, free thyroxine (T4), and thyroid-stimulating hormone (TSH) in 1752 consecutive patients prior to CA and free-iodide in five non-ionic CM. Urinary free-iodide before and 24 h after CA, and thyroid hormone profile 48 h after CA were also made in 17 patients with low T3 syndrome. Patients were followed up for an average duration of 63.5 months. Results The patients were divided into four groups: euthyroidism (60%), low T3 syndrome (28%), hypothyroidism (10%), and hyperthyroidism (2%). The free-iodide resulted far below the recommended limit of 50 μg/mL in all tested CM. In low T3 syndrome, 24-h free-iodide increased after CA from 99.9± 63 ug to 12276±9285 ug (P< 0.0001). A reduction in TSH (4.97±1.1 vs. 4.17±1.1 mUI/mL, P < 0.01) and free T3 (1.44±0.2 vs. 1.25±0.3 pg/mL, P < 0.01), with an increase in free T4 (11.3±2.9 vs. 12.5±3.4 pg/dL, P < 0.001), was found. Patients with functional thyroid disease in the follow-up had a significant lower rate survival compared to euthyroid patients (90.7 vs. 82.2%, P < 0.00001). Conclusion Thyroid dysfunction is frequent in patients who perform a CA, and low T3 syndrome is the predominant feature. The administration of contrast medium may further compromise the thyroid function.

scholarly journals SAT-518 Progression of Graves Disease to Hashimoto’s Thyroiditis Following Alemtuzumab Therapy for Multiple Sclerosis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Brandon Rapier ◽  
Frank Gargasz ◽  
Omar Suheil Zmeili
Keyword(s):  
Multiple Sclerosis ◽  
Thyroid Function ◽  
Hashimoto’S Thyroiditis ◽  
Thyroid Nodules ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Thyroid Function Tests ◽  
Thyroid Disorder ◽  
Free T4 ◽  
Free T3

Abstract Introduction: Alemtuzumab, an anti-CD52 monoclonal antibody used in the treatment of relapsing-remitting multiple sclerosis is most commonly associated with Graves disease, but autoimmune hypothyroidism may also be seen. We present an unusual case where both were present in the same patient and progression from hyperthyroidism to hypothyroidism was seen within only a few months. Clinical Case: A 33-year-old female referred to Endocrinology clinic for evaluation of hyperthyroidism. She was complaining of palpitations, tremors, increased sweating, heat intolerance, and unintentional weight loss for 3 months. She received 2 cycles of alemtuzumab treatments over the last 21 months for her multiple sclerosis. Last treatment was 8 months before she developed hyperthyroid symptoms. Patient had no prior history of thyroid disorder. Thyroid stimulating hormone (TSH) level was within normal range before alemtuzumab was administered. TSH was monitored periodically and was normal till 8 months after receiving alemtuzumab therapy. Physical exam was remarkable for diffuse enlarged thyroid, not tender, without palpated thyroid nodules but with thyroid bruit. No proptosis was present. Thyroid function tests obtained by her primary care physician were consistent with hyperthyroidism. Patient found to have suppressed TSH &lt;0.015 IU/mL [0.465 - 4.680IU/mL], elevated total T3 372ng/dL [97-169ng/dL], and elevated total T4 &gt;24.9 ug/dL [5.5 - 11.0 ug/dL]. Further workup revealed elevated Free T3, 10.90 [2.77 - 5.27 pg/mL] and elevated free T4 &gt; 6.99 ng/dL [0.78 - 2.19 ng/dL]. Thyrotropin receptor antibody (TR Ab) was elevated as well at 3.43 IU/L [&lt;1.75 IU/L]. Pregnancy test was negative. Thyroid ultrasound demonstrated goiter with no focal thyroid nodules seen. She was started on methimazole 10 mg daily. One month later, TSH was elevated at 31.58 though she only took methimazole for one week and then discontinued due to rash and pruritus. At that time, she reported severe fatigue and 25 lbs weight gain. Repeated labs one month later showed elevated TSH, 60.978 IU/ML, low free T4 0.08 pg/mL and low free T3 0.72 ng/dL. Thyroid peroxidase Antibody (TPO Ab) was obtained and was 5308.8 IU/mL [0.0 - 5.5 IU/mL]. She was started on levothyroxine 100 mcg daily. Two months later, levothyroxine dose was increased to 112 mcg daily due persistent TSH elevated. At subsequent visit, patient was euthyroid with normal TSH 3.191IU/mL and normal free T4 1.48 ug/dL. Conclusion: This case was unique in that the patient developed both TR Ab and TPO Ab after alemtuzumab therapy which resulted in Grave’s disease followed by Hashimoto’s thyroiditis. The case highlights the importance of continuous monitoring of thyroid function in patients treated with alemtuzumab given the unpredictable autoimmune phenomena which may occur.

scholarly journals SUN-504 A Case of T3 Thyrotoxicosis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Isabelle Daneault Peloquin ◽  
Matthieu St-Jean
Keyword(s):  
Thyroid Function ◽  
Thyroid Function Test ◽  
Nutritional Supplement ◽  
Thyroid Function Tests ◽  
Free T4 ◽  
Endocrine Society ◽  
Product Consumption ◽  
Function Tests ◽  
History Of ◽  
Receptor Antibodies

Abstract Clinical vignette ENDOCRINE SOCIETY 2020 Title: A case of T3 thyrotoxicosis induced by a dietary supplement. A 24 yo man consulted for a 2 weeks history of diaphoresis, fatigue, insomnia, palpitations and headache associated with a 20 pounds lost. The patient didn’t have a goiter or any signs of orbitopathy. The results revealed a free T3 level of 45.8 pmol/L upon arrival (normal (N) 3.4- 6.8 pmol/L), free T4 level of 6.4 pmol/L (N 11.0–22.0 pmol/L) and TSH level less than 0.005 mUI/L (N: 0.35 to 3.50 mUI/L). Facing those results, a complete review of the patient medication and natural product consumption was done. The patient revealed that he was using, since a month, a vegetable extracts nutritional supplement that didn’t included iodine. He was asked to stop the nutritional supplement and propranolol 10 mg twice daily was prescribed. Thyroid function tests were done 3 days after. The results demonstrate a fT3 level of 4.6 pmol/L, a fT4 level of 5.6 pmol/L and a TSH that still suppressed. A thyroid scintigraphy was performed 7 days later and showed a homogeneous uptake of 18.5% (N 7.0% – 35.0%). We saw the patient 2 weeks later and we ordered another thyroid function test with TSH receptor antibodies, TPO antibodies and thyroglobulin. The results were the following: fT3 of 5.1 pmol/L, fT4 of 12.1 pmol/L, TSH of 2.31 mUI/L, thyroglobulin of 19.8 ug/L (N: 1.4 – 78) and normal levels of antibodies against TPO and TSH receptors. To confirm the contamination of the nutritional supplement by fT3 we used a plasma pool of normal patients in which we measured thyroid function tests at baseline and after we have added the nutritional supplement powder to reflect the dose suggested by the manufacturer. The results showed that fT3 level increased by 36.5%, fT4 by 11.2% and TSH didn’t changed. The powder was then analyzed by an external laboratory that wasn’t able to demonstrate the presence of fT3 nor fT4. The two diagnostic possibility facing those results were that the powder induced an interference with immunoassay used to measure fT3 and fT4 but not TSH or thyrotoxicosis induced by the nutritional supplement with limitation in the technique that tried to identify fT3 in the powder. Given the presentation of the patient, we are convinced that this case represents a thyrotoxicosis induced by a nutritional supplement. In conclusion, Graves’ disease is responsible for 60–80% of the cases of hyperthyroidism. However, there are few cases reports of thyrotoxicosis induced by nutritional supplement1,2, but some studies demonstrate the presence of thyroid hormone in significant amounts in some commercially available health supplements3. This case highlights the importance of verifying exposition to medications and natural products when confronted to cases of thyrotoxicosis. 1.Regina A et al. MMWR Morb Mortal Wkly Rep. 2016 2. Panikkath R et al. Am J Ther. 2014 3. Kang GY et al. Thyroid. 2013

scholarly journals MON-480 Isolated Hyperthyroxinemia - Does Everyone Needs Treatment?

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Bilal Bashir ◽  
Moulinath Banerjee ◽  
Harnovdeep Singh Bharaj ◽  
Simmi Krishnan ◽  
Atir Khan ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Equilibrium Dialysis ◽  
Antithyroid Drugs ◽  
Thyroid Function Tests ◽  
Free T4 ◽  
Normal Thyroid ◽  
Function Tests ◽  
Tsh Levels ◽  
Roche Cobas ◽  
Assay Interference

Abstract Background: Raised free thyroxine (T4) with normal thyroid stimulating hormone (TSH) levels should be identified and interpreted with caution. Some of these conditions do not need treatment. We present three cases with similar biochemical abnormalities from three different causes. Case 1: A 62-year-old clinically asymptomatic lady was referred to us with Free T4 34.9 pmol/L (10.0 – 24.0 pmol/L), TSH 0.81 mU/L (0.2 – 5.0 mu/L) and negative TSH receptor antibodies (&lt;0.9 IU/L). She was trialled on antithyroid drugs for 6 months. Her Free T4 stayed elevated between 29.0 – 35.0 pmol/L with normal TSH. We worked up for assay interference by running tests on two analysers, Roche Cobas e801 and Siemens ADIVA Centaur CP, both yielded similar results. Alpha1 glycoprotein subunits and SHBG were normal with clinical euthyroid status making TSHoma less likely. Serum protein electrophoresis did not detect any abnormal albumin. We were unable to perform equilibrium dialysis due to non-availability of facility at our centre. Due to strong clinical suspicion and family history of thyroid dysfunction that never needed a treatment, we tested her genetically for familial dysalbumineic hyperthyroxinemia (FDH) using mutation surveyor and fluorescent sequence analysis showed her to be heterozygous for c.725G&gt;A ALB variant confirming diagnosis of FDH. Case 2: A 65-year-old clinically asymptomatic lady, was referred to us with Free T4 28.8 pmol/L (10.0 – 24.0 pmol/L) and TSH 2.50 mU/L (0.2 – 5.0 mu/L). Given inappropriately normal TSH levels, we repeated her TFTs using 3 different analysers, Roche cobas e801, Siemens ADIVA centaur CP and Abbot ARCHITECT i1000SR. Roche and Siemens assays yielded similar results, however Abbot assay showed normal thyroid function tests with TSH 1.01 mu/L (0.4-5.0 mu/L) and free T4 18.7pmol/L (9.0-19.0 pmol/L), confirming assay interference. As Siemens and Roche uses streptavidin-biotin immobilizing system while Abbot uses a magnetic bead-based capture system, the abnormal results could be due to biotin interference. Case 3: A 65-year-old lady, clinically asymptomatic was referred to us with Free T4 29.2 pmol/L (10.0 – 24.0 pmol/L) and TSH 1.59 mU/L (0.2 – 5.0 mu/L), 3 months after stopping amiodarone, which she took for 3 weeks for atrial fibrillation. This was thought to be due to amiodarone, owing to its long half-life of 58 days. We repeated thyroid function tests in 3 months from first clinical encounter i.e. 6 months after stopping amiodarone that showed Free T4 24.2pmol/L and TSH 2.30 mU/L and repeated further 3 months later that were normal, confirming amiodarone induced abnormal biochemical profile requiring no treatment. Conclusion: Hyperthyroxinaemia with normal TSH need to be interpreted with caution as illustrated above. Some of them do not need treatment and inappropriate interpretation can potentially cause anxiety for the patient and harm due to unnecessary treatment.

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