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 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 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 <0.015 IU/mL [0.465 - 4.680IU/mL], elevated total T3 372ng/dL [97-169ng/dL], and elevated total T4 >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 > 6.99 ng/dL [0.78 - 2.19 ng/dL]. Thyrotropin receptor antibody (TR Ab) was elevated as well at 3.43 IU/L [<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 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 Challenges in interpretation of thyroid hormone test results

2016 ◽  
Vol 144 (3-4) ◽  
pp. 200-203
Author(s):  
Tijana Lalic ◽  
Biljana Beleslin ◽  
Slavica Savic ◽  
Mirjana Stojkovic ◽  
Jasmina Ciric ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Genetic Disorder ◽  
Clinical Status ◽  
Nodular Goiter ◽  
Thyroid Function Tests ◽  
Thyroid Status ◽  
First Case ◽  
Secondary Hypothyroidism

Introduction. In interpreting thyroid hormones results it is preferable to think of interference and changes in concentration of their carrier proteins. Outline of Cases. We present two patients with discrepancy between the results of thyroid function tests and clinical status. The first case presents a 62-year-old patient with a nodular goiter and Hashimoto thyroiditis. Thyroid function test showed low thyroid-stimulating hormone (TSH) and normal to low fT4. By determining thyroid status (?SH, T4, fT4, T3, fT3) in two laboratories, basal and after dilution, as well as thyroxine-binding globulin (TBG), it was concluded that the thyroid hormone levels were normal. The results were influenced by heterophile antibodies leading to a false lower TSH level and suspected secondary hypothyroidism. The second case, a 40-year-old patient, was examined and followed because of the variable size thyroid nodule and initially borderline elevated TSH, after which thyroid status showed low level of total thyroid hormones and normal TSH. Based on additional analysis it was concluded that low T4 and T3 were a result of low TBG. It is a hereditary genetic disorder with no clinical significance. Conclusion. Erroneous diagnosis of thyroid disorders and potentially harmful treatment could be avoided by proving the interference or TBG deficiency whenever there is a discrepancy between the thyroid function results and the clinical picture.

scholarly journals Diverse Genotypes and Phenotypes of Three Novel Thyroid Hormone Receptor-α Mutations

2016 ◽  
Vol 101 (8) ◽  
pp. 2945-2954 ◽  
Author(s):  
Korcan Demir ◽  
Anja L. M. van Gucht ◽  
Muammer Büyükinan ◽  
Gönül Çatlı ◽  
Yavuz Ayhan ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Motor Development ◽  
Thyroid Hormone Receptor ◽  
Clinical Phenotype ◽  
Case Series ◽  
Detailed Knowledge ◽  
Thyroid Function Tests ◽  
Free T4 ◽  
Serum Free ◽  
Free T3

Context: Recently several patients with resistance to thyroid hormone (RTH)-α due to T3 receptor-α (TRα) mutations were identified. The phenotype of these patients consists of varying degrees of growth impairment, delayed bone, mental and motor development, constipation, macrocephaly, and near-normal thyroid function tests. Objective: The objective of the study was to describe the clinical phenotype of three new families with RTHα and thereby gain more detailed knowledge on this novel syndrome. Design, Setting, and Participants: RTHα was suspected in three index patients from different families. Detailed clinical and biochemical assessment and imaging and genetic analyses were performed in the patients and their relatives. In addition, functional consequences of TRα mutations were investigated in vitro. Results: We studied 22 individuals from three families and identified 10 patients with heterozygous TRα mutations: C380fs387X, R384H, and A263S, respectively. The frame-shift mutation completely inactivated TRα, whereas the missense mutations produced milder defects. These mutations were associated with decreasing severity of the clinical phenotype: the patient in family 1 showed severe defects in growth, mental, and motor development, whereas the seven patients in family 3 had only mild clinical features. The most frequent abnormalities were anemia, constipation, and a delay in at least one of the developmental milestones. Serum free T3 ranged from high-normal to high and serum free T4 and rT3 from normal to low. TSH levels were normal in all patients. Conclusions: This large case series underlines the variation in the clinical phenotype of RTHα patients. RTHα should be suspected in subjects when even mild clinical and laboratory features of hypothyroidism are present along with high/high-normal free T3, low/normal free T4, and normal TSH.

scholarly journals MON-475 Discrepant Thyroid Function Tests in Adenocarcinoma-Is This a True Thyroid Disorder?

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Mohammed Al Tameemi ◽  
Janice L Gilden
Keyword(s):  
Thyroid Function ◽  
Thyroid Function Test ◽  
Amiodarone Therapy ◽  
Thyroid Function Tests ◽  
Thyroid Disorder ◽  
Check Point ◽  
Free T4 ◽  
Function Tests ◽  
Function Test ◽  
Check Point Inhibitors

Abstract Background: Many causes of abnormal thyroid function tests (TFTs) occur that may or may not reflect a true thyroid disorder. The most common include: immune check point inhibitors therapies (ICI) used to treat various types of cancers; biotin supplements, which may interfere with thyroid function test assays; euthyroid sick syndrome; as well as amiodarone therapy for cardiac disorders. Clinical Case: A 67-year old female patient with type 2 diabetes mellitus, taking insulin and oral antihyperglycemic agents, with hyperlipidemia, hypertension and coronary artery disease, who had abnormal TFTs (TSH was 3.7 to 4.9 uIIu/ml; ref range 0.27-4.2 uIU/mL), and Free T4 was 0.92 to 1.06 ng/dL; ref range 0.55-1.6 ng/dl) prior to the diagnosis of metastatic adenocarcinoma of the lungs. She was initially treated with radiation. TFTs were unchanged. Her CEA was noted to be 129.5 (0-3.0 ng/mL). However, following chemotherapy with Tarceva (Erlotinib) 50 mg po daily, the TSH increased to 7.6 uIU/ml with Free T4 of 3.19 ng/dL. She remained clinically euthyroid. A thyroid ultrasound showed 1 -small sub centimeter nodule in each thyroid lobe. The patient later admitted to also taking biotin for an unknown period of time. TSH antibodies and TSI were both negative. Free T4 by dialysis was normal. While still taking Tarceva her TSH was noted to be 2.5 to 3.8 uIU/ml and both Free T4 and Free T3 were elevated and was 6.57 pg/ml;ref range=2.52-4.34 pg/mL). Six months later, the Free T4 decreased to 1.08 ng/dL. Thyroid antibodies and thyroglobulin remain normal. The patient remained clinically euthyroid. Conclusion: It is important to note that several factors can cause abnormal thyroid function tests, such as Immune check point inhibitors therapy, with the exact mechanism for abnormal TFTs unknown, and can also be associated with either Grave’s hyperthyroidism or Hashimoto’s hypothyroidism,as well as other autoimmune endocrine disorders. Biotin, a common supplement, has also been reported to interfere with the thyroid function test assays for free thyroxine (T4), total T4, free triiodothyronine (T3), total T3, TSH, and various cancer markers. However, It is important to clinically evaluate the patient for thyroid disorders, and recognize that therapy may not always be required, when discrepant and fluctuating thyroid function tests are obtained, such as in this patient. References: (1) Holmes EW, Samarasinghe S, Emanuele MA, Meah. Biotin interference in clinical immunoassays: a cause for concern. . Arch Pathol Lab Med. 2017;141:1459-1460. (2) Rossi E, Sgambato, De Chaira G, et al. Thyroid-induced toxicity of check-point inhibitors immunotherapy in the treatment of advance non-small cell lung cancer. J. Endocrinol Diabetes 2016;3:1-10.

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 Thyroid Function Status in Indian Adult Nonpregnant Females in Ranchi, India

2017 ◽  
Vol 21 (1) ◽  
pp. 25-29
Author(s):  
Nandita Hazra ◽  
Sarvinder Singh ◽  
Binay Mitra ◽  
Bhaskar Shahbabu
Keyword(s):  
Thyroid Function ◽  
Subclinical Hypothyroidism ◽  
Clinical Status ◽  
Study Group ◽  
Thyroid Disorders ◽  
Reference Ranges ◽  
Thyroid Function Tests ◽  
Thyroid Disorder ◽  
Female Population ◽  
Nonpregnant Adult

ABSTRACT Aim Thyroid disorders are one of the most common endocrine diseases in India. Thyroid disorders are more common in women than in men and contribute to significant morbidity. In this postiodization era, there is paucity of pan-Indian data of thyroid disorder status among adult nonpregnant women. This study was done to analyze the thyroid hormone levels in women of Jharkhand region, which is traditionally known to be an iodine-deficient area. Materials and methods Three hundred and forty nonpregnant adult females in Ranchi area who were consuming iodized salt formed part of the study group. Clinical evaluation was done by a gynecologist pertaining to thyroid illness. Thyroid function tests encompassing triiodothyronine, thyroxine, and thyroid-stimulating hormone were carried out by quantitative enzyme immunoassay method. Thyroid status of the population was defined as per kit reference range. Results Subjects with age range 20 to 67 years were divided into three groups as per clinical status of thyroid disorder, viz. total, disease free, and control. A total of 19.6% had biochemical evidence of thyroid disorder and 82.4% were euthyroid as per reference ranges in kit literature. Out of hypothyroid subjects, 3.2% had clinical and 14.4% had subclinical hypothyroidism. In the study group, no subjects were detected to have overt or subclinical hyperthyroidism. Multiple comparison analysis was done with Statistical Package for the Social Sciences version 20.0, a statistical software package. Discussion This is the first study in Jharkhand area on nonpregnant adult female population that are getting iodine sufficient foods in an iodine-deficient region. The study showed high prevalence of thyroid disorders in the study group. Hypothyroidism, predominantly subclinical hypothyroidism, is prevalent among women in this region. How to cite this article Chakrabarty BK, Mitra B, Shahbabu B, Hazra N, Singh S. Thyroid Function Status in Indian Adult Nonpregnant Females in Ranchi, India. Indian J Med Biochem 2017;21(1):25-29.

scholarly journals Thyroid function tests and its interpretation

2014 ◽  
Vol 4 (7) ◽  
pp. 584-590 ◽  
Author(s):  
KC Shiva Raj
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Screening Test ◽  
Thyroid Diseases ◽  
Thyroid Function Tests ◽  
Thyroid Disorder ◽  
Medical Conditions ◽  
Hormone Concentration ◽  
Function Tests ◽  
Thyroid Hormone Concentration

Abstract: Thyroid diseases are among the most prevalent of medical conditions. In the patients with obvious features of hypothyroidism or hyperthyroidism thyroid function tests only confirm the diagnosis. Though TSH is widely used as a screening test in suspicion with thyroid disorder, many times TSH alone may be misleading. In this situation TSH along with T4 and T3 should be performed which will resolve the problem. However, thyroid function tests may not concord with each other. Discordant results between TSH, T4 and T3 may be because of various conditions like subclinical hypo- or hyperthyroidism, non-thyroidal illness, drugs etc. Beside that antibody interference and special condition like pregnancy may alter the thyroid hormone concentration. DOI: http://dx.doi.org/10.3126/jpn.v4i7.10318 Journal of Pathology of Nepal (2014) Vol. 4, 584-590  

Interference in thyroid-function tests in postpartum thyroiditis

1991 ◽  
Vol 37 (8) ◽  
pp. 1397-1400 ◽  
Author(s):  
R John ◽  
S Othman ◽  
A B Parkes ◽  
J H Lazarus ◽  
R Hall
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Antibody Binding ◽  
Postpartum Women ◽  
Thyroid Autoantibodies ◽  
Thyroid Function Tests ◽  
Serum Concentrations ◽  
Free T4 ◽  
Postpartum Thyroiditis ◽  
Free Thyroid Hormone

Abstract Three women are described from a study of patients with postpartum thyroiditis whose sera gave spuriously increased concentrations of free thyroid hormone because of antibody binding of radiolabeled thyroxin (T4) and triiodothyronine (T3) analogs. All of the women showed increased serum concentrations of thyroid autoantibodies. The antibody binding of radiolabeled analogs and its effect on free T4 and free T3 assays disappeared by 48 weeks postpartum. Postpartum women who develop thyroid autoantibodies have approximately 2% prevalence of increased binding of radiolabeled analogs, which can result in an interference in thyroid hormone assays involving T4 and T3 analogs.

Sign in / Sign up

Export Citation Format

Share Document