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 ◽  
...  

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 (<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>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.

1987 ◽  
Vol 80 (12) ◽  
pp. 750-752 ◽  
Author(s):  
C Farror ◽  
M L Wellby ◽  
C Beng

Clinical and biochemical studies on a family in which 3 members have familial dysalbuminaemic hyperthyroxinaemia (FDH) are presented. They were clinically euthyroid with elevated serum thyroxine (T4) and free T4 indices but normal free T4 by equilibrium dialysis and normal serum triiodothyronine (total and free). All thyroid function tests on the remaining family members were normal. The inheritance is consistent with autosomal dominance. Also presented are data on 4 unrelated patients with FDH and two patients with T4 autoantibodies. The methods for detecting FDH, T4 antibodies and other causes of euthyroid hyperthyroxinaemia are now freely available. Since these anomalies may be more common than previously supposed, clinical awareness of the conditions is necessary to protect patients from the consequences of incorrect diagnosis of thyrotoxicosis.


2008 ◽  
Vol 21 (2) ◽  
pp. 179-182
Author(s):  
Carol F. Adair ◽  
John T. Preskitt ◽  
Kristin L. Joyner ◽  
Robin W. Dobson

2011 ◽  
Vol 26 (S2) ◽  
pp. 1515-1515 ◽  
Author(s):  
Y. Themeli ◽  
I. Aliko ◽  
A. Hashorva

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.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Robert P McEvoy ◽  
Anthony O’Riordan ◽  
Mark J Hannon

Abstract The population attending the Medical Assessment Unit at our hospital comprises patients attending electively for investigation and acutely unwell patients presenting for unscheduled care. The standard panel of blood tests taken on arrival includes thyroid function tests (TFTs, i.e. TSH and free-T4), despite a recent review questioning the clinical utility of this practice [1]. We performed a retrospective audit to determine what proportion of our patients had abnormal thyroid function on presentation, and whether these abnormal test results were being followed up. Using the iSoft Clinical Manager software, a list was generated of all patients who attended the hospital between January 2018 and June 2018 inclusive. For each attendance, we recorded the date, medical record number, patient age, gender, and TFT result. Abnormal TFT results were classified as overt or subclinical hyper- or hypothyroid, or non-thyroid illness syndrome (NTIS), based on their admission TSH and free-T4. We then examined the hospital and primary care records of patients with abnormal TFTs to determine if they had ongoing thyroid follow up post discharge. In total, 2,298 patients attended over the 6-month study period. The mean patient age was 67.2 years, and 49% were female. Thyroid function tests were ordered on the day of attendance for 1,688 patients (73%). Of these, 181 results (11%) were abnormal: 20 overt hyperthyroid (11%), 72 subclinical hyperthyroid (40%), 12 overt hypothyroid (7%), 35 subclinical hypothyroid (19%), and 42 NTIS (23%). Twenty of these patients died within 3 months of the abnormal TFT result (4 overt hyperthyroid, 3 subclinical hyperthyroid, 3 overt hypothyroid, 6 subclinical hypothyroid, and 4 NTIS). Of the remaining 161 patients, 74 (46%) had not been followed up within 3 months (4 overt hyperthyroid, 34 subclinical hyperthyroid, 3 overt hypothyroid, 15 subclinical hypothyroid, and 18 NTIS). The low percentage of abnormal TFTs (11%) in this audit is in keeping with similar studies where thyroid function testing was performed on unselected hospital populations [1]. Subclinical hyperthyroidism was by far the most common abnormality found. A high percentage of abnormal tests (46%) were not followed up, with poor compliance with thyroid management guidelines [2]. Future work will investigate adoption of an ‘opt-in’ order system [3] and electronic alerts to flag abnormal results for follow-up. [1] Premawardhana LD. Thyroid testing in acutely ill patients may be an expensive distraction. Biochemia medica. 2017; 27(2): 300-307. [2] Ross DS et al. 2016 American Thyroid Association Guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016 Oct; 26(10):1343-1421. [3] Leis B et al. Altering standard admission order sets to promote clinical laboratory stewardship: a cohort quality improvement study. BMJ Qual Saf. 2019; 28(10): 846-52.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A940-A941
Author(s):  
Nyembezi Dhliwayo ◽  
Rana Wajahat ◽  
Andriy Havrylyan ◽  
Alvia Moid ◽  
Walid Khayr ◽  
...  

Abstract There is considerable evidence that some Borrelial (Lyme spirochetal) proteins share significant antigenic properties with several thyroid-related proteins (e.g. TSH receptor, thyroglobulin, thyroid peroxidase) and can induce thyroid autoimmunity, sometimes associated with Hashimoto’s thyroiditis and perhaps also a “destructive thyroiditis” such as “silent” thyroiditis or “Hashitoxicosis.” As an acute illness, Lyme disease may also constitute a “non-thyroidal illness” capable of perturbing thyroid function tests without causing thyroid dysfunction. We report a 22-year old woman admitted with an acute paranoid schizophrenia, thyroid function tests consistent with autoimmunity, transient thyrotoxicosis (tachycardia, lid-lag, brisk DTR’s) and a greatly reduced radioiodine uptake. The thyroid was not palpably enlarged, nodular or tender. On screening assay, reactivity was demonstrated to 4 of 13 Borrelial proteins. Anti-Lyme IgM but not IgG, antibodies, were positive. This was consistent with recent Lyme disease infection. Serum TSH (NL: 0.358-3.74 mcU/ml), Free T4 (NL: 0.76-1.46 ng/dl), and Free T3 (NL: 2.18-3.98 pg/ml) were, respectively: Day1: 0.087 mcU/ml (suppressed), 1.52 ng/dl (slightly elevated), 2.07 pg/ml (slightly reduced); Day2: 0.148 (suppressed), 1.18 (normal), no FT3; Day4: 0.827 (normal), no FT4 or FT3; Day5: 1.66 (normal), 0.89 (normal), 1.77 (low). Anti-Tg and Anti-Peroxidase antibodies were both moderately elevated. Thyroid Stimulating Immunoglobulins were not elevated. The radioactive iodine uptake on Day4 was 2.8% (NL: 15-30% at 24 hr). Thyroid ultrasonogram was normal. An attractive explanation is that Lyme disease triggered a “destructive thyroiditis,” perhaps but not necessarily mediated by thyroid autoimmunity. This would account for the brief interval of thyrotoxicosis accompanied by a very low radioiodine uptake. Alternatively, Lyme disease, as an acute process, would expectedly be capable of eliciting the thyroid function abnormalities of “non-thyroidal illnesses” in general, as would acute psychosis, well-known to often resemble Graves’ disease at admission.


2021 ◽  
Vol 184 (5) ◽  
pp. 699-709
Author(s):  
Irene Campi ◽  
Ilaria Bulgarelli ◽  
Antonella Dubini ◽  
Giovanni Battista Perego ◽  
Elena Tortorici ◽  
...  

Objective Alterations in thyroid function tests (TFTs) have been recorded during SARS-CoV-2 infection as associated to either a destructive thyroiditis or a non-thyroidal illness. Methods We studied 144 consecutive COVID-19 patients admitted to a single center in intensive or subintensive care units. Those with previous thyroid dysfunctions or taking interfering drugs were excluded. Differently from previous reports, TSH, FT3, FT4, thyroglobulin (Tg), anti-Tg autoantibodies (TgAb) were measured at baseline and every 3–7 days. C-reacting protein (CRP), cortisol and IL-6 were also assayed. Results The majority of patients had a normal TSH at admission, usually with normal FT4 and FT3. Low TSH levels were found either at admission or during hospitalization in 39% of patients, associated with low FT3 in half of the cases. FT4 and Tg levels were normal, and TgAb-negative. TSH and FT3 were invariably restored at the time of discharge in survivors, whereas were permanently low in most deceased cases, but only FT3 levels were predictors of mortality. Cortisol, CRP and IL-6 levels were higher in patients with low TSH and FT3 levels. Conclusions Almost half of our COVID-19 patients without interfering drugs had normal TFTs both at admission and during follow-up. In this series, the transient finding of low TSH with normal FT4 and low FT3 levels, inversely correlated with CRP, cortisol and IL-6 and associated with normal Tg levels, is likely due to the cytokine storm induced by SARS-Cov-2 with a direct or mediated impact on TSH secretion and deiodinase activity, and likely not to a destructive thyroiditis.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A565-A565
Author(s):  
Alisha Hossain ◽  
Emily Skutnik ◽  
Arjan Ahluwalia ◽  
Lindor Gelin ◽  
Sonum Singh ◽  
...  

Abstract Background: Pituitary adenomas are usually benign tumors that arise from adenophypophyseal cells and produce one or two types of hormones. Plurihormonal adenomas are a rare subtype that produce two or more hormones and represent less than 1% of all pituitary adenomas. Clinical Presentation: A 76-year-old female presented for evaluation of abnormal thyroid function test results. She was found to have an elevated free T4 of 1.92 ng/dL and total T4 of 14.4 ug/dL with an inappropriately normal TSH of 2.11 uIU/mL. Physical examination was significant for tachycardia, tremors, diaphoresis, coarse facial features, and enlarged hands. Further biochemical evaluation of her pituitary hormone levels demonstrated an elevated prolactin (PRL) of 237.2 ng/mL, elevated insulin-like growth factor 1 (IGF-1) of 787 ng/mL, normal morning ACTH of 47 pg/mL, normal morning cortisol of 17.0 ug/dL, an inappropriately suppressed FSH of <5.0 mIU/mL, an elevated alpha subunit of pituitary glycoprotein hormones (PGH) of 6.9 ng/mL, and an elevated free T4 of 3.5 ng/dL by equilibrium dialysis. She underwent an MRI of the pituitary and brain which demonstrated a pituitary adenoma measuring 1.2 x 1.3 x 1.8 cm with a portion herniating into the sella turcica with no mass effect of the optic chiasm. A formal visual field examination was normal. The patient underwent workup for Cushing’s Disease with a low dose overnight dexamethasone suppression test, resulting in an appropriate response with an 8 AM cortisol of <1.0 ug/dL. Glucose suppression test confirmed the diagnosis of acromegaly with growth hormone at 120 minutes of 19.90 ng/mL. Neurosurgery performed a trans-sphenoidal pituitary adenoma resection. Thyroid function tests on post-operative day 4 demonstrated a suppressed TSH of 0.01 uIU/mL and an elevated free T4 of 2.30 ng/dL. Histological evaluation revealed dual expression of transcription factors pituitary-specific positive transcription factor 1 (PIT1) and steroidogenic factor 1 (SF1) as well as PRL, GH, TSH and FSH expression. Immunostaining for LH and ACTH were negative. Post-operative IGF-1 and GH levels were 106 ng/mL and 0.51 ng/mL at 17 weeks, respectively. Post-operative TSH normalized to 0.82 uIU/mL, free T4 normalized to 1.04 ng/dL, and PRL normalized to 8.1 ng/mL at 12 weeks. The patient remained symptom free after successful surgical resection. Discussion: Our case demonstrates the clinical course of a unique patient with clinical and biochemical manifestations of thyroid dysfunction and acromegaly with a pituitary adenoma immunoreactive for GH, TSH, FSH, and PRL. The co-secretion of GH, TSH, PRL, and FSH as well as positivity for the alpha-subunit is extremely unusual. This case emphasizes the importance of considering pituitary abnormalities as a cause for abnormal thyroid function tests.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jorge Pedro ◽  
Vanessa Gorito ◽  
Cristina Ferreras ◽  
Ferreira João Silva Maria ◽  
Sofia Ferreira ◽  
...  

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.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A948-A949
Author(s):  
Jordan Albrecht ◽  
Moeed Ahmed ◽  
Sudha Nandala ◽  
Saad Farooqi ◽  
Robert J Anderson

Abstract Introduction: Postpartum Thyroiditis (PPT) is an autoimmune disorder characterized by destruction of the thyroid gland within the first year after delivery. Systemic Lupus Erythematosus (SLE), another autoimmune disease, has been associated with a spectrum of thyroid disorders. While the prevalence of thyroid diseases in patients with SLE is increased, the association between SLE and PPT is not well known. The infrequency of encountering SLE and PPT makes abnormal thyroid tests in the postpartum period a diagnostic challenge. Clinical Case: A 27-year-old G1P1001 who was five months postpartum and not breast feeding was referred to Endocrinology clinic for evaluation of abnormal thyroid function tests. Past medical history was significant for SLE with renal and pericardial involvement. SLE was well controlled, treated with hydroxychloroquine. Family history was significant for hypothyroidism in her mother. She was asymptomatic and appeared clinically euthyroid. Vitals were stable and physical exam was negative for goiter, nodule or orbitopathy. Lab results at two months postpartum showed an elevated TSH of 3.87 UIU/mL (Normal 0.40-3.8 UIU/mL) and at four months postpartum TSH was low at 0.012 UIU/mL. Repeat labs at five months postpartum continued to show a low TSH at 0.007 UIU/mL with mildly elevated Free T4 at 1.7 ng/dL (Normal 0.6-1.6 ng/dL) and elevated Free T3 of 6.0 pg/mL (Normal 2.1-3.8 pg/mL). Anti-thyroid peroxidase antibodies (TPO), thyroid stimulating antibodies (TSI) and TSH receptor antibodies (TRAb) were negative. Thyroid Ultrasound with Doppler was within normal limits. Radioactive Iodine Uptake and Scan, obtained at 6 months postpartum, showed high normal uptake (17% and 32% at 4 hours and 24 hours respectively), suggestive of recovery phase of PPT. The most recent TSH was elevated at 8.5 UIU/mL and Free T4 was low at 0.7 ng/dL. Disease course was consistent with PPT. Conclusion: The Th1 (T-helper) lymphocyte immune predominance in autoimmune thyroid disease and SLE is the immune-pathogenetic base of the association between both diseases. Postpartum thyroiditis is a variant of chronic autoimmune thyroiditis. Serum anti-TPO antibodies vary during pregnancy and tend to increase early and may decline later. Immunologic tolerance increases during pregnancy, fades in the postpartum period and makes interpretation of thyroid function tests and disease process challenging. Pregnant and postpartum patients who have SLE have increased prevalence of thyroid disease. Causes are multifactorial with a higher prevalence of hypothyroidism and thyroid autoantibodies. Hyperthyroidism is much less likely. One comparable study found 6 of 43 (14%) women with SLE developed PPT and only one of these patients had positive thyroid antibodies. These reports and our patient illustrate the variability of thyroid function tests in patients with SLE.


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