scholarly journals Management of Atrial Flutter in Thyroid Storm

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A941-A941
Author(s):  
Theresa N Lanham ◽  
Farah Hena Morgan
Keyword(s):  
Atrial Flutter ◽  
Hot Flashes ◽  
Gastrointestinal Symptoms ◽  
Liver Function Tests ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Storm ◽  
Beta Blockade ◽  
Free T4 ◽  
Free T3 ◽  
History Of

Abstract Introduction: Thyroid storm, life-threatening hyperthyroidism, commonly presents with tachyarrhythmias. We present a case of hyperthyroid-induced atrial flutter, refractory to beta-blockade, successfully treated with electrical cardioversion (CV) while biochemically hyperthyroid. Case Description: A 49-year-old female with history of asthma and no family or personal history of thyroid disease presented with new-onset atrial flutter and heart failure. The patient endorsed weight loss, hot flashes, anxiousness, tremors, and palpitations. She denied gastrointestinal symptoms or visual changes. She was afebrile with normal mentation. Heart rate was found to be 260 beats per minute (bpm) in atrial flutter. Exam demonstrated bilateral lower extremity edema, and profound exophthalmos. Labs were remarkable for thyroid stimulating hormone (TSH) <0.01 [ref: 0.27-4.2] uIU/mL, free T4 4.5 [ref: 0.8-1.8] ng/dL, free T3 15.5 [ref: 2.0-4.4] pg/mL, thyroid stimulating immunoglobulin (TSI) of 379 [ref: <140] % and a thyroid receptor antibody (TRab) of 10.02 [ref:<=2.0] IU/L. White blood cell count and liver function tests were normal. Chest x-ray (CXR) showed bilateral pulmonary edema and ultrasound showed an enlarged heterogeneous hypervascular thyroid gland. The patient was initially started on Methimazole 30 mg daily and Metoprolol 25 mg every six hours but on day two, the patient was transitioned to Propylthiouracil (PTU) 250 mg every 6 hours given continued atrial flutter and concern for thyroid storm given Burch-Wartofsky score was 50. She was also given potassium iodide for three days. Cardioversion was deferred, as it was felt that the severity of thyrotoxicosis would limit success. On day six, TFTs were improved with a free T4 of 2.2, free T3 3.6. On day 8, because of continued tachycardia >130 bpm with limitation of beta-blockade due to hypotension, she underwent a cardioversion which was successful. On discharge, free T4 was 1.7 and she was transitioned to Methimazole 40 mg daily. Discussion: Thyroid storm has a mortality rate of 10-20%, often related to tachyarrhythmias which can be difficult to treat during a hyperthyroid state. Tachycardia should initially be treated with beta-blockade and antithyroid therapy. Amiodarone is avoided due to concern for worsening hyperthyroidism. A literature review suggests that electrical CV should not be attempted until a patient is euthyroid for four months, as a majority will spontaneously revert once thyroid levels normalize. Conversely, other studies have found that the rate of recurrence of atrial fibrillation between clinically hyperthyroid and euthyroid patients was not statistically significant, suggesting CV should not be delayed until a patient is euthyroid. This suggests that further studies need to be completed to better elucidate appropriate timing in hyperthyroid patient’s refractory to pharmacologic treatment alone.

scholarly journals Acute Iodine Toxicity from a Suspected Oral Methamphetamine Ingestion

2014 ◽  
Vol 7 ◽  
pp. CCRep.S20086 ◽  
Author(s):  
Marilyn N. Bulloch
Keyword(s):  
Case Report ◽  
Gastrointestinal Symptoms ◽  
Liver Function Tests ◽  
Oral Ingestion ◽  
Methamphetamine Abuse ◽  
Normal Limits ◽  
Naturally Occurring ◽  
History Of ◽  
Systemic Symptoms ◽  
Iodine Toxicity

Background Iodine is a naturally occurring element commercially available alone or in a multitude of products. Iodine crystals and iodine tincture are used in the production of methamphetamine. Although rarely fatal, iodine toxicity from oral ingestion can produce distressing gastrointestinal symptoms and systemic symptoms, such as hypotension and tachycardia, from subsequent hypovolemia. Objective The objective of this case report is to describe a case of iodine toxicity from suspected oral methamphetamine ingestion. Case Report A male in his early 20′s presented with gastrointestinal symptoms, chills, fever, tachycardia, and tachypnea after orally ingesting a substance suspected to be methamphetamine. The patient had elevated levels of serum creatinine, liver function tests, and bands on arrival, which returned to within normal limits by day 4 of admission. Based on the patient's narrow anion gap, halogen levels were ordered on day 3 and indicated iodine toxicity. This is thought to be the first documented case of iodine toxicity secondary to suspected oral methamphetamine abuse. Conclusion Considering that the incidence of methamphetamine abuse is expected to continue to rise, clinicians should be aware of potential iodine toxicity in a patient with a history of methamphetamine abuse.

scholarly journals TSH enhancement of FT4 to FT3 conversion is age dependent

2016 ◽  
Vol 175 (1) ◽  
pp. 49-54 ◽  
Author(s):  
David Strich ◽  
Gilad Karavani ◽  
Shalom Edri ◽  
David Gillis
Keyword(s):  
Age Groups ◽  
Thyroid Stimulating Hormone ◽  
Older Age ◽  
Age Group ◽  
Free T4 ◽  
Free T3 ◽  
Age Related ◽  
Differential Increase ◽  
Retrospective Examination ◽  
Tsh Levels

ObjectiveWe previously reported increasing free T3 (FT3) to free T4 (FT4) ratios as thyroid-stimulating hormone (TSH) increases within the normal range in children. It is not known if this phenomenon is age-related among humans, as previously reported in rats. This study examines the relationships between TSH and FT3/FT4 ratios in different ages.DesignRetrospective examination of thyroid tests from patients without thyroid disease from community clinics.MethodsFree T3, free T4, and TSH levels from 527 564 sera collected from patients aged 1 year or greater were studied. Exclusion criteria were the following: missing data, TSH greater than 7.5mIU/L, and medications that may interfere with thyroid hormone activity. A total of 27 940 samples remaining after exclusion were stratified by age. Samples with available anthropometric data were additionally stratified for body mass index (BMI). Correlations of TSH to FT4, FT3, and FT3/FT4 ratios by age group were examined.ResultsUp to age 40, for each increasing TSH quartile, FT3 and the FT3/FT4 ratio increased and FT4 decreased significantly (for both FT3, FT4 and FT3/FT4 ratio,P<0.05 for every TSH quartile when compared with the 1st quartile, except FT3 in the 30–40 age group). In older age groups, increasing TSH was not associated with increased FT3/FT4 ratio.ConclusionAs TSH levels increase, FT3/FT4 ratios increase until age 40, but this differential increase does not occur in older age groups. This may reflect a decrease in thyroxine (T4) to triiodothyronine (T3) conversion with age, which may be part of the aging process.

Graves’ Hyperthyroidism-Induced Psychosis Treated With Aripiprazole—A Case Report

2012 ◽  
Vol 26 (1) ◽  
pp. 59-61 ◽  
Author(s):  
Livia R. Macedo ◽  
Jehan Marino ◽  
Brady Bradshaw ◽  
Joseph Henry
Keyword(s):  
Atrial Fibrillation ◽  
Psychiatric Symptoms ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Long Term Effects ◽  
Free T4 ◽  
History Of ◽  
Antithyroid Peroxidase Antibody ◽  
First Time

Graves’ disease is an autoimmune syndrome with symptoms such as tachycardia, atrial fibrillation, and psychiatric symptoms. Limited evidence exists for the treatment of Graves’ hyperthyroidism-induced psychosis with atypical antipsychotics. A 47-year-old female with a psychiatric history of bipolar disorder presented for the first time to the psychiatric hospital. She was agitated and grossly psychotic with delusions. Electrocardiogram showed atrial fibrillation and tachycardia. Drug screen urinalysis was negative. Endocrine workup resulted in a diagnosis of Graves’ disease (thyroid-stimulating hormone [TSH]: 0.005 μIU/mL, triiodothyronine [T3]: 537 ng/dL, thyroxine [T4]: 24 mcg/dL, free T4: 4.5 ng/dL, positive antithyroid peroxidase antibody, and antinuclear antibody). Aripiprazole 10 mg daily was initiated and titrated to 15 mg daily on day 4. On day 16, her suspicious behavior, judgment, and insight improved. Other medications given included aspirin 325 mg daily, metoprolol 25 mg twice daily, titrated to 12.5 mg twice daily, and methimazole 30 mg daily, titrated to 20 mg twice daily, and discontinued on day 29. The patient received radioiodine I-131 treatment 1 week later. We report the first known case on the use of aripriprazole to treat Graves’ hyperthyroidism-induced psychosis. Further studies examining the long-term effects and appropriate dose and duration of aripiprazole in this patient population are needed.

scholarly journals SUN-524 Patient with Pseudohypoparathyroidism Type 1B, Graves Disease, and False Positive HIV Screen- a Rare Presentation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Viraj V Desai ◽  
Pratima V Kumar
Keyword(s):  
Western Blot ◽  
Autoimmune Diseases ◽  
False Positive ◽  
Thyroid Stimulating Hormone ◽  
Laboratory Evaluation ◽  
Graves Disease ◽  
Free T4 ◽  
Rare Presentation ◽  
Elisa Testing ◽  
History Of

Abstract Background: Pseudohypoparathyroidism 1B (PHP1B) is a disorder that can lead to thyroid stimulating hormone (TSH) resistance and hypothyroidism, although it is rarely associated with thyrotoxicosis. Clinical Case: A 25-year-old female with a history of PHP1B, seizures due to hypocalcemia, and family history of PHP1B in her three sisters and brother presented to our emergency room with a fever of 1030F and generalized malaise. Two months prior, she was seen at an outside hospital with palpitations and bulging of the left eye. There, she was diagnosed with hyperthyroidism, started on methimazole, and asked to continue levetiracetam and calcitriol upon discharge. On our exam, she had tachycardia of 120 beats per minute, left eye proptosis, positive Chvostek sign, and a large goiter with bruit. Reflexes were 3+. Laboratory evaluation revealed corrected serum calcium of 6.1 (8.5-10.5 mg/dL), TSH &lt; 0.01 (0.34-5.60 mU/L), free T4 2.81 (0.60-1.60 ng/dL), free T3 13.0 (2.4-4.2 ng/dL), and iPTH 131 (12-88 pg/mL). ELISA testing for screening of HIV was positive. She was treated with IV calcium gluconate, methimazole, propranolol, and hydrocortisone. Her home doses of calcitriol and calcium were resumed. She was referred for total thyroidectomy as an outpatient once she became euthyroid. The confirmatory Western blot test for HIV was negative. It was determined that presence of thyroid stimulating immunoglobulin resulted in the false positive ELISA test. Discussion: Hyperthyroidism with Graves disease seen in PHP has only very rarely been reported. (1) It has been postulated that abnormal electrolytes and elevated parathyroid hormone from PHP may lead to stimulation of the thyroid gland and perpetuate Graves disease symptoms. (2) Furthermore, the presentation of thyrotoxicosis despite TSH resistance in PHP indicates that there may be other mechanisms for TSH receptor antibodies to take effect in these patients which have not yet been determined. (3) Lastly, autoimmune diseases, including Graves disease, can cause a false-positive HIV ELISA as seen in our patient. Conclusion: Although rare, thyrotoxicosis may present in patients with PHP1B. Additionally, it should be kept in mind that autoimmune diseases such as Graves disease can cause a false positive HIV ELISA, and follow-up Western blot testing should therefore be performed. References: (1) Gerhardt A, Hackenberg K. 2002. Pseudohypoparathyroidism and Graves’ disease: a rare combination of two endocrinological diseases. Exp Clin Endocrinol Diabetes. 110:245-247 (2) Morón-Díaz et al. 2019. A rare case of Graves’ disease in a patient with type 1B pseudohypoparathyroidism and associated TSH resistance. Endocrine Abstracts. 63:96 (3) Richard Prokesch. 2010. Navigating False Positive Testing. HIV Specialist (AAHIVS). 2:27

scholarly journals Thyroid Storm Treated With Nonconventional Therapy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A962-A962
Author(s):  
Caroline Tashdjian ◽  
Paul Shiu ◽  
Tarandeep Kaur
Keyword(s):  
Atrial Fibrillation ◽  
Critically Ill ◽  
Liver Enzymes ◽  
Normal Liver ◽  
Ventricular Rate ◽  
Thyroid Storm ◽  
Free T4 ◽  
History Of ◽  
Chest X Ray ◽  
Iodine Treatment

Abstract Background: Thyroid storm is a rare sequela of thyrotoxicosis with mortality rate of 10-30%. Management of thyroid storm is heavily dependent on thionamides. Cholestyramine and potassium iodide (SSKI) are used as adjunctive therapy and not as the sole treatment for storm. We present a case of thyroid storm treated with cholestyramine and SSKI. Clinical Case: A 45 year old male with past medical history of atrial fibrillation, congestive heart failure, hypertension, substance abuse and grave’s disease presented to the emergency department (ED) for diarrhea. During the course of ED, patient went into atrial fibrillation with rapid ventricular rate. Chest X-ray showed pulmonary edema. Labs were: TSH &lt;0.0025 mIU/L (0.35-4.94 mIU/L) and free T4 3.52 ng/dl (0.7-1.40 ng/dl). Patient was noncompliant with methimazole. Upon admit, ACLS was initiated due to hypoxia and transferred to ICU for ventilator and pressor support. Wartofsky score was 60, suggestive of thyroid storm. Management included methimazole 20mg every 4hours, hydrocortisone 100mg every 8 hours, cholestyramine 4mg every 6 hours, and SSKI 250mg every 6 hours for thyrotoxicosis and amiodarone infusion for afib. Despite normal liver enzymes on admit, day 3 AST increased to 2740 U/L (5-34) and ALT 2684 U/L (0-55). Methimazole was stopped due to potential hepatotoxicity. Day 3 free T4 remained high at 4.16 ng/dl and patient remained critically ill. Plasmapheresis was offered as methimazole was stopped and patient was hemodynamically unstable to undergo surgery. However, family declined this intervention; SSKI and cholestyramine were continued. Free T4 was monitored over the course of treatment; by day 5 free T4 trended down to 1.93 ng/dl. SSKI was eventually stopped on day 8 of treatment as free T4 had normalized and cholestyramine reduced to 4mg twice daily. By day 15, free T4 was 0.8 ng/dl, so cholestyramine was stopped. Due to clinical improvement, patient was weaned off the ventilator and pressor support along with hydrocortisone. Liver enzymes normalized by Day 17. Patient was restarted on methimazole 5mg daily before discharge. Discussion: Thyroid storm is associated with varying degree of liver dysfunction, which can pose a challenge to treatment. In our case, acute fulminant liver failure was multifactorial in the setting of shock, thyroid storm and potential drug toxicity. Thus, thionamides were contraindicated. Radioactive iodine treatment was contraindicated due to use of amiodarone. Plasmapheresis and emergent thyroidectomy could not be done. Thus, nonconventional therapy was used and patient responded well to treatment. This case emphasizes the use of cholestyramine along with SSKI as an effective treatment in patients who are critically ill the setting of a thyroid storm, especially when thionamides are contraindicated and other avenues of treatment are limited.

scholarly journals Thyroid Storm: A Diagnostic Conundrum

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A963-A963
Author(s):  
Mashrutee S Maharaul ◽  
Maya P Raghuwanshi ◽  
Rehan Umar ◽  
Reza Pishdad
Keyword(s):  
Heart Failure ◽  
Atrial Flutter ◽  
Underlying Mechanism ◽  
Left Lobe ◽  
Clinical Syndrome ◽  
Thyroid Storm ◽  
Anterior Mediastinal Mass ◽  
Thyrotropin Receptor Antibodies ◽  
History Of ◽  
Venous Pulsation

Abstract Thyroid storm is a life threatening complication of hyperthyroidism which comes with multi-system involvement and is associated with a mortality of 8-25% despite modern advancements in treatment and supportive measures. A 47 year old woman with past medical history of hypertension and morbid obesity presented to the emergency room with 3 week history of shortness of breath and chest pain associated with productive cough, bilateral leg swelling, orthopnea and palpitations. Upon evaluation, she was in moderate respiratory distress, restless, tachypneic and tachycardic. She had bilateral proptosis and visible jugular venous pulsation along-with bibasilar crackles and pitting edema bilaterally. Lab tests revealed BNP 539 pg/ml and D-Dimer 6401 ng/ml. ECG showed atrial flutter, Chest X-Ray showed bilateral pleural effusions, and CT Chest was negative for pulmonary embolism but revealed anterior mediastinal mass, differential of which included thymoma or teratoma. She was admitted to CCU for aggressive diuresis, control of heart rate and was started on anticoagulation. A review of medical records from outside hospital revealed patient was hyperthyroid 8 months ago, however, was not on any medications. Given a Burch-Wartofsky score &gt;70, she was started on IV hydrocortisone and cholestyramine for severe thyrotoxicosis. Endocrinology was consulted and added PTU to management. TFTs revealed a TSH 0.006 IU/ml, FT4 4 ng/dL and T3 2.5 ng/ml. Bedside ECHO showed LVEF of 14% with global hypokinesis and thyroid ultrasound revealed an enlarged, heterogenous thyroid with a solid, isoechoic, calcified left lobe nodule measuring 0.8 x 0.4 x 0.5 cm. Her serum TSI and thyrotropin receptor antibodies were elevated at 17.20 IU/L and 20.20 IU/L, respectively. She responded to treatment and was discharged on metoprolol, losartan, spironolactone, and furosemide for new-onset heart failure, apixaban for atrial flutter, and PTU and cholestyramine for hyperthyroidism, with Cardiology and Endocrinology follow-ups. Thyroid disease is a common illness affecting 9 to 15 percent of the adults. Thyrotoxicosis refers to the clinical syndrome of hyper-metabolism due to excessive amount of circulating thyroid hormones. The incidence of thyroid storm is 0.57 to 0.76 per 100,000 people per year in the US. It most commonly occurs in women and is more common in patients with underlying Grave’s Disease. The exact underlying mechanism that leads to thyroid storm is not well understood but adrenergic activation seems to have a major role. Our patient had long standing untreated hyperthyroidism with a solid nodule which led to the crisis. The most common cause of death is cardiopulmonary failure and hence treatment should be initiated as soon as diagnosis is suspected owing to high mortality. Awareness of thyroid pathology affecting the heart is important to remember in evaluating the etiology of heart failure in patients.

scholarly journals THYROID ACROPACHY: A RARE MANIFESTATION OF GRAVES DISEASE IN JOINTS

2019 ◽  
Vol 5 (6) ◽  
pp. e369-e371 ◽  
Author(s):  
Nicolas Perini ◽  
Roberto Bernardo Santos ◽  
João Hamilton Romaldini ◽  
Danilo Villagelin
Keyword(s):  
Elevated Serum ◽  
Clinical Signs ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Free T4 ◽  
Tissue Edema ◽  
Rare Manifestation ◽  
Small Joint ◽  
History Of ◽  
Hands And Feet

Objective: The objective of this report was to describe a patient with Graves acropachy, a rare manifestation of Graves disease (GD) that is clinically defined by skin tightness, digital clubbing, small-joint pain, and soft tissue edema progressing over months or years with gradual curving and enlargement of the fingers. Methods: The patient was evaluated regarding thyroid function (serum free T4 [FT4] and thyroid-stimulating hormone [TSH] quantifications) and autoimmunity biomarkers (thyroid receptor antibody [TRAb]) as well as radiographic investigation of the extremities. Results: A 52-year-old man presented with a history of thyrotoxicosis and clinical signs of Graves orbitopathy. Laboratory tests showed suppressed TSH (0.01 UI/L; normal, 0.4 to 4.5 UI/L) and elevated serum FT4 (7.77 ng/dL; normal, 0.93 to 1.7 ng/dL), with high TRAb levels (40 UI/L; normal, <1.75 UI/L). A diagnosis of thyrotoxicosis due to GD was made and the patient was treated with methimazole. After the patient complained of swelling in hands and feet, X-ray evaluation was conducted and established the thyroid acropachy. Conclusion: We present a case of a patient with GD associated with worsening extrathyroid manifestations during orbitopathy, dermopathy, and developed acropachy in hands and feet.

scholarly journals Graves disease-induced thrombotic thrombocytopenic purpura: a case report

2019 ◽  
Vol 13 (1) ◽  
Author(s):  
Saira Chaughtai ◽  
Ijaz Khan ◽  
Varsha Gupta ◽  
Zeeshan Chaughtai ◽  
Raquel Ong ◽  
...  
Keyword(s):  
Thrombotic Thrombocytopenic Purpura ◽  
African American Woman ◽  
Case Reports ◽  
American Woman ◽  
Pulseless Electrical Activity ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Free T4 ◽  
Thrombocytopenic Purpura ◽  
History Of

Abstract Background Thrombotic thrombocytopenic purpura is an autoimmune disease that carries a high mortality. Very few case reports in the literature have described a relationship between Graves disease and thrombotic thrombocytopenic purpura. We present a case of a patient with Graves disease who was found to be biochemically and clinically hyperthyroid with concurrent thrombotic thrombocytopenic purpura. Case presentation Our patient was a 30-year-old African American woman with a history of hypertension and a family history of Graves disease who had recently been diagnosed with hyperthyroidism and placed on methimazole. She presented to our hospital with the complaints of progressive shortness of breath and dizziness. Her vital signs were stable. On further evaluation, she was diagnosed with thrombotic thrombocytopenic purpura, depending on clinical and laboratory results, and also was found to have highly elevated free T4 and suppressed thyroid-stimulating hormone. She received multiple sessions of plasmapheresis and ultimately had a total thyroidectomy. The patient’s hospital course was complicated by pneumonia and acute respiratory distress syndrome. Her platelets stabilized at approximately 50,000/μl, and her ADAMTS13 activity normalized despite multiple complications. The patient ultimately had a cardiac arrest with pulseless electrical activity and died despite multiple attempts at cardiopulmonary resuscitation. Conclusion Graves disease is an uncommon trigger for the development of thrombotic thrombocytopenic purpura, and very few cases have been reported thus far. Therefore, clinicians should be aware of this association in the appropriate clinical context to comprehensively monitor hyperthyroid patients during treatment.

Neurological and gastrointestinal symptoms as an initial presentation of pediatric thyroid storm: report of three cases

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Masao Nogami ◽  
Shadia Constantine ◽  
Shuji Sai
Keyword(s):  
Gastrointestinal Symptoms ◽  
Antithyroid Drug ◽  
Severe Case ◽  
Initial Presentation ◽  
Thyroid Storm ◽  
Gi Symptoms ◽  
Old Japanese ◽  
Threatening Condition ◽  
Life Threatening ◽  
History Of

Abstract Objectives Thyroid storm (TS) is a rare but life-threatening condition caused by decompensated hyperthyroidism. There is no consensus on how to diagnose pediatric TS. We report three pediatric cases of TS presenting with central nervous system (CNS) and gastrointestinal (GI) symptoms as the initial presentation of Graves’ disease. Case presentation They were previously healthy adolescents without family history of thyroid disease. CNS symptoms varied from agitation to coma. GI symptoms included abdominal pain, vomiting, and diarrhea. Their laboratory studies revealed thyrotoxicosis and positive result of thyroid-stimulating antibody (TSAb). They were admitted to the intensive care unit (ICU) and received the combination of an antithyroid drug, Lugol’s solution, a beta antagonist, and hydrocortisone. The most severe case was a 13 year-old Japanese girl who presented with loss of consciousness and hemodynamic shock. She died after 5 days of intensive treatment. Conclusions Pediatricians should consider TS in the differential diagnosis when a patient exhibits both CNS and GI symptoms.

scholarly journals Alteration of Thyroid-Related Hormones within Normal Ranges and Early Functional Outcomes in Patients with Acute Ischemic Stroke

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Xiao-yan Xu ◽  
Wen-yu Li ◽  
Xing-yue Hu
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Functional Outcome ◽  
Multiple Logistic Regression Analysis ◽  
Univariate Analysis ◽  
Thyroid Stimulating Hormone ◽  
Free T4 ◽  
Poor Functional Outcome ◽  
Free T3 ◽  
Normal Ranges

This study evaluated the prognostic value of thyroid-related hormones within normal ranges after acute ischemic stroke. This was a retrospective study and we reviewed 1072 ischemic stroke patients consecutively admitted within 72 h after symptom onset. Total triiodothyronine (T3), total thyroxine (T4), free T3, free T4, and thyroid-stimulating hormone (TSH) were assessed to determine their values for predicting functional outcome at the first follow-up clinic visits, which usually occurred 2 to 4 weeks after discharge from the hospital. 722 patients were finally included. On univariate analysis, poor functional outcome was associated with presence of atrial fibrillation as the index event. Furthermore, score of National Institutes of Health Stroke Scale (NIHSS), total T4, free T4, and C-reactive protein at admission were significantly higher in patients with poor functional outcome, whereas free T3 and total T3 were significantly lower. On multiple logistic regression analysis, lower total T3 concentrations remained independently associated with poor functional outcome [odds ratio (OR), 0.10; 95% confidence interval (CI), 0.01–0.84;P=0.035]. The only other variables independently associated with poor functional outcome were NIHSS scores. In sum, lower total T3 concentrations that were within the normal ranges were independently associated with poor short-term outcomes.

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