Thyroid Case Reports III (posters)

MON 184

Misdiagnosis of Graves’ Hyperthyroidism By Biotin Treatment
Eva Philipse, Yentl De Roeck, Theodorus B Twickler and Luc F Van Gaal

MON 186

Concurrence of Graves’ Disease and Cogan’s Syndrome in a Polyarthritis Patient
Takako Yonemoto, Kae Morishita, Rieko Kosugi, Tatsuo Ogawa, Takeshi Usui and Tatsuhide Inoue

MON 187

Reversible Mania: An Unusual Presentation of Hypothyroidism
Deepa Philip, Andrew J Bauman and Richard J Comi

MON 188

IgG4-Related Disease of the Thyroid Presenting As Profound Primary Hypothyroidism: Report of Two Cases
Satbir Kaur Singh, Kaitlin Ditch, Kathyrn Peterson and Devaprabu Abraham

MON 189

MON 190

RAI-Avid Warthin’s Tumor of the Parotid Gland
Daniel Cyrus Rafii and Jocelyne Georges Karam

MON 191

Disseminated Aspergillosis with the Involvement of Thyroid Gland
Vinita Singh, Arshi Basit and Pauline M Camacho

MON 192

A Case of Incidental Myxedema Hypothyroidism in a Patient with Impending Cardiac Tamponade
Wai Wai Lin, Janice L Gilden, Phyo Thazin Myint, Caroline Tomas and Katherine E Jackon-Flechet

MON 193

Rhabdomyolysis Caused By Profound Hypothyroidism
Stephanie Behringer-Massera and Hanna Lee

MON 197

Profound Hypothyroidism Causing Acute Tubular Necrosis
Arwa Mahmoud Elsheikh, Nawras Alshoubaki, Amol Shrikhande and Wagid Choudhry

MON 198

A “Graves” Manifestation of Hashimoto’s Thyroiditis
Pranjali Sharma, Paul Rosenberg and Krishnakumar Rajamani

MON 200

Myxedema Coma Secondary to Hypopituitarism in a Patient without Previously Known Pituitary Dysfunction
João Sérgio Neves, Ana Isabel Oliveira, Ana Varela and Davide Carvalho

MON 201

Uremic Encephalopathy Masking Myxedema Coma
Arman Mushtaq and Hiyam Bakhit

MON 202

MON 203

Title:  an Unusual Case of Recurrent Amiodarone Induced Thyroiditis      Katayoun Lotfi, Marina Basina  Department of Medicine Division of Endocrinology Stanford Health Care    Introduction   Amiodarone Is a Class III Antiarrhythmic Drug That Is Used in the Treatment of Recurrent Ventricular and Supraventricular Arrhythmias.  in Each 200mg of Amiodarone There Is a 75mg of Iodine, 10% of Which Is Released As Free Iodide Daily. While on Amiodarone Therapy 3% of the Patients in Iodine Sufficient Areas of the World, Such As North America and 10% of the Patients in Iodine Deficient Areas of the Works Develop Amiodarone Induced Thyrotoxicosis, Classified As Type I and Type II.  Type I Occurs in Patients with an Underlying Graves’ Disease or Autonomous Nodular Goiter, in Whom Iodine Load from Amiodarone Therapy Accelerates Thyroid Hormone Synthesis.  in Type II the Thyrotoxicosis Occurs in Patients without Underlying Thyroid Disease in the Setting of Destructive Thyroiditis That Results in Excess Release of Preformed T4 and T3 into the Circulation.  the Thyrotoxicosis Phase Usually Takes Several Weeks to Several Months and It Is Often Followed By a Hypothyroid Phase with Eventual Recovery Versus Permanent Hypothyroidism, What Is Thought of As Thyroid Burnout.    We Present a Case of Recurrent Thyrotoxicosis and Hypothyroidism in a Patient with Type 2 Amiodarone Induced Thyrotoxicosis on Continuous Amiodarone Therapy in a Young Patient with Non-Ischemic Cardiomyopathy. the Thyrotoxic and Hypothyroid Phase Has Recurred with No Permanence of Either State.    Clinical Case   Patient Was a 32-Year-Old Man with Severe Familial Dilated Cardiomyopathy Complicated By Recurrent Episodes of Ventricular Tachyarrhythmia (V-tach), on Heart Transplant List, Which Has Been Treated with Amiodarone Since Age 23, in 2008. the Patient Has Remained Stable with No Recurrent V-Tach.  Three Years after Treatment with Amiodarone, He Developed More Energy (usually fatigued in the setting of NYC HF IV), Heat Intolerance, Insomnia, Tachycardia, Weight Loss of 10 Lbs Despite Great Appetite.    the Patient’s Thyroid Function Tests Were Closely Monitored.  Electronic Records of Thyroid Function Tests Are Available Since 2008. TSH Was 1.38, Total T3 of 149, and Free T4 of 1.3. in 2009, His TSH Was 4 with Free T4 of 1.3. in 2010, a TSH of 4.69 with Free T4 of 1.5. in November of 2010, TSH of 3.98, Free T4 of 1.5. in June of 2011, His TSH Was 2.49 and Free T4 of 1.6. He Had His Regular Thyroid Level Checked on January 25, 2011, and the TSH Level Came Back As 0.01. the Patient Also Had an Additional Blood Test Done at an Outside Laboratory on January 27, 2012, Which Showed Free T4 of 6.3 with the Normal Range Being Between 0.8 and 1.8, Total T3 of 384 with Normal Range Between 76 and 181.  He Was Taken Off Transplant List Due to Severe Hyperthyroidism.    the Patient Had No Previous History of Thyroid Disease. the Patient Was Thought to Have Amiodarone Induced Thyrotoxicosis Type 2. His TSI Was Negative and No Thyroid Enlargement Was Noted on Physical Examination.   Hyperthyroid Phase  in Feb 2012, He Was Started on Methimazole and Prednisone. Although the Patient Was Thought to Have Type 2 Amiodarone Induced Thyrotoxicosis, Methimazole Was Added Due to Severity of the Patient’s Condition and in the Absence of Definitive Test to Confirm His Diagnosis. Initially, TSH and FT 4 Were Checked Every 2 Weeks. on March 2, 2012, TSH 0.01, Free T4 2.7 (down from 3.0 on February 23, 2012) Total T3 136 (down from 171 on February 23, 2012). the Methimazole Dose Was Decreased and Prednisone Was Tapered. the Patient’s Free T3 Rose 172, Hence the Prednisone Dose Was Increased and Eventually Tapered By Smaller Increments. Two Months Later on May 31, 2012 TSH Was 0.01 and Free T4 Was 2.0. after 4 Months of Methimazole and Steroid Therapy TSH Was 0.48 and Free T4 1.2.   Hypothyroid Phase  in August of 2012, TSH Dropped to 11.06 and Free T4 to 1.0. at This Point Both the Doses of Prednisone and Methimazole Were Decreased. on September 10, 2012, Tsh  25.8 and Free T4 0.9 Were Noted Hence Prednisone and Methimazole Dose Were Decreased. the Patient Developed Symptoms of Hypothyroidism and in October of 2012, Was Thought to Have Developed Thyroid Burnout.  the Methimazole Was Discontinued and Prednisone Was Tapered Further.  the Patient Was Started on Levothyroxine. in September 2012, TSH Improved to 5.77 and Free T4 to 1.4, Hence, Levothyroxine Dose Was Increased and Prednisone Was Further Tapered and Subsequently Discontinued. the TSH and Free T4 Remained in the Normal Range on Levothyroxine for over 3 Years and Monitored Every 2-3 Months While Continued on Amiodarone. He Was Re-Listed for Heart Transplant. Hypothyroid to Hyperthyroid  in March of 2016, Patient Reported Symptoms of Heart Palpitations.  in Early March of 2016, TSH Was 0.02 and Free T4 Increased to 6.3, Hence Prednisone and Methimazole Were Restarted. TSH and Free T4 Were Monitored Every 2 Weeks. on  March 28, 2016 TSH Decreased to 0.01, Free T4 Rose to 5.5, Prednisone Dose Was Increased.  Free T4 Remained Persistently High on Prednisone and Methimazole until 5/9/2016, When It Decreased to 3.2.  in July of 2016 When TSH Was Noted to be 0.01 Free T4 1.7, Hence Methimazole Was Discontinued. on 8/10/2016 TSH Was Noted to be 3.62 and FT4 1.1, When Prednisone Was Decreased.    Hypothyroid Back Again  on September 1, 2016, TSH Was Noted to be 10 and Free T4 1.0.  on September 20, 2016 TSH Increased to 13.19 and Free T 4 to 1.0, When Prednisone Was Further Decreased in Dose. on October 13, 2016 TSH 9.5 and Free T4 1.0 Were Noted. on October 25, 2016 TSH Was 13.9 and Free T4 Was 1.2. Prednisone Was Stopped and the Patient Is Being Closely Monitored.  He Is Clinically Euthyroid.   Clinical Conclusions  This Is a Unique Case of Recurrence of Destructive Amiodarone Induced Thyroiditis after Being Hypothyroid for over 3 Years and Treated with Levothyroxine.  Both Thyrotoxicosis and Hypothyroidism Reoccurred in This Patient While Being Continued on Amiodarone.  in Our Review of the Literature, There Are No Other Cases Reported of Such Pattern of Recurrence. in One Matched Retrospective Cohort Study, Five out of Eight Patients with Type 2 Amiodarone Induced Thyrotoxicosis on Continued on Amiodarone, Developed Recurrence of Thyrotoxicosis. Seven Percent of the Patients with Recurrence of Thyroitoxicosis Developed Permanent hypothyroidism1.  Recurrence of Thyrotoxicosis after Prolonged Hypothyroidism Was Not Reported. As per the Practice Guidelines of North American Society of Pacing and Electrophysiology, the Patients Requiring Chronic Amiodarone Therapy Should Have TSH at Baseline Checked and then Every 6 months2. Our Case, Emphasizes That Even If Patients Develop What Appears to be Persistent Hypothyroidism, They Are at Risk of Developing Recurrence of Thyrotoxicosis.  These Patients Should be Followed Vigilantly, with Low Threshold of Checking Thyroid Levels If Any Changes in Patient’s Status Including Worsening Cardiac Function. the Case Demonstrates the Importance of Close Monitoring of Patients with Amiodarone Induced Thyroiditis Who Require Amiodarone for Management Their Life Threatening Arrhythmias.     Referrenes 1.Bogazzi, Fausto, Bartalena, Luigi, Tomisti, Luca, Rossi, Giuseppe, Brogioni, Sandra and Martino, Enio. Continuation of Amiodarone Delays Restoration of Euthyroidism in Patients with Type 2 Amiodarone-Induced Thyrotoxicosis Treated with Prednisone: A Pilot Study. J Clin Endocrinol Metab, November 2011, 96(11):3374 –3380. 2. Goldschlager, Nora MD, Epstein, Andrew E. MD, Naccarelli, Gerald V. MD, Olshansky, Brian MD, Singh, Bramah MD, Collard, Harold R. MD, Harold R. Murphy, Harold R. MD, PhD. a Practical Guide for Clinicians Who Treat Patients with Amiodarone: 2007. Arch Intern Med. 2000 Jun 26;160(12):1741– 8
Katayoun Lotfi

MON 204

Development of Atypical Grave’s Orbitopathy during Pregnancy
Leticia Fernandes Facundo, Debora Soares de Araujo, Juliana de Sá Freire Medrado Dias, Isabel Silveira Dias Garcia and Marcus Vinicius Leitão Souza

MON 205

An Unrecognized Heart Failure in Elderly; The Myxedema Heart
Paula Jeffs Gonzalez, Alex Gonzalez Bossolo, Michelle M Mangual, Karen Torres and Jose Hernan Martinez