ResearchPad - thyroid-disorders-case-reports-ii Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[SAT-489 The Weary Beating Heart: Complications of Severe Hypothyroidism in a Mentally Ill Patient]]> Myxedema coma is a severe form of hypothyroidism representing a endocrinologic emergency. It requires prompt identification and management, as mortality rates exceed 50%. Its rarity stems from early recognition and thyroid medication availability. Its presentation can be non-specific, making it a challenging diagnosis.

This is a 67-year-old male inmate who was brought to the ED due to hypoactivity. He had a long-standing history of bipolar disorder, and hypothyroidism receiving oral levothyroxine.

On evaluation, patient had slowed mentation, GCS 14/15, sluggish reactive pupils, macroglossia, diffuse non-pitting edema, and delayed relaxation of the deep tendon reflexes in the extremities. Vital signs were abnormal; T: 35.2 °C, RR: 10 rpm, SpO2: 84 %, BP: 137/89 mmHg and HR: 42 bpm without chronotropism. 12-lead ECG revealed a complete atrioventricular block (AV block), with non-conductive P waves and idioventricular rhythm. Patient became hemodynamically unstable, transcutaneous pacemaker was placed. Dopamine infusion was initiated for adequate mean arterial pressure. Subsequently, a femoral transvenous pacemaker was performed. However, neurological deterioration prompted mechanical ventilation.

Exploring reversible AV block etiologies, laboratory results were markedly elevated for TSH at 184.775 ng/mL and decreased T4 at 1.5 ng/mL. Lithium levels were therapeutic.

Myxedema coma was identified and timely treatment was provided with intravenous thyroid hormone replacement, intravenous hydrocortisone, and supportive care. Patient was transferred to an ICU where TSH was monitored. After 5 days of receiving IV thyroid hormone replacement therapy, TSH improved. However, patient remained dependent on transvenous pacemaker, for which permanent pacemaker had to be placed. With further therapy, patient’s neurological status improved leading to extubation, and subsequent discharge.

Thyroid hormones play a vital role in the electrical current of the heart; hence, disturbances may potentiate cardiac arrhythmias. Sinus bradycardia and QT interval prolongation are commonly seen. As the severity of hypothyroidism progresses, high-grade AV block may be encountered, being third degree AV block the most challenging and severe.

Patients with high-degree AV block in the setting of reversible etiologies, commonly, do not need a permanent pacemaker. On the contrary, our patient developed complete dependence of the pacemaker for adequate cardiac synchrony, despite adequate replacement therapy.

With this case, we illustrate the importance of a thorough evaluation in patients with AV block of unknown origin, with special attention to reversible etiologies. Thyroid function abnormalities should be promptly identified and managed for better outcomes. Furthermore, it may decrease cardiac death risk and the need for invasive procedures, such as permanent pacemaker placement.

<![CDATA[SAT-500 Response to Tocilizumab Retreatment in Refractory Thyroid Eye Disease]]> Background: The current standard of care for moderate to severe thyroid eye disease (TED) is intravenous methylprednisolone (IVMP), though alternative immunosuppressive options are emerging. In a recent randomized trial, Tocilizumab (TCZ), an anti-IL-6 receptor antibody, demonstrated improved efficacy for corticosteroid-resistant TED compared to placebo. Clinical response to TCZ retreatment, however, has not been previously reported.

Clinical case: A 64-year old man presented with progressive diplopia, eyelid retraction and edema and retrobulbar pain. Initial labs revealed TSH 0.221 uIU/mL, free thyroxine (FT4) 1.11 ng/dL, total T3 172 ng/dL and a thyroid stimulating immunoglobulin (TSI) index of 329 (normal < 140). The patient was a former cigarette smoker who had recently transitioned to e-cigarettes. He was treated with 12 weeks of IVMP with improvement in ocular redness and swelling. Three months following completion of treatment, he presented with worsening left sided proptosis, restrictive strabismus, and compressive optic neuropathy (CON) evidenced by deteriorating central acuity and color vision. He underwent urgent surgical decompression for CON with full restoration of visual acuity. He then received a second 12-week course of IVMP with concomitant orbital radiation. Of note, his hyperthyroidism was well controlled with methimazole. Two months after his second IVMP course, he had a third flare of ophthalmic symptoms. He was then treated with TCZ 8 mg/kg (800mg) IV monthly for six months. The patient’s Clinical Activity Score (CAS) improved from 4 to 2 and TSI index decreased from 610 to 92 (normal). He had significant improvement in periorbital edema, caruncle/plica swelling, and conjunctival injection. However, ten months following completion of the TCZ course he again complained of worsening diplopia and left proptosis. Of note, relapse of his TED symptoms was preceded by an increase in TSI from 92 to 300 two months prior. Orbital CT demonstrated progression of left orbitopathy and increased orbital apex crowding. Following these CT findings he was restarted on TCZ, of which he has now completed 5 additional infusions. His CAS has improved from 3 to 2 and TSI index has decreased from 284 to 100.

Conclusion: This is the first reported case of response to successive courses of TCZ in relapsing, severe, corticosteroid-resistant TED. TCZ can be an effective option for refractory TED though retreatment may be necessary for recurrent inflammation. Further study of TCZ is required to determine its role in relapsing TED and the optimal duration of therapy needed.


Perez-Moreiras et al., 2018. Efficacy of Tocilizumab in patients with moderate to severe corticosteroid resistant Graves’ orbitopathy: a randomized controlled trial. Am J Ophthalmol 195:181

<![CDATA[SAT-490 A Case of Unilateral Exophthalmos Due to Thyroid Orbitopathy and Its Association with Chronic Kidney Disease]]> Graves ophthalmopathy(GO)is the most common extra-thyroidal manifestation of Graves’ disease (GD). Most cases of GO are bilateral which may be asymmetric, whereas unilateral ophthalmopathy is less common and has been observed in 9-15% cases. Association between chronic kidney disease and unilateral Grave’s ophthalmopathy in a clinically euthyroid patient is rare. We report a case of a 24-year-old male with no previous history of any chronic medical illnesses who presented with protruded right eye for the past 6 months. He did not have any other visual symptoms or symptoms related to thyroid disease. Laboratory results revealed low TSH, normal free T3 and free T4. TSH receptor antibodies were positive. He also had elevated serum creatinine at 418 umol/L (normal levels 64 - 110 umol/L). US KUB showed bilateral small sized kidneys and increased parenchymal echogenicity suggestive of chronic kidney disease. MRI Head showed features suggestive of unilateral thyroid associated orbitopathy. Patient received 1-week course of oral prednisolone 10 mg per day after which his exophthalmos improved.Case report: A 24 year old male with no previous history of any chronic medical illnesses, presented to the clinic with protruded right eye for the past 6 months that was progressively getting worse. There was no eye pain, visual changes, ophthalmoplegia, dryness or discharge from eye. Patient did not report any other symptoms, Physical examination revealed a comfortable man with protruded right eye, lid retraction, normal eye movements and no signs of orbital cellulitis. Neck examination was significant for a mild diffuse goitre. Laboratory studies were significant for haemoglobin of 12.1 g/dl (normal 13-17 g/dl). He also had elevated serum creatinine at 418 umol/L (normal 64 - 110 umol/L). Serum electrolytes, liver function tests and lipid profile were within normal range. 24 hr urine collection showed 3.08 gm/24 hr proteinuria. Serum TSH was 0.04 mIU/L (normal 0.45 - 4.5 mIU/L), free T4 was 13.8 pmol/L (normal 9 - 20 pmol/L) and free T3 was 4.56 pmol/L (normal 2.89 - 4.88 pmol/L). Thyrotropin Receptor Ab titre was 4.69 IU/L (normal 0.00 - 1.75 IU/L). ANA, ANCA, C3, C4, Anti thyroid peroxidase and Anti GBM antibodies were negative. Screening for hepatitis B, C and HIV was negative US KUB showed bilateral small sized kidneys and increased parenchymal echogenicity suggestive of CKD. MRI Head was remarkable for proptosis of the right eye with increased retro-orbital fat, thickening and T2 hyper-intensity with sparing of the tendinous insertion involving the right inferior, medial, superior and lateral rectus muscles with crowding at the orbital apex. Features were suggestive of unilateral thyroid associated orbitopathy. Patient received 1-week course of oral prednisolone 10 mg per day after which his exophthalmos improved. An association between CKD and GO in a clinically euthyroid patient is rare.

<![CDATA[SAT-498 Graves’-Associated Takotsubo Cardiomyopathy: An Uncommon Condition]]> Introduction Graves’ disease is an autoimmune disorder that causes excess thyroid hormone (T4 and T3). T4 is converted into T3 (active hormone) in the peripheral tissues by the deiodinase enzyme. T3 has an effect on the cardiac electrical system as well as myocyte contractility. Excess T3 can result in cardiac arrythmias as well as ventricular dysfunction (heart failure). Takotsubo cardiomyopathy is a subtype of nonischemic cardiomyopathy related to severe physiologic or mental stress. Excess catecholamine levels have been reported to cause this disease as well. Takotsubo cardiomyopathy has rarely been reported in Graves’-associated thyrotoxicosis.

Case report 55-year-old female who presented to the ED with palpitations and difficulty breathing. She had been seen by her PCP within the past two weeks with complaint of recent 30 lb weight. TSH was noted to be < 0.001 and a neck ultrasound revealed a diffusely enlarged, hypervascular thyroid. She was referred for outpatient endocrinology consultation for further workup. Prior to her initial endocrinology appointment, she developed palpitations and shortness of breath. She did not have any known family history of thyroid disease or other autoimmune conditions. She drinks 1-2 glasses of wine per week and quit smoking in 2017. Physical exam on admission revealed a heart rate of 133 bpm and a blood pressure of 145/93, normal temperature, and normal respirations. Thyroid was diffusely enlarged and without nodularity. No evidence of orbitopathy. Heart was tachycardic but without murmur. Lungs clear. Abdomen soft, nontender. No significant peripheral edema or pretibial rash. No neurological dysfunction. Labs revealed TSH < 0.001, Free T4 > 7.77, Free T3 12.0, TRAb 44.4%, TSI 433%, Anti-TPO 614, high-sensitivity troponin of 112. EKG showed nonspecific infero-lateral T wave changes, rate 123. Echocardiogram demonstrated left ventricular apical hypokinesis but preserved basilar contractility. Ejection fraction was estimated at 40-45%. Nuclear stress test did not reveal any indication of myocardial hypoperfusion.

Discussion/Conclusion Takotsubo cardiomyopathy can mimic acute myocardial infarction both clinically as well as on EKG/serum biomarkers. Troponin levels are typically elevated as a result of myocardial stretch and subsequent troponin “leak”. Echocardiogram demonstrates apical ballooning of the left ventricle, and by definition coronary arteries will be free of significant occlusive disease. A small number of cases have been reported in association with endocrine conditions including thyrotoxicosis due to Graves’ disease. The majority of cases associated with thyrotoxicosis will resolve spontaneously with 1-3 weeks. Treatment consists of medication to decrease cardiac preload as well as afterload (ACE inhibitor, beta blocker, diuresis as needed), similar to medical treatment of other nonischemic cardiomyopathies.

<![CDATA[SAT-LB81 Carbohydrate Crash: A Rare Case of Thyrotoxic Periodic Paralysis]]> IntroductionThyrotoxic Hypokalemic Periodic Paralysis (TPP) is an uncommon diagnosis in the western world and may be the initial presentation of hyperthyroidism. CaseA healthy 37 year old Asian male was visiting the US when he had sudden onset lower limb weakness after carbohydrate rich meal on Saturday night. He reported hand tremors for 1 month and a 10kg weight loss. On examination he was anxious with a fine hand tremor, BP 158/80mmHg, and HR 106bpm. He had grade 2/5 power to lower limb proximal muscles and brisk reflexes. Thyroid and eyes were normal. Laboratory results significant for potassium (K) 3.2mmol/l, TSH 0.005 (0.270-4.4uiu/ml), FT4 2.6 (0.8-2.2ng/dl), FT3 12.4 (2.77-5.27 pg/ml) and TSH Receptor antibody was 23.9% (<16%). Thoracolumbar MRI was normal. Repletion of K resulted in total resolution of paresis. He was given propranolol and methimazole and chose to complete workup in China.Clinical LessonTPP results in paralysis due to hypokalemia and hyperthyroidism and can be the initial presentation of hyperthyroidism. It is most common in Asian males 20-40 years with incidence 1.9%, but only 0.2% in the west. Proximal muscles are affected more. Attacks may be precipitated by carbohydrate load, rest after exercise, or stress. Patients tend to present on weekends between 2100-0900hrs. It is hypothesized that K metabolism is diurnal, with influx to muscle at night or at rest. Once euthyroid, TPP will not recur unlike familial hypokalemic periodic paralysis which is recurrent and of earlier onset. The underlying reason remains unclear. It may be related to the action of thyroxine on Na/K-ATPase pump. TPP is usually associated with Graves’ disease, but other causes of hyperthyroidism have been reported. TPP is a treatable rare illness in Asians, and very uncommon in the West. Physicians must be aware of its subtleties, as it may be confused with other more common conditions.ReferencesChang-Hsun Hsieh, Shi-Wen Kuo, Dee Pei, Yi-Jen Hung, Sandra Chyi-Fan, Ling-I Wu, Chih-Tsueng He, Tsao-Chin Yang, Wei-Cheng Lian, and Chien-Hsing Lee, Thyrotoxic periodic paralysis: an overview, Ann Saudi Med. 2004 Nov-Dec; 24(6): 418-422. doi:10.5144/0256-4947.2004.418Annie W. C. Kung, CLINICAL REVIEW: Thyrotoxic Periodic Paralysis: A Diagnostic Challenge, The Journal of Clinical Endocrinology and Metabolism 91(7):2490-2495, Copyright © 2006 by The Endocrine Society doi: 10.1210/jc.2006-0356

<![CDATA[SAT-508 Oh My Thyrotoxic Heart! An Uncommon Presentation of High Output Heart Failure]]> High output heart failure is an extremely rare manifestation of thyrotoxicosis in patients without heart disease. Thyroid hormone has a potent metabolic, vascular, positive chronotropic and inotropic effects. Thyrotoxicosis is accompanied by a reduction in systemic vascular resistance and an obligatory increase in cardiac output to compensate high metabolic state. Most of the patients had completed or near completed recovery of cardiac function after treatment to euthyroid status, if cut in time.

Case of 70 y/o female with past medical history of hypothyroidism, hypertension and chronic smoker, came to emergency room due to lightheadedness, weakness, shortness of breath, palpitations and acute bedridden for one week ago. Denied fever, nausea, vomiting or chest pain. On examination patient presented with 122bpm, 23rpm and normotensive. She was in acute respiratory distress requiring BiPAP. Lungs auscultation bilateral crackles, decrease sounds in the bases. Cardiac exam significant for tachycardia, lower extremity edema and JVD +. Laboratories significant for CKD stage 2, chronic anemia and hypoxemia. EKG no ST changes neither T depressions. CXR day #1 reported no cardiopulmonary disease. Basing in these she was admitted with Suspected Pulmonary Embolism. Well’s score was moderate risk; a Chest CTA and full anticoagulation were ordered. Later, venous duplex reported no DVT and D-dimer levels 1.65μg/ml. TSH levels significant decrease 0.0002mU/L and T4 1.800ng/dL. CXR Day#2 reported pulmonary edema and pleural effusion. ECHO2D moderate LVH and preserved systolic function. Patient referred her doctor recently increased thyroid medications from 50 to 100 mcg. Instead of presenting with pulmonary embolism, she has hyperthyroidal state causing cardiac failure. Levothyroxine, heparin and Chest CTA scan were cancelled. She was started in Atenolol and diuretics. Patient symptoms improved and was discharged home to be followed in the clinic. After one week, TSH levels were in 0.008mU/L and one month later in 3.032mU/L. She was started in Levothyroxine 50mcg, to maintain patient euthyroid state.

This case illustrates that sometimes tachycardia and tachypnea are symptoms which frequently presents as baffling diagnostic problems. The association of thyrotoxicosis and cardiovascular morbidity is well established. Thyrotoxicosis most common cardiac manifestation is high output heart failure. Patients presenting with heart failure may have thyrotoxicosis as the underlying cause. Treatment of the thyrotoxicosis can restore normal heart function. Hyperthyroidal state may be take into consideration as a differential of tachycardia and tachypnea even if it’s not one of the common causes. Awareness of this presentation may help identify patients with reversible dilated cardiomyopathy and other complications.

<![CDATA[SAT-501 Thyrotoxicosis with Pre-Ventricular Complexes Resulting in Thyroid Storm and Cardiac Arrest]]> Background: Ventricular arrythmias are a rare, often lethal complication of thyrotoxicosis. We describe a patient with uncontrolled hyperthyroidism and pre-ventricular complexes (PVCs) who presented with ventricular tachyarrhythmia cardiac arrest and was successfully resuscitated.

Clinical Case: A 64 year old woman was diagnosed with thyrotoxicosis secondary to Graves’ disease [TSH < 0.01 (0.40 – 4.5 mcIU/mL) and free T4 of 2.8 (0.8 – 1.8 ng/dL)] 1 year ago in the setting of a 6 month history of weight loss, palpitations, tremors, and a large goiter. She was started on methimazole and metoprolol XL and was intermittently compliant. During follow-up evaluation she complained of light headedness, developed agonal breathing, and became pulseless. Chest compressions were initiated. She regained spontaneous rhythm after receiving 1 shock with an Automated Electronic Defibrillator (AED). She was transferred to the Emergency Room (ER) and intubated for altered mental status.

Emergent CT Angiography and bedside echocardiogram showed no pulmonary embolism and normal biventricular function. Troponin T high sensitivity assay was negative and electrolytes were normal. Repeat thyroid function tests showed TSH <0.01, Free T4 of 5.6 and free T3 of 14.5 (2.0 – 4.4 pg/mL). She was started on propylthiouracil, glucocorticoids, potassium iodide and treated for thyroid storm. EKG in the ER showed sinus tachycardia with no ischemic ST changes but PVCs and fusion complexes were noted. These were also present on EKG at the time of her initial diagnosis of hyperthyroidism. EKGs prior to the diagnosis of hyperthyroidism showed normal sinus rhythm.

Cardiac arrest was attributed to thyrotoxicosis as there was no infectious nidus and no evidence of structural cardiac disease. The AED rhythm strips could not be obtained but she was presumed to have an appropriately shockable ventricular tachyarrhythmia such as ventricular tachycardia (VT) or ventricular fibrillation (VF).

Her thyroid hormone levels declined appropriately over the course of the hospitalization and PVCs were no longer noted on telemetry and daily EKGs. She was discharged on methimazole which she took consistently. She underwent RAI ablation several months after discharge.

Conclusion: Failure to achieve rapid euthyroidism in thyrotoxicosis is associated with increased cardiovascular morbidity and mortality (1). Most arrythmias associated with thyrotoxicosis are supraventricular and ventricular arrythmias are a rare sequela (2). This is one of the few cases reported of antecedent PVCs being noted on EKG. The PVCs resolved with anti-thyroid medications.

References: (1) Okosieme, O. E., et al. (2019) Primary therapy of Graves’ disease and cardiovascular morbidity and mortality: a linked-record cohort study. Lancet Diabetes Endocrinol 7, 278-287. (2) Marrakchi, S., et al. (2015) Arrhythmia and thyroid dysfunction. Herz 40 Suppl 2, 101-109.

<![CDATA[SAT-513 Thyroid Disease And Infrared Imaging Of Eyelids]]> Background: Thyroid eye disease is thought to present as proptosis and/or severe conjunctival chemosis. Severe dry eye disease and its symptoms of non-specific eye pain and foreign body sensation in the eye can be overlooked as an early biomarker of thyroid disease. New infrared imaging can be used to evaluate dry eye and eyelid gland anatomy. Infrared imaging and detailed history of thyroid eye symptoms may lead to subsequent testing of thyroid function and more referrals to thyroid specialists.

Purpose: Using infrared photography to evaluate dry eye complaints in patients: do they have thyroid disease?

Methods: A retrospective chart review (2017–2019) of patients with dry eyes, eyelid imaging with infrared photography and thyroid lab testing was performed. Infrared photography with 820 nm wavelength (Heidelberg Spectralis, Heidelberg, Germany). Percentage loss of Meibomian glands was identified for each eye, then analyzed, per patient. The control population consisted of patients with no dry eye complaints, no thyroid testing or thyroid history. Exclusion criteria: patients over the age of 90 years and patients with a history of glaucoma, diabetes, cataract surgery, and eyelid surgery. Age matching was done (±5 years).

Results: n=48 patients, avg age=57.73 years (sd=16.81, range 21–85 years). Thyroid patients: n=24 patients, male=10, female=14, avg age= 57.12 years (sd=16.65, med=55.5, range 23–83 years). Controls: n=24 patients, male=9, female=15, avg age=58.33 years (sd=17.30, med=58, range 21–85 years). Loss of Meibomian glands: thyroid=40.94%, control=5.10% (p<0.0001, t-test). Dry eye complaints: thyroid = 16/24, control = 0/24 (p<0.0001, x2).

Discussion: Meibomian glands are glands in the upper and lower eyelids. These glands provide the lipid component of the tear film, thus slowing the evaporation of the tears and stabilizing the tear film with each blink. Meibomian gland loss would explain the dry eye symptoms in an abnormal thyroid patient population. Infrared photography can be performed with a #87 camera lens filter (cost = $65). The loss of Meibomian glands may be an early sign for thyroid disease.

Conclusion: Infrared photography may be helpful in identifying severe dry eye, thus leading to increased awareness of thyroid eye disease symptoms in our patients in ophthalmology, endocrinology, and primary care.

<![CDATA[SAT-485 Variations in the Time Course of Pembrolizumab-Induced Thyroiditis: A Case Series]]> Variations in the Time Course of Pembrolizumab-Induced Thyroiditis: A Case Series


Thyroid dysfunction is reported in 5 - 9.5 % of patients treated with Pembrolizumab, one of the PD-1 immune checkpoint inhibitors. However, the underlying mechanism of Pembrolizumab-induced thyroid disorders remains unclear.

We present 3 clinical cases with Pembrolizumab-induced painless thyroiditis. They initially presented with thyrotoxicosis, but later converted to hypothyroidism. The onset of thyrotoxicosis after the treatment and time course of changing in thyroid function were varied among these cases. All three cases had normal thyroid function prior to the treatment.

Case 1: 63-year-old M with bladder cancer, NSCLC and multiple brain metastases developed overt thyrotoxicosis with TSH 0.02 (0.34 - 4.82 mIU/mL) and Free T4 2.2 (0.8 - 1.5 ng/dL) at 108 days after the first cycle of Pembrolizumab. He had high TgAb (856) and TPO antibodies (196). In 14 days, he converted to hypothyroidism confirmed by TSH 14.6 and Free T4 0.8. Patient was started on Levothyroxine.

Case 2: 69-year-old M with Stage IV NSCLC presented with thyrotoxicosis (TSH 0.01, Free T4 1.9) at days 41 after starting Pembrolizumab. TPO antibodies and TgAb were negative. During 51 days of follow up, he converted to hypothyroidism (TSH 8.89 and continued to trend up above 60). He eventually required levothyroxine therapy.

Case 3: 57-year-old M with invasive verrucous squamous cell carcinoma of the perineum, urethra and prostate had normal TSH at baseline. Within 39 days after the first dose of pembrolizumab, TSH dropped to 0.013 and Total T4 increased to 14.8 (4.5 - 12.1 ug/dL), consistent with overt hyperthyroidism. In 108 days, patient developed hypothyroidism with Free T4 0.7.


All 3 cases we present did not have overt signs or symptoms of hyperthyroidism. Thyrotoxicosis spontaneously resolved without requiring steroid treatment. Studies suggest symptomatic treatment of beta blockers in cases of tachycardia, otherwise steroid use is not routinely recommended in PD1-induced thyroiditis.

One cohort study analyzed the dynamic course of thyroid functions in patients receiving Pembrolizumab. Among the patients who developed thyrotoxicosis while on PD-1 inhibitor therapy, median onset time was 47 days (14–447 days). The median time for transition from thyrotoxicosis to hypothyroidism was 42 days (21–169 days).


Our case series highlight the variations in the time course and nature of the Pembrolizumab-induced thyroiditis. Clinicians should be aware of the relatively short period of fluctuations of thyroid functions in patients treated with PD-1 inhibitors.

References: Lee, Hyunju et al. “Characterization of Thyroid Disorders in Patients Receiving Immune Checkpoint Inhibition Therapy.” Cancer Immunology Research 5, no. 12 (2017): 1133–40.–6066.cir-17–0208.

<![CDATA[SAT-503 Levothyroxine Absorption Testing in Three Patients with Severe Hypothyroidism on Adequate Replacement]]> Background: Levothyroxine (L-T4) absorption is a concern in patients who report appropriate self-administration but remain clinically and biochemically hypothyroid. However, there are no established guidelines for L-T4 absorption testing.

Clinical Cases: Two women (A and B) with a history of Graves’ disease and radioactive iodine ablation (RAI) on weight-based L-T4 replacement presented to the hospital with severe fatigue and bilateral leg swelling. A third woman (C) with a history of papillary thyroid carcinoma, total thyroidectomy and RAI, on suppressive doses of L-T4 presented to the clinic with fatigue, constipation and weight gain. All patients reported compliance with taking L-T4 with appropriate technique. They had no known medical problems contributing to a malabsorptive state, and were not taking any medications known to interfere with L-T4 absorption.

Initial testing of thyroid function revealed TSH (0.57-3.5 μIU/mL)/Free T4 (0.61-1.18 ng/dL) levels of 10.12/0.249, 45.95/<0.2 and 142/<0.2 in patients A, B and C respectively. Patients A and B tested negative for Helicobacter pylori infection, celiac disease and lactose intolerance. Patient C had been successfully treated for H. pylori infection in the past. Celiac testing was negative, but the patient tested positive for anti-parietal cell antibodies and vitamin B12 deficiency. She was referred to Hematology & GI specialists. None of the patients had clinical evidence of heart failure and had normal echocardiograms.

In order to evaluate for poor absorption, all patients underwent L-T4 absorption testing. Based on published data, baseline TSH and Free T4 levels were obtained followed by administration of 1000 mcg of L-T4. Next, free T4 levels were obtained at 2 hours for all patients and at 4, 8 and 24 hours for patient A & B. Patients A and B underwent testing in the inpatient setting, while Patient C was tested in the outpatient clinic.

In all cases, a > 50% rise in free T4 levels was observed at 2 hours, suggesting non-adherence or “pseudo-malabsorption”. Patients were counseled extensively regarding proper technique and compliance with L-T4. Patients A and B demonstrated rapid clinical improvement in the hospital, and Patient C reported to her next clinic visit with clinical and biochemical improvement.

Conclusions: Though guidelines have not been established for L-T4 absorption testing, case reports exist exhibiting the safety and efficacy of L-T4 absorption challenge with a weekly weight-based dose or 1000 mcg of LT4. Our case series show the success of the latter with meaningful results in as little as 2 hours. Case C demonstrates that this test can be done safely and cost-effectively as an outpatient. Standardization of L-T4 absorption test will be of great utility in the management of this common problem encountered by endocrinologists.

<![CDATA[SAT-468 Anticoagulation Conundrum: A Case Of Embolic Stroke Due To Thyrotoxic Atrial Fibrillation]]> Background: Thyrotoxicosis is not incorporated into any of the atrial fibrillation (AF) CVA risk stratification methods, including CHADS2VASc, as neither the American College of Cardiology/American Heart Association nor the American College of Chest Physicians view it as an independent risk factor of CVA. However, the literature has reported numerous cases of patients with thyrotoxic AF and low CHADS2VASc scores who developed CVA. It is unclear which patients with thyrotoxic AF would benefit from prophylactic anticoagulation (AC).

Clinical Case: A 50-year-old male without past medical history presented for palpitations. He was found to be in AF with rapid ventricular rate. Labs revealed thyrotoxicosis (TSH <0.010 [RR 0.34-5.6 μIU/mL], FT4 3.57 [RR 0.61-1.64 ng/dL], FT3 5.26 [RR 2.5-4.5 pg/mL], and TSI negative). He was started on methimazole but no AC, as his CHADS2VASc score was 0. A few hours after admission, he developed a right-sided facial droop and weakness & aphasia. CT head showed acute left MCA infarct. CTA head/neck revealed occlusive embolus in the distal left M1 segment. He underwent IR-guided embolectomy and received intra-arterial tPA. Echocardiogram did not show thrombi or atrial level shunt but showed right atrial dilation. After extensive work-up, etiology of CVA was determined most likely a cardioembolic source due to thyrotoxic AF. Patient was treated with PTU and steroids initially for two days due to recent contrast exposure (CTA and embolectomy) and poor neurologic status, in order to obtain the added benefit of decreased T4 to T3 peripheral conversion. Patient was started on AC two weeks after his CVA (given initial risk of hemorrhagic conversion due to large CVA burden), at which time his weakness and aphasia were slowly improving, but he remained with significant neurologic deficits.

Discussion: The current thought that thyrotoxicosis is not an independent risk factor of CVA in patients with AF has led to recommendations against prophylactic AC for this specific group. Although recent research has suggested that patients with thyrotoxic AF are at a lower risk of CVA than patients with non-thyrotoxic AF, there have still been many reported cases of CVA in patients who have thyrotoxic AF but no other risk factors for CVA. This discrepancy in association between thyrotoxic AF and CVA needs to be clarified.

Conclusion: This case of a middle-aged man with thyrotoxic AF who developed a debilitating CVA after being treated according to his CHADS2VASC score of 0 (he was not given prophylactic AC) mirrors multiple cases in the literature. It highlights the potential benefit of examining thyrotoxic patients with AF more closely in order to more effectively risk stratify them for CVA or further exploring the relationship between thyrotoxicosis and CVA. This may help to identify more patients who could benefit from AC and thus prevent devastating consequences of CVA.

<![CDATA[SAT-515 Anorexia and Severe Hypothyroidism Driving Persistent Ascites and Liver Injury]]> Background Unintentional weight loss, ascites, and altered mental status typically raise concerns for hepatologic-cardiac-oncologic disease. Herein we present a case that after exhaustive workup the etiology of the aforementioned findings was attributed to a combination of anorexia and severe hypothyroidism, states where slowed metabolism and altered nutritional status can interact synergistically. Clinical Case A 71 y/o lady with a history of hypothyroidism after RAI for Graves’ disease, anxiety, depression, presented with 20-30 lbs unintentional weight loss over 5 months. She had poor appetite, nausea, constipation, increased abdominal girth, anasarca, fatigue, weakness, and altered mental status. On exam she had bradycardia, hypotension and hypothermia (BP 97/51, HR 54, RR 18, Temp 94, BMI 15.8). Labs revealed a TSH of 36, FT4 0.98, Tbili 0.3, alk phos 491, AST 435, ALT 651, gGT 151, albumin 2.3, prealbumin 14.7, INR 1.03, and pancytopenia. Treatment with IV levothyroxine resulted in mental status improvement. Over the next few months extensive testing revealed mild element deficiencies (zinc 44- nl range 60 - 130 mcg/dL, vit A 32- nl range 38 - 98 mcg/dL), no evident infectious/hematologic or inflammatory disease. Despite 3 paracenteses, 2 liver biopsies, multiple imaging studies (abdominal U/S, ECHO, XRs, CT chest/abdomen/pelvis, MRI abdomen/pelvis, enterography, MRI brain, PET scan), EGD/colonoscopy, bone marrow bx, and explorative laparoscopic abdominal surgery, no clear explanation was found. During the workup her liver enzymes remained elevated, TSH and fT4 normalized, but T3 remained low at 50 (76 - 181 ng/dL). Psychiatric evaluation revealed mild cognitive impairment, presumed to be secondary to depression and underlying disease. By exclusion, she was diagnosed with anorexia with a possible component of persistent hypothyroidism. She was fed through NG tube and followed closely by nutrition with a personalized high protein and calorie meal plan. Eight months later she had gained 5 lbs, her liver enzymes/electrolytes and CBC normalized, and most of her symptoms resolved. Conclusion Hypothyroidism can cause LFT abnormalities, and though rare, there are >50 cases of hypothyroidism induced ascites reported. Usually LFTs and ascites normalize promptly with hormone supplementation. However, our patient’s case was complicated by severe anorexia, with nutritional status essentially equivalent to kwashiorkor sufferers. Though extremely rare in the developed world and in adults, kwashiorkor like physiology has been described in patients with anorexia, with impressive liver abnormalities, presumed to be due to autophagy. Though certainly this is a rare diagnosis, it does point to the fact that in our test driven culture, it is worth pausing, re-evaluating history and physical and thinking outside the box prior to subjecting our patients to countless tests and procedures.

<![CDATA[SAT-469 Vitals for the Prompt Recognition of Myxedema Crisis in a Critically Ill Patient]]> Myxedema coma is a rare but life-threatening condition if not treated promptly. The time from initial presentation to diagnosis may be prolonged in patients with severe illness whose presenting features are common to myxedema crisis. A 94-year-old male admitted to the neuroscience intensive care unit for acute stroke monitoring after intra arterial thrombolysis was treated for myxedema three days after initial labs revealed severe hypothyroidism and a myxedema score greater than 60. A diagnostic scoring system for the diagnosis of myxedema coma gives points for the following to easily identify patients with high likelihood of decompensated state of extreme hypothyroidism. Given the potential for under recognition of myxedema crisis in severe illness the clinician must pay close attention to vital signs and have a high level of suspicion for myxedema crisis and low threshold for treatment if myxedema score indicates high likelihood despite concomitant critical illness

<![CDATA[SAT-483 Levothyroxine Absorption Test: A Potential Therapeutic Tool for Levothyroxine Malabsorption]]> INTRODUCTION

Persistent hypothyroidism (PH) even on high doses of levothyroxine is a common clinical problem and it is difficult to treat. Levothyroxine absorption test has been used to distinguish between pseudo-malabsorption and malabsorption as one of its causes. This test uses 1000 mcg of levothyroxine to calculate the percentage of levothyroxine absorbed. We present a case of malabsorption in which we used the levothyroxine absorption test to diagnose as well as treat malabsorption.


55-year-old male with history of papillary thyroid cancer status post total thyroidectomy, postsurgical hypothyroidism, recurrent small bowel obstruction, status post jejunal resection, complicated by high output entero-cutaneous fistula, distal high-grade obstruction status post placement of jejunal tube, chronic abdominal pain on narcotics, who initially presented with sepsis and was also found to be hypothyroid.

The thyroid stimulating hormone (TSH) level was 45.25 with free thyroxine (FT4) level of 0.54. He was adherent to his levothyroxine (LT4) 175 mcg once daily which is given one hour after tube feeds have been stopped or one hour prior to any administration of other medications.

Levothyroxine absorption test was done to distinguish between malabsorption versus pseudo-malabsorption. Three different doses of LT4 were used with results all consistent with malabsorption. The percentage of absorption with 175 mcg, 500 mcg, and 1000 mcg LT4 were 3.4%, 7.2%, and 18% respectively. The formula used to determine the percentage of absorption was (total T4 at 2 hour after LT4 administration - baseline total T4 prior to administration in mcg/L) x plasma volume in liter/dose of administered LT4 in mcg. The final prescription dose of 700 mcg once daily was then derived from the available data, which eventually corrected the patient’s hypothyroidism. Repeat testing after 2 weeks showed TSH of 0.17, FT4 of 1.29 and total T4 of 6.5. The suppressed TSH at this point was attributed to chronic narcotic use but FT4 and total T4 improved appropriately.


There is no gold standard protocol for levothyroxine absorption test so we used a different protocol for LT4 dosing compared to the conventional regimen (1000 mcg of LT4). Our patient did show appropriate levothyroxine absorption on the calculated dose. Hence, the Levothyroxine absorption test may be used both as a diagnostic as well as a therapeutic tool for the patients with LT4 malabsorption causing PH.


G.E. Sun, K.M. Pantalone, C. Faiman, M. Gupta, L. Olansky, B. Hatipoglu, The clinical utility of free thyroxine in oral levothyroxine absorption testing. Endocr. Pract. 20(9), 925–929 (2014)

<![CDATA[SAT-496 Acute GI Bleed Associated with Myxedemic Coma: Yes It Still Exists!]]> Introduction: Myxedemic coma is a life-threatening medical emergency. It needs to be treated emergently & carries very high mortality. It involves multi-organ failure at cellular level due to severe thyroid hormone deficiency. Most common clinical presentation involves CVS. With advancement in health care it is now uncommon to see myxedemic coma especially associated with GI Bleed. Here in we present an interesting case of GI bleed associated with myxedemic coma. Case: 84 years old male was discovered in home, minimally responsive. EMS intubated & brought him to ED with agonal respirations, hypotensive & unresponsive, He was admitted to ICU. Past medical history was significant for smoking & hypertension. Physical Exam was significant for dryness of skin, obtundation, hypothermia, tachypnea & BMI >30. Initial Labs revealed anemia with Hemoglobin of 5.1mg/dL, Hematocrit 17.5%, Hyponatremia-134meq/L, Hyperkalemia-K+ levels 5.3meq/L, BUN-84mg/dL & creatinine-4.1mg/dL, His serum TSH levels were 352 mIU/ml with low free T4 and T3 levels at 0.15ng/dl and 1.99pg/ml, respectively. Stool was positive with Blood. IV fluids were given.GI was consulted. He underwent emergent upper GI endoscopy, which found the Dieulafoy’s lesion at cardiac end of stomach & treated with a combination of epinephrine injection, argon laser, & 3 hemo-clips. He had 6 PRBCs transfused. He was started on IV Thyroxine, Liothyronine and Hydrocortisone. His mental status improved, & hemoglobin remained relatively stable. Later on, he decided to move to palliative care & was discharged to hospice. Discussion: Myxedemic coma is a term generally used to denote most severe decompensated hypothyroidism. The typical progression is lethargy evolving into a stupor & eventually into a coma with respiratory failure and hypothermia. It can lead to volume depletion, hyponatremia, & AKI, which can worsen to ATN if prolonged ischemia remains.GI bleed is a rare manifestation of myxedemic coma. Pathophysiology of GI bleed in these patients involves mucosal edema & mucopolysaccharide infiltration. Also, myxedemic coma is associated with neurological changes resulting in slow peristalsis & GI atony. This coupled with coagulopathy associated with decompensated hypothyroidism results in increased risk of bleeding. Dieulfoy’s lesion are rare cause of GI bleed. Stress & ischemic changes are one of the inciting factors for these lesions. These lesions are more common in elderly males & are associated with severe systemic illness similar to our patient. Treatment is usually supportive with goal of identifying the lesions, stopping the bleed & aggressively managing myxedemic coma. We present an interesting case of GI bleed associated with myxedemic coma now relatively uncommon with advancement in healthcare. It provides an excellent learning opportunity for clinicians to consider while managing these patients.

<![CDATA[SAT-475 New Breast Cancer Therapy Atezolizumab, Leads to Thyroiditis]]> Background: A NSABP B 59 trial is currently underway to check the efficacy of an experimental drug, Atezolizumab (Anti-PDL 1 monoclonal antibody) in the treatment of triple negative breast cancer. In the trail, the drug is added to the usual neoadjuvant chemotherapy given before surgery and prolonged treatment with it is continued after surgery to reduce the recurrence. Listed adverse effects are immune medicated hyperthyroidism in 2% of population.

Clinical Case:

32 y old Asian woman was diagnosed with triple negative left breast cancer in May 2018. She was started on paclitaxel, carboplatin and study medication Atezolizumab/Placebo in June 2018 and she received 4 cycles of the same and then it was stopped in August 2018. She was started back on the same in September 2018 which ended in November 2018. Patient tested positive for BRCA1 gene mutation and underwent bilateral mastectomy in December 2018. The study medication was restarted in January 2019.

Patient is received a total of 11 doses of study medication and was due to receive 16 doses if she had finished the trial in June 2019. Patient received radiation therapy starting in January 2019 till February 2019.

On her oncology visit in April 2019 patient was found to have a suppressed TSH of 0.009 with a high free thyroxine of 1.72 and an elevated free T3 of 5.4. She was referred to endocrinology for evaluation of thyroid abnormalities, as the study medication can cause thyroid problems. She denied symptoms of hyperthyroidism. TPO, TSI and anti-thyroglobulin antibodies were negative. Thyroid uptake scan showed uniformly decreased tracer distribution in both thyroid lobes consistent with thyroiditis.

As per the protocol for the study medication as well as recommendations by the American Society of oncology, we waited for normalization of the thyroid function test before resuming the study medication. In July 2019, TSH normalized to 2.99 and free T4 0.97.

She was noted to have low random cortisol level of 3.27 at 1000AM. ACTH stimulation test was performed and she responded appropriately.

Hence could not take the remainder of the study medication that were scheduled until June 2019. She is on observation phase since June 2019 and currently doing well.

<![CDATA[SAT-470 When The Heart Can’t Clap To The Thyroid’s Beat]]> Hyperthyroidism is associated with multiple cardiac pathologies including dilated cardiomyopathy, isolated right ventricular heart failure, and atrial fibrillation (AF). Long standing untreated hyperthyroidism in conjunction with AF can cause severe dilated cardiomyopathy with reduced ejection fraction that is completely reversible with treatment. We present the case of a previously healthy male who presented with florid congestive heart failure (CHF) as an initial presentation for hyperthyroidism. A 37-year-old male presented to the emergency department with progressively worsening dyspnea on exertion and lower extremity edema for one month. His heart rate was noted to be 172 bpm and an EKG was done that showed AF. He was clinically noted to be in heart failure and was admitted for further management. He was started on metoprolol with good heart rate control and was started on furosemide for diuresis. A transthoracic echocardiogram was done and showed severe global hypokinesis with left ventricular ejection fraction reduced to 20% along with bi-atrial enlargement and dilated left ventricular cavity. Ischemic cardiomyopathy was ruled out with left heart catheterization. A TSH level was checked as a part of workup for non-ischemic cardiomyopathy and atrial fibrillation and was markedly reduced to <0.01mIU/L with free T4 of 1.49ng/dL and free T3 of 6.7ng/dL. A diagnosis of hyperthyroid cardiomyopathy with concomitant tachycardia induced cardiomyopathy was made. Autoimmune workup was negative for anti-thyroid-peroxidase and anti-thyroid-stimulating antibodies. Ultrasound of his thyroid gland revealed multiple thyroid nodules concerning for toxic multinodular goiter. He was started on methimazole and discharged after volume optimization with diuresis to closely follow up with endocrinology and cardiology for further management. CHF can be the primary presentation in about 6% of patients with hyperthyroidism. T3 is the main thyroid hormone that binds to cardiomyocytes. It increases the expression of beta-adrenergic receptors on cardiomyocytes and subsequently increases heart rate and contractility. T3 can also cause atrial arrhythmias such as AF by decreasing the parasympathetic tone. Concomitant AF and hyperthyroidism can cause reduced ejection fraction due to tachycardia induced cardiomyopathy and dilated cardiomyopathy. Treatment mainly is with beta-blockers that slow down the heart as well decrease serum T3 levels by blocking 5-monodeiodinase which converts T4 to T3. Our patient was started on beta-blocker and methimazole with good reduction in heart rate and improvement of symptoms. Recovery of cardiac function will be assessed with longitudinal follow up. As hyperthyroidism is one of the few causes of CHF that is completely reversible, clinicians must maintain low degree of suspicion in patients with new onset heart failure especially when associated with AF.

<![CDATA[SAT-510 Association of Myotonic Dystrophy with Autoimmune Endocrinopathies and Thyroid Carcinoma]]> Myotonic dystrophy (MD) is a multisystemic, autosomal dominant disorder associated with progressive muscle weakness, premature cataracts, frontal baldness, and cardiac disturbances. MD has been associated with several endocrinopathies including primary testicular failure, autoimmune endocrinopathies (hypothyroidism, hyperthyroidism, multinodular goiter, and Addison’s disease), thyroid carcinoma (primarily papillary), insulin resistance, and type 2 DM. Development of diabetes is thought to be related to formation of an insulin-resistant receptor because of aberrant regulation of mRNA. We describe the first reported case of a patient with MD associated with type I diabetes mellitus, Hashimoto’s thyroiditis with hypothyroidism, and follicular variant of papillary thyroid cancer. A 49-year-old female presented with acute congestive heart failure. The patient had history of type I DM diagnosed at the age of 26, complicated by mild background retinopathy, peripheral neuropathy, and nephropathy with microalbuminuria. The patient first noticed proximal muscle weakness 1 year ago that gradually progressed resulting in multiple falls. She had history of bilateral cataracts status post cataract extraction at age 26. She also had progressive dysphagia requiring PEG placement, and cognitive dysfunction with mood disorder and depression. Family history was significant for myotonic dystrophy in both maternal aunt and uncle as well as 2 cousins. EMG confirmed myotonia however genetic testing was not obtained due to cost. Due to her cognitive dysfunction and depression, she had difficult to control diabetes with HbA1c of 9.9%, and multiple previous admissions for DKA. She was status post total thyroidectomy in 2008 for follicular variant of papillary carcinoma and Hashimoto’s thyroiditis followed by I-131 therapy in 2009 and maintained on levothyroxine suppression therapy. Most recent Tg and Tg Ab were undetectable. On physical exam, the patient had a narrow, sallow face with temporal muscle atrophy, percussion myoclonus involving the thenar eminence of the hands, but no frontal balding. Work up showed LVEF of 20-24% with regional hypokinesis that led to catherization and PCI to LAD. The patient had recurrent NSTEMI which eventually resulted in CABG 1 year after presentation. The association of autoimmune endocrinopathies, thyroid carcinoma and MD suggests a possible cause and effect relationship between these disorders. In patients with diabetes and MD, previously described insulin resistance as well as cognitive dysfunction can hinder good glycemic control increasing risk for complications. Although patients with MD are typically treated by neurologists, evaluation and therapy of endocrine dysfunctions are also necessary.

<![CDATA[SAT-492 Impending Thyroid Storm Induced by Checkpoint Inhibitors]]> Introduction:

Thyroid storm is a rare but life threatening condition due to thyroid hormone excess and is usually caused by Graves disease, toxic nodular goiter or rarely due to thyroiditis. Immune checkpoint inhibitors (ICI) are a novel choice for treating cancers, and carry a risk for development of endocrinopathies. We report a case of impending thyroid storm 5 weeks after initiation of ICI.

Case Presentation:

81-year-old Caucasian male with metastatic renal cell carcinoma presented with generalized weakness and fatigue 5 weeks after ipilimumab and nivolumab were started. He had no prior history of thyroid disease and had normal thyroid functions before the treatment. He complained of palpitations, heat intolerance and loose stools on admission. On examination he was disoriented, tachycardic (128bpm) with new onset atrial fibrillation, had moist skin and brisk reflexes. He had non-tender thyroid, no thyromegaly, and no nodules palpated. Burch-Wartofsky score was 35, suggesting impending thyroid storm. Laboratory investigation showed elevated free T4 (>7.77), elevated free T3 (8.6) with a suppressed TSH (< 0.02). He had positive anti-TPO but Thyrotropin receptor antibody was negative. He was treated with propranolol 40 mg three times daily, prednisone 40 daily, methimazole 30mg three times a day with significant improvement in free T4 (5.67) within first 48 hours.


Imipimumab and nivolumab are monoclonal antibodies against cytotoxic T-lymphocyte associated protein 4 (CTLA-4) and programmed death receptor-1 (PD-1) respectively. The reported incidence of thyroid dysfunction after combined imipimumab and nivolumab therapy can be as high as 22%1. Thyroiditis could present as early as 2-6 weeks 2 after treatment, and hypothyroidism tends to present between 5 months and 3 years3. According to a current consensus4, baseline TSH and FT4 should be drawn prior to initiating ICI. Thyroid storm is a clinical diagnosis and Burch-Wartofsky score can help in diagnosis. A high degree of suspicion and prompt diagnosis of thyroid storm and treatment is of utmost importance especially in this patient population. Rapid improvements in thyroid hormone levels suggest thyroiditis as a potential cause for thyrotoxicosis.


ICI induced thyroid disease is not an uncommon condition. It could present as either thyrotoxicosis or hypothyroidism. Both patient and clinician should be aware of potential signs and symptoms of thyroid storm for early recognition and timely treatment of this life-threatening condition.

[1] Byun DJ et al.Nat Rev Endocrinol. 2017 Apr;13(4):195-207 [2] Iyer PC et al. Thyroid. 2018 Oct;28(10):1243-1251 [3] Endocr Relat Cancer. 2014 Mar 7;21(2):371-81 [4] Puzanov et al. Journal for ImmunoTherapy of Cancer (2017) 5:95

<![CDATA[SAT-509 Sudden Onset of Malabsorption]]> Celiac disease (CD) is an immune-mediated enteropathy caused by a reaction to gliadin which responds to a restriction to dietary gluten. It has been traditionally recognized in children and young adults, although, recently, detection in the elderly population has increased. CD occurs in 2–5% of patients with autoimmune hypothyroidism, and is more prevalent in this group than in the general population

An 82-year-old Caucasian woman with primary hypothyroidism and a BMI of 16 is referred to our endocrinology clinic for help with the management of hypothyroidism. She had a history of well controlled hypothyroidism on weight-dosed levothyroxine for many years until several months prior when she developed sudden onset of diarrhea and weight loss. Since then, her thyroid function tests showed an elevated TSH despite medication adherence. Her levothyroxine dose was steadily increased to 300 mcg daily and yet, her TSH still remained elevated. Laboratory work up was done which revealed elevated transglutaminase antibodies, suggesting the diagnosis of CD. The patient refused an endoscopy for a tissue diagnosis. Even though the patient has been diagnosed with CD, she has trouble following a gluten free diet and still has intermittent diarrhea and high levothyroxine requirements.

Although lack of medication adherence is common, it is important to exclude gastric or intestinal causes of malabsorption in patients with high thyroid replacement requirements. Elderly patients often have paucity of symptoms, so high clinical suspicion is necessary to diagnose these patients.