bluuebunny/crossref_metadata_2025_split huggingface dataset:
Amiodarone-Induced Hypothyroidism Initially Presenting as Decompensated Heart Failure and Hyponatremia
Authors: Ayesh Hazem , Burmeister Cameron , Beran Azizullah , Akpunonu Basil 
Published: May 2021

Abstract
Introduction: Amiodarone is an effective antiarrhythmic, but it is associated with altering thyroid function, ranging from thyrotoxicosis to hypothyroidism. In this study, we discuss amiodarone-induced hypothyroidism (AIH) presenting with hyponatremia and myxedema.
Case Presentation: A 75-year-old Caucasian man with a history of ischemic heart disease with an ejection fraction of 55-60% was seen in the ED with complaints of worsening lower limb edema and shortness of breath. Associated symptoms of constipation, generalized weakness, daytime sleepiness, and increased urinary frequency were noted. He was recently diagnosed with atrial fibrillation with a CHA₂DS₂-Vasc score of 5 and started on amiodarone nine months ago. He weighed 235 lbs with a BMI of 33.85 and vital signs are as follows: blood pressure 90/64, heart rate 64, respiration rate 13, and a temperature of 36.6 °C. Physical examination revealed a well-developed man in mild distress and slightly lethargic, with a palpable thyroid gland, heart sounds revealed an irregularly irregular heart rate, elevated JVD, bilateral rales, and bilateral pitting edema. Labs showed mildly low HB of 11.7, low Na of 125 mmol/L, elevated creatinine at 1.67 mg/dl, low urine osmolality at 270 mOsm/kg, and BNP of 24 with negative troponin. Chest x-ray showed cardiomegaly. TSH was elevated at 93 uIU/mL and low free T4 at less than 0.25 ng/dL with a negative anti-TPO. A diagnosis of amiodarone-induced hypothyroidism was made, and the patient was started on increased furosemide and levothyroxine 25 mcg daily. Significant improvement was noted in mental status, sodium level, and volume status within three days; and the patient was discharged home on 50mcg of levothyroxine.
Discussion: This case illustrates the need to constantly investigate the etiology of decompensated heart failure, especially when new medications with potential culprit side effects are noted or suspected. Amiodarone which is helpful in the management of atrial fibrillation has been known to cause thyroid dysfunction as hypo or hyperthyroidism. What is not widely known is that these endocrine dysfunctions can occur just a few weeks after therapy initiation.
Conclusion: We recommend that patients who started on amiodarone be monitored for thyroid dysfunction; especially when they present with deterioration in the cardiac function or show symptoms of endocrinopathy.
Coexistence of Thyroid Hormone Resistance and Autoimmune Thyroid Disease: Not a Mere Coincidence
Authors: Gnanapragasam Helen Prathiba , Idupuganti Amrutha , Bhat Salman Zahoor 
Published: May 2021

Abstract
Introduction: The coexistence of thyroid hormone resistance and autoimmune thyroiditis was initially thought to be a chance event. In a large cohort study, Barcoff et al. demonstrated an increased likelihood of thyroid autoantibodies in patients with thyroid hormone resistance (RTH). We report a unique case to epitomize the coexistence of these two conditions and discuss the postulated mechanisms.
Clinical Case: A 22-year-old woman with a history of Hashimoto’s thyroiditis, attention deficit hyperactivity disorder, and migraine presented to the endocrinology clinic with symptoms of weight loss, fatigue, decreased appetite, and heat intolerance for 4 months. She was diagnosed with Hashimoto’s thyroiditis at age 12 with elevated TSH only and had been on levothyroxine 25 mcg since diagnosis. Physical exam demonstrated a body mass index of 34.14 kg/m2, blood pressure of 138/91 mmHg, pulse of 77 bpm, and an enlarged palpable thyroid gland. Laboratory investigations revealed elevated thyroid peroxidase (TPO) antibody at 234 IU/mL (&lt;9) and thyroglobulin Antibody at 3 IU/mL (&lt;1) with elevated free T4 of 3.76 ng/dL (0.61-1.36), elevated total T4 of 21.58 mcg/dL (6.09-12.23), increased T3 uptake of 51.2% uptake (32-48.4), and upper normal TSH of 3.99 uIU/mL (0.44-5.33). Elevated free T4 was confirmed by the equilibrium dialysis method at 6.2 ng/dL (0.9-2.2) with upper normal TSH at 3.77 uIU/mL. Thyroid ultrasound demonstrated thyromegaly and hypervascularity of the gland. TSH secreting pituitary adenoma was ruled out with a normal alpha subunit of 0.2 ng/ml (0.1-0.6) and molar ratio of the alpha subunit to TSH ratio &lt;1 along with a normal pituitary MRI. She was not taking other medications or supplements. She was diagnosed with thyroid hormone resistance and is undergoing genetic testing to differentiate the THRB genetic mutations from Non-TR-RTH. Her symptoms improved after discontinuing her levothyroxine.
Clinical Lesson: Our case highlights the importance of evaluating thyroid disorders properly before starting treatment and illustrates the coexistence of autoimmune thyroiditis with thyroid hormone resistance. Barcoff et al. demonstrated that there was an increased likelihood of thyroid autoantibodies with odds ratio = 2.36 (p = 0.002) in a large patient cohort with RTH, compared to their unaffected first-degree relatives. However, since there was no correlation in increased antibody with increased age and the duration of the disease, the proposed hypothesis did not substantiate chronic TSH stimulation inducing autoimmune response. The proposed mechanism is that the elevated TSH in RTH stimulates the immune system at the TRα level which was demonstrated in murine models with increased activation of thymic function in correlation with TSH level. More research is needed to understand the underlying mechanism of their coexistence.
How to Stop a Thyroid Storm When the Liver Is Bad: A Case Report and Literature Review
Authors: Saleh Ahmed Osman , Gul Wajiha , Hamad Mohammad Khair Ahmad Ibraheem , Naem Emad 
Published: May 2021

Abstract
Introduction: Patients with thyroid storm and resistance or contraindications to conventional medications may receive plasmapheresis until they have the definitive therapy.
Case Presentation: A 42 years old lady with no past medical history was brought by the EMS with palpitations, shortness of breath, vomiting, and profuse diarrhea. She was found to have an atrial flutter with low blood pressure, received synchronized cardioversion, but unfortunately, she developed ventricular tachycardia, tonic-clonic seizure and went to pulseless electrical activity (PEA). Upon examination, the patient was intubated, heart rate of 200 beats/min, blood pressure of 80/60 on vasopressors. She had exophthalmos and icteric eyes. Neck examination revealed palpable goiter. There was bibasal fine cracked and mild lower limb edema. Laboratory showed FT4 39 (11.6-21.9 pmol/L), FT3 5 (3.7- 6.4 pmol/L), and TSH &lt;0.01 (0.3-4.2 mIU/L). Burch- Wartofsky’s score was 55/140. Her presentation was suggestive of Graves’ disease with thyroid storm. Further labs showed high liver enzymes, high INR, ammonia as well as high creatinine.
She was started on IV hydrocortisone and cholestyramine. Thionamides were contraindicated due to liver impairment.
Extracorporeal membrane oxygenation (ECMO) was initiated for cardiopulmonary support and continued for 6 days. TSH receptor antibodies result was pending, thus a thyroid uptake scan was done while the patient connected to ECMO to confirm the diagnosis. Thyroid scan showed increased uptake suggestive of grave’s disease despite iodine contrast received for CT scan chest two days back. After 5 sessions of plasmapheresis, FT3 2.8, and FT4 30, Lugol’s iodine started and she underwent total thyroidectomy. She was successfully extubated and thyroxine replacement was started after normalization of thyroid hormones
Discussion: The raised liver enzymes (shock liver) were a barrier to thioamides. With the contraindication to antithyroid medications, plasmapheresis was a rapid and safe option before thyroidectomy. The mechanism of plasmapheresis is to eliminate thyroid hormones, TSH-receptor antibodies, and cytokines. The current guidelines lack clear indications, the timing of initiation, and patient selection for plasmapheresis.
Conclusion: Plasmapheresis should be considered as a stabilising measure, especially when patients cannot tolerate conventional medications. Plasmapheresis leads to rapid decline in thyroid hormone levels, providing a window to treat definitively with thyroidectomy.
Improvement of Treatment Resistant Depression in a Patient With Primary Hypothyroidism and Thr92Ala5’ Type 2 Deiodinase Gene Polymorphism With Multiple Daily Doses of Triiodothyronine
Authors: Ahmed Ziyan , Sherin Rinsha P V , Fonseca Tatiana De Lourdes , Hoang Thanh Duc , Shakir Mohamed K M 
Published: May 2021

Abstract
Introduction: The augmentation pharmacologic therapy used in patients with treatment-resistant depression (TRD) includes drugs such as lithium, buspirone, triiodothyronine (LT3) and other drugs. We report a patient with TRD and primary hypothyroidism who responded to a combination of LT3, given in divided doses, and levothyroxine (LT4), rather than LT4 alone, even though the serum TSH levels were in the normal range with these treatments. Interestingly, the patient had a Thr92Ala5’ type 2 deiodinase polymorphism. Case Report: A 54-year old male presented to our emergency room with suicidal ideation 8 years ago. The patient had severe depression and developed uncontrollable urges to surf the internet, generally prohibited sites, approximately 3 months prior to his visit to the emergency room. He had noted a 12-lbs weight gain, cold intolerance, dry skin, and excessive sleepiness for 3 months. Patient was admitted to the psychiatry ward and laboratory testing showed a serum TSH 180 µIU/mL, FT4 0.48 ng/dL, total T3 46 ng/mL, and TPO antibody 278 IU/mL. A thyroid ultrasound was consistent with Hashimoto’s thyroiditis. A diagnosis of major depressive disorder and primary hypothyroidism was made. He was started on citalopram (20 mg/day) and levothyroxine (175 mcg/day). The Beck Depression Scores (BDS) during the initial weeks was 37.5 ± 5.1 (Mean ± SD) (normal 0-9) with corresponding TSH 164 ± 133 µIU/mL, FT4 0.70 ± 0.25 ng/dL, and total T3 61 ± 7.9 ng/mL. Two weeks later the dose of citalopram was increased to 40 mg/day and then buspirone 10 mg/day was added. At the end of 11 months the BDS was 27.81 ± 2.1 with a corresponding TSH 1.5 ± 0.1 µIU/mL. After 4 months, 7.5 mg of aripiprazole was added. After 11 months of treatment, he was treated with a combination of LT4 + LT3 (5 mcg once daily) and TSH became 0.76 ± 0.1 µIU/mL with a corresponding BDS of 18.0 ± 1.9. Twelve months later, the patient was switched back to LT4 alone and during LT4 treatment the BDS score was 24.2 ± 22.2 with a TSH of 1.44 ± 0.11. Nine months later patient was changed to LT4 + LT3 (5 mcg three times daily) and his BDS score was 10.3 ± 1.2 with a TSH of 0.72 ± 0.09 µIU/mL. When he was on LT4 + LT3 TID he was able to discontinue all the antidepressant drugs and he had no urge to surf on internet. His depression was controlled by over-the-counter antidepressant drugs (S-adenosylmethionine and rhodiola). A genetic test confirmed Thr92Ala5’ type 2 deiodinase polymorphism. Discussion and Conclusion: In our patient, there was a good correlation between the BDS improvement and the serum T3 levels (r: -0.7 p-value: 0.01). Thus, in patient with Thr92Ala5’ type 2 deiodinase polymorphism TID T3 dosing may significantly improve depression. Additional studies are needed.
Management of Atrial Flutter in Thyroid Storm
Authors: Lanham Theresa N , Morgan Farah Hena 
Published: May 2021

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) &lt;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: &lt;140] % and a thyroid receptor antibody (TRab) of 10.02 [ref:&lt;=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 &gt;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.
Stopping Levothyroxine Therapy in Subclinical Hypothyroidism, Perhaps We Could Start a Trend
Authors: Albashaireh Arwa , Maraka Spyridoula 
Published: May 2021

Abstract
Introduction: Subclinical hypothyroidism (SCH) is diagnosed based on elevated thyrotropin (TSH) and normal thyroxine (FT4) levels. Previous guidelines recommended treatment of SCH with levothyroxine (LT4) when TSH is &gt; 10 uIU/mL or if TSH &lt;10 uIU/mL with symptoms suggestive of hypothyroidism, positive thyroperoxidase antibodies (TPO Ab) or evidence/risk factors of cardiovascular disease. There has been an increasing practice of LT4 prescription for SCH, which contributes to making LT4 the second most prescribed drug in the US. Case: This case reviews the course of a patient with SCH treated with LT4. A 68 year old woman with medical history of hyperlipidemia, osteoporosis, and non-toxic multinodular goiter was diagnosed with SCH due to Hashimoto’s thyroiditis based on TSH 9.59 uIU/mL (0.34 - 5.60), FT4 0.66 ng/dL (0.58 - 1.64), and +TPO Ab. The patient had similar thyroid function tests (TFT) 1 year ago. She reported symptoms of hair loss, dry skin, and fatigue. She decided to undergo a trial of LT4 50 mcg daily. Two months later, her TSH had normalized and she reported slight improvement of fatigue. After one year on LT4, the patient reported symptoms of anxiety and heat intolerance and decided to stop LT4. Laboratory work up revealed TSH 0.22 uIU/mL and FT4 1.03 ng/dL consistent with exogenous hyperthyroidism. At the time of her follow up, the patient had been off LT4 for about 3 weeks. She continued to have ongoing fatigue, but reported resolution of the hyperthyroid symptoms. She was advised to stay off LT4 and to have yearly TFT. Discussion This case illustrates that not only LT4 treatment for SCH did not result in apparent improvement of hypothyroid-related symptoms, but also caused iatrogenic hyperthyroidism. A recent meta-analysis of 21 randomized clinical trials including 2192 patients with SCH found that LT4 therapy is not significantly associated with improvement in general quality of life or thyroid-related symptoms. Additionally, there is evidence of potential harm associated with LT4 and added burden of lifelong management. In 2019, a new guideline panel issued a strong recommendation against thyroid hormones in adults with SCH. Patients who are already on LT4 therapy for SCH may benefit from LT4 deprescribing. Clinicians need to discuss with their patients if LT4 discontinuation is a reasonable consideration. Studies at low risk of bias assessing patient important outcomes after LT4 discontinuation are required imminently.
Storm’s a Brewing
Authors: Franquemont Stephanie , William Ronnie , Theckedath Boby 
Published: May 2021

Abstract
Intro: Thyroid storm is an often feared but overall rare complication of untreated hyperthyroidism. This severe presentation of thyrotoxicosis has multiple different treatment modalities with actual treatment directed by the patient’s clinical course. We present the case of a 34-year-old male who presents in thyroid storm. Case: A male presented to the emergency department in southern Arizona in July with complaint of dizziness and tachycardia after working outside in the sun all day. He was rehydrated with symptomatic improvement but had continued tachycardia. The patient refused admission and left the emergency department prior to his thyroid function tests resulting with a TSH of &lt;0.02 and FT4 of 7.43. He had no apparent follow-up or further symptoms until he presented back to the emergency department approximately one year later at age 34. He presented the second time with shortness of breath and palpitations and was found to have atrial fibrillation with rapid ventricular rate &gt;200, a TSH &lt;0.02, and TSH of 6.59. He was tachypneic, but his temperature and blood pressure were within normal limits. He had a CTA of the chest that showed bilateral pulmonary infiltrates. He was started on intravenous metoprolol and diltiazem without resolution of his tachycardia, so an amiodarone drip was started. Hours later, the patient became hemodynamically unstable and went into cardiac arrest. Return of spontaneous circulation was obtained and the patient was intubated with post-arrest cooling protocol initiated. The patient was clinically diagnosed with thyroid storm, which was supported by an elevated Burch-Wartofsky score. Post-arrest treatment of thyroid storm was complicated by acute liver failure, systolic heart failure with ejection fraction &lt;20%, and persistent tachycardia. The patient was treated with high dose methimazole, propranolol, potassium iodine drops, corticosteroids, and cholestyramine. Surgery was considered given the slow progression of medical treatment but no pursued due to cardiovascular risk. Plasmapheresis was considered but not available. The patient’s thyroid function was followed daily and improved over a week despite persistent tachycardia and delirium. Eventually, the patient was discharged home with daily methimazole 20mg and planned outpatient follow-up for definitive therapy. Discussion: This patient presented to the ED with evidence of thyrotoxicosis that was untreated for one year prior to returning with thyroid storm. This illustrates the ability of a young, otherwise healthy patient to compensate for a prolonged period with relatively few symptoms prior to decompensating. This also shows the importance of having a system in place to catch abnormal laboratory results even if the patient is no longer present in the facility; a project has already been completed to catch abnormal thyroid function testing at our facility in the future.
Sub-Acute Thyroiditis Presenting as Pyrexia of Uknown Origin
Authors: Bahl Suhani , Babu Priya Mohan , Capatana Florin , Khan Ishrat , Adlan Mohamed , Premawardhana Lakdasa D K E 
Published: May 2021

Abstract
Introduction: Pyrexia of unknown origin (PUO) is often a diagnostic challenge. Common causes currently reported include non-infectious inflammatory disorders (NIID) (30.6%), infections (23.1%), malignancy (10.7%) and miscellaneous (12.4%). However, 23.1% remain undiagnosed despite extensive investigations. Fever is a component of subacute thyroiditis (SAT) in 28-83% of subjects reported in the literature. But its presentation as a PUO is reported only in a handful of subjects.
Case Presentation: A 71-year-old Asian male presented with evening fevers of 2-3 weeks duration. He had no accompanying sweats, cough, breathlessness, or weight loss. He had a past history of TB, polio, hydatid cyst and hypertension for which he was on treatment. He was a teetotaler. Several family members living in his native land had active TB and he visited them often. Clinical examination at initial presentation was unremarkable. He interrupted investigations to go back to Asia, and became unwell for over 6 weeks with evening fevers and sweating, a weight loss of over 7 kg, and a poor appetite. At this point he had no neck pain, palpitations or bowel abnormalities. Clinical examination continued to be normal upon his return to the UK and in the Endocrine Clinic. Investigations: Investigations were done to exclude (a) infections - There was no growth of pathogenic organisms in repeated blood, urine and sputum cultures. Screening tests for TB, hepatitis, and glandular fever were negative. Blood screens for malarial parasites, amoebic and Brucella serology, and stools examination and culture were also negative. Echocardiography was normal. (b) Malignancy - Urine Bence Jones proteins and serum protein electrophoresis were normal. Bone marrow examination was suggestive of Leishmaniasis but a PCR test excluded this diagnosis. Humoral markers of malignancy were negative. CT scans of the thorax, abdomen and pelvis were normal and did not show any evidence of visceral abnormalities (c) NIID - CRP 120, ESR 130, with blood tests consistent with iron deficiency. Autoimmune screening for dsDNA, ANA, ANCA were negative. Upon return to the UK a PET/CT scan showed the diffuse tracer uptake in both thyroid lobes and changes consistent with a large left lobe. Free thryroxine was 28pmol/l (reference range 9-19.1), and TSH was undetectable (&lt;0.004 mU/l). Thyrotrophin receptor antibodies were negative. Management and conclusion He was given carbimazole initially but this was stopped as he became severely hypothyroid. This hypothyroidism persisted for several months even after stopping carbimazole but reversed spontaneously. He therefore had a biphasic pattern of thyroiditis typical of SAT. There are only 9 previous cases reported of SAT presenting as PUO. Although SAT is a rare cause of PUO, early thyroid testing and if necessary, functional thyroid imaging should be considered in subjects with PUO to confirm it.