Complication Of Hyperthyroidism Research Articles

8232 Therapeutic Plasma Exchange as a Bridge to Total Thyroidectomy in a Patient with Refractory Thyroid Storm

Abstract Disclosure: A. Sridhar: None. T. Chaudhary: None. S. Patil: None. A. Prabha Kumar: None. K. Djekidel: None. B.C. Jameson: None. Background: Thyroid storm is a rare life-threatening complication of hyperthyroidism with a mortality rate of 10-30%. Therapeutic plasma exchange (TPE) could be a bridge to definitive total thyroidectomy in patients with refractory disease who fail conventional therapy. Clinical case: Patient is a 31-year-old male with a past medical history of untreated hypertension, anxiety, alcohol use, substance abuse and a family history of Graves’ disease. He presented with complaints of breathing difficulty, back and shoulder pain for the past 1 day. In the ED he was found to be in respiratory distress with a rate of 40/min. He was started on a non-rebreather mask and was eventually intubated due to worsening distress. He was tachycardic with a heart rate of 130/min and had elevated blood pressure at 170/105 mm Hg. Physical examination was significant for diaphoresis, accessory respiratory muscle use, and diffuse swelling on the front of the neck. His blood work was significant for hemoglobin 11.1g/dL, TSH <0.01 uIU/mL, FT3 >32.6 pg/ml, FT4>7.8 ng/dL and urine drug screen was negative. Chest X-ray showed mild perihilar vascular congestion due to pulmonary edema. CT neck showed nonspecific diffuse enlargement of the thyroid gland without dominant thyroid nodule. The patient was admitted to the ICU for management of thyroid storm likely from Graves’ disease. Burch-Wartofsky Point Scale score on admission was 60. Endocrinology was consulted and the patient was started on IV hydrocortisone 100 mg and IV Methimazole 20 mg every 8 hours, propranolol 60 mg every 6 hours, and iodine drops 300 mg every 6 hours after the first dose of methimazole. Since repeat FT4 after 48 hours showed no improvement, he was switched to Propylthiouracil (PTU) with a loading dose of 500mg every 4 hours for 2 doses followed by 250 mg every 6 hours and cholestyramine 4 g orally 4 times daily to reduce enterohepatic circulation of thyroid hormone. After 3 days of PTU, the patient’s FT3 was improving but FT4 continued to be elevated. ENT was consulted for total thyroidectomy, but the patient required preparation to improve FT4 levels prior to surgery. He was transferred to a tertiary care center on Day 6 of admission to undergo TPE. After 3 sessions of TPE serum FT3 and FT4 decreased, patient’s mentation improved, and he was extubated on Day 10 of admission. He received a total of 5 sessions of TPE and underwent total thyroidectomy on Day 15 of admission without complications. Postoperatively he was started on oral Levothyroxine 125 mcg once daily and calcitriol 0.25 mcg twice daily. Patient continues to follow up with Endocrinology clinic for thyroid function monitoring and medication adjustment. Conclusion: Given the high mortality rate associated with thyroid storm, early recognition of refractory disease is imperative. Bridging with TPE while awaiting total thyroidectomy improved clinical outcomes in our patient and should be considered in such cases. Presentation: 6/3/2024

Ameliorating Effects of Intermittent Fasting on Cardiac Dysfunctions in Experimentally Induced thyrotoxicosis in Adult Rats. Role of Ghrelin Hormone

Abstract Background Cardiovascular complications of hyperthyroidism have high morbidity and mortality rates. The cardioprotective effect of intermittent fasting (IF) in addition to the concomitant rise of blood ghrelin hormone level during IF have gained attention, but their effects on thyrotoxic hearts are still unclear. Therefore, we aimed to investigate the impacts of IF on hearts of rats subjected to induced thyrotoxicosis (TH) elucidating the role of ghrelin hormone in the assumed cardio protection. Methods Forty-five adult male Wistar Albino rats in 3 groups: control group, thyrotoxic group, injected IP with L-thyroxine100 μg/kg/day, 5 days/week for 4 weeks and intermittent fasting-treated thyrotoxic group, subjected to alternative day fasting regimen for 4 weeks. cardiac functions were assessed by in-vivo studies (ECG recording and arterial blood pressure evaluation) and in-vitro studies (responses to isoproterenol infusion using Langendorff’s preparation). Results Compared to the TH rats, intermittent fasting showed significant body weight loss, decreased left ventricular and whole heart absolute weights, with significant decrease of heart rate (HR) and prolongation of P-R interval in ECG. The baseline values of PT/LV, HRT and MFR/LV as well as their maximal responses and their delta changes in response to isoproterenol infusion were increased and were positively correlated to ghrelin hormone. Ghrelin hormone was increased in IF rats reaching the control group value and showed positive correlation with GPx and BCL-2. Conclusions IF conferred partial cardioprotective effects against thyrotoxicosis. These effects were attributed – at least partially- to normalization of ghrelin hormone which has anti-inflammatory, antioxidant as well as anti-apoptotic effects.

Exploring the spectrum: complications of hyperthyroidism - insights from a series of 29 cases

Exploring the spectrum: complications of hyperthyroidism - insights from a series of 29 cases

Thyroid storm: Report of four cases in two health institutions, Barranquilla

Thyroid storm or thyrotoxic crisis is a life-threatening condition, characterized by signs and symptoms of thyrotoxicosis associated with multiorgan dysfunction, occurs as a complication of hyperthyroidism and due to its high risk of mortality, merits timely diagnosis and early treatment. Among the main causes of thyroid storm is Graves' Basedow's disease, which is associated with triggering factors such as non-adherence to medical therapy. The diagnosis is based on clinical manifestations and increased thyroid hormones, but thyroid hormone levels are not related to the severity of the condition, so sensitive scoring systems have been developed to support the diagnostic approach. In this review, we analyze a series of patients with thyroid storm in which half of the patients have a fatal outcome, demonstrating the association with high mortality.

Epidemiology, prognosis, and challenges in the management of hyperthyroidism-related atrial fibrillation.

Atrial fibrillation (AF) is a common condition with a global estimated prevalence of 60 million cases, and the most common cardiac complication of hyperthyroidism, occurring in 5-15% of overtly hyperthyroid patients. Additionally, subclinical hyperthyroidism and high-normal free T4 have been associated with an increased risk in the development of AF. Hyperthyroidism-related AF is a reversible cause of AF, and the majority of patients spontaneously revert to sinus rhythm in 4-6 months during or after restoration of euthyroidism. Therefore, restoring thyroid function is an indispensable element in hyperthyroidism-related AF management. Rate control with beta-blockers consists another first-line therapy, reserving rhythm control in cases of persistent hyperthyroidism-related AF. It is still controversial whether hyperthyroidism is an independent risk factor of stroke in nonvalvular AF. As a result, initiating anticoagulation should be guided by the clinical thromboembolic risk score CHA2DS2-VASc score in the same way it is applied in patients with non-hyperthyroidism-related AF. Treatment with the novel direct oral anticoagulants appears to be as beneficial and may be safer than warfarin in patients with hyperthyroidism-related AF. In this review, we address the epidemiology, prognosis, and diagnosis of hyperthyroidism-related AF, and we discuss the management strategies and controversies in patients with hyperthyroidism-related AF.

Cardioprotective effects of losartan and diminazene against the ischemia/reperfusion injury in hyperthyroidism rats.

Hyperthyroidism is a condition where the thyroid gland produces high levels of thyroid hormone. Heart diseases are one of the main complications of hyperthyroidism. Several studies have shown that losartan (LOS) and diminazene aceturate (DIZE) possess cardioprotection effects against cardiac hypertrophy, ischemic heart disease, and heart failure. The research aimed to investigate the cardioprotection of LOS, DIZE, and their combination in the case of levothyroxine (LT4)-induced cardiomyopathy in rats. Hyperthyroidism was induced by LT4 in drinking water (12mg/L) for 28 days. LOS (10mg/kg, orally) and/or DIZE (15mg/kg, subcutaneously) were administrated in rats with hyperthyroidism for 28 days. Decreased serum creatine kinase myoglobin and lactate dehydrogenase levels and cardiac hypertrophy by DIZE and combination therapy in hyperthyroidism rats have been reported. Cardiac hemodynamic findings showed that DIZE and its combination with LOS decreased the LT4-mediated left ventricular developed pressure (LVDP), rate pressure product (RPP), and RPP recovery percentage. Elevated cardiac oxidative stress and inflammation were confirmed by decreasing cardiac superoxide dismutase (SOD) activity and increasing the total oxidative stress and tumor necrosis factor-alpha (TNF-α) levels. SOD activity and TNF-α level were reversed by LOS and DIZE administration, respectively. Generally, DIZE and combination therapy with LOS improved cardiac dysfunction caused by hyperthyroidism in rats, whereas LOS alone has not been able to effectively respond to this dysfunction.

FRI497 Thyroid Storm And Recurrent Myopericarditis

Abstract Disclosure: D.J. Gomez D' Aza: None. T. Zahedi: None. F. Zhang: None. Introduction: Thyroid storm is an acute life-threatening complication of hyperthyroidism with high mortality rate. Plasmapheresis is often used in patients who are unresponsiveness to conventional treatment for thyroid storm. About 5% of thyroid storm patients present with heart failure while other cardiovascular dysfunctions include tachycardia, arrhythmias, hypertension, and pericardial disease. Myopericarditis is characterized by pericarditis associated with myocardial inflammation evident by elevated cardiac biomarkers. Thyrotoxicosis associated with pericarditis and myocarditis is rare. Here, we report a case of recurrent myopericarditis and thyroid storm in Grave’s disease treated with plasmapheresis. Case Report: A 47 years male with a history of Schizophrenia and Hyperthyroidism due to Grave’s disease was presented with poor oral intake, generalized weakness, and tachycardia with HR 180 bpm. Labs showed elevated troponin 0.505 ng/mL, Free T4 > 6.99 mg/dL, T3 > 651 ng/dL, and low TSH < 0.015 mg/dL. Burch-Warsofsky scale was 50 points which suggested thyroid storm. EKG revealed atrial fibrillation. Patient was managed with propranolol, propylthiouracil (PTU), iodine solution, hydrocortisone, and Diltiazem. However, his mental status deteriorated requiring intubation and patient developed cardiac shock with BP 77/53 mmHg. Troponin I trended up to 23.60 ng/mL and EKG showed ST-segment elevation in the anterior and inferior leads. Echocardiogram revealed severely reduced ejection fraction of 15 % and diffuse hypokinesis. Cardiac catheterization was unremarkable. PTU was discontinued due to liver dysfunction with AST and ALT levels above 1500 U/L and 2500 U/L. A session of plasmapheresis was initiated and the post labs showed an improvement of thyroid and liver function to Free T4 2.46 mg/dL, TSH 0.022 mg/dL, and ALT/AST 641/682 U/L. Patient was hemodynamically stable with normal sinus rhythm. Cardiac magnetic resonance images revealed left ventricular dilation with high T2 signal, late gadolinium enhancement in the pericardial region of basal inferolateral, inferior, and mid segments, consistent with pericarditis. Previous record showed patient had a similar admission 4 months ago with a diagnosis of myopericarditis. Discussion: The association of recurrent myopericarditis and hyperthyroidism may be related with the autoimmune dysfunction and underlying viral infection that precipitated inflammation of the thyroid gland, triggered thyroid storm, and caused cardiac event. Rapid correction of the hyperthyroid state is warranted in thyroid storm in addition to aggressive treatments for heart failure, arrhythmias, and myopericarditis. Our patient’s cardiac function improved rapidly after achieving euthyroidism by plasmapheresis. The treatment of hyperthyroidism is critical in preventing the recurrence of myopericarditis. Presentation: Friday, June 16, 2023

FRI499 The Importance Of Identifying Atypical Presentation Of Thyroid Storm

Abstract Disclosure: D.H. Sacoto: None. C.A. Villavicencio: None. A. Franco-Akel, MD: None. R. Belokovskaya: None. Thyroid storm is a rare and life-threatening syndrome. Despite treatment and supportive measures, it has an estimated mortality around 8–25%. Identifying atypical clinical presentation such as psychosis is crucial since prompt diagnosis and treatment is paramount for survival. We present an unusual case of psychosis as the manifesting symptom of thyroid storm.A 54-year-old female with a history of major depressive disorder, hypertension, and Graves’ disease presented to the ED with a 3-day history of bizarre behavior noted by the family. At the time of examination, the patient had pressured and circumferential speech, flight of ideas, labile mood, and paranoid ideations. On further questioning, patient reported palpitations and lack of sleep on days previous to presentation. Vital signs revealed hypertension (182/101 mmHg), tachycardia (176 beat per minute), tachypnea, and a temperature of 99.6 °F. Warm skin, fine tremors, and patellar hyperreflexia were noted on physical examination. Subsequent studies showed a suppressed TSH (<0.01uIU/mL), an elevated T3 (227ng/dL) and free T4 (2.1ng/dL). TSH receptor antibody was found positive. Patient’s clinical presentation combined with a Burch-Wartovsky scale of 55 stablished the diagnosis. Further history was notable for non-adherence to methimazole. Iodine-131 was administered. Further treatment with prednisone, propranolol, and cholestyramine was started. Patient showed subsequent clinical improvement. Thyroid storm is a rare complication of hyperthyroidism. It is commonly precipitated by infection, surgery, or medication non-adherence. Atypical presentation of thyroid storm can be disguised as psychiatric condition or substance abuse disorder. These manifestations can be the result of a generalized hypermetabolism generated by an increase in NA+/K+ ATPAse activity, raising the basal metabolism, resulting in thermogenesis. In addition, upregulation of beta-adrenergic receptors lead to increased central nervous system sympathetic response. This results in a catecholamine surge which may manifest as psychosis, mania, or coma. Being aware of atypical presentation in thyroid storm such as active psychosis is key in early diagnosis and prompt management. Presentation: Friday, June 16, 2023

THU228 Thyrotoxic Periodic Paralysis In Three Adolescent Males

Abstract Disclosure: E. Ra: None. J. Austin: None. Thyrotoxic periodic paralysis (TPP) is a rare but potentially fatal complication of hyperthyroidism associated with Graves disease. Paralysis is due to hypokalemia caused by overactivation of the sodium potassium adenosine triphosphatase (Na+/K+ ATPase). TPP is usually seen in males between 20 - 40 years of age who are of Asian descent. We report 3 Hispanic American adolescent males, as young as 13 years old, who presented with TPP without an existing diagnosis of Graves disease. All three presented with leg weakness and were found to be hypokalemic and ultimately diagnosed with hyperthyroidism. Each patient was supplemented with potassium, either intravenously or orally, with their symptoms resolving within 24 hours. Although TPP is most prevalent in Asian adult males, theorized to be due to an underlying genetic preposition related to a variant of the KCNJ18 gene, there are increasing reports of non - Asian adolescents presenting in TPP. Therefore, pediatric care providers should consider TPP in their differential if a patient presents with weakness and hypokalemia, even without a pre-existing diagnose of hyperthyroidism. Presentation: Thursday, June 15, 2023

Ultrasound measurement of vastus lateralis and vastus medialis muscle parameters to identify chronic thyrotoxic myopathy.

Chronic thyrotoxic myopathy (CTM) is a common, easily neglected complication of hyperthyroidism. There are currently no standard diagnostic criteria for CTM, and the ultrasonic characteristics of CTM-affected skeletal muscle remain unclear. Herein, we aimed to evaluate hyperthyroid patients for CTM by ultrasound and identify ultrasonic muscle parameter cutoffs for CTM diagnosis. Each participant underwent ultrasonography. The original (muscle thickness (MT), pennation angle (PA), and cross-sectional area (CSA)) and corrected (MT/height (HT), MT/body mass index (BMI), CSA/HT, and CSA/BMI) parameters of the vastus lateralis and vastus medialis (VM) were evaluated. The diagnostic effectiveness of ultrasound for predicting CTM was determined using receiver operating characteristic (ROC) curve analysis. Our study included 203 participants: 67 CTM patients (18 males, 49 females), 67 non-CTM patients (28 males, 39 females) and 69 healthy controls (20 males, 49 females). The CTM group had lower muscular ultrasonic and anthropometric parameters, higher thyroid hormone and thyroid-stimulating hormone receptor antibody (TRAb) levels, and a longer duration of hyperthyroidism than the non-CTM group (P < 0.05). The VM-PA, VM-CSA, VM-CSA/HT, and VM-CSA/BMI were lower in females than in males (P < 0.05). Free thyroxine (FT4) and TRAb both showed significant negative correlations with VM-MT, VM-MT/HT, VM-CSA, and VM-CSA/HT (P < 0.05). VM-MT/BMI and VM-CSA/HT, respectively, best predicted male and female CTM (AUC = 0.84, 0.85; cutoff ≤ 0.07, < 4.01). Ultrasound measurement of muscular parameters, especially in the VM, is a valid and feasible way of diagnosing and characterizing possible CTM in hyperthyroidism.

Hypothyroid Myopathy: A Commonly Missed Complication of Hypothyroidism

Muscle disease is a known complication of hyperthyroidism as well as hypothyroidism. The muscle disease is associated with elevated creatine kinase and pain. This the case of a 63-year-old female who presented to the ED from her cancer therapy with elevated creatine kinase of 2,000 IU/L (International units/Liter). She reports muscle pain in her shoulders and hips for the past 3 days. Patient was recently diagnosed with hypothyroidism and has started on levothyroxine 75 mcg. Her Thyroid Stimulating Hormone (TSH) stays elevated at 65 IU (international units). Other autoimmune causes of elevated creatine kinase were excluded via testing, leaving hypothyroid myopathy as the only possible probable cause of this patient elevated creatine kinase. Muscle pain and creatine kinase should resolve with proper levothyroxine dose and compliance to therapy when patient becomes euthyroid. Unfortunately, the patient passed away from complications related to fall.

Hypokalemic periodic paralysis as the first sign of thyrotoxicosis- a rare case report from Somalia

BackgroundThyrotoxic hypokalemic periodic paralysis (THPP) is a rare complication of hyperthyroidism characterized by thyrotoxicosis, hypokalemia, and paralysis. It is the most common form of acquired periodic paralysis. THPP is precipitated by strenuous exercise, a high carbohydrate diet, stress, infection, alcohol, albuterol, and corticosteroid therapy. It is most common in Asian men with hyperthyroidism and exceptionally rare in black people.Case PresentationA 29-year-old man was admitted to the emergency department in Somalia with a sudden onset of paralysis after a high carbohydrate meal. Laboratory investigations showed low serum potassium 1.8 mEq/l (3.5–4.5), and biochemical thyrotoxicosis with TSH 0.006 miu/l (0.35–5.1), total T3 3.2 ng/ml (0.9–2.8) and total T4 13.5 ng/ml (0.6–1.2). He was successfully treated with potassium chloride infusion and an antithyroid drug, methimazole.ConclusionTo prevent life-threatening cardiac and respiratory complications, it is critical to consider and diagnose THPP early, even in populations where the condition is rare.

HYPERTHYROIDISM SECONDARY TO GESTATIONAL TROPHOBLASTIC DISEASE : A LITERATURE REVIEW

Gestational trophoblastic disease (GTD) is a rare form of pregnancy-related cancer that is effectively treatable. GTD is accompanied by the potentially fatal complication of hyperthyroidism. We created a review consisting of five case reports. This case report was conducted on women who became pregnant when they were &gt;35 years old. They showed consistent laboratory results, in which there was an increase in hCG levels. TSH and thyroid stimulating antibodies cannot account for the hyperthyroidism associated with GTD. The source of the thyroid stimulating agent is trophoblastic tissue. The thyrotropic effects of ?-hCG mediate GTD hyperthyroidism. Other research examined the prevalence of hyperthyroidism in women with normal pregnancy, hydatidiform mole, and choriocarcinoma who had ?-hCG serum levels below 100,000 IU/ml. Early prenatal screening may significantly reduce hyperthyroidism rates. Thyroid hormone synthesis inhibitors treat hyperthyroidism in pregnancy. Thioamides, propylthiouracil (PTU), and methimazole (MMI) are the most prevalent U.S. antithyroid medications (ATD). Plasmaphoresis may be an option for people who are resistant to therapy or need emergency surgery. GTD can cause fatal hyperthyroidism. Anti-thyroid medicines can handle most GTD hyperthyroidism. Surgery may be a possibility for patients refractory to medical treatment.

Thyrotoxic periodic paralysis: a presentation of hyperthyroidism increasing in frequency around the world

Thyrotoxic periodic paralysis (TPP) is a complication of hyperthyroidism commonly seen in Asian populations. It presents as sudden-onset muscle paralysis and hypokalaemia. Diagnosis is often delayed due to the rarity of the disease, the subtlety of the hyperthyroidism and the fleeting nature of the clinical presentation. With global expansion, physicians outside Asia should be aware of this disease for early recognition and treatment as severe cardiac arrhythmias, which may prove fatal, can occur. Several breakthroughs have been made in identifying the pathophysiological mechanism resulting in the severe hypokalaemia, including mutations in the Kir2.6 channel, an inwardly rectifying potassium channel, which results in a massive intracellular potassium shift. Treating the underlying hyperthyroidism is the definitive treatment; however, beta blockers and potassium supplementation are vital in acute management of this condition. This is a report of a case seen in Cape Town, South Africa with a review of the literature regarding the clinical features, pathophysiology and treatment.

Cardiovascular Complications of Hyperthyroidism

Thyrotoxicosis is a clinical syndrome caused by an excess of thyroid hormones circulating in the body. Myocardium and blood arteries have thyroid hormone receptors; hence, an increase or decrease in thyroid hormone levels can alter cardiovascular function. Cardiovascular complications are obvious in-patient with hyperthyroidism. Palpitations, tachycardia, exercise intolerance, dyspnea with exertion, expanded pulse pressure, and on occasion atrial fibrillation are associated with hyperthyroidism, excessive endogenous thyroid hormone production, and thyrotoxicosis, the condition caused by excess thyroid hormone. In the early stages of hyperthyroidism, a high cardiac output and hypertrophy of the left ventricle are observed, followed by biventricular dilatation and congestive heart failure. Atrial fibrillation and pulmonary arterial hypertension can contribute to the higher morbidity associated with untreated hyperthyroidism. Therefore, early and effective treatment of hyperthyroidism is required to prevent thyrotoxic cardiomyopathy.

Cardiothyreosis: Epidemiological, clinical and therapeutic approach.

Cardiothyreosis corresponds to the cellular effects of free thyroid hormones on the vascular wall and the myocardium. We aim to describe the clinical, para-clinical and therapeutic aspects of cardiothyreosis and to detail prognostic factors. We conducted a descriptive retrospective study at the Endocrinology-Diabetology Department of the Hedi Chaker University Hospital in Sfax-Tunisia. We collected medical records of 100 patients with cardiothyreosis between January 1999 and December 2019. We included patients with cardiothyreosis who underwent adequate cardiac evaluation. We excluded patients with cardiac abnormalities related to conditions other than hyperthyroidism, patients who died and patients without cardiothyreosis. We included 100 adult patients (43 men and 57 women). The mean age was 49.3 ±12.9 years (20-79 years). The diagnosis of cardiothyreosis was concomitant with that of hyperthyroidism in 72% of cases. Weight loss and palpitations were the two most frequently reported signs in 91% of cases each. Hypertension was systolic in 15 patients. The average heart rate was 103.1 beats/min (52-182 bpm). The mean TSH and FT4 levels were 0.042 μIU/ml and 59.6 pmol/l, respectively. Rhythm disorders and heart failure were the most common cardiac complications with 81 and 56 cases, respectively. Cardiac ultrasound showed dilatation of the left atrium in 28.3% of patients. Pulmonary arterial hypertension was present in 43% of cases. 57 patients had been treated with benzylthiouracil at a mean dose of 157.45 mg/day. Radical treatment with radioactive iodine was indicated in 81 patients. The evolution of cardiothyreosis was favourable in 58 patients. Cardiothyreosis is a serious complication of hyperthyroidism. Future prospective studies will be of great help to better characterise and manage cardiothyreosis.

High-dose intravenous hydrocortisone for the treatment of hyperthyroidism: a rare precipitant of thyrotoxicosis periodic paralysis.

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism triggered by precipitants that increase the activity of the sodium-potassium pump in the skeletal muscle. In our case study, a previously healthy 34-year-old male presented to the emergency department with new onset thyrotoxicosis, secondary to Graves' disease. Given the severity of his triiodothyronine (T3) thyrotoxicosis, he was admitted and started on a high dose of beta-blocker, thioamides, and intravenous hydrocortisone. On the second day of his hospitalization, he developed acute flaccid paralysis of his lower extremities. Subsequent stroke workup was negative, and his electrolytes revealed severe hypokalemia and hyperglycemia consistent with TPP. He was treated with potassium and had a complete recovery of his paralysis and hypokalemia within hours. The patient has not had any recurrence since this singular episode in the hospital. This case highlights the scenario where the treatment of hyperthyroidism with high-dose corticosteroids to reduce the conversion of thyroxine to T3 inadvertently resulted in TPP. Clinicians should be aware of this potentially rare but serious consequence of using steroids to manage hyperthyroidism. High-dose steroids used to treat hyperthyroidism in hospitalized patients may rarely precipitate thyrotoxic periodic paralysis (TPP) by inducing hypokalemia and hyperglycemia. TPP should be included in the differential diagnosis for acute flaccid paralysis in hospitalized patients with hyperthyroidism. Since TPP is associated with trans-cellular shifts in potassium instead of total body potassium depletion, conservative repletion of potassium is recommended to avoid rebound hyperkalemia.

ODP526 Thyrotoxic Periodic Paralysis in Graves’ Disease: A rare presentation in an African American male

Abstract INTRODUCTION: Thyrotoxic Periodic Paralysis is a rare but life-threatening manifestation of hyperthyroidism characterized by hypokalemia, acute flaccid paralysis, and signs of hyperthyroidism. Despite being commonly seen in East Asian males, TPP has been increasingly reported in other parts of the world including western countries. Early recognition and prompt treatment of TPP is essential in preventing its grave and potentially life-threatening consequences. CASE PRESENTATIONA 21-year-old African American male patient with past medical history significant for hypertension and untreated hyperthyroidism presented to the emergency department with sudden onset bilateral lower extremity weakness and difficulty walking for one day. Upon arrival to the emergency department, vitals were unremarkable. On examination, patient had a decreased muscle tone in bilateral lower extremities with depressed deep tendon reflexes. The thyroid gland was diffusely enlarged. The remainder of physical exam was normal. Electrolyte abnormalities were also present with decreased serum potassium level of 1.2 mEq/L (3.6-5.1 mEq/L) and magnesium of 1.7 mg/dL (1.8-2.5 mg/dL). A low TSH level of &amp;lt;0. 010 mIU/mL (0.350-4.940 mIU/mL) with elevated free T4 levels of 4.30 ng/dL (0.70-1.48 ng/dL) were noted. CT Head/ Brain without contrast and Chest X ray were unremarkable. Potassium replacement was initiated with oral and intravenous potassium chloride. He was also started on oral atenolol (25 mg daily) and methimazole (10 mg daily). The patient's symptoms resolved in few hours after the treatment was started. An ultrasound of the thyroid gland showed diffuse heterogeneity of the gland most consistent with thyroiditis or similar abnormality. No definite focal abnormalities were noted. TSH receptor antibodies were also elevated with levels at 10.70 IU/L (≤1.75 IU/L) making Graves’ disease the most likely diagnosis. The patient's condition significantly improved along his hospitalization with complete resolution of symptoms and electrolyte abnormalities. He was subsequently discharged on atenolol and methimazole with outpatient follow up at the endocrinology clinic. DISCUSSION TPP is an underreported yet possibly fatal medical complication of hyperthyroidism. Prevalence is higher in Asia, however, incidence in Western countries has been increasing. While the underlying pathophysiology is poorly understood, h ypokalemia in TPP results from an intracellular shift of potassium induced by an increased adrenergic sensitization of Na + /K + –ATPase pump. Genetic and environmental factors may possibly play a role. Treatment of TPP entails beta-blockade to prevent intracellular shift of potassium, replenishing potassium stores, as well as correcting the underlying hyperthyroid state. Immediate diagnosis and initiation of treatment prevents serious cardiopulmonary complications and increases the probability of full recovery of muscle weakness. Presentation: No date and time listed

PSAT317 An Impending Thyroid Storm Caused by COVID-19 Infection

Abstract Background Thyroid storm is an acute, potentially fatal complication of hyperthyroidism, usually manifested with tachycardia, hyperthermia, and altered mental status. Despite medical advancements, the mortality associated with thyroid storms remained 5% to 25%. Previously, cases of thyroiditis following COVID-19 infection have been reported. But the manifestation of COVID-19 infection as a thyroid storm is infrequent, and less than 5 cases have been reported to date. Case A 72-year-old female with a remote history of breast cancer status post-mastectomy presented to the emergency department with the chief complaint of shortness of breath. She was found to have a history of fever eight days before the presentation; she was also complaining of non-productive cough, non-bloody, and non- bilious vomiting, myalgia, and fatigue. Home Covid Test was positive. On the day of the presentation, she received Regeneron infusion (casirivimab and imdevimab) and was discharged home. After a few hours, she represented to the hospital with chills and worsening of shortness of breath. She was found to be hypoxic on the presentation, was started on O2 supply, and transferred to the ICU. She received IV dexamethasone 6 mg and IV Remdesivir 200 mg on the first day, followed by 100mg for the next four days. On the fourth day following admission, she developed Atrial Fibrillation with a rapid ventricular response. The patient was somnolent and had loose bowel movements. Thyroid function tests were ordered; TSH was 0.02 and free T4 of 2.9. She stated she was never diagnosed with a thyroid disorder in the past. Thyroid function tests were ordered, which are mentioned in the table below. A thyroid-stimulating antibody assay was ordered to rule out Graves thyrotoxicosis, which turned out to be normal. Ultrasound of the thyroid gland didn't reveal any abnormalities. Conclusion Although most patients remain euthyroid during COVID-19 infection, some may have shown transient thyroid derangements during the illness, which later turns out to be normal. Our case shows that a clinician should not take the thyroid derangements in COVID-19 lightly, as they can be the early signs of an impending thyroid storm. Our case guides the clinician to evaluate the thyroid function as soon as possible in any signs of overt hyperthyroidism. Due to the high mortality associated with thyroid storm, a clinician should have a high index of suspicion to diagnose the storm, such as in our case where other signs of hyperthyroidism are absent. Early treatment of thyroid storms becomes necessary to mitigate the mortality in such cases. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

P223 THYROTOXIC DILATED CARDIOMYOPATHY

Abstract Hyperthyroidism can strongly impact cardiac function. Thyrotoxicosis enhances myocardiocytes metabolism and it can be responsible for hyperdynamic circulation state leading to heart failure with preserved ejection fraction, but also left ventricle dilatation and severe contractile function impairment. It can furthermore provoke arrhythmias, mostly atrial fibrillation, but, as we are going to discuss in this case, even ventricular arrhythmias. A 40–year–old woman came to our emergency department for chest pain. ECG showed reduced R waves voltage in precordial leads and troponin I values were normal. The echocardiogram showed severe left ventricle disfunction with global hypokinesia (EF 35%) and enlarged left ventricle (LVEDD 65 mm). Blood tests revealed severe hyperthyroidism with extremely low level of TSH, FT3 13,45 pg/ml, FT4 3,4 ng/ml and thyroid echography documented multiple solid nodular formations with hypo–isoechogenic signal. She underwent a coronary angiography that showed patent coronary arteries, and a cardiac magnetic resonance confirming severe contractile impairment and hypertrabeculation of the apex and lateral wall. On the assumption of a dilated cardiomyopathy secondary to hyperthyroidism, we started treatment with methimazole, ACE inhibitors and propranolol. During hospitalization, continuous ECG monitoring recorded several episodes of non–sustained ventricular tachycardia, the longest lasting 22 seconds, so the patient was discharged with a wearable cardioverter–defibrillator. It did not record any arrhythmias and it was dismissed a month later. After almost two months of therapy, the echocardiogram showed mild left ventricular contractility improvement (EF 45%), and blood tests documented partial reduction of hyperthyroidism. A 24–hour ECG Holter did not record any arrhythmias and the patient remained asymptomatic during all the period after discharge. Even if rare, scientific literature confirms that dilated cardiomyopathy with reduced ejection fraction can occur as a complication of hyperthyroidism. After the exclusion of an ischemic cause, we underline the need for adequate initiation of treatments for thyrotoxicosis and heart failure, in order to improve chance of left ventricular function recovery. In the case discussed, after two months of therapy, EF was still not completely restored but improved from 35% to 45%, and concurrently arrhythmic risk did clearly decrease.