Severe Hyperthyroidism Research Articles

PSAT337 Thyroid Storm Triggered by Thyroid Nodule Fine-Needle Aspiration Biopsy

Abstract Background Thyroid storm is a severe and life-threatening thyrotoxicosis precipitated by an acute event such as thyroid gland manipulation, infection, trauma, or an acute iodine load. Patients with known hyperthyroidism or low TSH with the presence of multinodular goiter should undergo radionuclide thyroid scan before deciding on fine-needle aspiration (FNA) biopsy. We present a case of a patient with history of multinodular toxic goiter disease, who had a thyroid storm after she underwent an FNA thyroid biopsy, requiring emergent total thyroidectomy. Clinical Case 62-year-old female patient with history of multinodular goiter (MNG) disease diagnosed in another country one year prior to admission. She was on methimazole for a few months but was off the medication upon presentation. She was admitted for evaluation due to worsening compressive symptoms. On presentation, she was hypertensive, tachycardic, with dysphonic voice and had a large goiter palpated bilaterally with extension over the sternocleidomastoid muscle. Laboratory results confirmed that she had thyrotoxicosis. TSH was 0.05 mclU/mL, n: 0.27-4.2mclU/mL; FreeT4 > 7.77 ng/dL, n: 0.93-1.70ng/dL; T3 was 552 ng/dL, n: 80-200 ng/dL; TSI and TRAB were elevated: 476 and 23 respectively. In view of this, methimazole 40 mg daily, prednisone 20 mg daily, cholestyramine 4 mg four times a day, potassium iodine 50 mg three times per day, and propranolol were started. Chest CT demonstrated a thyroid gland that was heterogeneous in appearance and markedly enlarged with a right thyroid lobe measuring approximately 6.2×5.8 cm and the left lobe measuring approximately 5.5×5.0 cm. Patient underwent ultrasound guided FNA biopsy of the right thyroid lobule ordered by another team two days after the medication regimen was initiated. One day after procedure, patient had altered mental status, stridor, acute respiratory failure, worsening of hypertension and tachycardia, requiring intubation. It was not possible to place an oral gastric tube, so propylthiouracil 400 mg was given via rectal route every 8 hours and her steroid dose was increased. Her FreeT4 decreased to 3.99 ng/dL and T3 to 165 ng/dL the following day. However, patient condition continued to deteriorate, and she underwent emergent total thyroidectomy, despite not being euthyroid. Patient tolerated the procedure and was able to be extubated the following day without postoperative complications. At the time of discharge, patient was on Levothyroxine 150 mcg oral daily. Conclusion FNA biopsy of toxic thyroid nodules are rarely indicated due to the risk of thyroid storm in patients with underlying hyperthyroidism. Control of the hyperthyroid state should be the priority prior to FNA of any thyroid nodule. Total thyroidectomy may be performed in the hyperthyroidism state as a life-saving procedure when there is failure control hyperthyroidism, as is the case here. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

PSAT360 Thyrotoxicosis as a Delayed Response to Amiodarone

Abstract Introduction Amiodarone is often used in the treatment of cardiac dysrhythmia, but has been associated with toxicity of multiple organ systems including the thyroid. Patients treated with amiodarone can develop hypothyroidism or hyperthyroidism, also known as amiodarone induced thyrotoxicosis (AIT). AIT is further categorized into type I or type II depending on pathogenesis of the disease: type I resulting from increased hormone synthesis and type II resulting from glandular destruction. We report a case of a 68-year-old male patient who developed type II AIT approximately four years after cessation of Amiodarone therapy. Case Presentation A 64-year-old man initially presented to an outpatient endocrinology clinic for evaluation of incidental thyroid nodules. He had a normal thyroid function. His significant past medical history included atrial fibrillation/atrial flutter status post ablation. Thyroid ultrasound revealed bilateral subcentimeter nodules which remained stable over the subsequent two years. Approximately four years after establishing care, he presented to the endocrinologist again with weakness, decreased appetite, fatigue, and weight loss. Thyroid function testing revealed new onset hyperthyroidism with suppressed TSH, <0.01 mU/L (normal 0.5-5.0 mU/L), elevated FT4 4.5 ng/dL (normal 0.7-1.9 ng/dL) and elevated FT3, 7.4 pg/mL (normal 2.3-4.1 pg/mL). He had normal TSI, normal ESR, and no history of recent viral infection. Thyroid ultrasound showed stable subcentimetric nodules. Evaluation with radioactive iodine uptake (RAIU) scan was not possible due to recent contrast exposure during CT spine imaging. The patient was started on methimazole therapy with an assumptive diagnosis of toxic multinodular goiter. The dose was rapidly increased, within weeks, to 60mg daily, due to persistent severe hyperthyroidism. He was hospitalized twice for exacerbation of atrial fibrillation with rapid ventricular rate requiring cardioversion and augmentation of medical therapy. Further investigation revealed the patient had received amiodarone therapy for approximately three months, almost four years prior to his current presentation. A trial of 40mg prednisone daily was started in conjunction with methimazole for possible delayed type II AIT, resulting in a rapid improvement of symptoms and Free T4 levels. Once the patient's urinary iodine levels returned to normal, he underwent RAIU scan which revealed low uptake supporting the diagnosis of type II AIT. Methimazole therapy was stopped, and prednisone therapy was tapered down slowly and then discontinued over the course of three months, with complete resolution of hyperthyroidism. Conclusion This report reiterates the difficulties clinicians are often faced with when diagnosing and treating AIT, which, in our case, occurred four years after the discontinuation of amiodarone therapy. It highlights the importance of obtaining a history of remote amiodarone therapy, and considering steroids treatment for type II AIT, especially in patients with no clear other etiology and no response to high dose methimazole. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Acute ST-Elevation Myocardial Infarction in Patient with Severe Uncontrolled Hyperthyroidism Complicated by Thyroid Storm

Acute ST-elevation myocardial infarction is a life-threatening medical emergency that needs to be recognized early and treated properly to prevent deleterious complications, including death. A thyroid storm (TS) is a rare but severe manifestation of uncontrolled hyperthyroidism that might present with serious cardiovascular or neurological problems. We described a case of a 40-year-old male patient, known to have uncontrolled hyperthyroidism, who presented with acute onset of central chest pain, agitation, tachycardia, and pulmonary congestion. Fast atrial fibrillation with ST-segment elevation in anterior leads was detected on electrocardiogram. Thyroxin level (T4) was very high with undetectable thyroid stimulating hormone. Initially, the patient refused any type of coronary revascularization; therefore, he was admitted to the cardiology intensive care unit, and medical treatment was commenced for both TS and acute coronary syndrome. High-risk coronary angiography was done 2 h later because he had worsening persistent chest pain and started to develop signs of heart failure. It showed embolic occlusion of the distal left anterior descending artery that was treated medically with anti-coagulation. There were no complications. Chest pain and thyroid function tests settled down during his hospital stay with close cardiology and endocrinology follow-up.

The Mediation Role of Thyrotropin Receptor Antibody in the Relationship Between Age and Severity of Hyperthyroidism in Graves' Disease.

Background: The severity of hyperthyroidism in Graves' disease (GD) has been reported to be worse in younger patients and to gradually improve with advancing age, accompanied by declining thyrotropin (TSH) receptor antibody (TRAb) values. This study was conducted to explore the extent to which the declining TRAb production may contribute to a decrease in severe hyperthyroidism with advancing age in patients with GD. Methods: This study was a cross-sectional analysis of retrospectively reviewed data. The medical records of patients newly diagnosed with GD at Ito Hospital, between January 2005 and June 2019, were examined. Patients were divided into age-stratified groups for evaluation. Multivariable logistic regression was performed to estimate the odds ratio (OR) of severe hyperthyroidism by increasing age. Mediation analyses were also conducted to quantify the association between age and declining severity of hyperthyroidism mediated through decreased TRAb productivity. Results: A total of 21,018 patients with newly diagnosed GD (3848 male and 17,170 female) were included. A correlation was observed between TRAb value and thyroid hormone values in each age-stratified group, which became weaker with an increase in age. Patients aged <40 years had a higher risk of severe hyperthyroidism (free thyroxine [fT4] level >7.0 ng/dL [n = 5616], OR [confidence interval, CI] = 1.80 [1.68-1.92]; free triiodothyronine [fT3] level >25 pg/mL [n = 4501], OR [CI] = 2.06 [1.92-2.23]) than those aged ≧40 years. In examining the relationship between age and severe hyperthyroidism, the proportion mediated through TRAb productivity was 8.5% and 8.4% using fT4 and fT3 as an outcome index, respectively. Conclusions: Declining TRAb value mediated only 8.5% of the negative association between age and severity of hyperthyroidism. The presence of other underlying mechanisms, such as the decline in the reactivity of thyrocytes to TSH stimulation, requires further investigation.

Thyrotoxic Periodic Paralysis in the Post-COVID Era: A Case Report with Literature Review

Thyrotoxic Periodic Paralysis (TPP) is an acute potentially lethal emergency in patients with hyperthyroidism who present with sudden muscle weakness and hypokalemia. It is commonly precipitated by high carbohydrate or high salt content meals, strenuous exercise, stress, trauma, glucocorticoids, epinephrine, alcohol, or respiratory infections. COVID-19 infection or vaccination may represent a novel trigger for TPP. Furthermore, COVID-19 infection or vaccination may incite inflammatory processes leading to thyrotoxicosis, which can manifest as TPP. While COVID-19 causing subacute thyroiditis, euthyroid sick syndrome, Hashimoto’s disease, or Graves’ disease have been well documented in the literature; there have only been six case reports of post-COVID-19 TPP. Notably, all cases thus far have been restricted to male patients, and there is paucity of literature from North America. The purpose of this paper is to outline the first case of post-COVID-19 TPP in a female patient, who presented to the emergency department with acute paralysis and severe hypokalemia (2.2 mmol/L) three months after COVID-19 infection. Investigations in the emergency department showed thyrotoxicosis. She was treated with potassium replacement, which improved her paralysis. Subsequent investigations revealed severe hyperthyroidism from Graves’ disease, which is currently managed with metoprolol and methimazole. Her hyperthyroidism improved without recurrent hypokalemia or paralysis. In addition, we outline the epidemiology, pathophysiology, precipitants, and management of TPP, with a particular focus on COVID-19 infection or vaccination precipitating TPP. We discuss post-COVID-19 TPP cases thus far described in the literature. Knowing that North American COVID-19 infection waves lagged Asia, we could anticipate additional future TPP cases.

TSH Receptor Antibody Testing in Early Pregnancy.

Graves disease (GD) is the leading cause of hyperthyroidism in women of childbearing age, and thus, low serum thyrotropin (TSH) during pregnancy might be expected to be largely secondary to GD. This is not the case for 2 reasons. First, autoimmunity frequently abates during pregnancy, including thyroid-specific autoimmunity (1), so that even those with previously diagnosed GD may go into remission during pregnancy. Second, the physiology of thyroid hormone regulation is altered as a result of the agonist activity of β-human chorionic gonadotropin (βhCG) at the TSH receptor (2). Under normal conditions this leads to a slight increase in thyroid hormone production, which is independent of pituitary TSH secretion. Serum TSH levels fall, resulting in a left shift of the TSH reference range in pregnancy, and a lower limit of 0.1 mU/L in most assays (3). In early pregnancy especially, elevations of serum βhCG above those typically seen can cause a further rise in serum free thyroxine and more dramatic suppression of the serum TSH, resulting in “gestational transient thyrotoxicosis” (GTT) (3). This is typically mild and resolves after the first trimester, and is not associated with adverse pregnancy outcomes (4). The very high levels of βhCG found in hyperemesis gravidarum are associated with more severe biochemical thyrotoxicosis, and extremely high levels seen with molar pregnancy and choriocarcinoma can require antithyroid drug therapy and other measures to mitigate thyrotoxicosis. Indeed, persistent thyrotoxicosis during pregnancy from any cause, especially GD, has been associated with poor outcomes including fetal loss, maternal heart failure, and preeclampsia (5).

Graves-Basedow disease treated by complementary medicine leading to severe thyrotoxicosis – a case report

Graves' disease is a common cause of hyperthyroidism. Inadequate treatment or non-compliance can lead to serious complications, including thyroid storm. &#x0D; We present the case of a 22-year-old woman who had been treated with antithyroid drugs (ATD) for almost 7 years, however decided to suspend conventional treatment and turned towards complementary and alternative medicine methods. Following the bioenergotherapist's advice, she began taking Lugol’s solution (LS) at a dose of 30 drops per day. After about one month of such therapy, the patient was urgently admitted to the Emergency Department with thyrotoxicosis with a high risk of thyroid storm development. With the implementation of intensive thyrostatic treatment and steroid therapy, euthyroidism was successfully restored.

Sinus Pauses and Asystole as a Rare Presentation of Thyrotoxic Crisis: A Case Report

INTRODUCTION: Thyroid crisis is a rare and life-threatening endocrine emergency characterized by exaggerated clinical manifestations of hyperthyroidism with cardiovascular manifestations being the most severe. Rhythm disturbances, sinus tachycardia and atrial fibrillation, are the commonest cardiac manifestations of severe thyrotoxicosis; however, asystole remains a very atypical and uncommon presentation. We present a case of thyrotoxicosis due to Grave’s disease complicated by multiple episodes of asystole. CASE PRESENTATION: A 65-year-old female recently diagnosed with Grave’s disease presented to the hospital with recurrent episodes of syncope. Her hospital course was significant for atrial fibrillation with subsequent progression to sinus pauses and asystole spontaneously reverting to atrial fibrillation. Her thyroid hormone levels were found to be markedly elevated at the time of presentation. She was initially managed with a temporary pacemaker but ultimately transitioned to a permanent dual-chamber pacemaker, in addition to concurrent anti-thyroid treatment with propylthiouracil and prednisone. She made an uneventful recovery and was discharged from hospital a few days later with scheduled outpatient follow-up. CONCLUSION: Asystole due to hyperthyroidism remains a very uncommon presentation of severe thyrotoxicosis, and in rarer situations can occur in hyperthyroid patients without any associated predisposing conditions such as infection, inflammation or medication use as previously reported. The mechanisms underlying this rhythm disturbance remain elusive, nevertheless, its management may require a permanent pacemaker placement in addition to concurrent medical treatment of the underlying cause and the thyroid hormone disturbance using standard hyperthyroid medications.

Steroid treatment in the management of destructive thyrotoxicosis induced by PD1 blockade.

ObjectiveDestructive thyroiditis is the most common endocrine immune-related adverse event (iRAEs) in patients treated with anti-PD1/PD-L1 agents. Given its self-limited course, current guidelines recommend no treatment for this iRAE. Nevertheless, in patients with enlarged thyroid volume and a poor performance status, thyrotoxicosis may be particularly severe and harmful. The aim of the study is to evaluate if steroid treatment might be useful in improving thyrotoxicosis in subjects with a poor performance status.MethodsWe conducted a retrospective study, comparing the course of thyrotoxicosis of four patients treated with oral prednisone at the dosage of 25 mg/day (tapered to discontinuation in 3 weeks) and an enlarged thyroid volume to that of eight patients with similar thyroid volume who were left untreated.ResultsThe levels of thyroid hormones were lower in subjects treated compared to those untreated at time of 7, 14, 21, 28, 35, 42, 60 and 90 days (P < 0.05 at each time). The time to remission of thyrotoxicosis was 24 days in patients treated with steroids and 120 days in untreated patients (P < 0.001). At 6 months, the rate of evolution to hypothyroidism was similar in the two groups (4/4 in the steroid group vs 7/8 in the untreated group, P = 0.74) and no difference was found in tumor progression (P = 0.89).ConclusionsOur preliminary data suggest that in patients with a poor performance status experiencing a severe destructive thyrotoxicosis induced by PD-1 blockade, a short period of administration of oral prednisone is effective in obtaining a quick reduction of the levels of thyroid hormones.

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.

Association of Human Leukocyte Antigen Genotypes with Severe Acute Respiratory Syndrome Coronavirus 2 Vaccine-Induced Subacute Thyroiditis.

Background: Despite mass vaccination, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine-induced subacute thyroiditis (SAT) is rarely seen as a complication. The reason why some individuals are susceptible to developing vaccine-induced SAT is not known. SAT develops in genetically predisposed individuals who carry specific human leukocyte antigen (HLA) haplotypes. It is unknown whether specific HLA alleles are associated with SARS-CoV-2 vaccine-induced SAT. Objective: This study compared the HLA profiles of patients with SARS-CoV-2 vaccine-induced SAT to controls, to assess whether there is an association between specific HLA genotypes and development of SAT. The relationship between HLA genotypes and the clinical course of SARS-CoV-2 vaccine-induced SAT was also evaluated. Methods: A case-control study was conducted in a Turkish tertiary care center. Fourteen patients with SARS-CoV-2 vaccine-induced SAT and 100 healthy controls were included. HLA-A, HLA-B, HLA-C, HLA-DQB1, and HLA-DRB1 frequencies were analyzed by next-generation sequencing. Results: The frequencies of HLA-B*35 and HLA-C*04 alleles were significantly higher in SARS-CoV-2 vaccine-induced SAT cohort when compared with controls (HLA-B*35: 13 [93%] vs. 40 [40%], p < 0.001; HLA-C*04: 13 [93%] vs. 43 [43%], p < 0.001, respectively). More severe thyrotoxicosis was seen in patients having HLA-B*35 and HLA-C*04 homozygous alleles (free thyroxine: 4.47 ng/dL [3.77-5.18] vs. 1.41 ng/dL [1.22-2.63], p = 0.048). Inflammation tended to be more severe in homozygous patients (C-reactive protein: 28.2 mg/dL [13.6-42.9] vs. 4.8 [1.2-10.5], p = 0.07). Conclusions: The frequencies of HLA-B*35 and HLA-C*04 alleles were higher in SARS-CoV-2 vaccine-induced SAT compared with controls. Homozygosity for HLA-B*35 and HLA-C*04 was associated with thyrotoxicosis and a greater inflammatory reaction. Our findings should be confirmed in studies of other populations.

Is there a familial predisposition to severe amiodarone-induced thyrotoxicosis? Report of two cases

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Role of plasmapheresis in the management of severe amiodarone-induced hyperthyroidism refractory to conventional medical treatment

Role of plasmapheresis in the management of severe amiodarone-induced hyperthyroidism refractory to conventional medical treatment

A case of severe thyrotoxicosis in acute setting presenting with hypercalcemia and deranged liver function test

A case of severe thyrotoxicosis in acute setting presenting with hypercalcemia and deranged liver function test

Abstract #1182688: Thyrotoxic Periodic Paralysis in an Active Duty Soldier

Thyrotoxic periodic paralysis (TPP) is a rare and life threatening presentation of thyrotoxicosis. Typically, patients present with severe hypokalemia, muscle weakness, and hyperthyroidism. It is reversible with judicious potassium replacement and antithyroid medication. Given the risk of cardiac arrhythmia and respiratory arrest, TPP is an important diagnosis to consider in the setting of thyrotoxicosis.

Abstract #1182431: Unilateral Massive Pleural Effusion as Manifestation of Severe Hyperthyroidism

Non-cardiogenic pleural involvement in hyperthyroidism is rare, with unilateral involvement being rarer still. We present the case of a patient with Graves’ disease (GD) with thyroid storm criteria who presented right pleural effusion compatible with exudate.

Severe thyrotoxicosis as initial presentation of gastric choriocarcinoma: a case report

BackgroundExtragonadal choriocarcinoma is rare and can be associated with hyperthyroidism when producing very high levels of human chorionic gonadotropin.Case presentationA 62-year-old Hispanic female presented with a 3-week history of shortness of breath, palpitations, extreme weakness, new-onset hot flashes, and right flank pain. Her physical examination was remarkable for tachycardia, hepatomegaly, hyperreflexia, and tremor; goiter was absent. Laboratory studies revealed increased lactate dehydrogenase, alkaline phosphatase, suppressed thyroid stimulating hormone, very elevated T4, and absent thyroid stimulating immunoglobulin. 18F-fluorodeoxyglucose positron emission tomography-computed tomography exhibited hepatomegaly with multiple large fluorodeoxyglucose-avid liver masses and a focus of fluorodeoxyglucose avidity in the stomach with no structural correlate. A thyroid scan (99mTcO4−) showed diffusely increased tracer uptake. She was started on propranolol and methimazole. Upon stabilization of severe thyrotoxicosis, upper endoscopy was performed, showing a ~ 5 cm bleeding lesion in the greater stomach curvature body; biopsy was consistent with choriocarcinoma; beta-human chorionic gonadotropin hormone was 2,408,171 mIU/mL. The patient received methotrexate followed by etoposide and cisplatin. Methimazole was titrated down, and upon liver failure the medication was stopped. The thyrotoxicosis was effectively controlled with antithyroid drug and concurrent chemotherapy. At ~ 1.5 months after initial diagnosis, the patient died due to bleeding/acute liver failure with coagulation defects followed by multiple organ failure.ConclusionsSevere thyrotoxicosis can represent an unusual initial presentation of metastatic choriocarcinoma in the setting of extreme elevation of beta-human chorionic gonadotropin. Primary gastric choriocarcinoma is an aggressive malignancy with very poor outcomes. The co-occurrence of severe thyrotoxicosis with advanced primary gastric choriocarcinoma and imminent liver failure complicates management options.

Increased Mean Cell Hemoglobin Concentration.

A 44-year-old man with a history of Grave disease presented with tachycardia, weight loss, and dysphagia. He was diagnosed with severe hyperthyroidism, diabetic ketoacidosis, and hyponatremia (Table 1). A complete blood count was performed and the hemoglobin, mean cell hemoglobin (MCH), and MCH concentration (MCHC) were flagged for review due to MCHC >37.5 g/dL. Smear review was normal, and the sample was prewarmed at 37°C with similar results. ... What are potential causes of an increased MCHC? Why does a markedly increased MCHC result serve as a flag for automated hematology analyzers? What is the most likely cause of the increased MCHC in this patient? The answers are below. Causes of high MCHC include red blood cell agglutination, hemolysis, lipemia, icterus, leukocytosis, spherocytosis, and electrolyte abnormalities (1). The high MCHC flag serves to detect interference in hemoglobin, hematocrit, mean cell volume, MCH, and MCHC. Hyponatremia can cause an artificially high MCHC and this was suspected in this patient. Hyponatremia can cause in vitro shrinking of the red blood cells due to osmolality differences between patient plasma and reagent diluent, leading to a falsely low hematocrit, low mean cell volume, and high MCHC (2–4).

Retrospective Evaluation of the Efficiency of Therapeutic Plasmapheresis in Thyrotoxic Patients

Background: Therapeutic plasma exchange (TPE) is a treatment method that can be used to provide euthyroidism before permanent treatment in patients with severe thyrotoxicosis, in cases of thyroid storm and in cases where antithyroid drug (ATD) cannot be used due to side effects or ineffectiveness. This study presented our results and experience on TPE in thyrotoxic patients.&#x0D; Material and Methods: The data of 10 patients who underwent plasmapheresis for thyrotoxicosis in Bursa Uludag University Faculty of Medicine Endocrinology Clinic were retrospectively analyzed and compared with the literature.&#x0D; Results: Ten patients, 6 female and 4 male, were included. The cause of hyperthyroidism was Graves’ disease in 8 patients and toxic multinodular goiter (TMNG) in 2 patients. It was observed that the reason for applying plasmapheresis in the patients was primarily due to toxic hepatitis. The mean number of plasmapheresis required to maintain euthyroidism was 4 (1-8). While no difference was found between the thyroid-stimulating hormone (TSH) results before and after TPE, free T4 (fT4) and free T3 (fT3) values were statistically significantly lower after TPE. It was observed that the leukocytes were considerably higher after TPE and the sodium and calcium values were markedly lower after TPE in the patients. After TPE, 7 patients underwent total thyroidectomy, 1 patient received radioactive iodine (RAI) treatment, and 2 were discharged with ATD treatment.&#x0D; Conclusions: TPE is an effective and safe treatment option that can be applied in cases where it is necessary to provide rapid euthyroidism before permanent treatments or non-thyroid surgical procedures or to treat life-threatening thyrotoxicosis. It requires experience in application and follow-up and provides rapid euthyroidism when performed in experienced centres.

Efficacy of preoperative therapeutic plasma exchange in patients with hyperthyroidism and factors affecting the number of sessions

Achieving preoperative euthyroidism in patients with hyperthyroidism for whom antithyroid drugs (ATDs) cannot be used for treatment is a serious clinical problem. We aimed to evaluate the effectiveness of therapeutic plasma exchange (TPE) in hyperthyroid patients scheduled for surgery and predictive factors for a high number of TPE sessions. We retrospectively analyzed the data of 21 patients with hyperthyroidism who were treated with TPE for preoperative euthyroidism in our institution. Pre- and post-TPE thyroid function tests were compared to assess efficacy. Binary logistic regression analysis was applied to determine predictors of patients requiring a high number of TPE sessions. All patients (20 patients with Graves' disease and 1 patient with toxic multinodular goiter; 12 women and 9 men; mean age 35.71 ± 12.38 years) had severe hyperthyroidism before TPE. The changes before and after TPE in fT3, fT4, and TSH levels were statistically significant (p < 0.001, p < 0.001, p = 0.002, respectively). The median number of TPE sessions was 8 (range: 1-24). Levels of fT3 before TPE were significantly higher in patients for whom higher numbers of TPE sessions were required (≥8) (OR: 1.427, 95% CI: 1.038-1.961, p = 0.028). Receiver operating characteristic curve analysis revealed an optimum cut-off value of 12.8 pg/ml for fT3 before TPE (91% sensitivity, 80% specificity, area under the curve: 0.927). TPE should be considered as an effective alternative treatment option that can be used to rapidly achieve euthyroidism before surgery when ATDs cannot be used. Pre-TPE fT3 levels of >12.8 pg/ml may be an independent factor predicting the need for higher numbers of TPE sessions (≥8).