Free T4 Research Articles

Outcomes of Radiofrequency Ablation for Autonomously Functioning Thyroid Adenomas-Mayo Clinic Experience.

Autonomously functioning thyroid nodules (AFTNs) constitute 5% to 7% of thyroid nodules and represent the second most common cause of hyperthyroidism following Graves' disease. Currently, radioactive iodine (RAI) and surgery are the standard treatment options, and both incur a risk of postprocedural hypothyroidism and other surgery and radiation-related complications. This work aimed at assessing the efficacy of radiofrequency ablation (RFA) as an alternative treatment option for resolving hyperthyroidism and the nodule volume rate reduction (VRR) and its associated adverse events. A total of 22 patients underwent RFA for a solitary AFTN. Seventy-two percent (n = 16) had subclinical hyperthyroidism, 9% (n = 2) had overt hyperthyroidism, and 18% (n = 4) were biochemically euthyroid on antithyroid medication. Average pretreatment TSH was 0.41 mIU/L (SD = 0.98) and free T4 1.29 ng/dL (SD = 0.33). Following a single RFA session, hyperthyroidism resolved in 90.9% (n = 20) and average VRR (61.13%) was achieved within 3 to 6 months following the ablation. Except for 1 nodule, none of the nodules grew during the follow-up period (16.5 months). Two patients (9%) developed transient tachycardia requiring short-term beta-blocker therapy, and 2 developed mild hypothyroidism requiring levothyroxine therapy. Two patients developed recurrent hyperthyroidism and elected to undergo lobectomy and repeat RFA respectively. No serious adverse effects were noted in this cohort. RAI and/or surgery represent the standard of care for toxic adenomas, but RFA shows excellent efficacy and safety profile. Therefore, at centers with RFA expertise, it should be considered an alternative treatment strategy, avoiding radiation and surgery-related complications.

Radiation Induced Thyroid Gland Changes in Nasopharyngeal Carcinoma Patient after Chemoradiotherapy in DR Sardjito Public Hospital

Objective: The objective of this study was to determine the volumetric change in thyroid gland in nasopharyngeal carcinoma patients after undergoing chemoradiotherapy that could alter thyroid gland function. Furthermore, this study correlates the mean dose effect towards the decrease in thyroid volume to predict the outcoming clinical signs of radiation induced hypothyroidism (RHT). Methods: This study consists of a cross sectional retrospective evaluation of multiplanar image that comprised three planes of axial, coronal, and sagittal of all NPC patients who underwent chemoradiotherapy and received a computed tomography (CT) imaging before and three months after completing treatment to the evaluate the alteration of thyroid volume. Result: A significant decreased in thyroid volume between pre and 3 months post chemoradiotherapy was obtained in the result with p value < 0.001, along with the mean dose of 58 Gray effect towards the decreased thyroid volume with p value = 0.005. Conclusion: Our study demonstrated that reduction in thyroid volume may be seen as early as 3 months after chemoradiotherapy in nasopharyngeal carcinoma that correlates with mean dose effect towards the thyroid volume. This volume changes also accompanied by the alleviation of free T3 and free T4 before and after chemoradiotherapy. Therefore, efforts should be made to do an early evaluation of radiation induced hypothyroidism (RHT). Early treatment and additional evaluation might be considered to enhanced the quality of life of the nasopharyngeal carcinoma patient. Highlights/Key points: Significant decreased in thyroid volume and its function among NPC patients evaluated by CT imaging and thyroid panel. Correlation of the mean dose volume effect towards the decrease in thyroid volume. Prediction of the outcoming clinical signs of radiation-induced hypothyroidism in NPC patients after chemoradiotherapy.

Defining Gestational Thyroid Dysfunction Through Modified Nonpregnancy Reference Intervals: An Individual Participant Meta-analysis.

Establishing local trimester-specific reference intervals for gestational TSH and free T4 (FT4) is often not feasible, necessitating alternative strategies. We aimed to systematically quantify the diagnostic performance of standardized modifications of center-specific nonpregnancy reference intervals as compared to trimester-specific reference intervals. We included prospective cohorts participating in the Consortium on Thyroid and Pregnancy. After relevant exclusions, reference intervals were calculated per cohort in thyroperoxidase antibody-negative women. Modifications to the nonpregnancy reference intervals included an absolute modification (per .1 mU/L TSH or 1 pmol/L free T4), relative modification (in steps of 5%) and fixed limits (upper TSH limit between 3.0 and 4.5 mU/L and lower FT4 limit 5-15 pmol/L). We compared (sub)clinical hypothyroidism prevalence, sensitivity, and positive predictive value (PPV) of these methodologies with population-based trimester-specific reference intervals. The final study population comprised 52 496 participants in 18 cohorts. Optimal modifications of standard reference intervals to diagnose gestational overt hypothyroidism were -5% for the upper limit of TSH and +5% for the lower limit of FT4 (sensitivity, .70, CI, 0.47-0.86; PPV, 0.64, CI, 0.54-0.74). For subclinical hypothyroidism, these were -20% for the upper limit of TSH and -15% for the lower limit of FT4 (sensitivity, 0.91; CI, 0.67-0.98; PPV, 0.71, CI, 0.58-0.80). Absolute and fixed modifications yielded similar results. CIs were wide, limiting generalizability. We could not identify modifications of nonpregnancy TSH and FT4 reference intervals that would enable centers to adequately approximate trimester-specific reference intervals. Future efforts should be turned toward studying the meaningfulness of trimester-specific reference intervals and risk-based decision limits.

Thyrotoxic periodic paralysis - a retrospective study from Southern India.

Thyrotoxic periodic paralysis is a rare manifestation of thyrotoxicosis. Here, we describe the clinical and biochemical features and treatment outcomes of this disorder. This retrospective study was conducted at a tertiary care centre in southern India. The clinical and biochemical features, treatment received, and therapeutic outcomes of all patients with thyrotoxicosis and acute flaccid paralysis without any other identifiable causes (cases for the study) were compared with an equal number of consecutively selected patients who presented with thyrotoxicosis but without features of paralysis (controls for the study) during the same period. In total, 41 cases and controls were included in this study. The proportion of males was 92.6% and 43.9% in the cases and controls, respectively. The mean age was 32.8 (±7.6) years (cases) and 39.7 (±11.3) years (controls). In the cases, 20% of patients presented without clinical thyrotoxic features. Graves' disease was the most common aetiology of thyrotoxicosis in both groups (92.6% of cases and 87.8% of controls). The prevalence of goitre was significantly higher among controls (90.2%) than among cases (53.7%). The mean serum potassium, free T4, total T4 and total T3 levels were significantly lower in the cases than in the controls. In these cases, two patients had an additional aetiology for persistent hypokalaemia, likely Gitelman's syndrome. This is one of the largest series of thyrotoxic periodic paralysis cases in India. In subjects with thyrotoxicosis, serum potassium, free T4, total T4 and total T3 levels were significantly lower in those with periodic paralysis than in those without.

SAT-560 Real or Not Real? An Elevated TSH

Abstract M.E. Sevilla-Alsina: None. A. Salvat: None. M. Saiful Islam: None. J. Yang: None. M.J. McPhaul: None. R.E. Weiss: None. Macro-thyroid-stimulating hormone (macro-TSH) is a rare, under-recognized cause of elevated thyroid-stimulating hormone (TSH) in presence of normal free T4 and T3 concentrations. The binding of glycoproteins, particularly antibodies, to TSH results in the formation of inactive macromolecular complexes, resulting in a falsely elevated TSH. Macro-TSH has very low biological activity but can represent a diagnostic challenge due to its measurement by TSH immunoassays. In many cases, it can be misdiagnosed as subclinical hypothyroidism or other causes of euthyroid hyperthyrotopinemia. As a consequence, patients may receive unnecessary treatment. We present a case with macro-TSH to guide the diagnostic approach and awareness of the condition. A 19-year-old male undergoing a “routine workup” was found to have a serum TSH of 85 mIU/l (Reference interval [RI] 0.36-4.0) measured by immunoassay (IA), with no specific symptoms and normal free T3 and T4. The patient was taking biotin supplements for hair growth. He was referred for endocrine evaluation and had suspended the biotin supplement several weeks prior to visit. He denied hypothyroid symptoms except for mild fatigue and chronic constipation. He was clinically euthyroid with an unremarkable physical exam, and the following test results were obtained: TSH 94.7 mUI/L (RI 0.40-4.50), Free T4 1.36 ng/dL (RI 0.8-1.8)., Total T3 93 ng/dL (RI 76-181), negative TPO, and thyroglobulin antibodies. Additional testing revealed a serum Free T4 direct by dialysis 1.3 ng/dL (RI 0.9-2.2), Alpha-Subunit 0.2 ng/mL (RI 0.1-0.5), Prolactin 11.5 ng/mL, cortisol 7.5 mcg/dL, and ACTH 13 pg/mL. Sequencing of the THRB gene was negative and ruled out resistance to thyroid hormone beta. Human anti-mouse IgG antibody (HAMA) testing identified no interference. The presence of TSH antibodies was assessed by demonstrating the presence of antibodies capable of immunoprecipitating radiolabeled TSH, absent from control serum. The positive TSH antibody test suggested the elevated TSH was due to macro-TSH. Gel filtration chromatography with a 23 x 3 cm Sephadex G-100 column demonstrated that a large proportion of the circulating TSH was contained within large molecular weight complexes, consistent with macro-TSH. The biochemical findings were discussed with the patient, avoiding initiating unnecessary treatment. Macro-TSH is an uncommon condition with a prevalence of 0.6-1.6%. Elevated TSH with normal free thyroid hormones in an asymptomatic patient raises the suspicion macro-TSH. Size fractionation chromatography of TSH is the gold standard method to confirm macro-TSH. Unfortunately, this test is unavailable commercially. The use of a TSH antibody test (available commercially at Quest Diagnostics), can help to identify immunoglobulins causing of macro-TSH, as presented in this case, preventing unnecessary medical intervention. Saturday, June 1, 2024

7617 Two Cases of Severe Beta-hCG-Mediated Hyperthyroidism with Gestational Trophoblastic Disease

Abstract Disclosure: A. Morvant: None. M. Mashayekhi: None. Introduction: Hyperthyroidism is most commonly caused by Graves’ disease and toxic nodules and affects 2.5% of the world’s population. Hyperthyroidism due to elevations in beta-hCG (b-hCG), which has thyroid-stimulating activity due to homology with TSH, is a rare process that requires high clinical suspicion. We present two cases of hyperthyroidism caused by severely elevated b-hCG due to gestational trophoblastic disease (GTD), with rapid resolution of hyperthyroidism after treatment of the underlying conditions. Clinical Cases Case 1: A 35-year-old at 28-weeks gestation presented with dyspnea, palpitations, and 6-pound weight loss over the prior month. Labs revealed b-hCG 5.2 million (0-5 mIU/mL), TSH <0.015 (0.35-3.6 mcU/mL), and free T4 2.42 (0.7-1.37 ng/dL). Imaging revealed extensive pulmonary lesions concerning for metastatic disease and a 2.4 cm ovarian mass. Due to worsening respiratory distress and the need to start chemotherapy urgently, she underwent Cesarean section to deliver the viable infant and take out the ovarian mass. Pathology confirmed choriocarcinoma. Methimazole was started post-operatively, and she started chemotherapy. Labs after cycle one of chemotherapy showed b-hCG 1.3 million, TSH <0.015, and free T4 1.46. The methimazole dose was decreased and ultimately stopped as free T4 levels decreased with subsequent chemotherapy cycles. After three cycles, labs showed b-hCG 4,652, TSH 1.55, and free T4 0.68. She was discharged without thyroid-targeting therapy. Case 2: A 33-year-old woman at 12-weeks gestation presented with nausea, vomiting, and 10-pound weight loss over 1 month. Labs showed TSH <0.015, free T4 2.39, and total T3 351 (58-160 ng/dL), which were thought to be due to hyperemesis gravidarum. Two months later she presented with vaginal bleeding and imaging showed an enlarged placenta with a moth-eaten appearance and theca lutein cysts concerning for partial molar pregnancy. Beta-hCG level was 3.3 million, TSH <0.015, free T4 1.76, and total T3 289. She underwent dilation and evacuation and pathology confirmed partial hydatidiform mole. Beta-hCG level decreased to 1.8 million and free T4 normalized after surgery, with b-hCG 3,300, normal TSH, and normal total T3 one month later. Conclusion: These cases highlight the importance of considering possible GTD when evaluating a patient with hyperthyroidism, particularly in women of childbearing age and cases of early pregnancy when the degree of hyperthyroidism seems out of proportion to that expected. Clinicians should consider checking a b-hCG level in consultation with an obstetrician when indicated. Treatment is aimed at the GTD and can yield rapid resolution of hyperthyroidism.

7314 The Thyroid Tetralogy: Hypothyroidism, Graves' Disease, AFTN, and Thyroid Cancer in a Single Patient

Abstract Disclosure: F. Sajid: None. F. Mohammadrezaei: None. K. Tiwari: None. J. Shapiro: None. F. Mohsin: None. T. Lin: None. Introduction: In this case, we explore a rare and complex situation involving a patient's shift from hypothyroidism to hyperthyroidism. This transition led to the diagnosis of Marine Lenhart Syndrome (MLS), an uncommon condition characterized by the coexistence of Graves' disease and autonomously functioning thyroid nodules (AFTNs). Adding to the complexity of the case, the patient was also diagnosed with papillary thyroid carcinoma (PTC). Case Presentation: A 47-year-old woman with a history of hypothyroidism, treated with levothyroxine for 14 years, presented with palpitations, weight loss, and insomnia for a few months. Her levothyroxine dose was gradually reduced and eventually discontinued by her primary care physician due to low TSH and high free T4 levels. Post-discontinuation, her symptoms were improving. Laboratory tests showed TSH 0.01 mIU/mL (0.39-4.08), Thyroglobulin (TG) 72 ng/mL (3-40), Free T4 2.5 ng/dL (0.8-1.8), Free T3 11.5 ng/dL (0.2-0.5ng/dL). Furthermore, Thyrotropin Receptor Antibody (TRAb), and Thyroid Peroxidase Antibody (TPO Ab) were positive leading to a diagnosis of Graves' Disease and initiation of Methimazole. After three months on Methimazole, her TSH remained suppressed with normalized free T4 and T3 levels. A thyroid ultrasound revealed bilateral nodules, with a calcified well-circumscribed nodule in the right mid-pole. A Radioactive iodine uptake (RAIU) scan showed a hyperfunctioning right mid-pole thyroid nodule. Fine-needle aspiration biopsy was consistent with Bethesda V, suggestive of possible malignancy. Consequently, she underwent a total thyroidectomy, with pathology confirming multifocal classic PTC, stage pT1bN0. Post-surgery, she developed hypothyroidism and was started on levothyroxine. Four weeks later, her TSH remain suppressed, other thyroid function tests and calcium levels were within normal range: TSH 0.01 mIU/mL, Free T4 1.0 ng/dL, TG 4.6 ng/mL, Thyroglobulin antibodies 1 IU/mL (less than or equal to 1), PTH intact 43 pg/mL (16-77), and Calcium 8.9 mg/dL (8.6-10.2). Conclusion: This case represents a complex and unusual medical scenario where a patient transitioned from hypothyroidism to hyperthyroidism, ultimately leading to the diagnosis of MLS in conjunction with PTC. The exact mechanism behind this transition is not fully understood. In the management of hypothyroidism, adjustments in thyroxine dosage are common, but significant tapering of the dose should prompt further investigation. The presence of PTC in AFTNs is considered rare, as AFTNs are typically characterized as hot nodules, implying they are hyperfunctioning and generally considered to be less likely malignant compared to cold nodules. This case underscores the need for comprehensive evaluation and follow-up in patients with thyroid disorders, especially when there is a change in thyroid function or the presence of nodules. Presentation: 6/3/2024

8087 A Case Series on Thyroid Eye Disease Precipitated by the COVID Vaccine in Patients with Long-Standing Primary Hypothyroidism

Abstract Disclosure: R. Hassan: None. J. Islam: None. Background: Thyroid eye disease (TED) is an autoimmune disease characterized by progressive inflammation and damage to the tissues around the eyes, especially extraocular muscle, connective, and fatty tissue. It is most commonly seen in patients with Graves' disease. Less commonly, TED may occur in patients with hypothyroidism. Case Discussion We are presenting a case series on TED precipitated by the COVID vaccine in three patients with known cases of long-standing hypothyroidism. References ranges:TPO Ab: (Ref range: <9.0 IU/mL)TSI: (Ref range: <=1.3 TSI index)TRAb : (Ref range: 0.00-1.75 IU/L)TSH: (Ref range: 0.450-4.500 uIU/mL)Free T4: (Ref range: 0.82-1.77 ng/dL)T3: (Ref range: 87.00 - 178.00 ng/dL) CASE 1: 59 year-old female patient with 18-year history of primary hypothyroidism on levothyroxine who presented with a 5 month history of progressive ocular symptoms of double vision and “puffy eyes” along with other thyrotoxic symptoms. These occurred after receiving her second COVID-19 vaccine. Labs showed elevated TSI and TRAb (3.0, 6.32). TPO antibody was within normal limits at 0.5. Patient had undetectable TSH and free T4 within normal range (162, 1.08). CASE 2: 70 year-old female patient with 25-year history of primary hypothyroidism on levothyroxine who presented with a 4 month history of eye discomfort, eyelid blistering and ocular swelling after she receiving her first dose of COVID-19 vaccine. She was found to have increased ocular pressure per her ophthalmologist. On lab work, she was found to have elevated TSI and TRAb (7.1, 2.60). TPO antibody was within normal limits at 0.8. TSH was undetectable and free T4 were within normal range (159.76, 1.49). CASE 3: 82 year-old female with 30-year history of primary hypothyroidism on levothyroxine who started developing diplopia and proptosis over a 6 month course after she received her first COVID-19 vaccine.Labs showed elevated TSI and TRAb (5.1, 17). Her TPO antibody was within normal limits at 0.4. Her TSH was undetectable, and free T4 was within normal limits (71.76, 1.32). All three patients were started on low-dose methimazole, prednisone, and completed an eight week infusion course of Teprotumumab (Tepezza) with subsequent improvement of proptosis and diplopia. Conclusion Providers should be aware that patients with long standing hypothyroidism, who suddenly require less to no thyroid hormone replacement along with new onset ocular symptoms could be developing TED. This had previously been thought to be solely associated with Graves’ Disease but now has been seen with an uptick in incidence in patients with chronic hypothyroidism during the COVID pandemic. This is likely related to immune response that been associated with vaccines. Presentation: 6/3/2024

6784 A Case of Euthyroid Hyperthyroxinemia due to Thyroid Binding Globulin Excess Syndrome

Abstract Disclosure: A.S. Iyer: None. Background: Congenital thyroid binding globulin (TBG) excess is a rare phenomenon associated with elevated serum total T3 and total T4 concentrations but normal serum concentrations of free thyroid hormones, with clinically euthyroid patients. While TBG excess can be caused by pregnancy, estrogen-secreting tumors, and estrogen therapy, congenital TBG excess follows an X-linked pattern, with hemizygous males most affected, and heterozygous females showing a spectrum of disease due to random inactivation of one X chromosome. Clinical Case: A 39-year-old Caucasian female presented as a referral from the Gastroenterology clinic due to concern for thyroid resistance syndrome. Symptoms included chronic constipation (improving with Miralax®), gradual weight gain of 8 pounds in one year, fatigue, and palpitations. She reported that her total thyroid hormone levels have always been elevated, with other thyroid labs remaining within normal limits, along with family history of similar labs noted in her two sons, father, and paternal grandmother. Upon initial encounter, TSH was 1.637 (0.430-3.550 uIU/mL), total T4 15.4 (4.8-11.7 ug/dL), total T3 231 (80-200 ng/dL), free T4 0.97 (0.70-1.25 ng/dL), free T3 3.2 (1.7-3.7 pg/mL), and albumin 4.2 (3.5-5.0 g/dL). The patient was not on oral contraceptive pills and she denied any pregnancies in the last three years. Thyroid ultrasound showed a normal-appearing homogeneous thyroid gland with a small cyst with colloid and no cervical lymphadenopathy. Initial differential diagnosis included TBG excess syndrome versus familial dysalbuminemic hyperthyroxinemia. Permission was obtained from the patient to access one of her son’s medical records from age 8-weeks old when he was also evaluated for abnormal thyroid labs. TSH was 2.144 (0.350-6.500 uIU/mL), total T4 28.2 (5.0-12.0 ug/dL), free T4 1.55 (0.8-1.8 ng/dL), and free T3 4.0 pg/mL (no reference available). Thyroid binding globulin was found to be elevated at 81 (12-26 mcg/mL) in her son and found to be elevated to 78.0 (13.5-30.9 mcg/mL) in this patient, confirming a diagnosis of TBG excess syndrome. Conclusions: TBG excess syndrome should be considered in the differential of patients with high total T3 and total T4 levels with normal levels of free T3, free T4, and TSH, especially in individuals who have a known family history and who have minimal or nonspecific symptoms. Definitive diagnosis will make further testing and treatment unnecessary. However, if these patients develop hypo- or hyperthyroidism, then use of TSH and free levels of T4 and T3 is necessary to direct management and avoid confusion. Reference: Pappa, T., and S. Refetoff. “Thyroid hormone transport proteins: Thyroxine-binding globulin, transthyretin, and albumin.” Reference Module in Neuroscience and Biobehavioral Psychology, 2017, https://doi.org/10.1016/b978-0-12-809324-5.03494-5. Presentation: 6/2/2024

6441 Hyperthyroidism in a patient with Lyme disease

Abstract Disclosure: J. Epstein: None. C. Berman: None. Background: Lyme disease is known to cause inflammation in many organs. There are few case reports in the literature that discuss the association between Lyme disease and thyroiditis. This case underscores the need to further research the association between Lyme disease and thyroid physiology. Clinical Case: A 15-year-old female with a history of polycystic kidney disease is referred to a pediatric endocrinologist for primary amenorrhea and hyperthyroidism. Initial thyroid function tests demonstrated suppressed TSH of 0.03 mIU/L with an elevated free T4 level of 4.0 ng/dL and total T3 of 437 ng/dL. The patient was asymptomatic with normal vital signs, and physical exam was normal without goiter, tremor, tongue fasciculations, or exophthalmos. Thyroid ultrasound demonstrated a mildly heterogenous appearance without nodules. Incidentally, Lyme disease was concurrently diagnosed based on a positive screen confirmed with immunoblot. There was no known tick exposure or rash, but the patient had recently spent time outdoors in upstate New York. Doxycycline was started for the treatment of Lyme disease and repeat thyroid tests one week later showed a decrease in free T4 and total T3 levels, although still elevated. Thyroid antibodies including thyroid peroxidase (TPO), thyroglobulin and thyroid-stimulating immunoglobulin (TSI) were negative. After finishing doxycycline treatment, she developed a hypothyroid state with a TSH of 6.39 mIU/L, free T4 of 0.6 ng/dL, and a normal total T3 of 148 ng/dL. Free T4 has since normalized however TSH remains elevated. The patient continues to be monitored closely without pharmacologic treatment. The evolution of this patient’s thyroid function is consistent with thyroiditis and appears similar to the course of Hashitoxicosis, however antibodies remain negative. There is literature that suggests molecular mimicry between Borrelia proteins and thyroid autoantigens due to amino acid sequence homology. Some Borrelial proteins are found to share antigenic properties with multiple thyroid related proteins, specifically the TSH receptor, TPO, thyroglobulin and sodium iodine symporter, potentially leading to thyroiditis. Three case reports describe adults with hyperthyroidism in the setting of Lyme disease, however in these cases thyroid antibodies (TPO +/- thyroglobulin) were positive. Two of these patients were asymptomatic, similar to our patient. This phenomenon has never been described in a pediatric patient and illustrates the need to consider Lyme disease as a potential cause of destructive, transient, thyroiditis. Presentation: 6/1/2024

6622 Severe Primary Hypothyroidism in a Child Presented as a Pituitary Tumour; a case Report

Abstract Disclosure: S.S. Awadalla: None. A 9-year-old patient showed up to the emergency department due to a headache that had been going on for a month without other symptoms and no neurological alterations. Complete blood count and glycemia were normal. A Cerebral MRI was requested and showed a pituitary adenoma. The patient was initially evaluated by neurosurgeons and referred to a pediatric endocrinologist. TSH, free T4, IGFI, and cortisol were evaluated, TSH was found to be high at 936 (normal, 0.4-4.2), free T4 < 0.4; suggestive of severe primary hypothyroidism. The case was analysed with the neurosurgery department, and a joint decision to start therapy with LT4 was taken, whilst monitoring the evolution of the pituitary adenoma. TSH and Free T4 were normal, and the MRI of Sella Turcica three months later showed complete pituitary normality. The presentation of this case is of relevance as the primary modality of treatment is thyroid hormone supply and not surgery. Interprofessional team integration is recommended for the treatment of patients with this condition. Presentation: 6/1/2024

7099 Severe Hypothyroidism from Potassium Iodide Supplements: A Case of Failure to Escape from Wolf- Chaikoff Effect

Abstract Disclosure: M.G. Hamilton: None. A. Kulkarni: None. P. Lekprasert: None. Introduction: The Wolf-Chaikoff effect (WCE) is a physiological response of the thyroid gland to supraphysiologic iodide levels. Failure to escape the WCE can lead to thyroid dysfunction, and we present such a case in a patient with Hashimoto’s thyroiditis taking high-dose potassium iodide (KI). Case Description: A 44-year-old female with hypothyroidism secondary to Hashimoto’s thyroiditis presented with 10-pound weight gain, extremity swelling, fatigue, and abnormal menstruation. She was prescribed Levothyroxine several years ago but stopped taking it shortly after as she felt no improvement. On physical exam, she was bradycardic with heart rate of 58 bpm. There is no goiter but dry skin and edematous lower extremities. Labs revealed TSH of 127 pg/mL (0.35-4.94), free T4 0.1ng/dL (0.8-1.8), TPO Ab 645 (<9) IU/mL in comparison to her labs 2 months ago of TSH 11 pg/mL and free T4 0.9 ng/dL. Suspicion for worsening hypothyroidism from Hashimoto’s was low given this dramatic change on labwork and clinically. On further questioning, she had been taking KI 130 mg/day (Iodine 100 mg, daily requirement 150 mcg/day) as advised by her homeopathic doctor. The supplements were stopped, and she was re-started on Levothyroxine. After 8 weeks, she reported improvement of symptoms and weight loss. TSH is normal at 3.54pg/ml and free T4 1.2 ng/dL. Discussion:The WCE serves as a protective mechanism to decrease thyroid hormone production in the setting of high iodide levels to prevent development of hyperthyroidism. WCE is explained by the formation of Iodopeptides inhibits thyroid peroxidase (TPO) mRNA and protein synthesis resulting in an inhibition of thyroglobulin iodination. WCE is temporary and expected to wane over a few days to weeks and is known as the Wolf-Chaikoff escape due to down regulation of the sodium iodine symporter (NIS) thereby decreasing the intrathyroidal inorganic iodine concentration and permitting normal TPO activity. Rarely, failure to escape WCE can lead to hypothyroidism due to continued suppression of thyroid hormone synthesis. Risk factors include underlying thyroid diseases i.e. Hashimoto’s or other causes of thyroiditis, use of Amiodarone, Lithium or Iodine-containing radiocontrast media and KI supplements. In our case, Hashimotos’ thyroiditis predisposed her to thyroid dysfunction and failure to escape from WCE after taking high-dose KI supplements causing severe hypothyroidism. Thus, this report highlights that in clinical practice, especially in patients with pre-existing thyroid dysfunction, a significant TSH increase, a high suspicion index is needed to investigate for other causes like concurrent use of iodine-containing food/drug leading to the failed escape from WCE apart from verifying compliance to thyroid replacement therapy. Presentation: 6/3/2024

SUN-010 A Unique Case of Central Hypothyroidism Due to Infective Endocarditis Presenting as Myxedema Coma

Abstract B. Godasi: None. N.R. Jannareddy: None. C. Lovato: None. Introduction: Central hypothyroidism is characterized by a deficiency of thyroid hormone either by insufficient production of thyrotropin releasing hormone and/or insufficient production of thyroid stimulating hormone from the pituitary. Acquired central hypothyroidism can result from invasive or compressive lesions of the sella, iatrogenic causes, trauma, vascular accidents, autoimmune diseases, infiltrative diseases, and infections. Clinical Case: A 31-year-old Hispanic female patient with a past medical history of end-stage kidney disease on hemodialysis, hypertension, non-ischemic cardiomyopathy, and cirrhosis was transferred from an outside hospital to our facility for MSSA endocarditis with multiple cerebral and pulmonary embolic abscesses from an infected dialysis catheter, new-onset seizures, and right frontal lobe intra-parenchymal hemorrhage secondary to mycotic aneurysm. At the time of presentation, the patient’s TSH was mildly elevated at 6.710 uIU/ml (n 0.270-4.20 uIU/ml), and free T4 was normal at 1.3 ng/dl (n 0.9-1.7 ng/dl). Eight days later, repeat TSH was inappropriately normal at 3.300 uIU/ml with undetectable free T4 < 0.2 ng/dl. She was discharged from the hospital without any levothyroxine supplementation. She was hospitalized 3 weeks later due to hypotension and somnolence. She developed bradycardia and hypoxia. Repeat labs showed undetectable free T4 < 0.2 ng/dl and mildly high TSH 5.710 uIU/ml. The patient was started on treatment for myxedema coma with IV hydrocortisone, IV levothyroxine, and IV liothyronine. The patient began to improve clinically and was transitioned to oral levothyroxine and was titrated off hydrocortisone. However, her free T4 levels did not improve into the normal range, likely secondary to poor absorption from gut edema and anasarca. She was transitioned back to IV levothyroxine with normalization of free T4 levels. Morning serum cortisol was 34.8 µg/dL (n 6.0-18.4 µg/dL) and prolactin was 18.7 ng/ml (n 4.8-23.3 ng/ml). MRI of the brain without contrast did not show a pituitary mass. However, the pituitary was T1 hyperintense and thought to potentially reflect sequelae of prior apoplexy/hemorrhage, prior hypophysitis or protein deposition. We suspect that the patient had a septic embolism to the pituitary that resulted in central hypothyroidism. The patient ultimately died from other medical complications during her hospitalization. Discussion: This is a rare case of central hypothyroidism resulting from infective endocarditis. To our knowledge, there is only one other case of endocarditis that resulted in hypopituitarism. Our case is unique as it resulted in an isolated central hypothyroidism. Physicians should be aware of potential pituitary complications of endocarditis, as these hormonal deficiencies can cause significant morbidity and mortality. Sunday, June 2, 2024

5128 Role of Plasmapharesis- A Tale of Two Thyroid Storms

Abstract Disclosure: Z. Zhang: None. S. Joseph: None. A.M. Kodali: None. D. Eagerton: None. Background: Thyroid storm is an acute life threatening endocrinological emergency. The standard treatment for a thyroid storm is antithyroid medication, iodine, beta blockers and corticosteroids. However, when patients are refractory to standard treatment, plasmapheresis may be an effective and safe intervention. Case 1: A 49-year-old male with typical symptoms of hyperthyroidism, presented with a Ventricular tachycardia arrest. After the return of spontaneous circulation, he was febrile, and developed new onset atrial fibrillation (AF) and Amiodarone drip was started. Physical exam showed a thin gentleman with an enlarged thyroid. ECHO showed LVEF 50% with moderate to severe dilatation of left atrium and mild mitral and tricuspid valve regurgitation. CT abdomen/pelvis and CTA chest did not show any pathology. Labs showed TSH of 0.02 (reference range: 0.465-4.68); Free T 4 >6.99 (reference range: 0.78- 2.19). He was started on Propylthiouracil (PTU), Hydrocortisone, Potassium Iodide, and Cholestyramine. His blood pressure was too low to tolerate a beta blocker. He developed increased liver enzymes thought to be due to shocked liver. PTU was switched to Methimazole due to less risk of hepatotoxicity. A Thyroid Stimulating immunoglobulin was 13.40 (reference range 0.00-0.55), confirming Graves’ disease. He developed multiorgan failure and plasmapheresis was initiated. His Free T4 level prior to his first apheresis was still >6.99 but improved to 6.20 after two days. After the second session, free T4 level drastically improved to 2.65. He sustained a level of 2.09 until his hospital discharge. Case 2: A 59-year-old male with untreated hyperthyroidism and AF, who presented with shortness of breath. He was tachycardic, febrile and developed AF with rapid ventricular response. A TSH and free T4 level showed <0.02 (reference range: 0.465-4.68); and >6.99 (reference range: 0.78- 2.19), respectively. Physical exam shows a cachectic man with an enlarged thyroid. ECHO showed reduced ejection fraction of 35% with biventricular failure. He was initially started on PTU, Potassium Iodide, hydrocortisone and esmolol drip and eventually Cholestyramine. Patient developed multisystem organ failure and PTU was switched to methimazole due to continued deterioration of his liver enzymes. Plasmapheresis started with a total of 3 sessions. His free T4 improved from 4.32 to 3.59 by the second session. Round three was performed when his Free T4 increased back to 4.56. Unfortunately, he had a sudden decline in mentation and CT head showed an acute/subacute left anterior parietal stroke and after family discussion, was palliatively extubated and expired. Discussion: This case series shows two cases of thyroid storm treated with plasmapheresis and had two stark contrasts. Further studies should be done to elucidate the usefulness of plasmapheresis for thyroid storm when refractory to standard of treatment. Presentation: 6/2/2024

6771 New onset Graves’ Disease in a Patient with Hashimoto's Thyroiditis and Positive Thyroid Peroxidase Autoantibodies. Case Report

Abstract Disclosure: M.M. Eid: None. J.L. Zapater: None. Introduction: Hashimoto’s Thyroiditis (HT) and Graves’ Disease (GD) are the most common thyroid autoimmune disorders. Transition of GD to HT is common, but transition of HT to GD is rare. Case: A 55 year old, female with depression, HTN and fibromyalgia. She was referred for evaluation of chronic fatigue and reduction in functional capacity. Five years earlier, she had also been evaluated for fatigue. Labs at that time: TSH 3.80 µIU/ml (0.35-3.74 µIU/ml), free T4 0.8 ng/dl (0.76-1.46 ng/dl), thyroid peroxidase antibody (anti-TPO) 605.6 U/ml (0-60 U/ml), and anti-thyroglobulin antibody (anti-TG) 37.2 U/ml (0-60 U/ml). Subclinical hypothyroidism was diagnosed, but no levothyroxine was initiated. Her TSH was found to be normal in 2019 and 2021. At the current clinical encounter, other than fatigue she denies weight/voice change, tremor, palpitation, anxiety, recent flu like illness or radiation exposure, neck swelling/pain, heat intolerance, or difficulty swallowing. Her daily medications are amlodipine 10mg and duloxetine 20mg. She had menopause 2 years ago. She has no known allergy. She has a brother with rheumatoid arthritis. She denies smoking or alcohol consumption. On exam, vital signs are normal, and BMI is 28.1. There is diffuse, firm thyromegaly without a palpable nodule. There is no cervical lymphadenopathy, tremor, neck tenderness, exophthalmos, or lid lag. Creatinine, liver enzymes are normal but hemoglobin is 9gm/dl. Anti-tissue transglutaminase and anti-gliadin antibodies were negative. Her thyroid labs were: TSH <0.008 uIU/ml, free T4 1.06ng/dl, free T3 4.07 pg/ml (2.3-4.2 pg/ml), total T3 1.74 ng/ml (0.60-1.81 ng/ml), anti-TPO antibody 12,414 U/ml, anti-TG antibody 22 U/ml, thyrotropin receptor antibody (TRAB) 15.24 IU/L (0-1.75 IU/L), and thyroid stimulating immunoglobulin (TSI) 331% (<130%). Thyroid uptake scan showed 49% iodine-131 uptake in symmetric and homogenous uptake, and no hot or cold nodules. GD was diagnosed, methimazole 5mg daily was initiated. Conclusion: Our case had subclinical HT with positive anti-TPO antibodies 5 years preceding the onset of GD. Causes of autoimmune conversion are not well understood. Viral infection or radiation exposure in genetic susceptible patients have been assumed as triggers (1). The blocking and stimulating action of TRAB on TSH receptors is considered as a possible mechanism of switching between hypothyroidism and hyperthyroidism. Clinical and biochemical evaluation for possible conversion to GD in patients with HT is recommended (2).

6618 Risks for Cardiovascular Comorbidities Associated with Desiccated Thyroid Extract Administration

Abstract Disclosure: S.C. De La Torre: None. C. Godar: None. K. Flynn: None. A.A. Patel: None. D. Maxwell: None. M.K. Shakir: None. T.D. Hoang: None. Introduction: Levothyroxine (LT4), synthetic thyroid hormone (T4), is considered the standard of care for the management of hypothyroidism based on the current American Thyroid Association (ATA) guidelines. However, there is a small subset of patients demonstrating symptomatic improvement with desiccated thyroid extract (DTE), which is composed of desiccated porcine thyroid containing T4 and triiodothyronine (T3). Limited data or studies are available exploring long-term cardiovascular effects associated with DTE use. In this retrospective review, we aim to identify possible cardiovascular comorbidities associated with DTE use. Methods: The charts of 77 patients at a tertiary hospital center (64 females and 13 males) over the age of 18 who were prescribed DTE were reviewed. Data collected include duration of treatment, dose of treatment, pre-treatment and current weight, blood pressure (BP), TSH, free T4, and total T3 levels. New cardiovascular and other events following initiation of treatment (hypertension, coronary artery disease (CAD), myocardial infarction (MI), stroke, transient ischemic attack (TIA), atrial fibrillation, type 2 diabetes, fractures) were also obtained. Averages, medians, and totals of patient data were used for analysis. Results: Average patient age was 54 years, average duration of therapy was 77.5 months, and median DTE dose was 75 milligrams per day. Review of chart documentation from DTE initiation compared to current values identified a 2.5% increase in weight, 3.6% increase in systolic BP, 0.8% decrease in diastolic BP, 60.9% decrease in TSH, 5.2% decrease in free T4, and 14.4% increase in total T3. 19.5% patients (15 total, 80% of which were female) had recorded new cardiovascular events at any time following initiation of therapy. 15 patients developed HTN, 5 developed CAD, 2 developed atrial fibrillation, 5 developed type 2 diabetes, 5 new fractures, 0 MI, 0 stroke, and 0 TIA. Conclusion: These results demonstrate new cardiovascular events in our study population following the initiation of DTE, but it is unclear whether these events were directly associated with DTE use versus other factors based on our available data. Limitations of our study include small study size, uneven gender distribution, and data significance would be improved with comparison to a control group. Additional studies are needed to further evaluate long-term cardiovascular risk factors associated with DTE use. Presentation: 6/2/2024

6575 From Tonsils to the Thyroid: A Rare Case of Acute Suppurative Thyroiditis in an Immunocompetent Adult

Abstract Disclosure: F. Sajid: None. A. Mubashir: None. F. Mohsin: None. M. Sattar: None. Introduction: Acute suppurative thyroiditis (AST) is a rare infection of the thyroid gland due to its high vascularity, protective encapsulation, and high iodine content. Most AST cases occur in children with anatomical aberrations or in immunosuppressed adults. Here, we describe a case of AST in an immunocompetent woman. Case: A 54-year-old woman with no medical history presented to the emergency department due to dyspnea, dysphagia, and odynophagia for two days. She reported a four-day history of sore throat, fever, and chills. She was saturating well on room air but was sitting in a tripod position. She had erythema, swelling, tenderness to palpation in the anterior neck with a hoarse voice, and moderate trismus. Nasopharyngoscopy revealed no mass, but the scope could not pass beyond the velum due to edema. The patient’s condition quickly deteriorated, necessitating emergent intubation for acute hypoxic respiratory failure. After intubation, the patient had cardiac arrest with asystole requiring resuscitation and successful ROSC. The initial CT scan showed extensive soft tissue abnormalities in the nasopharynx and parapharyngeal tissues, extending to the thyroid gland and mediastinum with the possibility of developing abscesses. A thyroid ultrasound showed a heterogeneous thyroid gland without nodules or increased vascularity. Treatment commenced with ampicillin-sulbactam. Laboratory results showed Free T4 of 4.74 ng/dL (0.58-1.64), TSH 0.03 MCIU/mL (0.39-4.08), Total T3 1.56 ng/dL (0.72-1.35), WBC 19.3 K/UL (4.8-10.8), and elevated ESR and CRP levels. Thyroid-stimulating Immunoglobulin (TSI), Thyroid Peroxidase (TPO) Antibody, and Thyrotropin Binding Inhibitory Immunoglobulin (TBII) were negative, making AST the top differential. Methimazole was initiated due to concerns of thyroid storm, but it was quickly tapered due to a significant decrease in Free T4 levels and suspicion of AST. A repeat CT scan revealed more defined abscesses along the bilateral pharyngeal walls extending to the thyroid bed. The patient underwent bilateral tonsillectomy and drainage of the abscesses. She was extubated the following day. Cultures from the abscesses grew rare Klebsiella pneumoniae, susceptible to Ampicillin-sulbactam. A barium swallow on day 14 showed no evidence of a pyriform sinus fistula. She was discharged on day 15 with Augmentin for 7 days. On discharge, free T4 decreased to half (2.39 ng/dL), and Total T3 normalized (1.08ng/dL). Conclusion: This case presents a rare instance of AST in an immunocompetent patient without anatomical anomalies, stemming from the spread of peritonsillar and parapharyngeal abscesses into the thyroid bed. AST should be considered in cases of deep neck infections, as it is a potentially life-threatening disease. It is crucial to identify and treat AST early to prevent complications. The primary treatment involves antibiotics, incision, and drainage. Presentation: 6/1/2024

12214 Metastatic Functional Thyroid Carcinoma As An Unusual Cause Of Hyperthyroidism

Abstract Disclosure: S. Jimenez Salazar: None. N. Aristizabal Henao: None. C. Aguilar Londoño: None. N. Buitrago Gómez: None. S. Saldarriaga Betancur: None. D.L. Beltran: None. J.L. Torres: None. Background: Differentiated thyroid carcinoma (DTC) represents the most prevalent endocrine neoplasm. Less than 10% present distant metastases, with the lung (50%), and skeleton (25%) being the most frequently affected sites. The location of bone metastases predominates in the spine and pelvis; usually as osteolytic lesions, being more frequent in follicular thyroid cancer (FTC) (7-28%) than in patients with papillary thyroid cancer (PTC) (1.4-7%). In rare cases this metastasis can be functional and trigger a thyrotoxicosis syndrome with or without recombinant human TSH injections prior to therapy with 131-I. Clinical case: 59-year-old woman with a history of bone metastatic follicular thyroid cancer (FTC) presented with 1 month of palpitations, 4 kg weight loss, non-dysenteric diarrhea and progressive dyspnea. Her FTC had been diagnosed 8 years prior her consultation. In that time iodine refractoriness was considered due to the progression of bone lesions, and Sorafenib 800 mg per day was initiated, which was not tolerated due to severe dermatological manifestations, and the patient decided not to continue with TKI therapy. Since then, she has been treated with zoledronic acid and local radiotherapy as part of palliative care. On physical examination, she was tachycardic (150 bpm), and hypertensive (BP 160/100 mmHg). A suppressed TSH (<0.01 uUI/mL, n: 0.4-4 uUI/mL) with elevation of thyroid hormones (free T4 3.99 ng/dL, n: 0.8-2 ng/dL and total T3 480 ng/dL, n: 45-140 ng/dL) was documented, associated with a patient who had required a dose adjustment of levothyroxine from 700 mcg to 350 mcg weekly 2 months prior to admission. Additionally, she had a significantly elevated thyroglobulin (>5000 ng/mL, n: 0.1-64.1 ng/mL) with undetectable antithyroglobulin antibodies (1.09 UI/mL, n: 0-4.11 UI/mL). Considering the history of total thyroidectomy and the high tumor burden, secondary thyrotoxicosis due to functioning bone metastases of DTC was considered. Levothyroxine was discontinued, and propranolol was initiated for the control of adrenergic symptoms, along with methimazole, cholestyramine, and systemic steroids to control thyroid hormone production. 3 days after therapy adjustment dyspnea, palpitations, and thyroid function tests improved significantly (free T4 1.43 ng/dL, n: 0.8-2 ng/dL and total T3 178 ng/dL, n: 45-140 ng/dL). A new administration of therapy with 131-I 200 mCi was indicated. Antithyroid therapy and beta-blockers were continued with sustained biochemical control. Conclusion: Functional bone metastases of FTC can lead to high morbidity and mortality. Treatment consists of surgical cytoreduction of any large accessible metastatic lesion, therapy with 131-I, and high-dose antithyroid drugs to control hyperthyroidism. It is important to avoid the use of recombinant human TSH due to the risk of secondary thyrotoxicosis following its administration. Presentation: 6/2/2024

7650 Thionamide Induced Pancreatitis and Agranulocytosis, a Rare Case of Concurrence

Abstract Disclosure: J. Lin: None. J. Shariff: None. Introduction: Thionamides are considered first line in the treatment of Graves’ Disease due to their efficacy and safety. We present a case of Graves’ in which methimazole resulted in not only agranulocytosis but also pancreatitis. Case Report: A 29yo female was diagnosed with Graves’ 5 months postpartum by her PCP. Her labs at diagnosis revealed a TSH <0.01 uIU/mL, free T4 of 6.4 ng/dL, and positive TRAb. She was started on methimazole 10mg and propranolol 20mg three times a day by her PCP. One month after starting treatment, she presented to the ED due to throat pain/fevers and was diagnosed with tonsilitis. She was given a 10mg dose of dexamethasone and sent home with antibiotics. No labs were drawn that visit. She went to her PCP 3 days later due to persistent symptoms and nausea/vomiting. A CBC revealed she had a WBC of 0.7 K/uL and an absolute neutrophil count (ANC) of 0.1 K/uL. Her last dose of methimazole had been the day prior to seeing her PCP. It was recommended she be seen in the ED due to concern for agranulocytosis where she was started on antibiotics and a CT abdomen pelvis with contrast revealed she had acute pancreatitis. She was admitted and started on filgrastim 5mcg/kg daily for thionamide-induced agranulocytosis. Her pancreatitis improved with conservative measures. Her propranolol was resumed at 30mg three times a day with symptom improvement. On her fifth hospitalization day, her ANC had recovered to 2.22 K/uL, WBC was 6 K/uL. Her free T4 was 1.65 ng/dL, free T3 4.1 pg/mL, TSI >40 IU/L. This change was suspected to be from propranolol, steroids, iodine load from her CT, and prior methimazole use. It was strongly recommended she pursue surgery that hospitalization given inability to treat her Graves’ medically. The patient refused, stating she wished to consider her options further outpatient. She would be seen one week later in a satellite ED. Her free T4 was 5.9 uIU/mL, T3 >30 pg/mL, TSH <0.010 uIU/mL. She left against medical advice. She subsequently declined further endocrine follow-up. Clinical Lessons: Thionamide-induced agranulocytosis is a rare but known complication of use, with some studies showing a prevalence as low as 0.2-0.5% [1]. Pancreatitis is a lesser-known complication of thionamides. There are several case reports of its occurrence, with the European Medicines Agency even listing it in the potential adverse reaction. Absolute risk of occurrence remains low, some studies showing <0.4% [1]. This case shows a rare concurrence of two uncommon complications from thionamide use and brings awareness to both pancreatitis and agranulocytosis as potential adverse events.

7504 A Case of Methicillin Sensitive Staphylococcus Aureus Thyroiditis

Abstract Disclosure: K. Patel: None. P. Kachhadia: None. S. Khan: None. F. Akanbi: None. A. Abu Limon: None. S.A. Aldasouqi: None. Introduction: Acute suppurative thyroiditis refers to bacterial infection of the thyroid gland. It is rare as the thyroid gland is typically protected from infection due to isolation of the gland from neighboring structures as well as its rich blood supply and adequate lymphatic drainage. It shares characteristics with subacute and autoimmune thyroiditis which make for difficult diagnosis. Here we present a case of acute suppurative thyroiditis in the setting of methicillin sensitive staphylococcus aureus (MSSA) bacteremia. Case Presentation: We have a 45 year old gentleman with a history of polysubstance abuse who was admitted after a drug overdose. He was being treated for rhabdomyolysis and approximately ten days after admission he became febrile with Tmax 103.3 Farenheit with a sore throat and dysphagia. Workup showed leukocytosis, ESR 86 mm/h [0-15], CRP 45.5 mg/dL [0-1], blood cultures with MSSA, negative viral upper respiratory panel, throat culture, Syphilis and HIV testing. He had a positive Hepatitis C antibody without a detectable viral load. Echocardiogram ruled out vegetations. He was treated with cefazolin. CT neck was obtained and showed thyroid enlargement. Subsequent ultrasound showed heterogeneous echotexture and increased color flow and a left inferior pole nodule 2.3 x 2.1 x 2.0 cm. Thyroid labs showed TSH 0.16 [0.35 - 4.01 u[IU]/mL,] Free T4 3.91 ng/dL [0.61 - 1.37], TPO <0.3. The nodule was biopsied and endocrinology was consulted. On exam thyroid was nontender. He was started on beta blockers and thyroid labs were monitored. TSI and TRAB were negative. TSH, Free T4 and Free T3 improved to normal range. Nodule biopsy results showed benign follicular cells with abundant acute inflammation suggestive of an abscess. Metronidazole was added after biopsy results. Post antibiotic therapy, CRP improved to 1.7 mg/dL. Discussion/Conclusion: Incidence of acute suppurative thyroiditis has been published as occurring <1% of all thyroid diseases. One systematic review found 200 cases reported from January 2000 to January 2020. Prior case reports have described acute suppurative thyroiditis in adult patients with prior thyroid gland pathology or an immunocompromised state and some demonstrated a correlation with intravenous drug users. The most common culprits include Staphylococcus spp, Streptococcus spp, Salmonella spp, Escherichia spp. Management includes antimicrobial therapy and/or needle aspiration. Non-responders can undergo incision and drainage of abscess or thyroidectomy. Mortality was reported in about 8% of the reported 200 cases. In our patient, his history of drug use and Hepatitis C likely made him prone to infection. Although there was no description of pus during biopsy, pathology suggested acute inflammation. This along with elevated inflammatory markers led to the diagnosis. This case highlights an uncommon but potential cause of thyroiditis. Presentation: 6/3/2024