T4 Levels Research Articles

7618 Thyroid Nodules, Normal Thyroid Levels, and Chronic Anxiety: A Case for Sub-Clinical Toxic Multinodular Goiter

Abstract Disclosure: C.M. Barrera: None. Introduction: Chronic anxiety and panic disorders, as described in the Diagnostic and Statistical Manual of Mental Disorders (DSM-V), are the most common psychiatric conditions. Hyperthyroidism is a known cause of both chronic anxiety and panic disorder. Case 1: A 36-year-old overweight Latin female is referred for evaluation of multiple thyroid nodules. The thyroid ultrasound was heterogeneous, with multiple bilateral nodules. In her history, the patient has chronic anxiety with panic attacks resulting in frequent emergency room visits. The TSH and T4 levels were TSH 0.59 mIU/L (0.40-4.5) and T4 10.7 mcg/dL (5.1-11.9). An I[1]23- Thyroid Scan showed a hot nodule with mild suppression and an uptake of 31.8% (The top limit is 35%). The patient started methimazole 2.5 mg daily, and after two months, her chronic anxiety and panic attacks resolved. Post-methimazole TSH rose to 1.18 mIU/L, and T4 10.0 mcg/dL and she has weaned off anxiety medications. Case 2: A 49-year-old overweight Latin female is referred for increased thyroid nodules. She complained of six months of tachycardia and anxiety. The TSH and T4 levels were TSH of 0.828 mIU/L (0.40-4.5) and T4 of 7.9 mcg/dl (4.5-12.0). An I[1]23-Thyroid Scan showed no dominant hot or cold nodules, with an uptake of 36.4% (The top limit is 35%, within normal error limits). She started methimazole 5 mg daily, resolving her tachycardia and anxiety within five weeks. Post-methimazole TSH was 1.64 mIU/L (0.45-4.5), and T4 6.7 mcg/dL (4.5-12.0). Case 3: A 60-year-old overweight Latin female is referred for evaluation of multiple thyroid nodules of ten years. She complained of chronic anxiety and panic attacks for two years. The TSH and T4 were normal at TSH 0.36 mIU/L (0.35- 5.50) and T4 9.7 mcg/dL (4.5-10.9). The thyroid ultrasound showed multiple bilateral nodules. An I[1]23-Thyroid Scan showed a suspected hot nodule without appreciable suppression and an uptake of 33% (The top limit is 35%). The patient started methimazole 5 mg daily. After eight weeks, she reported the resolution of most of her chronic anxiety with post-methimazole TSH 2.39 mIU/L and T4 7.1 mcg/dL (4.5-12.0). Discussion: The normal range of TSH, typically from 0.4-4.5 mIU/L, is calculated by measuring the TSH levels among a normal population. The group range then determines the laboratory reference range. This contrasts with individual values, which have a narrower range, suggesting that each person has a unique thyroid level. This suggests that TSH levels at the extremum, associated with hyperfunctioning nodules contributing to a rise in uptake, may not be normal for that patient and may explain the anxiety and other symptoms. Learning Points: Evolving multiple autonomous thyroid nodules lowers TSH levels while raising thyroid uptake. Symptoms of chronic anxiety and panic attacks can predate abnormal thyroid levels and resolve with low-dose methimazole. Presentation: 6/1/2024

12611 The Thyroid Adapts Remarkably to Overnutrition to Mitigate Hypothyroidism

Abstract Disclosure: J. Rampy: None. A. Torres Manzo: None. K. Hoffsmith: None. M.A. Loberg: None. H. Wang: None. V.L. Weiss: None. N. Carrasco: None. Obesity affects >40% of the U.S. population and is one of today’s biggest public health concerns. Losing weight is challenging, and maintaining weight loss even more so, owing to the many biochemical and hormonal changes that occur in the pathogenesis of obesity, some of which do not reverse after weight loss. Thyroid hormones (THs) have far-reaching effects on whole-body energy balance. Their synthesis and release by the thyroid are finely regulated by central mechanisms to control serum TH levels. THs are also regulated by nutrient sensing, so that their levels modulate energy expenditure to match energy intake. Given the reciprocal and fine-tuned relationship between THs and energy balance, one would expect strong upregulation of TH levels to counteract diet-induced weight gain, but this is not consistently reported in obesity studies. Thus, we hypothesized that overnutrition impairs thyroid function, preventing a sustained increase in TH levels. We tested this hypothesis in male C57Bl/6J mice fed a high-fat diet and sucrose water. Strikingly, overnutrition decreased T4 levels after just 5 days—and within 3 weeks, we observed mild hypothyroidism, with increased thyroid stimulating hormone (TSH) levels and goiter. After 6 weeks, intrathyroidal T4 levels were significantly decreased, whereas the expression of the TH precursor thyroglobulin (TG) was unchanged, despite high TSH stimulation. Furthermore, we found increased expression of several ER stress-related proteins, including BiP, p-eIF2α, and PDI. These results suggest that TG was not upregulated because overnutrition-induced ER stress impaired protein translation. Remarkably, even though T4 levels were low, the thyroid maintained normal T3 levels, likely due to the pronounced histological and vascular changes we observed, which should promote TH availability. Some changes were consistent with the classical growth effects of TSH stimulation, while others were likely due to upregulation of adrenomedullin 2, a TSH-responsive angiogenic vasodilator. Preliminary studies in female mice showed similar results. Notably, we have observed similar histological changes in human thyroids, which strongly correlate with BMI. Collectively, our results, despite the unchanged T3 levels, are consistent with a struggling thyroid and a mildly hypothyroid state. Existing data suggest that low T4 can itself be problematic, particularly in metabolic tissues that generate T3, the more biologically active form, from T4 to levels beyond those of the T3 available from the bloodstream. Reversibility of this state is being investigated in ongoing experiments. The causal role that overnutrition plays in thyroid impairment and decreased TH availability in the pathogenesis of obesity has scarcely begun to be elucidated. Our work sheds new light on how overnutrition changes thyroid function and highlights the remarkable adaptability of the thyroid. Presentation: 6/1/2024

8534 Comorbid Autoimmune Thyroid Disease in a Parent-Child Pair with Resistance to Thyroid Hormone Beta

Abstract Disclosure: A.H. Smith: None. E. Grethen: None. Resistance to Thyroid Hormone Beta (RTHβ) is an inherited disorder caused by mutations in the gene encoding the thyroid hormone receptor beta protein, resulting in decreased binding affinity to triiodothyronine in certain tissues. An asymptomatic individual with RTHβ may demonstrate abnormalities in serologic evaluation of thyroid hormone markers. When other thyroid pathologies present with RTHβ, however, the diagnosis and management can quickly become complex. Below we discuss two cases, a parent-child pair, with different presentations of presumably the same RTHβ gene. Patient 1 is a 61-year-old male with a history of autoimmune thyroiditis several years ago, presenting for continuation of care; he has had levothyroxine doses gradually uptitrated to over 3 mcg/kg to normalize TSH despite persistently high free T4 levels. He also has a family history notable for six out of seven siblings with autoimmune thyroid disease. Patient 2 is a 44-year-old male who was evaluated for hypothyroidism and difficulty with levothyroxine titration. Prior to consultation, he underwent radioactive iodine ablation for presumed Grave’s disease, followed by total thyroidectomy due to persistent symptoms. Post-operatively, he required high doses of levothyroxine to maintain normal TSH levels; however T4 and T3 levels remained high. Both patients confirmed proper levothyroxine supplementation. Further analysis of both patients demonstrated mildly elevated TBG and normal alpha subunit. Patient 2 pursued genetic testing while patient 1 declined, revealing a heterozygous R320S mutation in the TR-beta protein. Further testing and genetic counseling were offered to other family members. Propranolol and levothyroxine supplementation were titrated accordingly; triiodothyronine administration was attempted but did not alleviate symptoms. These two cases demonstrate the increased risk of autoimmune thyroid disorders in patients with RTHβ and the unique challenges they pose in accurate diagnosis. Autoimmune thyroiditis in RTHβ, with goiter, elevated T4 and elevated T3 levels, can be easily confused with Grave’s disease, especially when TSH is suppressed during active thyroiditis. Timely diagnosis can aid in targeted management of sequelae, prevent ineffective treatments for comorbid conditions which may mimic other diseases, and provide anticipatory/preventive guidance for family members to help with screening. Presentation: 6/1/2024

6430 SAT-534 Evaluating the Effectiveness of Combined T4 and T3 Therapy or Desiccated Thyroid Versus T4 Monotherapy in Hypothyroidism: A Systematic Review and Meta-Analysis

Abstract Disclosure: M. Nassar: None. A. Hassan: None. M.T. Desouki: None. S. Ramadan: None. M.A. Hassan: None. A. Chaudhuri: None. Background: Many patients with hypothyroidism experience persistent symptoms despite normalized TSH levels, which highlights the need for alternative treatment strategies. This study aims to evaluate the effectiveness of combined T4 and T3 therapy or desiccated thyroid (DTE) compared to T4 monotherapy, with a focus on thyroid profile, lipid profile, and quality of life metrics, including the 36-point thyroid symptom questionnaire (TSQ-36), Beck Depression Inventory (BDI) scores, and General Health Questionnaire (GHQ)-28 scores. Methods: A systematic literature search was conducted using a Boolean strategy on the following databases: Embase, Medline/PubMed, and Web of Science. The search included results from the inception of each database until 11/23/2023. We used the following keywords: "Armour Thyroid," OR "Thyroid Extract," OR "Natural Desiccated Thyroid," OR "Nature-Throid," "Desiccated Thyroid," OR "NP Thyroid," OR "Synthroid," OR "Levothyroxine," OR "Liothyronine," "Cytomel," OR "Thyroid USP," OR "Unithroid." AND "hypothyroidism. " We only included RCTs. We excluded non-English articles. Results: Initially, 6,394 records were identified. After removing 477 duplicate records, 5,917 records underwent title and abstract screening, excluding 5,874 records. The full texts of the remaining 43 articles were examined for eligibility, excluding 27 articles. Ultimately, 16 studies met the inclusion criteria and were incorporated into our analysis. We included two studies on desiccated thyroid and 15 studies on combined therapy. In this meta-analysis, combination therapy with T4+T3 revealed a significant reduction in free T4 levels (mean difference (MD): -0.34; 95% CI: -0.47, -0.20), total T4 levels (mean difference: -2.20; 95% CI: -3.03, -1.37), and GHQ-28 scores (MD: -2.89; 95% CI: -3.16, -2.63) compared to T4 monotherapy. Total T3 levels increased significantly in combined therapy (MD: 29.82; 95% CI: 22.40, 37.25). The analyses demonstrated moderate to high heterogeneity. There was no significant difference in heart rate, SHBG, TSH, lipid profile, TSQ-36, or BDI score. DTE significantly increased serum total T3 levels (MD: 50.90; 95% CI: 42.39, 59.42) and significantly decreased serum total T4 (MD: -3.11; 95% CI: -3.64, -2.58) and free T4 levels (MD: -0.50; 95% CI: -0.57, -0.43) compared to T4 monotherapy. Moreover, DTE treatment showed a modest increase in TSH levels (MD: 0.49; 95% CI: 0.17, 0.80). The analyses indicated low heterogeneity. There was no significant difference in heart rate, SHBG, lipid profile, TSQ-36, GHQ-28, or BDI score. Conclusions: Our study revealed that combined therapy and DTE lead to higher T3 and lower T4 levels compared to T4 monotherapy in hypothyroidism. However, no significant effects on heart rate, lipid profile, or quality of life were noted. Given the heterogeneity of results, personalized treatment approaches are recommended. Presentation: 6/1/2024

8500 Fvb/Ant Mice Carrying the Thr92Ala-Dio2 Polymorphism Have a Goiter

Abstract Disclosure: A. Batistuzzo: None. B. Bocco: None. E. McAninch: None. M.O. Ribeiro: None. A.C. Bianco: Consulting Fee; Self; Abbvie. Fvb/Ant Mice Carrying the Thr92Ala-Dio2 Polymorphism Have a Goiter Introduction: The Thr92Ala-DIO2 polymorphism is prevalent worldwide, with about 50% of the population carrying at least one polymorphic allele. Ala-D2 is ectopically located in the Golgi apparatus and causes endoplasmic reticulum (ER) stress. It is also about 40 % less active than Thr92-D2, thus T3 production could be compromised in carriers of the polymorphism. Objective: C57BL/6J (B6) mice carrying the Ala92-DIO2 polymorphism exhibit no significant thyroid phenotype as compared to control Thr92-Dio2 mice. Here we wished to test whether changing the genetic background of mice can influence the thyroidal impact of the Thr92Ala-DIO2 polymorphism. Therefore, we backcrossed B6-Thr92Ala-Dio2 mice to the FVB/Ant background for 8 generations. Methods: Mice were killed by asphyxiation in a CO2 chamber and blood collected from 7-18 weeks old female and male FVB/Ant Ala-Dio2 mice to measure plasma levels of TSH, T4, T3, and rT3. The thyroid gland was dissected, weighed and processed for histological analysis. The weight of the thyroid gland was normalized by femoral length. The QuPath Software was used for measuring follicular area, cell height, and the number of internalized follicular cells. Thr92-Dio2 mice of the same age and sex were used as controls. Data were analyzed using PRISM software and expressed as mean±SE (TH plasma levels and thyroid weight) or mean±SD (thyroid histology). A Student t-test was used to compare 2 groups. Results: Male and female Ala mice had significantly higher levels of TSH (males: 0.36±0.04 vs 1.1±0.21 ng/ml; p<0.01 and females: 0.017±0.006 vs 0.12±0.06 ng/ml; p<0.01), lower levels of plasmatic T4 (males: 2.9±0.2 vs 1.3±0.25 µg/dl; p<0.01 and females: 2.1±0.16 vs 1.15±0.16 µg/dl; p<0.001) and lower levels of rT3 (males: 23.8±2 vs 14.2±1.3 ng/dl; p<0.001 and females: 16.45±1.4 vs 10.4±1.17 ng/dl; p<0.01). Additionally, the thyroid gland of female polymorphic mice was heavier (4.3±0.39 vs 1.8±0.17 mg/cm; p<0.001) and both sexes presented enlarged thyroid follicle area (males: 1464±1464 vs 2055±2443 µm2; p<0.0001 and females: 1519±1364 vs 2597±2624 µm2; p<0.0001) and a higher number of internalized follicular cells (females: 0.06±0.007 vs 0.17±0.008 internalized cells/follicle; p<0.0001). No differences in the follicular cell height were observed. Discussion: In contrast to B6, FVB mice carrying the Thr92Ala-D2 polymorphism exhibit goiter, increased follicular area, slightly reduced serum T4 levels, and elevated serum TSH levels. These findings suggest that the impact of the Thr92Ala polymorphism varies according to the genetic background. They may explain why clinical studies of patients carrying the Thr92Ala-DIO2 polymorphism have yielded inconsistent results when different populations are analyzed. 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

6669 Association Between Serum Levels of Thyroid Function and Per- and Polyfluoroalkyl Compounds Concentrations in Central Precocious Puberty in Girls

Abstract Disclosure: Y. Li: None. Y. Xing: None. X. Yin: None. J. Yang: None. S. Zang: None. T. Dong: None. Y. Pan: None. J. Dai: None. P. Li: None. Background: Exposure to per- and polyfluoroalkyl substances (PFASs) may interfere with thyroid function in the general population and disturb the timing of puberty onset. Objectives: We investigated the possible relationship between PFASs and thyroid hormone (THs) exposure in girls with central precocious puberty (CPP). Methods: In a prospective study initially established for assessing CPP, 627 serum samples were collected with (n = 226) and without (n = 401) CPP. The concentrations of 25 PFASs, thyroxin (T4), 3,5,3’-triiodothyronine (T3), and 3,3’,5’-triiodothyronine (rT3) were measured. We used logistic regression to examine the association of THs with the odds of having CPP and multiple linear regression to analyze the associations between THs and various PFASs in the CPP and control groups. Results: The levels of T4 in the CPP group were significantly lower than those in the control group, and the levels of T3 and rT3 were significantly higher than those in the control group. After adjusting for confounders, T3 concentrations were associated with 1.526-fold increased odds of having CPP [odds ratio (OR) = 1.526, 95% confidence interval (CI):1.216-1.914]. In the CPP cohort, perfluoroheptanoic acid (PFHpA), perfluoro (2-ethoxyethane) sulphonic acid (PFEESA), and fluorotelomer phosphate diester (6:2/8:2 diPAP) were inversely associated with T3; perfluorobutanoic acid (PFBA) was inversely associated with T4, and PFEESA and 6:2/8:2 diPAP positively associated with T4; PFBA was positively associated with rT3, and perfluorooctane sulfonic acid (PFOS) was inversely associated with rT. In the control cohort, perfluorobutanesulfonic acid (PFBS) was positively associated with T3, and PFEESA and 6:2/8:2 diPAP were inversely associated with T3, and these PFASs had an adverse association with T4. Perfluorohexanoic acid (PFHxA) was positively associated with rT3, and 6:2/8:2 diPAP was negatively associated with rT3. Conclusion: In this study, different measurements of PFASs and THs were observed in the CPP and control groups. Discrepancies in exposure to PFASs were associated with THs in the CPP cohort and healthy girls. Further research is necessary to investigate the mechanism by which PFASs affect the timing of puberty onset and thyroid function. Presentation: 6/1/2024

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

8124 Prevalence and Characteristics of Patients with Hypothyroidism in the Danish Blood Donor Study

Abstract Disclosure: N.L. Frisk: None. J.R. Shorter: None. O.B. Pedersen: None. L.T. Dalgaard: None. Introduction: While impaired thyroid function leading to subclinical hypothyroidism and overt hypothyroidism is common in Denmark, the knowledge about the paths by which patients’ progress to impaired thyroid function is limited. Undiagnosed hypothyroidism as well as subclinical hypothyroidism constitute serious risk factors for development of cardio metabolic disease. The Danish Blood Donor Study (DBDS) is a large longitudinal cohort and biobank containing information and samples dating more than 10 years back. Blood donors donate blood every 3-6 months and each time provide a sample for research. Research question: The aim of the study was to obtain up-to-date information about prevalence and characteristics of patients with hypothyroidism in a Danish longitudinal cohort of blood donors. Methodology: The study employed a cross-sectional design. Hypothyroidism was defined based on at least two prescriptions of levothyroxine (LT4) and used for calculations of prevalence. Case numbers were compared to all controls that were currently not being prescribed LT4 nor anti-thyroid drugs (carbimazole, propylthiouracil, thiamazole). We compared cases of hypothyroidism to two different control (ctrl) groups: 1) All the participants of the DBDS having TSH levels in the normal range, and 2) Normothyroid participants matched to hypothyroid cases based on age and sex. Incidence was determined based on DBDS participants developing hypothyroidism after being enrolled into the DBDS during a 10-year follow-up. Men and women were compared separately among cases and controls. Students’ t-test was used to compare cases and controls, and corrected using Bonferroni. Major results: There were 3397 cases of hypothyroidism and 153791 ctrl subjects in the DBDS, giving a prevalence of 2.2%. 85% of cases were female, while among ctrl 50% were female. Average age of cases was 52±13 years (mean±SD) for women and 58±13 for men, while ctrls were 45±13 and 48±14 years, respectively (both P<0.001). BMI among cases were: 25.8±4.7 for women and 26.8±3.9 kg/m2, while cases were 25.1±4.4 and 26.0±3.6, respectively (both P<0.001). TSH levels were, for female cases: 4.6±4.0 iu/mL and 5.7±4.9 for men, while ctrls were 1.8±1.1 and 1.7±1.1, respectively (both P<0.001). Free (F) T4 levels were, for female cases: 14.4±6.4pmol/L and male: 14.0±4.6, while ctrls were: 14.8±4.5 and 15.0±3.9 respectively (P<0.003 for females, P<0.0001 for males), while FT3 levels were for cases: 4.3±1.7 and 4.3±1.4 pmol/L and 4.5±2.0 and 4.7±1.5 for ctrls (both P<0.0001). Conclusion: Hypothyroidism is less prevalent among blood donors than reported in the general Danish population, which is accordance with ‘the healthy donor’ bias. Hypothyroid donors were on average older and with higher BMI than normothyroid controls. Donors with hypothyroidism were generally well regulated, but despite that FT4 and FT3 levels were lower than ctrls. Presentation: 6/1/2024

7647 Myxedema Coma- A Rare and Fatal Manifestation of Severe Hypothyroidism

Abstract Disclosure: B.K. Ray: None. R. Kaur: None. L. Kaur: None. M. Thakur: None. Introduction: Myxedema coma is a severe and life-threatening form of hypothyroidism. It is a rare occurrence with an incidence of 0.22 per million per year, associated with a high mortality rate ranging from 30 to 60% even with early diagnosis and treatment. This condition arises when the body's response to hypothyroidism is overwhelmed by factors like infection, surgery, and medication noncompliance. The definitive management is with thyroid hormones but supportive measures and identification and treatment of the precipitating factors is also vital. The case discussed concerns an elderly woman with myxedema coma due to noncompliance to Levothyroxine. This case stresses the importance of consistent medical follow-ups. Case Presentation: A 73 year old female presented to the hospital with altered mental status for about 32 hours. Vital signs at presentation showed hypotension (80/50 mmHg), bradycardia (54 beats per minute), tachypnea (32 breaths per minute) and hypothermia (33.2 °C). A computed tomography scan of the brain and Computed tomography angiography of the head/neck showed no stenosis or large vessel occlusion of the vasculature. Initial pertinent laboratory test results revealed a white blood cell count of 6.1 (3.7–11.0×103/uL), hemoglobin level of 14.3 (11.5–16.0 g/dL), sodium level of 131 (136–145 mmol/L), glucose level of 142 (65–125 mg/dL). Troponin, lactate and procalcitonin were normal. She was intubated and transferred to the Intensive care unit. Thyroid function tests revealed a markedly elevated TSH of 37.9 (0.4 to 4.0 mIU/L) and a decreased T4 of 0.3 (0.9-1.7 ng/dL). She was immediately started on hydrocortisone 100 mg Three times daily and initiated on intravenous levothyroxine monotherapy with a loading dose of 200 mcg followed by 100 mcg daily. Her T4 level was trended daily and she demonstrated gradual improvement. She was successfully extubated. On discussion she reported noncompliance with her medications. Hydrocortisone was tapered and she was started on her home dose of oral Levothyroxine (200 mcg) after four days of Intravenous levothyroxine. She was counselled on medication compliance and discharged to home. Conclusion: Myxedema, an extreme form of hypothyroidism, is life-threatening and requires immediate admission to intensive care. Symptoms are usually vague, and require a high degree of suspicion. Treatments include thyroid hormone supplementation, steroid replacement and supportive care. Early detection and quick intervention are crucial for survival. Patient education on medication compliance, regular testing, and reporting new medication to prevent interference with thyroid metabolism is crucial. Presentation: 6/1/2024

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

8319 Pituitary Apoplexy Leads to the Spontaneous Resolution of Hypercortisolism Secondary to Cushing Disease: A Clinical Case

Abstract Disclosure: N. Sweis: None. J. Sanchez Perez: None. M. Fariduddin: None. R.M. Sargis: None. D.J. Toft: None. S. Reutrakul: None. Background: Pituitary apoplexy is a potentially fatal condition involving the infarction or hemorrhage of the pituitary gland. Rarely, it can occur in the setting of an ACTH-secreting pituitary adenoma. Clinical Case: A 27-year-old female with a past medical history of obesity, spontaneous miscarriages, and amenorrhea presented to the ER with an acute onset frontal headache of throbbing quality, associated with nausea and vomiting. The headache began two days prior, rapidly intensified, and did not improve with oral acetaminophen. CT of the head revealed an enlarged pituitary gland, while neurovascular imaging showed no abnormalities. Her neurologic examination was normal. She denied visual changes, photophobia, neck rigidity, fevers, chills, or recent infections. Furthermore, she endorsed a weight gain of about 40 pounds over the past year despite no change in dietary habits. This was accompanied by amenorrhea, hair thinning, itchy comedonal acne, hirsutism, and a loss of libido. Her physical examination was remarkable for the presence of cushingoid features including violaceous abdominal striae, facial acne, moon facies, a dorsal fat pad, and acanthosis nigricans around the neck and axillae. Pituitary MRI with and without contrast showed an enlarged sellar and suprasellar macroadenoma measuring approximately 2.1x1.4x1.2 cm abutting the optic chiasm. The visualized lesion contained hemorrhagic products, suggesting pituitary apoplexy. Biochemical testing on admission included a low morning plasma cortisol of 6.5 ug/dL (ref. range: 6.7-22.6 ug/dL), a 24-hour urine free cortisol of 12.0 (<=45.0 ug/24 hour), and an elevated ACTH of 145.0 pg/mL (7.2 - 63.3 pg/mL). A1c was 5.8% (<5.7%). Serum levels of prolactin, IGF1, GH, LH, FSH, TSH, Free T4, estradiol, total and bioavailable testosterone were within normal limits. She was evaluated with an ACTH stimulation test, which showed a morning cortisol level of 1.2 ug/dL at baseline, lower from prior. Cortisol levels were adequately increased at 19.6 ug/dL and 22.6 ug/dL, 30 and 60 minutes after the administration of Cosyntropin 250 mcg, respectively (>=18 ug/dL after 30-60 mins). The level of ACTH at the time was also decreased to 76.6 pg/mL. The patient was therefore started on steroid replacement therapy with hydrocortisone and later underwent transsphenoidal resection of the pituitary mass without complications. Histopathological examination of the resected mass showed pituitary adenoma cells with diffuse weak to moderate ACTH staining, most consistent with a sparsely granulated corticotroph pituitary adenoma. Conclusion: We report an interesting case of Cushing disease that spontaneously resolved after pituitary apoplexy. Our case underlines the importance of close monitoring of such patients who may rapidly undergo a period of adrenal insufficiency after hypercortisolism. Presentation: 6/3/2024

8412 Resolution of Central Hypothyroidism shortly after Transsphenoidal Surgery For Cushing’s Disease

Abstract Disclosure: L. Esper: None. A. Ibrahim: None. N. El Asmar: None. Background: Cushing's disease is a rare endocrine disorder characterized by excessive cortisol production, resulting in various metabolic disturbances. Hypercortisolism is known to cause central hypothyroidism. The mechanism is complex and involves hypercortisolism mediated decreased TRH and TSH secretion in addition to inhibition of peripheral deiodination. This case details the successful management and recovery of a patient with Cushing's disease and reversal of central hypothyroidism after pituitary surgery.Case:A 43-year-old man was evaluated for central hypogonadism, 20 pound weight gain with central weight distribution, and the development of purple abdominal striae for the past year. He had a normal thyroid exam and appeared euthyroid. He was alsodiagnosed with hypertension and prediabetes in the past yearrequiring medical therapy.A low dose dexamethasone suppression test (DST) resulted in AM cortisol of 12.9 mcg/dl. Two adequate 24hr Urinary cortisol measurements showed elevated cortisol excretion at 458 and 378mcg/24. Lab evaluation revealed elevated cortisol levels along with elevated adrenocorticotropic hormone (ACTH) levels(ACTH of 172 pg/ml with a cortisol level of 23.9 mcg/dl). A high dose DST demonstrated suppression of cortisol to 3.4 mcg/dl. MRI pituitary was performed which showed a clearright sided 7mm pituitary adenoma.Thyroid function tests performed were consistent with central hypothyroidism, with low levels of free thyroxine (FT4) at 0.67ng/dl along with an inappropriately low normal thyroidstimulating hormone (TSH) at 0.596 uIU/ml. Total T4 was low at 4 ug/dl in addition to a low total T3 of 66 ng/dl. Remaining labs revealed central hypogonadism along with slightly elevated prolactin of 16 ng/ml. He was not started on thyroid hormone.He then underwent transsphenoidal surgery for tumor removal. He developed post-operative adrenal insufficiency (cortisol 2.12 mcg/dl) 16 hours post-op after which he was started on hydrocortisone replacement, indicating remission. 12 hours post-op, his TSH was 0.656 uIU/ml with a free t4 of 0.79 ng/dl, both in the normal range. 36 hours post-op, TSH was 0.524 uIU/ml and free t4 was 1.15 ng/dl. Histopathological examination confirmed the diagnosis of an ACTH-secreting pituitary adenoma.At 4 weeks post-op, thyroid labs showed normal FT4 (1.07ng/dl) and TSH (2.06uIU/ml). Conclusion: Hypercortisolism causes a global inhibition of the thyroid axis, with decreased levels of TSH, T4, and T3 (1). Previous studies suggest the monitoring of thyroid function at 6 and 12 months after surgical cure of hypercortisolism. Our case suggests that the resolution of hypothyroidism occurs shortly after surgery for Cushing’s disease and the need for earlier monitoring. Presentation: 6/3/2024

12475 Revisiting Myxedema Coma

Abstract Disclosure: M.H. Islam: None. D.R. Jimenez Corado: None. S. Siddiqui: None. M.F. Aquino Camey: None. S. Yeasmin: None. Background: Myxedema coma is a rare and life-threatening complication of hypothyroidism.Although it is rare in the era of better diagnostics and treatment modalities, its life-threatening nature mandates its timely recognition and better understanding. Case:81-year-old female with a history of hypothyroidism (unclear medication compliance) and alcohol use disorder was admitted due to alcohol withdrawal and treated with benzodiazepines. A few days prior to the presentation, she was found to have worsening confusion, unsteady gait, and multiple falls. On presentation, she was hemodynamically stable, tremulous, anxious, and oriented to person only. Blood work was remarkable for mild transaminitis. CT scan of the head revealed sequelae of microvascular disease. The day after admission, she was noted to be lethargic, and benzodiazepines were held. Later, she became hypothermic, hypotensive, bradycardic, and hyponatremic. Further investigation was pursued, revealing a TSH of 55 (normal 0.27 to 4.2 mlU/L), free T4 of <0.10 ng/dL (normal 0.8-1.7 ng/dL), free T3 of <1.0 pg/mL (normal 2.2-4 pg/mL), and cortisol of 10.7 ug/dL. Due to concerns of myxedema coma, she was started on stress dose steroids and IV levothyroxine. She was transferred to the ICU as her mental status continued to deteriorate; she underwent endotracheal intubation and received additional doses of IV levothyroxine and liothyronine. After a few days, her clinical condition and her cortisol, free T4, and free T3 levels improved; she was extubated and later discharged with an adjusted levothyroxine dose. Conclusion: It is of absolute importance to keep myxedema coma as a differential diagnosis when evaluating encephalopathic elderly patients, especially those with a history of thyroid disorders.There is a paucity of evidence to suggest a clear benefit of combining levothyroxine-liothyronine over levothyroxine alone. Treating initially with intravenous levothyroxine over oral is beneficial, as GI absorption and bioavailability are likely variable and unpredictable. In this case, oral liothyronine was used with IV levothyroxine to speed up clinical and biochemical recovery.Adrenal insufficiency often coexists with hypothyroidism, with considerable overlap in clinical features like hypotension, hypoglycemia, and hyponatremia. Administration of levothyroxine before steroids can lead to a rapid increase in metabolic rate and subsequent depletion of the existing reserves. Considering this, it can be said with fair confidence that patients need prior or concomitant stress doses of corticosteroids on an emergent basis. Later, biochemical testing can be done to evaluate the functioning of the hypothalamic-pituitary-adrenal axis and then adjust steroid doses accordingly. Presentation: 6/1/2024

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

7982 Is there a Connection between Alpha Thalassemia and Thyroid Disorders

Abstract Disclosure: W. Akhter: None. V. Taqi: None. J.L. Gilden: None. IntroductionA number of case reports suggest an association between thalassemia and autoimmune diseases through specific mutations and molecular pathways. An example is thyroid disease in thalassemia patients. Due to factors such as age, ethnicity and treatment protocol differences, the frequency of hypothyroidism in thalassemia patients is a wide range of 4 to 29% based on free T4 and TSH levels. Subclinical hypothyroidism is more common in thalassemia patients as compared to overt hypothyroidism. 90% of morbidity and mortality in B-Thalassemia patients is attributed to iron overload, anemia and hypoxia. Understanding this possible mechanism helps guide treatment and monitoring. Case PresentationWe present the case of a 26-year-old African American with Haitian ethnicity female, who upon routine testing was found to have a very high TSH level of 79.084 uIU/ml (nl=0.550-4.780 uIU/ml) for which 125 mcg of Levothyroxine was started, and then she was referred to the endocrine clinic. Past history was notable for sickle cell trait and alpha thalassemia trait. Patient stated that at age 12, she developed fatigue and low energy and was found to have hyperthyroidism which was treated with RAI ablation. After that, no follow up or lab tests were done until recently. The patient denied symptoms of hypo or hyperthyroidism or enlargement of the thyroid gland. She denied any family history of thyroid disorders. After presenting to the endocrine clinic a few days later, she was diagnosed with postprocedural hypothyroidism and the same dose of levothyroxine was continued. Physical exam was unremarkable and no thyromegaly was appreciated on exam. Labs were notable for decreased Hemoglobin of 11.4 g/dL (nl=12-16 g/dL) and CMP was unremarkable except low glucose of 65 mg/dL (nl=70-99 mg/dL). The patient’s most recent labs after 8 weeks of taking Levothyroxine were notable for TSH of 14.65 uIU/ml (nl=0.550-4.780 uIU/ml) and free T4 of 1 ng/dL (nl= 0.89-1.76 ng/dL) and the patient admitted to having still no thyroid symptoms and a little more energy. ConclusionEndocrinopathies are common complications of thalassemia with hypothyroidism being the second most common endocrine disorder in thalassemia patients after hypogonadism, reported in 5.6-17% of patients. In thalassemia patients, endocrine disorders have to be managed as early as possible. Therefore, it is recommended that an endocrine evaluation be carried out in thalassemia patients at a young age.Monitoring for glucose homeostasis, hypothyroidism and hypoparathyroidism is also warranted. Physicians caring for thalassemia patients should perform routine screening for and treat thyroid dysfunction appropriately. Reference: De Sanctis V, Soliman AT, Canatan, et al.. Thyroid Disorders in Homozygous β-Thalassemia: Mediterr J Hematol Infect Dis. 2019 May 1;11(1):e2019029. doi: 10.4084/MJHID.2019.029. PMID: 31205633; PMCID: PMC6548211. Presentation: 6/2/2024

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

6601 A Case of Recurrent Painless Thyroiditis and Discussion of Management

Abstract Disclosure: M.C. Slack: None. S. Grock: None. Introduction: Painless (silent) thyroiditis is characterized as a subacute and generally self-limited disease process in which patients develop transient thyrotoxicosis, which is often followed by a hypothyroid phase before entering the recovery euthyroid phase. Given high frequency of positive thyroid antibodies, it may be autoimmune-mediated; recurrence is rare. Here we present a case of recurrent painless thyroiditis and discuss management options. Clinical Case: A Korean woman was followed by endocrinology from age 38 to 60 and experienced at least seven episodes of painless thyroiditis over this time. The episodes occurred without an identifiable trigger and were not preceded by viral illness. During episodes she developed palpitations, hair loss, and dyspnea on exertion and biochemical evidence of thyrotoxicosis with TSH suppressed to <0.2 mIU/mL (normal 0.3-4.7) and elevated free T4 levels as high as 5.4 ng/dL (normal 0.8-1.7). TSI, TPO, and TSH receptor antibodies were checked during multiple episodes and resulted negative, though thyroglobulin antibody was significantly elevated. A radioactive iodine uptake scan was obtained during an active episode of thyroiditis and revealed diffusely low uptake. The patient’s episodes lasted approximately two to three months before normalization of her TSH and FT4. She had at least one instance of transient hypothyroidism after thyrotoxicosis with a TSH of 13.2 and FT4 of 0.6 which subsequently normalized 6 weeks later. The patient did not have known cardiovascular disease and DXA scans revealed mild osteopenia with the lowest T-score -1.3. RAI was considered for the patient based on the total number and increasing frequency of her episodes. She ultimately declined treatment with RAI and continues to follow with endocrinology. Clinical Lessons: While the deleterious effects of prolonged hyperthyroidism (e.g. osteoporosis, arrhythmia, cardiovascular disease) are well known, it is unclear what risk recurrent painless thyroiditis episodes pose. As there are no guidelines regarding treatment, clinical gestalt incorporating frequency and duration of episodes, as well as symptoms, is often used to determine if definitive management is indicated. There are case reports in the literature of treatment of recurrent thyroiditis with RAI ablation performed during a euthyroid state, which eliminated recurrence of episodes but did lead to permanent hypothyroidism necessitating hormone replacement. Surgical thyroidectomy may also be considered in select patients. This case highlights the challenges in treating rare cases of recurrent painless thyroiditis given the lack of research or established guidelines. It is reasonable to consider the frequency, severity, and total number of episodes, as well as patient risk factors, symptoms, and preferences when making recommendations regarding management. Presentation: 6/1/2024

8278 Myxedema Coma With COVID-19 Infection

Abstract Disclosure: R. Kalas: None. V. Manohar: None. N.S. Bapat: None. Y. Kim: None. Myxedema coma is a rare medical emergency that occurs in severe hypothyroidism with a mortality rate reaching 60%. The hallmarks include depressed mental status and hypothermia, but hypotension, hyponatremia, bradycardia, and hypoventilation can also occur. This complication can occur in patients with a longstanding history of severe hypothyroidism especially when precipitated by an acute event such as infection, myocardial infarction, or surgery. Prompt recognition and treatment of the condition is important to prevent fatal outcomes. We present a case of myxedema coma in the setting of COVID-19 infection and nonadherence to medication. A 91-year-old woman with history of hypothyroidism, hypertension, coronary artery disease, cardiomyopathy, and chronic obstructive pulmonary disease presented with dyspnea. Her home medications included levothyroxine 75 mcg daily, which she reported not taking for at least 3 weeks. Vital signs revealed a normal heart rate and blood pressure of 84 beats/min and 137/78 mmHg, but the patient was hypothermic to 35.7 °C. On exam, she was somnolent. Labs were notable for markedly elevated TSH level of 111 (0.380 - 4.700 uIU/mL), low free T4 level of 0.57 (0.93 - 1.70 ng/dL), random cortisol level of 25.5 (6.2-18.4 ug/dL), and positive SARS-COV-2 PCR test. Chest x-ray revealed bilateral lower lung parenchymal consolidations and arterial blood gas revealed a pH of 7.29 and pCO2 of 52.5 (35-45 mm Hg), indicating hypercapnia. She was treated for COVID pneumonia and given concern for COVID induced myxedema coma she was given IV levothyroxine 100 mcg for 2 days, after which the patient’s hypothermia and somnolence improved, with an improved repeat free T4 level 0.87 ng/dL. She was subsequently transitioned to oral levothyroxine 112 mcg daily and discharged after improvement of her COVID symptoms. Myxedema coma is a rare complication of decompensated hypothyroidism, frequently triggered by an infection. Thyroid hormone plays an important role in regulating both the innate and adaptive immune systems. As a result, individuals with hypothyroidism are at increased risk of acquiring infections, which can further lead to myxedema coma. COVID-19 infection has been associated with thyrotoxicosis, thyroiditis and hypothyroidism. Given the associated high mortality rate, regardless of the underlying precipitant, prompt diagnosis and early administration of thyroid hormone replacement therapy is crucial to improve outcomes. Presentation: 6/3/2024

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