bluuebunny/crossref_metadata_2025_split huggingface dataset:
LBSAT247 Factors Guiding Successful Treatment Discontinuation In Levothyroxine Replacement Therapy Overuse: Short And Long-term Observation Data Of 802 Subjects.
Authors: Livadas Sarantis , Androulakis I , Kollias A , Paparodis R D , Angelopoulos N , Boniakos A , Askitis D , Anagnostis P , Duntas L 
Published: November 2022

Abstract

Background
Levothyroxine (LT4-Rx) is one of the most commonly prescribed drugs worldwide and the vast majority of patients receive long-term treatment. However, in a recent study of LT4-Rx withdrawal in 291 subjects, it was found that 60% of those remained biochemically euthyroid two months after LT4-Rx discontinuation1.

Aim of the study
A prospective clinical cohort follow-up study was carried out to address this issue. We registered all patients presented in our clinical practice who were not on LT4-Rx for a solid diagnosis of hypothyroidism and abruptly discontinued treatment. All subjects underwent weight, height, TSH, TPO, Tg-Abs and free T4 measurement and thyroid ultrasound on enrolment, 2-4 months later, and at the end of follow up. A TSH value of ≥4.5IU/mL was considered as underlying hypothyroidism.

Results
We enrolled 802 consecutive subjects (83% females) aged 48±16 (range 18-84 years) with 8.8±7.3 years on LT4-Rx. The treatment indications and corresponding percentage for LT4-Rx were classified as a nodule(s) (35%), indefinite (25%), post-partum (7%) and Hashimoto's (33%); 48% of subjects were part of Group A and long-term follow-up up to 5 years was achieved in the remaining. Among the entire cohort, n=182 subjects became hypothyroid, while the remaining n=620 remained euthyroid off LT4-Rx (23 vs. 77%, p&lt;0. 001). On subgroup analysis, 40% of subjects comprising Group A became hypothyroid, whereas the corresponding value for Group B was 7%. In Group A, the reason for LT4-Rx, LT4 dose, LT4 dose/BMI, TSH levels and the presence of increased thyroid autoantibodies titers (ATA) were significantly different in those who became hypothyroid, whereas only the reason for LT4-Rx differed in Group B. Subjects with a diagnosis of nodules, negative ATA, lower TSH values and lower LT4 dose during treatment had significantly lower probability to become hypothyroid. Furthermore, in Group A, 14.8% became hypothyroid with baseline TSH&gt;3IU/mL vs. 5.2% with baseline TSH&lt;3IU/mL (p&lt;0. 001); the corresponding values for Group B were 22.2% vs. 8.8%, (p&lt;0. 001), respectively.

Conclusions
These findings suggest considerable overuse of thyroxine therapy. In cases of uncertainty, the existence of nodules, a low-normal TSH value, a relatively small T4 dose, and the absence of ATA are strong predictors of euthyroidism, and accordingly a treatment discontinuation trial is recommended. Furthermore, if hypothyroidism does not ensue 2-4 months post-treatment discontinuation, the likelihood to develop hypothyroidism in the long term is minimal.1. Livadas S, et al. Thyroid 2018.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
LBSAT292 A Rare Case Of Co-existent Grave's Disease Complicated By Non Medullary Thyroid Carcinoma And Primary Hyperparathyroidism In A Young Male
Authors: Arora Gunjan , Patel Toral 
Published: November 2022

Abstract

Introduction
The relationship between medullary thyroid carcinoma and parathyroid adenoma is well recognized and has been described in connection with MEN syndromes; however, co-existing Grave's disease with underlying non medullary thyroid carcinoma and primary hyperparathyroidism remains a rare phenomenon. The basis of this entity remains yet to be deciphered. With this case we wish to highlight that synchronous abnormalities of thyroid and parathyroid should always be considered and further testing to evaluate for underlying genetic abnormalities should be offered on a case by case basis. In addition, since both Grave's disease and hyperparathyroidism contribute to hypercalcemia, their interplay must be considered in interpretation of serum calcium and parathyroid function.

Case presentation
A 44 year old male with no significant medical history presented to the PCP with chest pain and dyspnea on exertion. EKG showed sinus tachycardia. Labs showed Calcium 11.1 mg/dl (8.6 - 10.3), Albumin 4 g/dl (3.5 - 5.7), TSH &lt;0. 010 uIU/ml (0.27 - 4.20), Free T4 3.71 ng/dl (0.5 - 1.6). Repeat labs confirmed these findings. Additional tests included: PTH 105.9 pg/ml (12 - 88), Ionized calcium 6.4 mg/dl (4.5-5.4), TPO antibody positive and TSI antibody positive. Propranolol was started and Endocrinology was consulted. Thyroid ultrasound showed hyperechoic gland and 24 hour radio-active Iodine uptake was abnormally increased to 67.8% (8 - 33%), consistent with Grave's disease. Options for treatment were discussed. Decision was made to start Methimazole to achieve euthyroid state followed by repeat PTH (104.1 pg/ml) and Calcium (calcium 10.6 mg/dL) testing. Due to persistent hypercalcemia with inappropriately elevated PTH, surgical intervention was planned. Pre-operative localization studies were ordered: thyroid ultrasound showed two hypoechoic thyroid nodules in the superior right thyroid lobe and inferior left thyroid lobe, and sestamibi scan did not show any focus of increased activity to suggest a parathyroid adenoma. Total thyroidectomy with parathyroid exploration was planned. Surgical pathology was consistent with three foci of papillary thyroid carcinoma measuring 5 mm, 3 mm and 1 mm in size in the right thyroid lobe and right inferior parathyroid adenoma. Post-operatively, thyroid hormonal supplementation was initiated and thyroid and parathyroid function panel normalized.

Discussion
Our patient had concurrent non medullary thyroid carcinoma and primary hyperparathyroidism. Concurrent thyroid carcinoma should always be considered in patients presenting with parathyroid abnormalities, and a complete pre-surgical screening evaluation must be done. Genetic testing should be considered. And since hyperthyroidism and hyperparathyroidism both can lead to hypercalcemia, their interplay must be considered in interpretation of serum calcium and parathyroid function.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
LBSAT310 A Rare Disease Engulfing Thyroid And Masquerading As Common Thyroid Disorders
Authors: Myint Myat Su Mon , Pinero-Pilona Antonio 
Published: November 2022

Abstract

Introduction
– Langerhans cell histiocytosis (LCH) is a rare clonal disorder caused by the CD207+ Langerhans cells derived from the myeloid origin. We present a case of LCH where it mimicked Hashimoto's and Riedel's thyroiditis and completely infiltrated the thyroid gland.

Case description
– A 54-year-old female was initially diagnosed with hypothyroidism, goiter, and bilateral parotid and submandibular glands enlargement. CT imaging revealed a diffuse goiter which imposed infraglottic airway narrowing and a suspicious left inferior thyroid nodule. Biopsy revealed atypia of undetermined significance. GSC showed a 50% suspicion of malignancy with a negative BRAF. Follow up imaging revealed increased infiltrative masses within the salivary glands, enlarging thyroid gland, and increased infiltration of the superior component of the right thyroid lobe into the submandibular space. A core needle biopsy revealed a background of acute and chronic inflammation without evidence of malignancy. Sjogren's, sarcoidosis and IgG4 diseases were ruled out. She was then referred to us after a myriad of work up. She had a diffusely enlarged goiter with a crusted area of skin over the thyroid gland and significant bilateral parotid swelling. We repeated a thyroid ultrasound which revealed diffusely enlarged and heterogeneous thyroid glands with pseudo-nodules and 3 suspicious nodules greater than 1cm on right and left lobes. She also had prominent reactive lymphadenopathy. Her submandibular glands were hypoechoic, avascular, markedly enlarged and abnormal appearing. She underwent total thyroidectomy. Pathology revealed proliferation of histiocytes, few islands of lymphoid tissue, and eosinophilic micro abscesses without any identifiable thyroid parenchyma in the entire resected specimens. Immunohistochemistry confirmed the diagnosis of Langerhans Cell Histiocytosis with atypical features. BRAF (V600E/V600K) mutation was again not detected. Flow cytometry showed no evidence of neoplastic myeloid blast population. She was referred to an oncologist for further management of LCH.

Discussion
– Our patient had a remarkably diffuse goiter with a sonographic appearance mimicking Hashimoto's thyroiditis or Riedel's thyroiditis. Initial thyroid FNA failed to reveal LCH. The diagnosis was reached only after total thyroidectomy. Treatment depends on single or multi-system involvement, presence or absence of risk organ involvement, and presence or absence of BRAF mutation.

Conclusion
In the cases of infiltrated thyroid diseases, Langerhans cell histiocytosis should be on the differential diagnosis, especially if there is concomitant infiltrative process in other organs. The sonographic finding can mimic Hashimoto's or Riedel's thyroiditis which may lead to misdiagnosis and treatment delay.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
ODP448 A Case of Lithium-Induced Silent Thyroiditis
Authors: Dawahir Wafa , Gilden Janice , Moid Alvia , Trendafilova Victoria 
Published: November 2022

Abstract

Background
Lithium is a drug used in the management of psychiatric condition such as acute mania and bipolar disorder. Lithium is generally known to decrease thyroid hormone synthesis and release, causing hypothyroidism and thyromegaly. Much less commonly, lithium can cause elevated thyroid function tests; we describe such a case.

Clinical Case
A 21-year-old man with bipolar disorder and polysubstance abuse, presented with acute mania and was started on Lithium. Baseline TSH was 1.42 [0.358-3.74 µIU/mL], but one week after starting Lithium, TSH was 0.1 uIU/mL [0.358 - 3.74 µIU/mL] with free T4 of 0.95 [0.76-1.46 ng/dL]. Three weeks later, TSH was 0. 01 µIU/mL [0.358 - 3.74 µIU/mL], FT4 1.52 ng/dL [0.76 - 1.46 ng/dL], FT3 6.16 pg/mL [ 2.18 - 3.98 pg/mL], total T3 221 ng/dL [76–181 ng/dL]. Six weeks after starting Lithium, TSH remained suppressed at &lt;0. 005 µIU/mL [0.358 - 3.74 µIU/mL], FT4 1.66 ng/dL [0.76 - 1.46 ng/dL], FT3 6.21 pg/mL [ 2.18 - 3.98 pg/mL]. During this time the patient's only complaint was tremor, with no other symptoms of hyperthyroidism. Physical exam showed mild tachycardia, with no evidence of thyroid eye disease, and the thyroid gland was normal size and nontender. TSI was negative with normal thyroglobulin and iodine levels, negative thyroglobulin and peroxidase antibodies. Lithium was in the therapeutic range. Thyroid US was normal without thyromegaly, normal echogenicity and color flow and without nodules or masses. I-123 thyroid uptake and scan showed low uptake and no nodules. The patient was diagnosed with Lithium-induced silent thyroiditis. He was treated with propranolol 10 mg PO BID for tremors, which was stopped later, due to bradycardia and dizziness. Due to persistent suppression of TSH and elevated FT4 and FT3 eight weeks after initiation of Lithium, this was discontinued, and Depakote was started.

Conclusion
Prior studies have shown that Lithium-induced thyrotoxicosis occurs in 2.7 cases/per 1000 person-years, with Lithium-associated Graves’ disease in 1.4 cases/1000 person-years, and silent thyroiditis only in 1.3 cases/per 1000 person-years. Although rare, our case highlights the importance of considering silent thyroiditis in patients treated with lithium and hyperthyroidism. References: K. K. Miller and G. H. Daniels, Association between lithium use and thyrotoxicosis caused by silent thyroiditis. Clinical Endocrinology 2001; 55, 501-508Kibirige et al. Spectrum of lithium induced thyroid abnormalities: a current perspective. Thyroid Research 2013; 6: 3
Presentation: No date and time listed
ODP449 A Case of Malignant Struma Ovarii
Authors: Alhusseini Maha , Daher Mona , Mehanna Reem 
Published: November 2022

Abstract
A 45 year old female presented to the ER with pelvic pain. Ultrasound of the uterus revealed a left ovarian 8 cm dermoid cyst. She underwent a unilateral salpingo-hysterectomy. During the operation, no high risk features were seen including no ascites or adhesions. Final pathology revealed a 2.2 cm papillary thyroid cancer with no other worrisome features (no angio-invasion or lymphatic invasion). A diagnosis of malignant struma ovarii was made, and the patient was referred to endocrinology for further work up. A neck US was performed revealed a benign looking, partially cystic, 0.8 cm right thyroid nodule. An FNA attempted came back non-diagnostic. Thyroid functions and baseline thyroglobulin were normal. The clinical dilemna that came up was how to approach the thyroid gland status since in the majority of thyroid cancer cases, the thyroid gland is removed. On review of over 200 cases reported in the literature of localized malignant struma ovarii, the majority of the cases were treated with pelvic surgery alone, and the thyroid gland was left in place. There is no available data that removing the thyroid gland in these patients decreases the risk of recurrence of thyroid cancer. Given the lack of any high risk features in our patient, it was decided not to pursue further adjuvant treatment and to continue surveillance with a repeat of thyroglobulin level in 6 months.
Presentation: No date and time listed
ODP459 Adiposity Rebound in Japanese Patients with Congenital Hypothyroidism Detected by Neonatal Screening
Authors: Nakayama Kanako , Kaneko Naoya , Hishimura Nozomi , Yamaguchi Takeshi , Ishizu Katsura , Tajima Toshihiro , Nagasaki Keisuke , Nakamura Akie 
Published: November 2022

Abstract

Background
More than 40 years have passed since the introduction of newborn screening programs (NBS) for congenital hypothyroidism (CH), and there have been many reports on the long-term outcome of CH identified by NBS. There are some reports that CH is associated with early adiposity rebound and adult obesity. On the other hand, the association between AR and CH has not been revealed in Japan.

Objective
The aim of this study was to evaluate the timing of AR in individuals with CH detected by NBS in our institution, furthermore, to find out the risk factors of early AR in CH individuals.

Patients and Methods
The study included 212 CH children (105 female/107 males) who were ten years of age or older as of September 2021. We retrospectively collected height and weight data from one to ten years of age, and the timing of AR was visually determined. We examined the association between the AR age and the severity of hypothyroidism at NBS and at the first visit.

Results
The median AR age was 5.6 years for boys and 6.2 years for girls, which was unexpectedly not unexpectedly younger than that of the general Japanese population reported by Koyama (4.8 ± 1.4 years for boys, 4.7 ± 1.5 years for girls). Data from 115 patients (107 males, 105 females) whose physique data between the age of 15 and 18 were available showed that body mass index (BMI) was 21.1±3.2 kg/m2 for males and 20.6±2.7 kg/m2 for females, positively correlated with AR age, and not significantly different from BMI at 15-19 years of age (21.1±3.6 for males and 20.2±2.2 for females) in the 2019 National Nutrition and Health Survey (p=0.790, p=0.619). NBS-FT4 was slightly positively correlated to AR age (r=0.234, p=0. 0315). We found that the AR age may be earlier and adult BMI may be higher in CH patients without ossification of the distal femoral epiphyseal nucleus at first evaluation.

Discussion
Severe fetal hypothyroidism may cause an absence of mineralization of the distal femoral epiphyses in the neonatal period. Our results indicate that severe fetal hypothyroidism, even if diagnosed and treated at neonatal, contributes to the development of adult obesity.

Conclusion
The AR age and BMI at 15-18 years of CH are not significantly different from the general population. However, severe fetal hypothyroidism could result in adult obesity.
Presentation: No date and time listed
ODP462 Amiodarone Induced Thyrotoxicosis-Treatment Challenges
Authors: Firak Gabriela , Gabriely Ilan , Leu James , Zahedpour Sara , Magaji Vasudev , Singh Vinita , Sherpa Chheki , Shrestha Bishow 
Published: November 2022

Abstract
Amiodarone induced thyrotoxicosis (AIT) presents a diagnostic and treatment challenge. Importantly, uncontrolled thyrotoxicosis can be associated with significant morbidity and mortality. The following presentation depicts a case of AIT with persistent thyrotoxicosis despite optimal and prolonged medical therapy. The case was complicated by patient's high-risk cardiovascular profile postponing definitive therapy with thyroidectomy. Patient was a 58-year-old female with past medical history of coronary artery disease, severe systolic heart failure, atrial fibrillation, and ventricular tachycardia maintained on amiodarone therapy since 2019, who was noted to have abnormal thyroid function labs in 2021 with TSH of 0. 04 uIU/mL (0.45-5.3), free T3 of 4.6 pg/mL (2.2-4.1) and free T4 of 2.7 ng/dL (0.58-1.64) indicative of hyperthyroidism. Her evaluation included negative family history of thyroid disorder, negative thyroid antibody profile, as well as a thyroid ultrasound that demonstrated no thyroid enlargement, no nodules and normal vascularity. At the time of initial evaluation, patient was suffering from episodes of atrial fibrillation with rapid ventricular response. Patient was diagnosed with AIT (presumably type 1). Amiodarone was discontinued and patient was initiated on methimazole 10 mg twice daily. Unfortunately, three weeks after initiation of methimazole treatment, patient's clinical status deteriorated and she was hospitalized for multifactorial shock requiring multidisciplinary approach and vasopressor/ionotropic support. At that time her free T4 had risen to &gt;5.6 ng/dL and free T3 peaked at 6.17 pg/mL. The most probable diagnosis was AIT type 2 and her medical therapy was augmented to methimazole 20 mg three times daily and prednisone 50 mg daily. After clinical stabilization, she was discharged home on this regimen. Unfortunately, her thyroid function tests remained persistently elevated for almost three months despite maximum medical therapy. At that point, patient was referred for thyroidectomy despite severe cardiomyopathy and high-risk surgical profile. Fortunately, her thyroid function tests began to improve prior to planned surgery and medical therapy was successfully de-escalated, precluding the need for surgical intervention. While most cases of AIT can be successfully treated with medical therapy, refractory cases can present a clinical challenge, especially in patients at high risk for thyroidectomy. Weighing the risks and benefits of each treatment plan requires a multi-disciplinary approach and close communication with all parties involved.
Presentation: No date and time listed
ODP464 Association between preoperative vitamin D insufficiency and postoperative symptomatic hypocalcemia in patients with thyroid cancer
Authors: Ram Hong A , Choi Wonsuk , Park Ji Yong , Yoon Jee Hee , Kim Hee Kyung , Kang Ho-Cheol 
Published: November 2022

Abstract

Background
It is controversial whether vitamin D insufficiency (VDI) increases the risk of postoperative hypocalcemia and decreases the predictive power of parathyroid hormone (PTH) for postoperative hypocalcemia in patients undergoing total thyroidectomy (TT). Here, we investigated the role of VDI in the development of postoperative symptomatic hypocalcemia and assessed its effect on the predictive power of PTH as a marker for postoperative symptomatic hypocalcemia in thyroid cancer patients who underwent TT plus central compartment neck dissection (CCND).

Methods
All consecutive differentiated thyroid cancer patients who underwent TT plus CCND between January 2017 and December 2020 at a single tertiary referral hospital were retrospectively reviewed. Patients were divided into two groups according to their preoperative 25-hydroxyvitamin D (25(OH)D) levels (&lt; 20 vs. ≥ 20 ng/ml). Postoperative symptomatic hypocalcemia was defined as ionized calcium &lt; 2.2 mEq/l on postoperative day 1 and positive symptoms or signs of hypocalcemia. The effects of exposure on postoperative symptomatic hypocalcemia were analyzed using a multivariate logistic regression model.

Results
The incidence of postoperative symptomatic hypocalcemia was comparable between patients with and without VDI (P= 0.252). Preoperative VDI was not associated with the development of postoperative symptomatic hypocalcemia (OR = 1. 07, 95% CI 0.73 to 1.56, P= 0.744). Postoperative hypoparathyroidism (iPTH &lt; 15 pg/ml) was associated with the development of postoperative symptomatic hypocalcemia in both VDI and non-VDI patients (OR = 6.78, 95% CI 3.88 to 11.85, P&lt; 0. 001 and OR = 9.68, 95% CI 3.86 to 24.28, P&lt; 0. 001, respectively).

Conclusions
VDI did not predict postoperative symptomatic hypocalcemia after TT plus CCND in thyroid cancer patients and did not influence the predictive power of postoperative PTH for postoperative symptomatic hypocalcemia. Therefore, prophylactic calcium and vitamin D supplementation in patients with VDI should be carefully considered in thyroid cancer patients.
Presentation: No date and time listed
ODP475 Developing suppurative thyroiditis
Authors: Katwal Dilasha , Aziz Shima , Lequerica Joe , Steinberg Helmut 
Published: November 2022

Abstract

Suppurative thyroiditis is rare and associated with significant mortality. A high level of suspicion and aggressive management is needed to reduce the risk of serious outcomes. A 67-year-old male with a medical history including diabetes type 2, cognitive impairment, and ESRD presented with decreased appetite and lethargy for a few days. He presented with fever, tachycardia, and hypertension. There was a non-tender fullness around the anterior neck region. Initial laboratory tests revealed leukocytosis to 24K/uL, lactic acid of 5. 0 mmol/L, ESR 100 mm/hr, CRP 419 ng/dl, and blood culture was positive for gram-positive cocci in clusters for which he was started on iv vancomycin and piperacillin/tazobactam. CT scan on admission showed a probable inflammatory process in the neck originating from the thyroid bed, concerning acute thyroiditis and developing abscess/abscesses vs. very atypical presentation of thyroid cancer. Thyroid ultrasound showed diffuse thyroid enlargement with heterogeneous echogenicity. Repeat CT obtained due to apparent thyroid enlargement with erythema and tenderness on examination and fever on day 7 showed extensive heterogeneous thyroid enlargement with ill-defined margins to the adjacent soft tissue structures. A modified barium swallow revealed severe oropharyngeal dysphagia leading to thyroid fine-needle aspiration of both thyroid lobes by interventional radiology and subsequent urgent incision and drainage (I&D) of the right neck and thyroid biopsy under general anesthesia by ENT. I&D showed purulent drainage from the thyroid. Cultures were positive for MRSA. Surgical pathology reported a necrotic muscle and abscess and fragment of thyroid tissue. Thyroid function tests (TFTs) on admission revealed a TSH 0.31 mcIU/ml (reference: 0.30 - 5. 0 mcIU/ml) and a free T4 of 2.21 ng/dl (reference: 0.76- 1.46 ng/dl) and repeat TFTs with a TSH of 0.30 mcIU/mL, free T4 of 1.87 ng/dL, free T3 of 2.15 pg/ml (reference: 2.18- 3.98 pg/ml), consistent with sick euthyroid syndrome. TPO and TSI were negative. Subsequently, the patient's fever resolved, and the neck swelling improved. He continued IV vancomycin for a month. TFTs six weeks later showed an elevated TSH of 13.10 mcIU/ml and normal free T4 of 1. 03 ng/dl.

Conclusion
MRSA suppurative thyroiditis is rare, and its diagnosis may be delayed due to its indolent course, especially in immunocompromised patients. Therefore, a high index of clinical suspicion is needed for this endocrine emergency in a patient presenting with fever and neck swelling. While an early FNA of the thyroid is likely to aid in diagnosing thyroid infection, TFTs may be variable and not helpful.
Presentation: No date and time listed