bluuebunny/crossref_metadata_2025_split huggingface dataset:
LBSAT291 Familial Papillary Thyroid Carcinoma
Authors: Arora Gunjan 
Published: November 2022

Abstract

Introduction
Familial papillary thyroid carcinoma is a rare entity; however, it must be considered if a strong family history of non medullary thyroid carcinoma is noted. As this cancer presents earlier and with more aggressive features with each subsequent generation, a targeted diagnostic and management approach should be utilized.

Case Presentation
A 26 year old female presented to the PCP after sustaining head trauma while kickboxing. During the visit, she requested for thyroid evaluation due to a strong family history of thyroid cancer in her mother, maternal aunt, maternal uncle and maternal grandfather. She reported that her mother was diagnosed with thyroid cancer at the age of 40 years; however, she was unaware of further details. She denied any personal history of cancer or exposure to radiation. An extensive review of systems was negative. TSH was within the normal range 2.65 uIU/ml (0.40 - 4. 0). Thyroid ultrasound showed a 1.1 cm nodule in the right thyroid lobe with microcalcifications suspicious for malignancy. Fine needle aspiration cytology of the nodule confirmed papillary thyroid carcinoma. A preoperative CT neck and soft tissue was negative for cervical lymphadenopathy per size criteria. She underwent a total thyroidectomy with neck dissection. Surgical pathology report showed 1.8 cm right thyroid lobe papillary carcinoma and 13 lymph nodes positive for metastatic carcinoma, the largest measuring 0.4 cm. Post-operatively, she underwent radio-active iodide therapy and was started on Levothyroxine supplementation. She was closely monitored with serial thyroid function tests, thyroglobulin levels and thyroid ultrasound examinations. Tempus XT positive for BRAF and FOXP1. Approximately one year after the surgery, serum thyroglobulin levels started to plateau. A surveillance thyroid ultrasound was concerning for left lobe thyroid tissue remnant/cancer. Thus, a radio-active iodine total body scan was planned to locate the remnant thyroid tissue followed by biopsy and excision in case of recurrent cancer.

Discussion
Papillary thyroid cancer runs in families and becomes more aggressive with each subsequent generation. The American Thyroid Association guidelines detail that screening with thyroid ultrasound should be considered in families with three or more family members affected by familial non medullary thyroid cancer. In addition, certain mutations such as the BRAF mutation are associated with aggressive clinicopathological characteristics and high tumor recurrence. There is limited data available on the FOXP1; however, it may also be linked to an aggressive course. Therefore, screening ultrasound should be offered in such patients and FNAC samples should be sent for genetic analysis to help formulate an appropriate treatment plan. These patients benefit from receiving early screening, more intensive management and frequent follow up.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
LBSAT313 Hashimoto Encephalitis Presenting With Stroke-like Symptoms In An Adult Male
Authors: Canales Shellsea Portillo , Loria Gloriana Madrigal , Sanchez Valenzuela Maria C , Fernandez Felix Daniel A , Castano Yennifer Gil , Sharma Sapna , Arias Morales Carlos E 
Published: November 2022

Abstract
Hashimoto encephalopathy (HE) is a term used to describe an encephalopathy of presumed autoimmune origin characterized by high titers of antithyroid peroxidase antibodies, an essential feature of this disorder. Pertinent laboratory findings include an elevated serum level of antithyroid peroxidase antibody (TPOAb) and/or antithyroglobulin antibody (TgAb) and negative autoimmune markers of encephalitis in cerebrospinal fluid (CSF). The analysis of CSF may show increased cellularity due to lymphocytic pleocytosis. However, there is no clear relationship between the severity of neurologic symptoms and the type or serum concentration of antibodies. Approximately two-thirds of patients of HE will experience seizures. Patients can present with a recurrence/remission or a diffuse, progressive pattern characterized by slowly progressive cognitive impairment with dementia, confusion, or hallucinations. We present a rare case of Hashimoto's encephalopathy associated with hyperthyroidism in a 61-year-old man evaluated for left facial droop and right upper extremity weakness, successfully treated with corticosteroids and methimazole. We conclude that the diagnosis of HE should be suspected early and be on the differential in patients who present with encephalopathy, which workup shows positive anti-thyroid antibodies and CSF with lymphocytosis. Treatment for meningitis or other life-threatening conditions should never be postponed, as HE is a diagnosis of exclusion that usually requires an extensive laboratory and diagnostic workup. Early diagnosis has an excellent outcome once treatment is started as it is a steroid-responsive encephalopathy associated with autoimmune thyroiditis.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
ODP453 A Lady Changes from Hypothyroid to Hyperthyroid State during Pregnancy
Authors: Ho Cheuk Wah 
Published: November 2022

Abstract
A 34-year-old lady presented to the Endocrine Clinic in 2021 initially for hypothyroidism complicated pregnancy. She volunteered history of Graves’ disease at age 11 and went into remission after taking anti-thyroid medication for 1-2 years. She did not have family history of thyroid disease. She was found to have hypothyroidism during pre-pregnancy check-up in 2017 and started thyroxine (LT4) replacement. The anti-thyroid peroxidase antibody was elevated to 358 (&lt; 35) kIU/l. She had first pregnancy in early 2018 and LT4 was increased to 128 microgram daily which was reduced to 50 microgram daily after delivery. Before the second pregnancy, her TSH was decreasing. The family doctor reduced LT4 to 25 microgram 5 days per week. The TFT just before the patient became pregnant showed TSH 0. 08 (0.35-3.8)mIU/l, fT4 15 (9.5-18.1) pmol/l. At 8th week of pregnancy, her TSH became undetectable, while fT4 was 20.8 (11.8-25.7)pmol/l. At 17th week, her fT4 further increased to 19.9 (10.1-19.4) pmol/l and fT3 was 7.3 (3.25-5.2)pmol/l. TSH remained undetectable. Clinically, she complained of palpitation. She had goiter but no thyroid bruit. Her pulse rate was 118 bpm. LT4 was stopped. She was suspected to have relapse of thyrotoxicosis. Anti-TSH receptor antibody was raised to 3.3 (&lt;1. 0) IU/l. The thyroid stimulating immunoglobulin (TSI) was raised to 155% above baseline activity (nl&lt;140%). At 22th week, her fT4 remained elevated at fT4 19.1 (9.2-17.44), fT3 7.6 (3. 03-4.75) pmol/l. Carbimazole was started at 5mg daily for 2 weeks then 5mg alternate day. At 28th week, her fT4 was still elevated fT4 17.7 (9.2-17.4), fT3 6.9 (3. 03-4.75) pmol/l. She was also noted to have poor maternal weight gain from 61kg pre-pregnancy to 62.4kg at 22th week. She had nausea and vomited once per week. She had iron deficiency anaemia requiring iron supplement. Carbimazole was increased again to 5mg daily for 3 weeks then tailed down to 5mg alternate day. At 33th week, her anti-TSH receptor antibody level reduced to 1.9. At 36th week of gestation, her fT4 level came down to mid normal range 14.1 (9.2-17.4)pmol/l. She delivered at 40th week uneventfully. There are a number of clinical challenges. Usually, the dose of thyroxine is increased by 30% in early pregnancy with TSH aim of 0.5-2. 0mIU/l. But in this patient, the TSH was already low before pregnancy and then became undetectable so LT4 was not increased. Gestational thyrotoxicosis is a differential diagnosis but seldom persisted towards second trimester and TSI is expected to be normal in such case. Graves’ disease usually becomes quiescent during pregnancy due to immunosuppression or haemodilution of autoimmune antibodies. Changing from hypothyroidism to hyperthyroidism is a rare phenomenon. It is related to the concentration and the affinity of anti-thyroid stimulating antibodies and blocking antibodies. The outcome depends on which antibodies predominate.
Presentation: No date and time listed
ODP586 Analysis of Adrenal Vein Sampling (AVS) Success: A Retrospective Study of Primary Aldosteronism Patients at the National University of Malaysia (UKM) Medical Center
Authors: Azizan Elena Aisha , Sukor Norlela , Zakaria Rozman , Nazri Syed Mohammed , Khadijah Siti 
Published: November 2022

Abstract
Currently, the gold standard for identifying a unilateral Primary Aldosteronism (PA) is adrenal vein sampling (AVS), an invasive and technically challenging procedure. In this study, we aim to identify the clinical-laboratory characteristics associated with successful AVS, and clinical parameters associated with PA patients that had successful AVS (on 1st, 2nd, or 3rd attempt), or had rejected further attempts after a failed AVS attempt.100 records of AVS from eighty-three AVS patients conducted between 2015 and 2020 at the National University of Malaysia (UKM) Medical Centre, Kuala Lumpur, Malaysia were analysed retrospectively. Of the 83 PA patients studied, 47 were performed on men and 36 were on women. Variables significantly associated with patients who booked for a further attempt of AVS was having a serum aldosterone of &lt;300pg/ml compared to those who rejected further attempts. There was also a trend for those who rejected further attempts to have a shorter duration of hypertension. Over one third of patient's have a failed AVS on 1st attempt and more than half do not wish to reattempt this invasive procedure. A biomarker for those that achieve complete cure should be identified to give incentives to the PA patients to proceed with AVS.
Presentation: No date and time listed
ODP466 Case of Sporadic Medullary Thyroid Cancer Detected by Serum Calcitonin Measurement
Authors: Juneau Andrea Kate , McMullen Kyle , Uwaifo Gabriel 
Published: November 2022

Abstract

Introduction
Thyroid nodules are common and their prevalence has increased with more widespread neck sonography. While most thyroid nodules are benign their evaluation and surveillance is centered around identifying nodules that harbor malignant growths. While secular trends suggest progressively increasing prevalence of thyroid cancer, it is largely an indolent generally curable disease. Medullary thyroid cancer (MTC) is comparatively rare (3-5% of all thyroid cancer) and significantly more virulent than the common papillary thyroid cancer. Guidelines regarding screening for potential MTC remain controversial. We describe the case of a patient with sporadic MTC detected by routine serum calcitonin measurement. Clinical case; The patient is a 52 yr old Caucasian man referred after a serendipitous finding of thyroid calcifications found on Neck and Chest CT done for radiculopathy evaluation. He had no neck symptoms and no anomalies on clinical neck examination nor history of radiation exposure nor relevant family neoplastic history. The neck ultrasound showed a multinodular goiter with a dominant hypoechoic 1.4 cm nodule in the right hemi-thyroid with microcalcifications (TIRADS 5). The nodule biopsy showed pauci-cellular specimen with abundant colloid and the patient had opted for repeat serial sonography rather repeat biopsy because of his unpleasant experience with the first biopsy. Routine initial endocrine evaluation included thyroid function tests (normal) and a random serum calcitonin; 267 (n; &lt;15pg/ml). This degree of elevation was confirmed on repeated measures. A calcitonin stimulation test with calcium gluconate showed a peak stimulated calcitonin of 786 pg/ml. Total thyroidectomy and central neck dissection, confirmed a diagnosis of MTC (T1a N1a Mx). Only one of six sampled neck lymph nodes showed metastatic disease. RET mutation testing was -ve and 4 months post surgery his calcitonin is 97pg/ml with no radiologic evidence of any residual or recurrent disease.

Discussion
The patient's clinical presentation is typical of sporadic MTC (found serendipitously) which while uncommon is more prevalent than familial MTC and has a significantly more virulent clinical course than the much more prevalent classic papillary thyroid cancer. It also has significantly less cure potential and greater morbidity and mortality risk making early detection and aggressive management even more vital. Despite not being included in many guidelines for standard evaluation of thyroid nodules the random calcitonin obtained in the patient was central to the prompt and correct diagnosis of the patient.

Conclusions
Despite the limitations and caveats to its interpretation, our case highlights the potential utility of routine serum calcitonin measurement as part of the routine screening work up of thyroid nodules even in so called "low risk" clinical presentations with no clinical flags suggestive of possible familial MTC or MEN 2.
Presentation: No date and time listed
ODP468 Checkpoint Inhibitor Immunotherapy- related Thyroid Disorders and Iodine Contrast Studies
Authors: Borges Espinosa Luis , Dicenso Daniela , Rodriguez Valentina 
Published: November 2022

Abstract

Introduction
Checkpoint Inhibitor Immunotherapy (CII) has been linked to multiple endocrinopathies. Thyroid dysfunction is more frequently associated with anti-PD-1 and anti-PD-L1 monoclonal antibody use, yet there are no good predictors for the development of thyroid complications after immunotherapy treatment. Iodinated contrast studies have been related to the development of thyroid dysfunction, and are frequently used in the oncology patient population for surveillance of malignancy and response to treatment.

Methodology and Results
We conducted a retrospective observational study to identify any potential association between the development of thyroid dysfunction and exposure to iodinated contrast studies in patients receiving CII. A chart review was conducted from 2012-2020. Data analysis was performed using Chi-square. Using ICD codes, 236 patients with new thyroid dysfunction after initiation of CII, and no alternative etiology for the thyroid dysfunction, were included. Out of these, 162 (68.6%) patients developed hypothyroidism, 71 (30%) developed thyrotoxicosis initially and subsequently developed hypothyroidism, and 3 (1.27%) developed hyperthyroidism. Of the total patients who developed thyroid dysfunction following CII, 145 vs.91 patients received ≥3 contrast studies, (p. 0. 0004).

Discussion
These findings suggest that there is an association with the use of three or more iodinated contrast studies and the development of thyroid dysfunction in patients receiving CII. More research is needed to identify additional predictors that could be utilized in clinical practice for earlier detection of patients at risk of developing CII related thyroid dysfunction.

Conclusion
Thyroid dysfunction following the use of CII, namely anti-PD-1 and anti-PD-L1 therapies, remains prevalent; however, it has been difficult to identify who is most at risk for this complication. This is the first study examining exposure to iodinated contrast and its potential contribution to CII thyroid endocrinopathy, and it warrants further investigation.
Presentation: No date and time listed
ODP596 Central Adrenal Insufficiency After Intra-Articular Triamcinolone Injection In A Patient On Dolutegravir And Cobicistat Boosted Darunavir
Authors: Chen Ying , Wong Beatrice Y , Shah Sejal 
Published: November 2022

Abstract

Background
Central adrenal insufficiency from drug-drug interaction between steroids and HIV anti-retroviral medications is a well-documented phenomenon in the literature, but in clinical practice making this diagnosis can prove challenging.

Clinical Case
58-year-old woman with well-controlled HIV on dolutegravir and cobicistat/darunavir, type 2 diabetes mellitus, and chronic kidney disease presented to our emergency department with 3 days of polyuria, polydipsia, headaches, nausea, and decreased appetite. She also noticed that her glucose readings have been much higher than usual. 5 days prior to presentation, she received a 40 mg triamcinolone acetonide injection into her right subacromial bursa for chronic shoulder pain. For diabetes, she had been on the same dosage of weekly dulaglutide with good control. Initial laboratory evaluation revealed elevated serum glucose of 763 mg/dl (70 - 140 mg/dL) without an elevated anion gap, sodium of 124 mEq/L (135 - 145 mEq/L) and potassium of 5.9 mmol/L (3.6 - 5.2 mmol/L). Morning cortisol was sent as part of the workup for hyponatremia and returned low at 1.2 ug/dL (4 - 20 ug/dL). A 250 mcg cosyntropin stimulation test was performed, with baseline cortisol at 1.3 ug/dL and one-hour post-stimulation cortisol of 8.8 ug/dL. Pre-stimulation ACTH was &lt; 5. 0 pg/mL (10 - 60 pg/mL). A synthetic glucocorticoid panel were sent on the 11th day after her injection and detected triamcinolone acetonide at 3.3 mcg/dL (cutoff: 0.1 mcg/dL) in urine and 0.85 mcg/dL (cutoff: 0.1 mcg/dL) in serum. She was diagnosed with iatrogenic adrenal insufficiency from intra-articular triamcinolone injection, the effect of which had been potentiated by her HIV medications cobicistat and dolutegravir (both CYP3A4 inhibitors). She was started on hydrocortisone and experienced improvement in appetite and fatigue. A plasma renin activity assay was elevated at 7.66 ng/mL/h (0.25 - 5.82 ng/ml/h) with 15 ng/dL of aldosterone (3 - 16 ng/dL). While awaiting the ACTH result, we discussed the possibility of primary adrenal insufficiency given persistent hyponatremia despite improved glucose control. However, given recent normal cross-sectional abdominal imaging, the history of steroid exposure, and lack of opportunistic infections in the past, central adrenal insufficiency remained the leading diagnosis. Further workup, including urine anion gap, eventually determined the cause of her hyponatremia to be a type 4 RTA likely related to her longstanding history of diabetes. The patient was discharged home on hydrocortisone with plan for repeat stimulation test in 6 weeks.

Conclusion
1. Keep primary adrenal insufficiency in mind in a patient with HIV who presents with hyponatremia and low cortisol. 2. Steroid injections carry risks of significant hyperglycemia and iatrogenic adrenal insufficiency in patients receiving cobicistat and integrase inhibitor.
Presentation: No date and time listed
ODP490 Levothyroxine Dosing Based on BMI and Different Causes of Hypothyroidism
Authors: Darquea Andres , Izquierdo Roberto , Huang Danning , Greenfield Margaret 
Published: November 2022

Abstract
While several approaches can be used when initiating levothyroxine therapy, it is commonly stated that total levothyroxine dose can be calculated as a function of the person's body weight. 1.6 mcg/kg of body weight. But studies have suggested that other factors must be assessed when trying to calculate a total daily dose. The cause of a patient's hypothyroidism may have an effect on their actual replacement needs. It is not the same to consider a patient with postsurgical hypothyroidism who has had all thyroid tissue completely removed versus Hashimoto's or Radioactive Iodine ablation where some thyroid function may be preserved. It is also important to consider a patient's ideal body weight as studies have shown that ideal body weight rather than actual body weight may be more useful in determining a patient's ultimate levothyroxine requirements. As the prevalence of obesity is increasing in the United States and worldwide, factors such as BMI may start playing a more important role when deciding initiation dosage in these patients. We conducted a retrospective chart review with a total of 260 hypothyroid patients on levothyroxine and with two stable TSH values on the same dose. We divided the patient into three BMI categories. &lt;= 24.9, 25-29.9 and &gt;=30. Patients with BMI &lt;= 24.9 had a levothyroxine mean (SD) dose of 1.5 MCG/KG (0.63), those with a BMI 25-29.9: 1.3MCG/KG (0.44), and those with a BMI &gt;=30: 1.1MCG/KG (0.45). P Value &lt;0. 001. When further subdivided into the cause of hypothyroidism (Hashimoto's, post surgical and radioactive iodine), the effects of BMI on levothyroxine dose seem to also be affected. In postsurgical hypothyroidism, patients with BMI &lt;= 24.9 had a levothyroxine mean (SD) dose of 1.8 MCG/KG (0.47), BMI 25-29.9: 1.5MCG/KG (0.21) and BMI &gt;=30: 1.4MCG/KG (0.38). P Value &lt;0. 001. Patients with Hashimoto's with BMI &lt;= 24.9 had a levothyroxine mean (SD) dose of 1.3 MCG/KG (0.65), BMI 25-29.9: 1.1MCG/KG (0.50) and BMI &gt;=30: 0.9MCG/KG (0.44). P Value &lt;0. 001. In patients with hypothyroidism due to radioactive iodine therapy, the levothyroxine dose for those with BMI &lt;= 24. was 1.4 MCG/KG, BMI 25-29.9: 1.2MCG/KG (0.53) and BMI &gt;=30: 1.2MCG/KG (0.39). P Value 0.883 These results suggest that when initiating levothyroxine therapy, a starting dose of 1.6 MCG/KG is not adequate for all patients and that BMI and cause of hypothyroidism should be considered before making this decision.
Presentation: No date and time listed
ODP500 Nephrotic syndrome as a cause of worsening hypothyroidism due to Hashimoto's thyroiditis
Authors: Thewjitcharoen Yotsapon , Nakasatien Soontaree , Butadej Siriwan , Veerasomboonsin Veekij , Himathongkam Thep 
Published: November 2022

Abstract

Background
Thyroid function has been reported to worsen when urinary protein levels increase from the loss of protein-bound thyroid hormones, such as thyroxine-binding globulin, transthyretin, and albumin, into the urine. In patients with previously undiagnosed Hashimoto's thyroiditis, subclinical hypothyroidism and overt hypothyroidism might develop at the onset of nephrotic syndrome. Here, we present an interesting case of Hashimoto's thyroiditis aggravated by newly developed nephrotic syndrome. Clinical case: A 43-year-old woman with no known underlying disease presented with generalized edema and weight gain of 5 kgs over 2 months. Physical examination revealed slightly enlarged thyroid goiter and pitting pedal edema. Thyroid function tests revealed hypothyroidism (FT4 0.71 ng/dL; reference range 0.93-1.70 ng/dL, TSH 8.32 uIU/mL; reference range 0.27-4.20 uIU/mL). Anti-thyroid peroxidase was negative but anti-thyroglobulin was positive. Thyroid ultrasound showed diffused heterogeneous parenchymal echotexture at both thyroid lobes, compatible with Hashimoto's thyroiditis. Subsequent investigations showed nephrotic range proteinuria (urine protein/creatinine ratio 7.5 grams), low serum albumin 2. 0 g/dL, and hypercholesterolemia 421 mg/dL. Viral infections including HIV, hepatitis B and C were negative. Kidney biopsy showed the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane, confirming membranous glomerulonephritis as a cause of nephrotic syndrome. Further investigations did not show potential secondary causes of membranous glomerulonephritis. Oral prednisolone and cyclosporin was given to treat nephrotic syndrome and levothyroxine 350 µg/week was initiated to treat hypothyroidism. Over the next 6 months, nephrotic syndrome went into remission and thyroid function tests showed stabilization. During a 3-year follow-up period, patient is still in stable condition with levothyroxine 450 µg/week.

Conclusion
Nephrotic syndrome may trigger the onset of hypothyroidism or aggravate preexisting hypothyroidism, with subsequent increase in thyroid hormone requirements. Careful history taking and physical examination are necessary when evaluating the patients with new-onset hypothyroidism or patients with worsening hypothyroidism. The diagnostic workup of patients with increasing requirements of thyroid replacement therapy should not be concentrated on the digestive system alone.
Presentation: No date and time listed