bluuebunny/crossref_metadata_2025_split huggingface dataset:
7385 Prevalence of Central Hypothyroidism in Cushing Syndrome and Thyroid Function Tests After Cushing Treatment
Authors: Kunavisarut Tada , Sriwijitkamol Apiradee 
Published: October 2024

Abstract
Disclosure: T. Kunavisarut: None. A. Sriwijitkamol: None.
Cushing syndrome can be associated with thyroid dysfunction. We investigated the association between Cushing syndrome and thyroid dysfunction. We conducted a retrospective study at Siriraj Hospital in Thailand and analyzed thyroid function tests in 80 Cushing's patients. The inclusion criteria were patients diagnosed with Cushing syndrome with thyroid function tests recorded at diagnosis of Cushing syndrome. Patients who had an abnormal thyroid function test at diagnosis of Cushing syndrome must have a thyroid function test after treatment of Cushing syndrome. Of the 80 patients, sixty-five patients (81.2%) had normal thyroid function at diagnosis, 12 patients (15%) had central hypothyroidism and three patients (3.8%) had subclinical hyperthyroidism.Interestingly, among 12 patients who had central hypothyroidism, eight patients (66.7%) were diagnosed with Cushing disease. Three patients (25%) were diagnosed with adrenal Cushing syndrome and one patient (8.3%) was diagnosed with ectopic Cushing syndrome. This finding suggested that central hypothyroidism may not be exclusively due to the mass effect of the pituitary tumor on the normal pituitary because adrenal Cushing syndrome and ectopic Cushing syndrome can also cause central hypothyroidism. Among 12 patients with central hypothyroidism at diagnosis of Cushing syndrome, nine patients (75%) normalized their thyroid function after remission of Cushing syndrome without Levothyroxine replacement. Moreover, patients with central hypothyroidism had significantly higher median 24-hour urine-free cortisol levels than euthyroid patients (1030.5 ug/day vs. 404.5 ug/day, p=0.017), indicating a potential correlation between cortisol excess and low FT4 levels. These findings suggest that hypercortisolism in Cushing syndrome can suppress the hypothalamic-pituitary-thyroid axis, but this suppression is often reversible with successful Cushing's treatment. This study highlights the importance of central hypothyroidism, which can occur in all types of Cushing syndrome. If the patients did not have hypothyroid symptoms, Levothyroxine replacement may not be necessary. For patients who already received Levothyroxine and had normal thyroid function tests, Levothyroxine can be carefully tapered and potentially discontinued because successful Cushing syndrome treatment can ultimately normalize thyroid function tests.
Presentation: 6/1/2024
8751 Radiofrequency Thermal Ablation in 32 Patients with Toxic Adenomas with Resolution of Hyperthyroidism in All Cases
Authors: Lima Amato Lorena Guimaraes , Martinho Volpi Erivelto , Moura Volpi Leonardo De , Machado Carani Pedro Henrique , Rahal Antonio 
Published: October 2024

Abstract
Disclosure: L.G. Amato: None. E.M. Volpi: None. L.D. Volpi: None. P.M. Carani: None. A. Rahal: None.
Introduction: In the general population, thyroid nodules are found in 3-7% of individuals on physical examination and in 20-76% on ultrasound. Around 8-10% of benign nodules may present autonomous behavior, being called hot nodules, causing symptoms of hyperthyroidism and being called toxic adenomas (TA). In TAs, autonomous hormone production can be caused by somatic activating mutations of genes regulating thyroid growth and hormone synthesis caused by somatic activating mutations of genes regulating thyroid growth and hormone synthesis. Classically, the proposed treatment for autonomous nodules was surgical resection or radioiodine ablation (RAI). In this context, the prevalence of hypothyroidism after the procedure varies from 2% to 3% following lobectomy, and lower after isthmusectomy in the unique circumstance in which the TA is confined to the thyroid isthmus. A study following 684 patients with TA treated with RAI reported a progressive increase in overt and sub-clinical hypothyroidism. Potential complications following near-total/total thyroidectomy include the risk of permanent hypoparathyroidism (&lt; 2.0%) or recurrent laryngeal nerve injury (RLN) (&lt; 2.0%). A small risk of permanent RLN injury exists with surgery for TA. Following RAI therapy, there have been reports of new-onset Graves Disease (up to 4% prevalence) as well as concern for thyroid malignancy and a very minimal increase in late non thyroid malignancy. Radiofrequency ablation (RFA) has been a precise and effective alternative for the treatment of many benign thyroid nodules over the past ten years, including hot nodules. RFA could preserves normal thyroid function compared to surgery or RAI. Clinical case: We evaluated the effectiveness of a single session of RFA in 32 patients with TA, through hormonal status, achieving normalization of thyroid and volumetric reduction of the nodule. Among the 32 patients included in this study, aged between 25 and 88 years, of these, 31 were women and 1 was a man, all of whom underwent a single RFA procedure (“moving shot” technique associated with hydrodissection). We had a single case of a reversible complication: a patient who had transient vocal cord paralysis, with total reversal. There was a reduction in the volume of all nodules as well as all patients progressed to a state of euthyroidism within 60 days of follow-up. Conclusion: A single session of RFA was effective in treating autonomous nodules, restoring euthyroidism in all patients.
Presentation: 6/3/2024
7009 Resistance to Thyroid Hormone
Authors: Gill Simranpreet , Chavez Luis F 
Published: October 2024

Abstract
Disclosure: S. Gill: None. L.F. Chavez: None.
Resistance to thyroid hormone is a unique phenomenon presenting with a variety of clinical findings due to biochemical elevations in thyroid hormones. We describe a case of a 52 year old male diagnosed with hypertension at age 25 followed by atrial flutter resulting in tachycardia induced cardiomyopathy who presented to the emergency department for lightheadedness and palpitations. He was found to be in atrial flutter and converted to normal sinus rhythm after receiving diltiazem. Labs showed a T4 of 17.4 with a TSH of 2.48. On examination, he was back to baseline and denied heat intolerance, changes in bowel habits, weight loss, hair loss, sweating, recent falls or fragility fractures, and in fact felt cold. Physical exam was remarkable for goiter. Patient was previously referred to endocrinology given an elevated FT4 and total T3 with a non-suppressed TSH level concerning for a TSH producing adenoma. He underwent extensive hormonal workup that revealed normal pituitary functioning apart from elevated FT4, FT3, and FT4 by dialysis. MRI of the brain was performed on two occasions, last done a few months prior to hospitalization which showed no focal lesions in the sella or parasellar regions. Given normal TSH and elevated FT4 levels in the setting of negative imaging, patient thought to likely have resistance to thyroid hormone (RTH). RTH is a rare inherited condition seen in as few as 1 in 40, 000 live births. It stems from an inability of target cells to respond appropriately to thyroid hormones due to dysfunction of thyroid hormone receptors (TRs). The most common variant of RTH is due to a mutation in the THRB gene encoding thyroid hormone receptor beta (RTH beta) located on chromosome 3 followed by defects in the THRA gene encoding thyroid hormone receptor alpha (RTH alpha) located on chromosome 17. Others may not have an identifiable genetic defect and are thought to be due to alterations in TR cofactors. Elevations of all three serum iodothyronines with non-suppressed TSH is seen with RTH beta while borderline high T3 and normal or slightly elevated TSH is seen in RTH alpha. Inadequate response to thyroid hormones can lead to feedback mechanisms attempting to resolve this relative deficiency by promoting synthesis of higher than normal thyroid hormone levels. Treatment is usually not required due to this adaptive mechanism but on occasion levothyroxine is supplemented to normalize the TSH in patients with limited thyroid reserve. Despite elevated circulating thyroid hormones, individuals can be clinically euthyroid or experience symptoms of thyroid hormone excess or deficiency. Conditions mimicking RTH including TSH producing adenomas should be ruled out which present with overt hyperthyroidism as opposed to the more subtle symptoms that can be seen with RTH. Overall, clinicians should be aware of RTH to prevent misdiagnosis and pursue treatment modalities that may otherwise not have been needed.
Presentation: 6/1/2024
6415 Resistance to Thyroid Hormone -A Challenge to Manage
Authors: Altaf Areeba , Iqbal Fizzah , Hamoudeh Eyad , Coyne Christopher , Anne Kiraithe , Buckley Lisa 
Published: October 2024

Abstract
Disclosure: A. Altaf: None. F. Iqbal: None. E. Hamoudeh: None. C. Coyne: None. K. Anne: None. L. Buckley: None.
Background: Resistance to thyroid hormone (RTH) or Refetoff syndrome was first introduced in 1967. It is an autosomal dominant or recessive genetic disease with a mutation in the thyroid hormone receptorβ (THR-β) gene or the thyroid hormone receptorα (THR-α) gene. The distinguishing biochemical feature of RTHβ is an elevated level of circulating free thyroid hormones with normal or high TSH concentration and decreased peripheral tissue response to thyroid hormone. Common signs and symptoms in patients with RTHβ are short stature, attention deficit disorder, and resting tachycardia and many patients might be asymptomatic. Case: We report a case of a 36-year-old patient with past medical history of congenital bilateral hearing loss, atrial fibrillation, CHF, and slow learning/comprehending who presented to the ER with shortness of breath and atrial fibrillation with tachycardia. Admission labs revealed elevated TSH 3.9, elevated fT4 3.28, and elevated TT3 205. He reported that for the past year, he has been on levothyroxine 50mcg for abnormal TSH. Levothyroxine was stopped and the patient was discharged on methimazole 10mg daily. Further workup revealed negative thyroglobulin and thyroid peroxidase antibodies. Thyroid ultrasound with Doppler demonstrated a mildly hypervascular thyroid gland without evidence of nodules. Brain MRI was negative for any pituitary abnormalities. HAMA testing continued to show elevated TSH. Patient was followed by cardiology and due to continued atrial fibrillation, had multiple cardioversions and was managed on a beta blocker. Due to his atrial fibrillation, endocrinology service continued his methimazole till his genetic testing came positive for an autosomal dominant heterozygous pathogenic mutation in THRB c.1373 T&gt;C (p. Val458Ala). His thyroid hormones and TSH continue to be elevated. Currently, he is not on thyroid medication and getting monitored. The need for multiple cardioversions for atrial fibrillation in this patient makes resistance to thyroid hormone management challenging. Discussion: Hyperthyroidism is commonly mistaken for RTH. However, the lack of TSH suppression should be further investigated. Most patients with RTHβ are adequately compensated by the increased endogenous supply of thyroid hormone showing increased serum fT3 and fT4 levels and normal or near normal TSH levels. Beta Blockers like atenolol cannot inhibit the conversion of T4 to T3 and can be used for RTHβ with tachycardia. Triiodothyroaceticacid (TRIAC) or dextrothyroxine (DT4) have also been used to treat thyrotoxicosis. In summary, treatment for RTHβ remains a challenge for clinicians, especially in patients with atrial fibrillation and many patients are misdiagnosed and managed as hyperthyroidism.
Presentation: 6/3/2024
7684 Resistance to Thyroid Hormone Beta Mistaken as Primary Hypothyroidism: Variable Phenotypes and Diagnostic Dilemmas
Authors: Belal H F , Mukhtar A N , Chehade J M 
Published: October 2024

Abstract
Disclosure: H.F. Belal: None. A.N. Mukhtar: None. J.M. Chehade: None.
Background: The differential diagnosis of hyperthyroxinemia and nonsupressed TSH includes assay interference, resistance to thyroid hormone beta (RTHb) and TSHoma. Correlation of laboratory findings with clinical presentation is crucial to avoid misdiagnosis. Clinical Case: A 50 year old female presented with palpitations, tremors, headaches, diarrhea, heat intolerance, chronic attention difficulty, pre-syncope and fatigue over several years. She had regular menses with no birth control use. There was no amiodarone, lithium or biotin use. Exam: vitals stable, no thyromegaly, no hand tremors, no exophthalmos. At 26 years old she was started on Levothyroxine (LEVO) 50 mcg for elevated TSH; FT4 was not measured. Over the past 10 years her labs demonstrated elevated FT4, elevated FT3, elevated FT4 by direct dialysis, normal TBG and inappropriately normal/elevated TSH while on LEVO 75 - 175 mcg. On LEVO 75 mcg: elevated TSH 5.94 uIU/mL (0.27-4.2), elevated FT4 2.2 ng/dL (0.8-1.7), elevated FT3 6.0 pg/mL (2.0-4.4), elevated FT4 direct dialysis 2.9 ng/dL (0.8-1.7), normal pituitary panel (including alpha subunit), low alpha subunit/TSH molar ratio (0.71). During an ED visit for chest pain, EKG revealed poor R wave progression, non-specific T wave abnormality. She was also found to have hepatic steatosis. RTHb was diagnosed and her LEVO was gradually tapered. Conclusion: TSH receptor beta is expressed in hypothalamus, pituitary, cochlea, retina, liver and kidney. TSH receptor alpha is expressed in skeletal muscle, heart, brain and bone. RTHb occurs at a frequency of 1 in 19,000 to 40,000 leading to resistance to thyroid hormone action at the HPA axis and liver. This produces higher FT4 and FT3 that act on normal TSH alpha receptors. Clinical phenotypes vary from euthyroid to hyperthyroid. Mistreating RTHb as hypothyroidism can worsen the thyrotoxic state. Testing for RTHb genetic mutation is available, yet 15% of RTHb patients do not have an identifiable pathogenic variant[1]. Treatment of RTHb ranges from observation, beta blockade, antithyroid drugs or TRIAC, a thyroid hormone analog which act at the HPA axis to inhibit TSH secretion.[1] Life threatening cases may require total thyroidectomy or radioiodine ablation; often avoided due to difficulty managing thyroid hormone replacement afterwards. Cases of goiter and ADHD in RTHb have been successfully treated with supraphysiologic every-other-day liothyronine.2 Management should be patient tailored and symptom specific. References: 1. Moran, Carla. “Syndromes of Resistance to Thyroid Hormone.” 2023 Endocrine Case Management: Meet the Professor, Endocrine Society, Washington, DC, 2023, pp. 311-319. 2. Pappa T, Refetoff S. Resistance to Thyroid Hormone Beta: A Focused Review. Front Endocrinol (Lausanne). 2021 Mar 31;12:656551. doi: 10.3389/fendo.2021.656551. PMID: 33868182; PMCID: PMC8044682.
Presentation: 6/2/2024
7668 Rhabdomyolysis Associated with Severe Hypothyroidism
Authors: Naing Soe Htut , Mikkilineni Pushyami 
Published: October 2024

Abstract
Disclosure: H. Soe: None. P. Mikkilineni: None.
Background: Over 70% of the patients with newly diagnosed hypothyroidism can present with muscle complaints such as weakness, fatigability, cramps, myalgia. However, rhabdomyolysis, which is the rapid breakdown of skeletal muscle cells, is the rare presentation. Clinical Case: A 70-year old male patient with history of rheumatoid arthritis, hyperlipidemia, prior CVA (left hemispheric subcortical stroke) 6 months ago without residual deficit presented to the hospital with poor oral intake and generalized muscle weakness for 3 weeks. He was unable to get out of bed without assistance and also needed adult diapers. Found to have new-onset severe hypothyroidism with TSH 228 uIU/ml (Ref: 0.350-4.940) and FT4 &lt;0.40 ng/dL (Ref: 0.70-1.50), positive TPO antibody 197 IU/ml (Ref: 0-34). No prior thyroid labs were available and no known history of thyroid disorder was recorded. He has never been on Amiodarone or Lithium before. On physical exam, he was alert and oriented. There was no goiter or palpable thyroid nodule. There was no focal neurological deficit and no peripheral edema. There were no other signs and symptoms pertinent to hypothyroidism except mild bradycardia (HR 56-60) and borderline low blood pressure. AM cortisol was 10.1 ug/dL (Ref: 3.7-19.4). EKG showed low-voltage sinus bradycardia. Echocardiogram was normal. Urinalysis was positive for large blood but only 3 RBCs were present which raised the suspicion of rhabdomyolysis. Creatinine kinase (CK) was 15,584 IU/L (Ref: 30-200). Other laboratory studies were significant for acute renal failure with mild hyperkalemia and mild hypocalcemia, also transaminitis; BUN 130 mg/dl (Ref: 8-26), Creatinine 9.51 mg/dl (Ref: 0.72-1.25), eGFR 5 ml/min/1.73 m2 (Ref: &gt;59), AST 435 IU/L (Ref: 5-34), ALT 269 IU/L (Ref: &lt;55), ALP 171 IU/L (Ref: 40-150). On medication review, he was started on Atorvastatin 80 mg daily during prior admission for CVA 6 months ago. He received IV fluids, s/p 1 dose of Hydrocortisone 100 mg IV, Levothyroxine IV 200 mcg, followed by Levothyroxine IV 50 mcg daily x 3 days and switched to Levothyroxine PO 100 mcg daily (weight-based dose). Atorvastatin was on hold. He became anuric during the hospital course and received 2-3 sessions of hemodialysis. 3-4 days later, CK was trending down to 3000 IU/L, FT4 improved to 0.54 ng/dl and there was also significant improvement in kidney and liver functions. The patient was diagnosed with acute renal failure secondary to rhabdomyolysis associated with severe hypothyroidism caused by Hashimoto's thyroiditis, in the setting of high dose statin use. Conclusion: Clinicians should raise the suspicion of rhabdomyolysis in a patient with severe hypothyroidism, especially in patients with recent high dose statin use as rhabdomyolysis can be a rare and fatal complication of severe hypothyroidism, in the presence of precipitating factors.
Presentation: 6/2/2024
12511 Rhabdomyolysis Related Acute Kidney Injury Presenting as First Manifestation of Autoimmune Hypothyroidism: A Case Report
Authors: Tiwari Apoorv , Mantravadi Sushmita , Doshi Nivedita , Dabaja Abed , Saad Chadi 
Published: October 2024

Abstract
Disclosure: A. Tiwari: None. S. Mantravadi: None. N. Doshi: None. A. Dabaja: None. C. Saad: None.
Introduction: Autoimmune thyroiditis is the predominant cause of primary hypothyroidism, with an incidence of estimated 0.3-1.5 cases per 1000 people, with female to male predominance of 7-10[1]. Hypothyroid myopathy affects 79 % of the affected population. Its common presentation is fatigue and cramp but in rare instances rhabdomyolysis can occur with trivial triggers like alcohol, exercise2, Case Presentation: A 32-year-old male with no significant medical history, presented with generalized weakness, myalgia, and facial puffiness for last three months. The patient engaged in regular-intensity workouts and reported consuming 12 beers several times a week for past 5 years. Physical examination revealed facial puffiness and proximal muscle weakness. Initial Laboratory findings showed elevated creatinine (1.68 mg/dL, baseline 1.0 mg/dL in April 2020), CK (8113 U/L), AST (260 U/L), ALT (129 U/L). Urinalysis revealed hematuria and mild proteinuria. Serum electrolytes were unremarkable. Abdominal ultrasound showed diffuse hepatic steatosis with normal kidney appearance. This could not explain the reason for the Acute Kidney Injury and further workup showed TSH (&gt;150 mIU/L) and TPO antibodies (197.9 U/mL). Autoimmune panel was unremarkable. Thyroid ultrasound done subsequently revealed a markedly heterogeneous gland. Treatment included parenteral crystalloids, low-dose prednisone which was empirically added for suspected autoimmune myositis and was later discontinued once the autoimmune panel was negative, and Levothyroxine at the recommended dose. At the time of discharge, his creatinine was reduced to 1.33 mg/dL and CK to 2,298 U/L. Discussion: Severe rhabdomyolysis is a rare but significant complication of autoimmune thyroiditis, potentially leading to acute kidney injury (AKI) if not promptly diagnosed and treated. Resident physicians often attribute symptoms like myalgia and generalized weakness in males to clear evident rhabdomyolysis if they find a cause like alcohol consumption and exercise, potentially overlooking the actual etiology. We recommend thyroid workup in such patients to promptly detect and manage underlying etiology predisposing to muscle damage and subsequent kidney injury. Our patient never had any Physician encounter as his prior medical history was unremarkable, however we suggest thorough family history and thyroid profile should be a part of outpatient workup as well for patients who show other risk factors for rhabdomyolysis like daily alcohol consumption, vigorous workout, consume medications like HMG CoA inhibitors, antipsychotics etc.
Presentation: 6/3/2024
6618 Risks for Cardiovascular Comorbidities Associated with Desiccated Thyroid Extract Administration
Authors: De La Torre Sebastian C , Godar Cassandra , Flynn Kathryn , Anit Patel Arjun , Maxwell Devin , Shakir Mohamed K M , Duc Hoang Thanh 
Published: October 2024

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