bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Case of Recurrent Paralysis and Low Potassium: Is It the Thyroid?
Authors: Do Justin , Mufti Hoveda 
Published: May 2021

Abstract
Introduction: Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that is characterized by episodes of hypokalemia and acute weakness. Although hyperthyroidism is more common in females, over 95% of cases of TPP have been observed in males, especially in Asian males with an incidence of 2% among hyperthyroid patients. In non-Asian populations, the incidence in hyperthyroid patients is estimated to be around 0.1 to 0.2% [1]. We describe a case of TPP seen in a Hispanic male.
Case Report: A 36-year-old Hispanic male with no past medical history presents with weakness in all extremities and difficulty breathing after consuming a carbohydrate heavy meal the night prior. He reports a recent, similar episode evaluated in another ER, which resolved after given potassium supplementation. He denied any vomiting, diarrhea, polyuria, diaphoresis, use of insulin or other medications, or any family history of paralysis.
His labs were significant for hypokalemia of 1.9, TSH of &lt;0.005 (0.358-3.740), free T4 of 2.22 (0.76-1.46), and total T3 of 2.7 (0.60-1.81). Thyroid stimulating immunoglobulin was 0.12 (0.0-0.55). His symptoms improved and potassium levels normalized following the administration of potassium chloride. He was discharged on propranolol and advised to follow up for further workup of his hyperthyroidism with radioactive iodine uptake scan.
Discussion: Thyrotoxic periodic paralysis is a potentially life-threatening condition associated with cardiac arrhythmias and respiratory failure. Hyperthyroidism increases response to β-adrenergic stimulation, which increases activity of the sodium-potassium ATPase and causes hyperpolarization of skeletal muscle [2]. Hyperthyroid patients are prone to episodes of paralysis due to their increased susceptibility to the hypokalemic action of insulin, which activates the sodium-potassium ATPase pump, and epinephrine, which stimulates β-adrenoreceptors. Management of an acute attack of TPP includes potassium administration. In cases where paralysis and hypokalemia are not reversed, intravenous propranolol has been shown to resolve the attack by blocking the β-adrenergic receptors. Definitive treatment of TPP includes managing the hyperthyroid state with medical therapy, radioactive iodine therapy, or surgery. Until the euthyroid state is reached, a β-blocker can prevent episodes of acute paralysis. Avoidance of carbohydrate heavy meals, exercise, and stress are recommended as these factors can potentially exacerbate hypokalemia. In patient with acute paralysis, it is important to consider the diagnosis of TPP as this condition can be prevented once euthyroidism is achieved. Diagnosis and management will lead to prevention of morbidity and mortality associated with the hypokalemia.
References: 1.Vijayakumar A, et al. J Thyroid Res. 2014;2014:649502. 2.Layzer RB. Annals of Neurology. 1982;11(6):547–552.
A Case of Rhabdomyolysis in a Patient With Hashimoto’s Thyroiditis
Authors: Ataallah Basma , Abdulrahman Mustafa , Kulina Georgia 
Published: May 2021

Abstract
Introduction: Hashimoto’s thyroiditis (HT) is an autoimmune disease that presents with musculoskeletal symptoms like proximal muscle weakness, stiffness, pain or cramps in the majority of patients. Rhabdomyolysis which is a breakdown of the skeletal muscles, is a rare but serious manifestation of hypothyroidism and if occurs, it is usually related to trauma, strenuous exercise or use of statins. We report a patient with unrecognized Hashimoto’s thyroiditis who presented with severe rhabdomyolysis without reported history of strenuous exercise, seizures or statin use and surprisingly, He did not have any complications from rhabdomyolysis like electrolytes abnormalities or acute kidney injury. Case Report: A 56-year-old man with no reported past medical history who presented with severe generalized weakness, bilateral leg pain, and recurrent falls for three months. He also reported constipation, fatigue and dry skin. Denied any prior personal or family history of thyroid disease, seizure disorder, statin use, trauma or tick bite. He was afebrile with a heart rate of 80 beats/minute, a blood pressure of 126/71mmHg. Initial laboratory testing showed normal metabolic panel, elevated thyroid stimulating hormone 30.6 uIU/mL (Range 0.27-4.2 uIU/mL), FT4 0.1 ng/dL (Range 0.93-1.7ng/dL), TPO Ab 300IU/mL (N&lt;43IU/mL), Creatine Kinase (CK) level 10,000U/L (N&lt;200U/L), ESR 27 mm/Hr (N&lt;20mm/Hr) and Lactate Dehydrogenase 621U/L (N &lt;225U/L). A muscle biopsy was done to rule out polymyositis as a cause of his severe muscle pain, weakness and tenderness and it was negative. Patient was diagnosed with HT with associated rhabdomyolysis after excluding other causes of rhabdomyolysis. Supportive treatment with intravenous fluids and Levothyroxine were initiated and resulted in dramatic clinical improvement. Conclusion: Rhabdomyolysis is a rare but potentially a serious complication of hypothyroidism. Screening for hypothyroidism in patients with elevated muscle enzymes should be considered, as early diagnosis and prompt treatment of hypothyroidism is essential to prevent rhabdomyolysis and its consequences like acute kidney disease and electrolytes abnormalities. Appropriate fluid resuscitation is the mainstay therapy for AKI prevention and should be initiated in a timely manner. Key Words: HT: Hashimoto’s Thyroiditis, ESR: Erythrocyte Sedimentation Rate, TPO Ab: Thyroid Peroxidase Antibody, TSH: Thyroid Stimulating Hormone, FT4: Free Thyroxine level, AKI: Acute Kidney Injury.
A Grave Case of COVID-19: SARS-CoV-2 Induced Autoimmune Hyperthyroidism
Authors: Matos Moises , Merino-Chavez Hilda Maria , Martinez Suzanne 
Published: May 2021

Abstract
Background: Autoimmune hyperthyroidism also known as Graves’ disease is the leading cause of hyperthyroidism. The pathogenesis of Graves’ disease is still an area of active research. We present a case of Graves’ disease, which developed following SARS-CoV2 infection. Clinical Case: A 43-year-old man with no prior history of thyroid disease, presented for evaluation due to fatigue palpitations, tremors, and hair loss in June 2020. Earlier that month, he was diagnosed with SARS-CoV2 infection and his thyroid function tests (TFTs) during a visit to the emergency department revealed thyroid stimulating hormone (TSH) level of &lt;0.010 mIU/L (0.35-4.94) with a free T4 (FT4) 1.4 ng/dL (0.7-1.5); consistent with subclinical hyperthyroidism. He continued to report palpitations and tremors and further workup was done. A thyroid ultrasound showed two sub-centimeter nodules. A thyroid uptake scan followed, which showed heterogeneous activity in the thyroid gland, (12% and 32% uptake at 6 and 24 hours respectively) with focal increased uptake in the medial lobes, without cold nodules or hot nodules. Repeat TFTs one month later showed a suppressed TSH &lt;0.010 mIU/L, and a normal FT4 1.3 ng/dL. Given suspicion for Graves’ disease, further labs were ordered. Thyroid stimulating immunoglobulin (TSI) were found to be elevated at 173 % baseline (&lt;=140). Thyroid peroxidase (TPO) antibodies and thyroglobulin antibodies were also elevated at 362 IU/mL H* (&lt;=9) and 2 IU/mL H* (&lt;=1) respectively. The overall picture was consistent with evolving early Graves’ disease. Conclusion: Multiple factors are frequently cited in the pathogenesis of autoimmune hyperthyroidism including viral and bacterial infections1 and there have been several reported cases of autoimmune disease related to SARS-CoV2 infection2. This case is one of several emerging cases of autoimmune hyperthyroidism possibly linked to COVID-19. References: 1. Smith, T. J . Graves’ Disease. New England Journal of Medicine. 2016 October 20; 375:1552-1565 2. Mateu-Salat, M., Urgell, E., Chico, A. SARS-COV-2 as a trigger for autoimmune disease: report of two cases of Graves’ disease after COVID-19. Journal of Endocrinological Investigation. 2020 July 19
A Grave Turn on Hashimoto’s Thyroiditis - A Case Series on Four Patients With Autoimmune Hypothyroidism that Converted to Grave’s Disease
Authors: Lee Michelle N , Colburn Jeffrey A 
Published: May 2021

Abstract
Disclaimer: The view(s) expressed herein are those of the author(s) and do not reflect the official policy or position of Brooke Army Medical Center, the U.S. Army Medical Department, the U.S. Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, or the Department of Defense or the U.S. Government.
Introduction: The most common cause of hypothyroidism is Hashimoto’s thyroiditis, a destructive autoimmune injury to the thyroid gland. Rarely, autoimmune hypothyroidism can be caused by thyroid-stimulating hormone (TSH) receptor blocking antibodies (TSHRab), and can be difficult to differentiate clinically from Hashimoto’s. Grave’s disease is the most common etiology of hyperthyroidism, and is typically caused by activation from TSHRab acting as an agonist for the TSH receptor. Patients with autoimmune thyroiditis, whether from TSHRab or Hashimoto’s, have been infrequently reported to convert to Grave’s disease1–3. Presentation: We present four cases whom initially presented with typical symptoms of hypothyroidism, were diagnosed with autoimmune hypothyroidism and started on levothyroxine. All four cases were later found to be hyperthyroid and ultimately diagnosed and treated for Grave’s disease.
Conclusion: Primary hypothyroidism can rarely transition to a hyperthyroid state, although these cases may be underreported. The mechanism isn’t well understood, but is hypothesized to be from a switch of a predominance of TSH receptor blocking antibodies (TBAb) to that of thyroid stimulating antibodies (TSAb)1. Assays using competitive binding for TSH receptor antibodies will not differentiate between blocking and stimulating antibodies4. A high index of suspicion is needed to diagnose these individuals.
References: 1. McLachlan SM, Rapoport B. Thyrotropin-blocking autoantibodies and thyroid-stimulating autoantibodies: Potential mechanisms involved in the pendulum swinging from hypothyroidism to hyperthyroidism or vice versa. Thyroid. 2013;23(1). doi:10.1089/thy.2012.03742. Takasu N, Matsushita M. Changes of TSH-stimulation blocking antibody (TSBAb) and thyroid stimulating antibody (TSAb) over 10 years in 34 TSBAb-positive patients with hypothyroidism and in 98 TSAb-positive graves’ patients with hyperthyroidism: Reevaluation of TSBAb and TSAb in TSH-receptor-antibody (TRAb)-positive patients. J Thyroid Res. 2012;2012. doi:10.1155/2012/1821763. Gonzalez-Aguilera B, Betea D, Lutteri L, et al. Conversion to graves disease from hashimoto thyroiditis: A study of 24 patients. Arch Endocrinol Metab. 2018;62(6). doi:10.20945/2359-39970000000864. Li Y, Kim J, Diana T, Klasen R, Olivo PD, Kahaly GJ. A novel bioassay for anti-thyrotrophin receptor autoantibodies detects both thyroid-blocking and stimulating activity. Clin Exp Immunol. 2013;173(3). doi:10.1111/cei.12129
A Rare Case of a Toxic Thyroid Nodule Found in a Hypothyroid Patient on Levothyroxine Therapy
Authors: Purewal Tiffany , Lesniak Christopher , Ravin Andrew , Cheng Jennifer 
Published: May 2021

Abstract
Introduction: A hyperfunctional thyroid nodule can lead to symptoms of overt or subclinical hyperthyroidism but the association between a hyperfunctional thyroid nodule and hypothyroidism has not been well reported. We present a patient with a prior history of hypothyroidism previously controlled on Levothyroxine who later presented with an enlarging hot nodule. Case Presentation: A 62-year-old female with a history of factor V Leiden, hypothyroidism on levothyroxine therapy, and a meningioma presented to an outpatient clinic with complaints of fatigue, constipation, and 37-pound weight loss in one year. She was diagnosed with hypothyroidism 7 years ago after delivering her third child, but the underlying cause of her disease was unknown. She began taking levothyroxine 50mcg every morning after her diagnosis. She reported compliance and proper pill taking technique. Physical examination revealed a palpable thyroid nodule. The patient had a previous work up for thyroid nodules with a thyroid uptake and scan a few years prior, which showed a 1.42 x 0.96 x 1.87 cm hot nodule at the right middle lobe with a 24-hour uptake of 15.3%. The patient was asymptomatic at that time and thyroid function tests were within normal limits. She was instructed to continue taking levothyroxine. Repeat RAI Uptake scan at the time of her presentation to our office again showed the right middle lobe hot thyroid nodule with an increased 24-hour uptake of 27.5%. Ultrasound showed bilateral thyroid nodules and a hypervascular solid nodule measuring 2.28 x 1.27 x 1.9 cm that has increased in size. Lab work at this visit revealed a TSH of 0.329 uIu/mL, and free T4 of 1.25 ng/dL. Due to her low TSH and clinical presentation, the levothyroxine was discontinued. Anti-thyroid peroxidase antibodies were obtained to assess for Hashimoto’s Thyroiditis but were found to be normal. The patient was later referred to an endocrine surgeon for a total thyroidectomy. Conclusion: Although uncommon, hyperfunctional nodules in hypothyroid patients can create a confusing clinical picture with overlapping symptoms of underactive and overactive thyroid disease. It has been reported that patients with Hashimoto’s Thyroiditis can have hot nodules and coexisting hypothyroidism but the prevalence of hyperfunctional nodules in hypothyroid patients without Hashimoto’s Thyroiditis, as in this case, is not well-documented. Patients with hypothyroidism are treated with Levothyroxine but if coexisting hyperfunctional nodules are not detected, the patient may develop thyrotoxicosis. Clinicians should be aware of this rare but potentially life-threatening clinical condition.
A Severe Case of Hypothyroidism: Immunotherapy Induced
Authors: Chunchulu Srivani 
Published: May 2021

Abstract
Background: Immune check point inhibitors are playing a crucial role in the treatment of many cancers. Their primary role is to reactivate anti tumor cytotoxic T cells. Programmed cell death 1(PD 1) is a transmembrane protein expressed on T cells, B cells and Natural killer cells. PD 1 ligand is expressed in many tumor cells along with hematopoietic cells and their interaction directly inhibits apoptosis of the tumor cell. Pembrolizumab binds PD1. FDA approved pembrolizumab initially for nonsquamous cell lung cancer and metastatic melanoma that express PD1 ligand which showed improved survival compared to standard therapy. Additionally it has been used in several others tumors with more than 50% PD L1 expression. Although well tolerated, these agents can cause immune related adverse events. Thyroid dysfunction is reported to range between 3.2-10.1% patients receiving pembrolizumab. Clinical Case: 86 year old Caucasian female with past medical history of hypertension and osteoarthritis was diagnosed with stage III metastatic colon cancer in the hepatic flexure and underwent hemicolectomy. Pathology showed 6.5cm mass and 2/30 lymph nodes positive. Due to fear of side effects from chemotherapy, patient refused further treatment. Her follow up labs showed elevation of carcinoembyronic antigen (CEA). Her oncologist suggested Pembrolizumab, immunotherapy. She was started on 5 cycles every 3 weeks. She had fatigue and fell twice after first cycle, but her CEA levels were improving, so it was decided to continue treatment. Soon after fifth cycle she became extremely weak, lethargic, and unable to do any ADLS and was exhausted all the time. Her labs showed TSH 137, free T4 0.4. At that point decision was made to stop pembrolizumab. She was started on levothyroxine 25mcg by her oncologist and referred to me few months later. She complained of tiredness, low energy. On exam Pulse 78, Blood pressure 152/77. Her labs showed TSH 106 and Free T4 0.45. Her levothyroxine dose was increased to 75mcg and followed her 6 weeks later. Her energy levels improved significantly and she is back to her normal self. Her thyroid function was normal. At this point patient has decided not to undergo any treatments for colon cancer. Conclusion: Immune related thyroid events are increasingly noticed with wide use of pembrolizumab. There is insufficient evidence to suggest the cause of these events. Reversible destructive thyroiditis and overt hypothyroidism are the common clinical presentations. It is important to recognize patients at high risk for these adverse events so these highly efficacious agents can be safely used in patients. Thyroid has been a frequent target for anti PD 1 treatments, further research can be of benefit to use against thyroid cancers.
Call for Emergency Room Guidelines to Identify Hyperthyroid Patients Prior to Contrast Imaging
Authors: Bassin Sandhya , Amorosa Louis F 
Published: May 2021

Abstract
Background: Thyrotoxicosis can be mistaken for conditions such as atrial fibrillation and pulmonary embolism (PE) given the nonspecific symptoms of fatigue, palpitations, and dyspnea. Patients often undergo further imaging on presentation to the emergency room (ER), many of which use iodine for contrast. This can put patients at increased risk for iodine induced hyperthyroidism and delay definitive treatment in patients with Graves’ disease, the most common cause of hyperthyroidism.
Clinical Case: A 53-year-old male with history of hyperthyroidism, atrial fibrillation, and prior PE presented with palpitations to the ER. He developed worsening dyspnea on exertion and palpitations over the last three days. He was unable to afford his medications, including methimazole, for the last nine months. In the ER he was in atrial fibrillation with rapid ventricular response. Due to concern for PE, he underwent a CTA with contrast, which was negative. His physical exam was notable for a diffusely enlarged goiter. His labs showed low TSH &lt;0.01 (norm 0.35-5.50mIU/L) and high free T4 &gt;7.77 (norm 0.9-1.8ng/dL). TSH stimulating antibodies were elevated at 1.9 (norm &lt;1.3 TSI index), consistent with Graves’ hyperthyroidism. Endocrinology was then consulted for severe thyrotoxicosis, initially treating the patient with PTU and propranolol. The patient was transitioned to methimazole and continued propranolol on discharge. Since he was given contrast, plan was for repeat thyroid uptake scan and iodine ablation in 3 months. However, patient was not compliant with medications, resulting in readmission for thyrotoxicosis 3 months later.
Conclusion: This case highlights the impact of increased use of contrast in imaging in hyperthyroid patients. Hyperthyroid patients are at an increased risk for emboli. However, iodine can cause contrast-induced hyperthyroidism and delay definitive treatment of Graves’ disease. As almost half of thyrotoxic patients receive iodinated contrast prior to an endocrine consultation, endocrinologists should work with emergency physicians to develop a set of guidelines to identify at risk populations for hyperthyroidism (1). We advocate for urgent thyroid testing in patients with new onset atrial fibrillation, a history of Graves’ disease, specific symptoms of Graves’, or those taking thyrotoxic-inducing medications. This will assist in determining if patients should receive a prophylactic dose of anti-thyroid medication prior to iodinated contrast imaging. These guidelines can help prevent contrast induced hyperthyroidism and disruptions in treatment of Graves’ while still imaging patients for other diagnoses on the differential.
Reference: (1) Giacomini A, et al. Urgent thyroid-stimulating hormone testing in emergency medicine: A useful tool? J Emerg Med. 2015;49(4):481-487.
Case Report of Postpartum Thyroid Nodule Size Reduction
Authors: Havranova Jana , Gallagher Thomas , Arastu Mohammad Ishaq 
Published: May 2021

Abstract
Introduction: Thyroid nodules are very common. They occur more commonly in women with an increased prevalence of thyroid nodules reported in pregnancy. Most thyroid nodules diagnosed during pregnancy are benign. Pregnancy causes major physiological changes including changes in the levels of thyroid hormones and the elevation of thyroid binding globulin. Thyroid nodules may also occur in people with abnormal thyroid function tests manifesting as hyperthyroidism or hypothyroidism. We present a unique case of a new diagnosis of a large thyroid nodule that has significantly decreased in size after 20 months postpartum. Case description: Patient is a 31 year old female with past medical history of anxiety and white coat hypertension who was diagnosed with a 3.3 x 2.3 x 2.1 cm thyroid nodule a month following delivery. Patient did not have any abnormalities in her thyroid function tests before, during, or after pregnancy. She remained euthyroid throughout the pregnancy and in the postpartum period. Fine needle aspiration biopsy of the nodule showed atypia of undetermined significance (Bethesda Category III). The specimen was further analyzed by afirma testing that confirmed benign pathology. Twenty months postpartum, the thyroid nodule significantly decreased in size to 1.9 x 1.4 x 1.2 cm. Conclusion: Thyroid hormone levels physiologically change during pregnancy and this may affect the growth of thyroid nodules. We just presented a patient who exhibited a significant decrease in the size of her thyroid nodule. Sahin et al. showed that while the size of the thyroid nodule increases during pregnancy the number of nodules remains unaffected. Kung et al. showed that pregnancy is associated with an increase in the size of preexisting thyroid nodules as well as the number of newly developed thyroid nodules. Vanucchi et al. showed that although the thyroid gland becomes larger, particularly in late pregnancy, the sizes of any preexisting thyroid nodules remained unchanged and patients’ thyroid gland size returned to normal after delivery. The current literature provides conflicting data on this topic. The true association between pregnancy and thyroid nodules is unknown. Contemporary literature is ambiguous on this topic and more scientific studies are required to find the true association between pregnancy, the formation of thyroid nodules, and increase in the size or number of thyroid nodules.