bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Million Reasons for Hyperthyroidism. Reporting a Case of Thyrotoxicosis in a Setting of Metastatic Choriocarcinoma
Authors: Ahmed Ali Samim , Siraj Elias Said 
Published: May 2021

Abstract
Background: Human chorionic gonadotropin (hCG) induced transient hyperthyroidism is often seen during pregnancy. Other rare causes of beta hCG induced hyperthyroidism include trophoblastic tumors (hydatidiform mole and choriocarcinoma) and in men, germ cell tumors. The mechanism for hCG induced thyrotoxicosis lies in the structural similarity between TSH and hCG molecules leading to the direct stimulation of the TSH receptors. In regard to treatment, while gestational thyrotoxicosis is usually mild, self-limited and does not need medications, the hyperthyroidism of trophoblastic tumors may require antithyroid medications in addition to treating the underlying tumor. Thionamide use is reserved for moderate to severe cases of hyperthyroidism and for presurgical optimization. In our case report, we present a 22-year-old African American female with choriocarcinoma induced thyrotoxicosis requiring thionamide therapy. Clinical Case: A 22-year-old African American female presented to our emergency room after a witnessed generalized tonic-clonic seizure. Her brain CT scan showed a 4 CM mass concerning for AVM malformation with a subsequent brain MRI confirming parenchymal hematoma with surrounding vasogenic edema. Past medical history was significant for molar pregnancy managed with dilation and curettage followed by laparotomy to remove the pelvic mass. Given her history of molar pregnancy, pelvic ultrasound was performed which showed complex heterologous structure of uterine origin concerning for malignancy. Additional imaging studies of the lung, brain, abdomen and pelvis were performed, which showed possible metastasis to the lung, adnexa, and to the brain. Her clinical exam showed heart rate of 130 beats/min with a normal rhythm, fine tremors, aphasia, and a decrease grip strength in her right upper extremity. Her thyroid gland was slightly enlarged with no tenderness. Laboratory tests showed hCG of &gt;1,000,000 mIU/mL, TSH of &lt; 0.01mcU/mL, free T4 of 5.1ng/dL. Her TPO and TSI were negative. With a diagnosis of hyperthyroidism due to trophoblastic disease, she was treated with methimazole and propranolol resulting in rapid clinical and biochemical improvement. Later, left frontal craniotomy and hematoma evacuation was performed with histology confirming the diagnosis of metastatic choriocarcinoma. She was later transferred to a specialized center where she received chemotherapy. Her hCG subsequently dropped down to 699 mIU/mL. Conclusion: We report a rare case of metastatic choriocarcinoma causing symptomatic hyperthyroidism. The diagnosis is made by excluding other common causes of hyperthyroidism and it should be considered in females of childbearing age. Methimazole is an effective agent to control the hyperthyroidism while waiting for treatment of the underlying cancer.
A Rapidly Enlarging Thyroid Nodule- Aspergillus Abscess
Authors: Sheu Ivana , Idriss Almoatazbellah M 
Published: May 2021

Abstract
Introduction: Acute suppurative thyroiditis is a rare thyroid disorder with high mortality often due to bacterial or fungal infection. Here we present a case of a rapidly enlarging thyroid nodule in the setting of disseminated aspergillosis.
Case: A 31 year old female with lupus on immunosuppressants first presented with weakness to the emergency department with workup finding multiple pulmonary, intracranial and vertebral lesions and a left thyroid nodule. On thyroid ultrasound the nodule was solid, hypoechoic, 1.5x2.3x2.7cm with irregular margins and no echogenic foci. Thyroid function tests: Total T3 52ng/dL (80-210ng/dL), Free T4 2.26ng/dL (0.6-1.12ng/dL), TSH 0.015µIU/mL (0.45-4.12µIU/mL). The patient was started on voriconazole for disseminated aspergillosis with plan for outpatient thyroid workup. However with further brain lesion growth, the patient was readmitted with incidental finding of thyroid nodule developing into a multiloculated, septated, fluid filled 5x2.9x4cm lesion after 3 months. Fine needle aspiration of the thyroid lesion resulted in negative bacterial and fungal cultures, no malignant cells, positive fungal elements consistent with aspergillus on cytology. The patient was continued on antifungal therapy (switched to cresemba due to voriconazole side effects) with thyroid lesion regression to 2.4x0.6x1.3cm at 6 months and 1.8x1.1x1.6cm at 12 months. Her thyroid function test normalized ~ 1 month after initial set of labs and the patient remained clinically euthyroid throughout her course.
Discussion: Thyroid infections are limited due to the thyroid’s high iodine content, capsular encasement and rich vascularity. Acute suppurative thyroiditis (AST) due to aspergillus is a rare finding that can present solo or as a part of disseminated infection especially in immunocompromised individuals. Early presentation is often asymptomatic with possible thyroid function test abnormalities that self resolve in a couple weeks. Occasionally patients present with obstructive symptoms or findings of thyroid storm. Diagnosis is done through fine needle aspiration or autopsy, with treatment options including surgery, antifungals or both. Due to the high mortality of fungal AST, with improved outcomes with early diagnosis, it is important to consider AST as a part of the differential diagnosis in immunocompromised patients with systemic illness.
Alemtuzumab-Induced Hypothyroidism Presenting in Pregnancy - the First 2 Reported Cases
Authors: Scott Rebecca , Cornish Emily , Williams Daivd 
Published: May 2021

Abstract
Introduction: Alemtuzumab is a monoclonal antibody that improves outcomes in patients with relapsing-remitting multiple sclerosis. It binds to CD52 and causes a profound depletion of B and T lymphocytes. Autoreactive T cells often form as the immune system repopulates, causing autoimmune thyroid dysfunction in approximately 35% of patients. Alemtuzumab has been associated with new-onset hyperthyroidism during a subsequent pregnancy. Here, we present the first two cases of alemtuzumab-induced hypothyroidism diagnosed in pregnancy. Diagnosing and treating de novo thyroid dysfunction in pregnancy is essential for optimal fetal development and maternal wellbeing.
Clinical Cases: Case A: A 28-year-old woman conceived 26 months after alemtuzumab therapy. Prior to pregnancy, routine TFTs showed euthyroidism. At 17 weeks’ gestation she presented with fatigue, and blood tests confirmed overt hypothyroidism (TSH &gt;100mIU/L (&lt;4IU/L), fT4 3.7pmol/L (9-15pmol/L)). TRABs were positive. She was treated with levothyroxine, and TFTs normalised by 38 weeks’ gestation. Serial fetal ultrasounds showed constant growth velocity and no fetal goitre or tachycardia. The baby was born at term with birthweight on the 30th centile. On day 5 postpartum, the baby had a normal TSH of 3.1mIU/l (0.27-4.20mIU/l) but elevated fT4 of 31.5pmol/L (12-22pmol/L), which fell spontaneously to 22.0pmol/L by day 11.
Case B: A 37-year-old woman conceived 19 months after alemtuzumab therapy. Prior to pregnancy, routine TFTs had been within normal limits. However at 5 weeks’ gestation, blood tests showed overt hypothyroidism (TSH 47.9mIU/L (&lt;4iU/L)), fT4 8.8pmol/l (10-16pmol/L)). Her only symptom was fatigue. TRABs were elevated. She was treated with levothyroxine, and TFTs normalised by 16 weeks’ gestation. Serial fetal ultrasound scans showed constant growth velocity and no fetal goitre or tachycardia. The baby was born at term with birthweight on the 25th centile. On day 1 postpartum, the baby had a normal fT4 (16.5pmol/l)but elevated TSH 13.02mIU/L, which normalised spontaneously by day 11 tp 1/64mIU/l.
Conclusion: To optimise pregnancy outcomes, we recommend that women previously treated with alemtuzumab should be screened monthly for thyroid dysfunction during a subsequent pregnancy. The neonatal team should be alert to transient neonatal thyroid dysfunction, which, like spontaneous alloimmune neonatal thyroid disease, appears to settle spontaneously. References: Garrahy et al. JCEM, 2019, 104 (9), 3624-3625Thakar et al. JCEM 2019, 104 (9), 3626-3627
An Unusual Cause of Thyrotoxicosis and Gynacomastia
Authors: McDonnell Tara Muire , Donald Darran Mc , Behan Lucy-Ann , Gibney James 
Published: May 2021

Abstract
We describe the case of a 24 year old man with metastatic non-seminomatous germ cell tumour who presented with hyperthyroidism and gynaecomastia associated with elevated human chorionic gonadotrophin(HCG). Following a 3 month history of gynaecomastia, flank pain, nausea and 7kg weight loss, the patient attended the emergency department with persistent vomiting. Initial laboratory investigations reported TSH &lt;0.05mU/L (normal range 0.3-4.3) and free T4 29.5pmol/L (12-22), TPO antibodies negative, FSH &lt;1 and LH 1 U/l, testosterone &gt;52 nmol/L (9-29.0), bioactive prolactin 1048mU/L (63-245), SHBG 110.6 nmol/l (18.3-54.1), and oestradiol 3935pmol/L (&lt;223). Clinical examination revealed bilateral tender gynaecomastia and supraclavicular lymphadenopathy. Testicular examination identified a left testis irregularity that was confirmed on ultrasound. Chest Radiograph revealed multiple bilateral opacities measuring up to 6 cm. Initial urine HCG was negative when tested on two occasions; however given suspicion for a HCG-secreting tumour, serum HCG was measured and reported as 503,944 IU/ml (&lt;5) and AFP 17.6 IU/ml (0-5.0). The negative urine HCG is believed to be due to “hook effect”. CT revealed bulky retroperitoneal lymphadenopathy measuring 13 cm consistent with metastatic spread from the non-seminamatous germ cell tumour of testicular origin. Up front chemotherapy protocol with 4 cycles cisplatin based therapy was initiated given his disease burden and degree of symptoms. Radical orchidectomy was deferred until after chemotherapy - at which time germ cell tumour was only identified on immunohistochemistry staining. Over the 2 months following chemotherapy, all endocrinopathies resolved with corresponding reduction of HCG to 65.0 IU/ml. Symptoms of hyperthyroidism abated with treatment and his TFTs were biochemical normal. Oestrogen level also normalised with treatment. HCG-induced hyperthyroidism is a rare cause of hyperthyroidism. Endocrine manifestations occur in &lt;5% germ cell tumour presentation but should be considered particularly when multiple endocrine abnormalities are present.
COVID-19 Induced Myxedema Madness
Authors: Tal Noa , Veriker Robbie , Averbukh Yelena 
Published: May 2021

Abstract
Background: Corona Virus Disease 2019 (COVID-19) pandemic was first reported in December 31st, 2019 in Wuhan, China. The clinical presentation is variable, including a variety of neuropsychiatric related symptoms. Myxedema Madness is a rare and severe neuropsychiatric complication of hypothyroidism manifested as psychosis.
Case Presentation: A 25-year-old female with past medical history significant for treated Papillary Thyroid Cancer, presented with near syncopal event associated with weakness, lower extremity swelling, constipation, cold intolerance and dry skin. The patient was not compliant with her thyroid replacement therapy. Upon collateral history taken from the patient’s mother; the patient became dysphoric and tearful. On examination, patient had slightly decreased blood pressure and non-pitting edema on lower extremities. On neurological evaluation she exhibited forgetfulness and retardation of speech and motoric activity. Lab was remarkable for TSH greater than 100 uU/mL (reference range 0.30-4.20 uU/mL), FT4 0.4 ng/dL (reference range 0.6-1.5 ng/dL), and FT3 0.7 pg/mL (reference range 2.3-4.2 pg/mL). Patient tested negative for COVID-19 PCR. She was started on her home dose of Levothyroxine 150 mcg daily. Patient was discharged home after she was assessed by a psychiatrist, with no further interventions. Three days later, the patient was readmitted for confusion, disorientation and memory loss. Patient was found to be positive for COVID-19 PCR and negative for SARS-CoV-2 antibodies. She was found to be disoriented with paranoid delusions. Laboratory studies showed negative urine drug screen, syphilis and NMDA antibodies. CSF analysis were within normal ranges. Brain Magnetic resonance imaging was only positive for pituitary hyperplasia. Patient was started on T4 and T3 replacement therapy (Levothyroxine 50 mcq Intravenous, Liothyronine 5 mcg daily orally, respectively) followed by Risperdal 1 mg nightly. After
significant improvement in her mood and delusions, patient was discharged home on Levothyroxine 150 mg daily and Risperdal 1mg for two weeks. Patient and family members were counseled on medications compliance. In a two-week follow-up visit, patient reported to be compliant with medications and improvement of mood. She denied hallucination or delusions. Her lab work was significant for TSH 5.57 uU/mL, FT4 1.3 ng/dL and FT3 3.2 pg/mL.
Conclusion: Both psychosis secondary to COVID-19 and Myxedema Madness are rare conditions. Appropriate and timely supplementation of thyroid hormone facilitated speedy return of patient’s cognitive and psychiatric functions to appropriate baseline. This case report may increase physician’s awareness for potentially increased susceptibility of patients with severe hypothyroidism to neuropsychiatric manifestations of COVID-19.
COVID19 Associated Painful Subacute Thyroiditis
Authors: Bhargava Pooja , Steenkamp Devin Warren 
Published: May 2021

Abstract
Objective: Physicians should be aware that thyroiditis is a potential sequela of COVID-19 infection. Discussion: A 49-year-old female without any prior history of thyroid dysfunction presented with clinical and biochemical hyperthyroidism after a diagnosis of COVID-19 illness four months ago. At the time of thyroiditis diagnosis: free T4 was 1.52 ng/dL (normal, 0.76-1.46 ng/dL), TSH &lt;0.005 uIU/mL (normal, 0.358-3.74 uIU/mL), Thyroglobulin antibodies 2 IU/mL (normal, &lt;=1 IU/mL), TPO antibody 1 IU/mL (normal, &lt;9 IU/mL), ESR 5 mm/hr (normal, 0-20 mm/hr). Thyroid US showed no nodules or evidence of autoimmune thyroid disease or abnormal vascular flow. A radioactive iodine uptake test was performed through the primary care office. The test demonstrated symmetric, uniform radiotracer uptake in the right and left lobe. 24-hour uptake was low at 0.1% (normal 15-25%) indicating thyroiditis. Patient features consistent with the diagnosis of subacute thyroiditis include suppressed TSH, diffuse tenderness on thyroid palpation, absent TPO/TG antibodies, and suppressed I-123 RAI uptake (&lt;1%) on 24-hour scan. Conclusion: There is limited data surrounding thyroid disease and COVID-19. It has been suggested that a possible sequela of COVID-19 is thyroiditis. Physicians caring for recovering COVID-19 patients should be aware of possible painful subacute thyroiditis and to check thyroid studies in persons with symptoms of thyrotoxicosis post-COVID-19.
Discordant Thyroid Function Tests in Patients With HIV: A Case Report and Discussion of Diagnostic Approach
Authors: de Souza Tamara Gizelle , Hannoush Zeina Carolina 
Published: May 2021

Abstract
Background: TFT patterns correlate directly with clinical symptoms in most patients with thyroid disease. However, some patients have TFTs which are at odds to clinical findings, posing a diagnostic challenge. Such cases warrant careful evaluation with a structured, rational approach to avoid misdiagnosis and mistreatment.
Clinical Case: A 48-year-old female liver transplant recipient with HIV presented with an asymptomatic multinodular goiter, low TSH and low/normal fT4. Her medications were nadolol, Bactrim, ursodiol, azithromycin, tacrolimus, efavirenz, emtricitabine, tenofovir and zolpidem. Thyroid US showed 3 dominant nodules with benign pathology on FNA. Uptake scan showed diffuse increased uptake consistent with Grave’s disease. She tried MMI for one year, then opted for RAI ablation and was started on LT4 with titration of dose. fT4 remained low/normal regardless of receiving LT4, MMI or no therapy over the following eight years. TSH was appropriately suppressed from 1.42 to 0.160 (0.45 - 4.500 mIU/L) when LT4 weekly dose was increased from 175 mcg to 350 mcg. On lower dose LT4 (150 mcg to 250 mcg weekly) her fT4 stayed low, 0.50 - 0.74 (0.82 - 1.777mg/dL) with normal TSH of 0.73 - 1.42. She remained clinically euthyroid throughout. Serial yearly thyroid US showed no significant change. Pituitary hormonal work-up (IGF-1, FSH, LH, ACTH, estradiol and cortisol) was appropriate for age. fT4 by direct dialysis assay was low with normal TSH. tT4, T3 uptake, rT3, TBG and TPO Ab were normal. HAMA antibodies were negative. LT4 was stopped and she remains clinically euthyroid with low fT4 0.56 and normal TSH 1.73.
Conclusion: The pattern of low fT4 with normal TSH is uncommon. Potential causes that were systematically evaluated include non-thyroidal illness, central hypothyroidism and assay interference. Normal pituitary function and appropriate TSH suppression while on LT4 ruled out central hypothyroidism. Her overall profile suggested fT4 assay interference. Commonly known interference factors were ruled out; biotin, HAMA Ab, pregnancy, renal failure, TBG excess, familial dysalbuminemic hyperthyroxiemia and trans-thyretin-associated hyperthyroxidemia. Direct dialysis is the gold standard fT4 assay but does not detect agents displacing T4 from TBG. It is less commonly recognized that low fT4 with normal TSH has been described amongst clinically euthyroid persons with HIV, at a prevalence of 1.3%–6.8%. Low fT4 is associated with didanosine, stavudine, and ritonavir, but not her anti-virals. The significance of low fT4 in patients with HIV is unclear, because they do not have a higher rate of hypothyroid symptoms. In the absence of clinical hypothyroidism, such as in this patient, LT4 treatment is not recommended. This case uniquely spans eight years and therefore offers valuable insight into the appropriate work-up, management and long-term natural history of low fT4 in persons with HIV.
Factitious Total Triiodothyronine(T3) Elevation in a Euthyroid Patient With Paraproteinemia
Authors: Mandal Kaushik , Asharobi Damilola , Kumar Salini Chellappan , Liao Huijuan , Resenthal David 
Published: May 2021

Abstract
Background: We report a rare case of a patient treated with levothyroxine for hypothyroidism who also had paraproteinemia and was found to have a clinically inconsistent elevation of T3 by RIA. Clinical Case: A 72 Year old African American female with a history of hypothyroidism and IgG kappa Multiple Myeloma (MM) was admitted to the hospital for altered mental status. Her hypothyroidism had been well controlled for years on a stable dose of levothyroxine 0.075mg daily. Review of systems were negative pertinent to thyroid dysfunction. Family history: negative for thyroid disease. On physical exam, an elderly female clinically euthyroid without palpable thyromegaly but was confused and disoriented. Initial Vital signs: BP 117/67, HR 62, RR 14, T 98, SpO2 99% on room air. BMI 19. EKG: normal sinus rhythm, CXR: normal, TSH: 6.27 (0.55-4.78 uIU/mL), total T3: &gt;600 (60-181ng/dL), total T4: 4.5 (3.2-12.6 ug/dL), FT4: 1.22 (0.89-1.76 ng/dL), hemoglobin: 6.6 (12-16 g/dL), hematocrit: 20.9 (38-47 %), Na: 132 (136-145 mmol/L), K: 4.0 (3.5-5.1 mmol/L), Cl: 104 (98-10/ mmol/L), BUN: 45 (20-31 mmol/L), creatinine: 2.8 (0.6-1.0 mg/dL), total protein: 10.1 (5.7-8.2 g/dL), albumin: 1.8 (3.4- 5.0 g/dL), A:G ratio: 0.22 (0.60-1.50 mmol/L). Serum protein electrophoresis revealed Gamma Globulin 5.8 (0.8-1.7 g/dL), Kappa 9270 mg/L (3.3 -19.4 mg/L) Lambda 9.3 (5.7-26.3mg/L), K/L 996.7 (0.26 -1.65), B2 - macroglobulin: 17.9 (ref: &lt;or= 2.51mg/L) which is consistent with an M- spike migrating in the gamma globulin region. Serum TPO, TG, TSI antibodies were negative. Further testing again reported Total T3 &gt;600 with normal reverse T3 21(8-25 ng/dL). Conclusion: Rare cases of factitious elevations of thyroid hormone have been reported in patients with elevated abnormal IgG or IgA proteins having high binding affinity for thyroid hormone.[1] This hypothyroid patient was clinically and biochemically euthyroid except for a dramatic but clinically inconsistent elevated total T3. She also had multiple myeloma with paraproteinemia (IgG Kappa M spike). The few cases reported to date have shown factitious elevation of either or both total T4 and total T3. In our case the factitious elevation was limited to total T3. We alert clinicians to be aware of factitious elevation of thyroid hormones due to high affinity binding to immunoglobulins. In our case this caused spurious elevation of total T3, but not total T4, in a patient with multiple myeloma and an IgG kappa M spike paraprotein. Reference: 1: Marianna Antonopoulou, Arnold Silverberg, “Spurious T3 Thyrotoxicosis Unmasking Multiple Myeloma”, Case Reports in Endocrinology, vol. 2013, Article ID 739302, 3 pages, 2013. https://doi.org/10.1155/2013/739302
Gestational Thyrotoxicosis in a Patient With Hyperemesis Gravidarum
Authors: Alameddine Hind , Palani Gurunanthan , Zekarias Kidmealem 
Published: May 2021

Abstract
Untreated or inadequately treated overt hyperthyroidism in pregnancy can have devastating consequences for both mother and fetus. At the same time antithyroid drugs (ATDs) are known for their teratogenic effect and should be avoid when possible; once the diagnosis of hyperthyroidism is made in a pregnant woman, attention should be focused on determining the etiology of the disorder and whether it warrants treatment. Here, we report a case of hyperemesis gravidarum patient presenting with significant elevation of thyroid hormones and a review on diagnosis and management of gestational transient thyrotoxicosis. A 33-year-old female, G4P3 at 8 weeks pregnant admitted for nausea and vomiting. Thyroid labs showed TSH &lt; 0.01 (Reference: 0.4-4.0mU/L) and free T4 is 3.53 (Reference: 0.76-1.46ng/dl). Patient was discharged on antiemetics with a diagnosis of hyperemesis gravidarum. She was re-admitted at 9 weeks pregnant with ongoing nausea and vomiting. She had palpitations, fatigue and reported 15 pound weight loss in 2 weeks. Past medical history included thyroid hormone abnormality noted during pregnancies of 2011 and 2017. Physical exam was significant for tachycardia and diffusely enlarged thyroid gland. Repeat labs showed TSH &lt;0.01, free T4 5.81, total T3 of 317 (Reference: 60-181ng/dl). Thyroid ultrasound showed multiple nodules. Considering significant elevation in free T4 and total T3; empiric therapy with propylthiouracil was recommended. Patient declined anti-thyroid therapy. TSI and TRH antibodies came back later as negative. Patient was treated with enteral feeding for hyperemesis gravidarum. Thyroid labs 3 weeks later improved; FT4 down to 1.63 and TT3 down to 250. Patient delivered healthy baby at 40 weeks of gestation. Although the differential diagnosis of thyrotoxicosis in pregnancy includes any cause that can be seen in a nonpregnant patient, the most likely causes for hyperthyroidism in pregnancy are gestational thyrotoxicosis (GTT) with or without hyperemesis gravidarum or Graves’ disease. GTT is described as an hCG-mediated hyperthyroidism that occurs in the first trimester of pregnancy; it is generally asymptomatic with mild biochemical hyperthyroidism. Distinguishing true overt hyperthyroidism from GTT in a setting of hyperemesis gravidarum is challenging. The absence of clinical signs of hyperthyroidism and negative thyroid antibodies supports the diagnosis of GTT. T3 tends to be disproportionately elevated more than T4 in patients with overt hyperthyroidism. HCG level has not been found to be useful in distinguishing between GTT and GD. Overt hyperthyroidism is treated using anti-thyroid drugs (ATD) whereas supportive therapy without ATD is the accepted standard of treatment of patients with hyperemesis gravidarum and GTT. More studies addressing the best management of these group of patients is needed.