bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pancytopenia in a Patient With Severe Hypothyroidism: A Case Report
Authors: Bulut Aysegul , AlSibai Khaled , Norman Catalina 
Published: May 2021

Abstract
Introduction: Hypothyroidism usually affects red blood cell line most commonly seen as normochromic normocytic anemia. We present a unique case of a patient with pancytopenia in the setting of severe hypothyroidism, which improved following IV thyroid hormone replacement.
Case: An 85-year-old female with history of type II diabetes mellitus and hypothyroidism who was admitted for open reduction and internal fixation (ORIF) of a displaced left femur fracture following a mechanical fall. Patient has a long-standing history of hypothyroidism on replacement with levothyroxine 75 mcg, which was inadvertently discontinued at the nursing home 2 weeks prior to presentation. CBC on admission was notable for pancytopenia with macrocytic anemia with hemoglobin of 6.2 g/dl (baseline of 11), leukopenia with WBC of 4.2 x103/ul and thrombocytopenia with platelet of 77 X 103 /ul. TSH was 83 uIU/mL (reference range: 0.34 - 5.6) and Free T4 was &lt; 0.11 ng/dl (reference range: 0.93 - 1.7). Patient was on the verge of developing myxedema coma as she presented with hypotension with blood pressure of 103/55 mmHg, hyponatremia 133 mmol/L and mild change in mental status. There was no evidence for hypothermia or bradycardia. Presence of a small thigh hematoma on examination partially explained the acute drop in hemoglobin. Iron panel, folic acid and vitamin B12 levels were found to be within normal range. Patient had no active of infection to suggest sepsis and she did not receive any myelosuppressive medication. Rapid replacement with IV levothyroxine was started before proceeding with surgery to prevent development of myxedema coma. Free T4 normalized at 1.05 ng/dl after receiving a total of 700 mcg of IV levothyroxine on day 5 of hospitalization. ORIF was done with no complications. Pancytopenia resolved upon thyroid replacement therapy and she was discharged on her regular dose of levothyroxine 75 mcg daily.
Discussion: Most common hematologic abnormality associated with hypothyroidism is normochromic normocytic anemia. Currently, there are less than 10 reported cases of pancytopenia associated with hypothyroidism. The exact mechanism is unclear but proposed hypothesis is transient bone marrow hypoplasia. The most common clinical presentation, as seen in our patient, is profound hypothyroidism with ultimate outcome of myxedema coma. Most of these patients had resolution of pancytopenia following adequate thyroid hormone replacement. Interestingly, all cases have been reported in female patient population. Further research is needed to understand pathophysiology, risk factors, prognosis and the risk of pancytopenia recurrence in patients with severe hypothyroidism. More importantly, hypothyroidism must certainly be entertained as a differential diagnosis of pancytopenia.
Postpartum Thyroid Abnormalities and Systemic Lupus Erythematosus: Is There a Link?
Authors: Albrecht Jordan , Ahmed Moeed , Nandala Sudha , Farooqi Saad , Anderson Robert J 
Published: May 2021

Abstract
Introduction: Postpartum Thyroiditis (PPT) is an autoimmune disorder characterized by destruction of the thyroid gland within the first year after delivery. Systemic Lupus Erythematosus (SLE), another autoimmune disease, has been associated with a spectrum of thyroid disorders. While the prevalence of thyroid diseases in patients with SLE is increased, the association between SLE and PPT is not well known. The infrequency of encountering SLE and PPT makes abnormal thyroid tests in the postpartum period a diagnostic challenge.
Clinical Case: A 27-year-old G1P1001 who was five months postpartum and not breast feeding was referred to Endocrinology clinic for evaluation of abnormal thyroid function tests. Past medical history was significant for SLE with renal and pericardial involvement. SLE was well controlled, treated with hydroxychloroquine. Family history was significant for hypothyroidism in her mother.
She was asymptomatic and appeared clinically euthyroid. Vitals were stable and physical exam was negative for goiter, nodule or orbitopathy. Lab results at two months postpartum showed an elevated TSH of 3.87 UIU/mL (Normal 0.40-3.8 UIU/mL) and at four months postpartum TSH was low at 0.012 UIU/mL. Repeat labs at five months postpartum continued to show a low TSH at 0.007 UIU/mL with mildly elevated Free T4 at 1.7 ng/dL (Normal 0.6-1.6 ng/dL) and elevated Free T3 of 6.0 pg/mL (Normal 2.1-3.8 pg/mL). Anti-thyroid peroxidase antibodies (TPO), thyroid stimulating antibodies (TSI) and TSH receptor antibodies (TRAb) were negative. Thyroid Ultrasound with Doppler was within normal limits. Radioactive Iodine Uptake and Scan, obtained at 6 months postpartum, showed high normal uptake (17% and 32% at 4 hours and 24 hours respectively), suggestive of recovery phase of PPT. The most recent TSH was elevated at 8.5 UIU/mL and Free T4 was low at 0.7 ng/dL. Disease course was consistent with PPT.
Conclusion: The Th1 (T-helper) lymphocyte immune predominance in autoimmune thyroid disease and SLE is the immune-pathogenetic base of the association between both diseases. Postpartum thyroiditis is a variant of chronic autoimmune thyroiditis. Serum anti-TPO antibodies vary during pregnancy and tend to increase early and may decline later. Immunologic tolerance increases during pregnancy, fades in the postpartum period and makes interpretation of thyroid function tests and disease process challenging.
Pregnant and postpartum patients who have SLE have increased prevalence of thyroid disease. Causes are multifactorial with a higher prevalence of hypothyroidism and thyroid autoantibodies. Hyperthyroidism is much less likely. One comparable study found 6 of 43 (14%) women with SLE developed PPT and only one of these patients had positive thyroid antibodies. These reports and our patient illustrate the variability of thyroid function tests in patients with SLE.
The Dexamethasone-CRH Stimulation Test: A Single-Center Experience
Authors: Wehbeh Leen , Alwahab Ula Abed , Mikhael Alexandra , Dobri Georgiana , Kennedy Laurence , Hamrahian Amir Hekmat 
Published: May 2021

Abstract
Background: The diagnostic value of adding a Corticotropin Releasing Hormone (CRH) Stimulation Test to the 2-day Low Dose Dexamethasone Suppression Test (Dex-CRH Test) has been debated in the literature. We hypothesized that adding CRH to LDDST would provide additional case detection in patients suspected of having Cushing’s disease (CD).
Methods: We identified 118 patients who underwent the Dex-CRH test to evaluate ACTH-dependent CS from a prospectively maintained pituitary database over 12 years. Seven patients were excluded (2 lost to follow up, 2 were on Dilantin with no available Dexamethasone (Dex) level, 2 had cyclic CD, and 1 suspected noncompliance with Dex intake). Three patients with ectopic ACTH Syndrome had very high cortisol levels after both LDDST and Dex-CRH tests. The remaining 108 patients are the subjects of this analysis. Patients were instructed to take 8 doses of Dex 0.5 mg PO every 6 hours starting at noon with the last dose of Dex taken at 6 AM. Ovine CRH injection (1 µg/kg, max 100 mcg) was given IV 2 hours afterwards. Cortisol was measured 2 hours after the last Dex dose prior to and 15 minutes after CRH administration. CD diagnosis was made based on positive ACTH staining on pituitary pathology and/or development of hypocortisolism postoperatively. Patients with no Cushing disease (NCD) are the group of patients in whom CD diagnosis could not be confirmed after a minimum follow up of 30 months.
Results: Among 108 patients who underwent Dex-CRH test, 66 had CD and 42 had NCD. The female sex ratio, and median (range) for each of age, BMI, and follow-up duration in months were as follows with no statistically significant difference between the two groups: CD: 83%, 40 (15–82), 34 (30–42) and 63 (24–102). NCD: 88%, 40 (20–71), 37 (31–43) and 52 (30–67). Among 66 patients with CD, 5 patients (7.6%) had a cortisol level ≤ 1.4 µg/dl after LDDST but were appropriately classified as CD with a cortisol level &gt;1.4 µg/dL at 15-min post CRH stimulation. In contrast, 3/42 patients (7.1%) in NCD had an abnormal Dex-CRH test. In only one of these three patients the LDDST was normal (cortisol post-Dex was 1.4 µg/dL and increased to 3.1 µg/dL 15-min post CRH). A cortisol cut-off value of &gt; 1.4 µg/dL at 15 min during Dex-CRH test provided a sensitivity of 100%, specificity of 93%, and diagnostic accuracy of 97% to diagnose CD. When patients without a Dex level were excluded from the analysis (n=74), the sensitivity did not change but specificity and accuracy of Dex-CRH test further increased to 97% and 99%, respectively.
Conclusion: The CRH test addition to the 2-day LDDST provided additional case detection in 5/66 (7.6%) of patients with CD. It resulted in one additional false-positive case compared to LDDST. Measurement of Dex level provided improved diagnostic accuracy of DEX-CRH test.
Regrowth of Thyroid Gland: Is This Possible????
Authors: Techathaveewat Pawarid , Alhakim Manal , Correa Ricardo Rafael , Vinales Karyne Lima 
Published: May 2021

Abstract
Introduction: Adult Thyroid gland which derived from primitive pharynx and neural crest is considered a non-regenerative organ. In this nature, partial or total thyroidectomy is considered a curative treatment for compressive non-malignant goiter. While there is a potential regrowth from stimulating by pituitary thyroid stimulating hormone (TSH), such growth is rarely significant and suppressive TSH therapy is currently indicated only for thyroid malignancy. We present an unusual case of rapid regrowth of normal thyroid tissue that expanded both of the lobes from a single unilateral remnant.
Case: 58-year-old male with prior history of multinodular goiter status post subtotal thyroidectomy due to compressive symptoms in 2006 present to our clinic for follow up. Post-operatively, case was complicated with Iatrogenic Hypoparathyroidism thus on replacement of calcium and calcitriol. Follow up neck ultrasound (US), showed no thyroid gland with minimal residual tissue in the right fossa and pathology was benign. In 2011, patient complained of new onset globus sensation, and voice changes which initially concern for gastroenterology issue as the etiology. A neck US unexpectedly revealed normal right thyroid lobe of 5.7 cm without any tissue on the left and no nodule. FNA subsequently performed which was benign tissue. Due to high risk of complication for repeat surgery, annual US was planned for monitoring. In 2013 there was a significant new growth of left thyroid of 1.7 cm in size, no nodules. A repeat US six months later revealed an increase in size in the right from 5.7 to 6.1 cm as well as 1.7 to 2.1cm on the left. Patient denied any compressive symptoms, so we continue with neck US surveillance. By 2020, the right lobe was 6.4 cm and left lobe at 2.4 cm. Within both lobes, now multiple nodules start appearing. FNA were performed on several of those nodules with a benign cytopathology in all of them. Of note, other than regrowth of his thyroid, it is also physiologically functional as patient is euthyroid without levothyroxine replacement since 2013.
Discussion: When patient underwent thyroidectomy for benign multinodular goiter, thyroid function test is the only routine test for follow up without additional further images. While it is considered a curative treatment, some regeneration or recurrence is still a possibility which is shown in our case. This is one of the few cases in the literature that we could found about normal thyroid tissue regrowth. It is still unclear how the mechanism for this phenomenon occurs. Further studies may need to be pursued with regards to suppressive TSH therapy or even radioactive iodine ablation for benign goiter that have regrowth potential. It is crucial that physicians become aware of such occurrence may happen since new thyroid nodules can also develop in the new thyroid tissue and fine needle aspiration should be performed accordingly.
Reverse T3 in Patients With Hypothyroidism, Helpful or a Waste of Time?
Authors: Wilson Julian Bryant , Friedman Theodore C 
Published: May 2021

Abstract
Background: Reverse T3 (rT3) is a biologically inactive form of T3 that is created by peripheral 5 deiodination of T4 by type 1 and type 3 deiodinases and may block T3 binding to the thyroid hormone receptor. As about 15% of patients on L-T4 replacement with a normalized TSH report continued fatigue and other hypothyroid symptoms, efforts are needed to understand why this occurs and how it can be corrected. Decades ago, endocrinologists realized that in severe illnesses, rT3 is often high and T3 is often low and termed this “sick euthyroid syndrome”. However, more recently, alternative doctors, including functional medicine doctors, have argued that high rT3 is detrimental and can block T3 from binding to the thyroid hormone receptor. Without peer-reviewed publications, these functional medicine doctors rely heavily on rT3 levels to treat patients that may have no other laboratory findings of hypothyroidism and often prescribe them L-T3-only preparations to try to lower the rT3. Also poorly characterized in the literature are the effects of hypercortisolism and hypopituitarism, both of which should modulate the expression of deiodinases to increase rT3. Hypotheses: 1) Patient rT3 levels will vary significantly with the type of thyroid medication taken. 2) Patient rT3 levels will be clinically significant in the management of patients on thyroid medications. 3) Hypercortisolism and hypopituitarism will increase rT3 levels. Methods: The most recent rT3 measurements were analyzed from 621 patients currently being managed by TCF. The upper limit of normal for rT3 at either Quest or LabCorp, which is usually 24.1 ng/dL was used as a cut-off for a high result and below 9.2 ng/dL as the low cut-off. Results: Elevate rT3 levels was seen in 3% of patients of patients not on thyroid replacement (5/143), seen in 8% of patients (17/203) taking desiccated thyroid. It was more prevalent in patients taking desiccated thyroid with synthetic T3 (27%, 7/26) or T4 (15%, 16/104) and was seen in 15% of patients (9/58) taking synthetic T4 alone. Changes were made to the amount or type of medications in 199 patients. Levels of rT3 levels were outside the normal range in 27% of these patients (54/199), being above normal range in 16% of these patients (32/199). Hypercortisolism was seen in 37 patients, 36 from Cushing’s disease, however above normal rT3 was seen in only 2 patients. Hypopituitarism was diagnosed in 22 patients, only one had above normal rT3 levels because they couldn’t afford their growth hormone replacement. Conclusion: Measuring rT3 may be helpful in patients who are already on thyroid treatments, and is of greater importance in patients taking synthetic preparations. It is not recommended in patients who are not taking thyroid medicine (even if experiencing hypercortisolism) or in patients with hypopituitarism that are taking adequate hormone replacement.
Subacute Thyroiditis After mRNA Vaccine for Covid-19
Authors: Franquemont Stephanie , Galvez Juan 
Published: May 2021

Abstract
Introduction: Subacute thyroiditis is a well-documented clinical condition which typically presents 1-2 weeks after an acute viral illness. Presenting symptoms are classically those of thyrotoxicosis but with associated tenderness in the thyroid. Treatment of acute symptoms is possible and the thyroid function will generally normalize with time. Subacute thyroiditis has rarely been reported after administration of viral vaccinations such as the seasonal flu vaccine. We present a case of subacute thyroiditis which presented after administration of the mRNA COVID-19 vaccine.
Case: Patient is a 42yo female with no past medical history. She received the first dose of the Pfizer/BioNTech mRNA vaccine for COVID-19 on 12/22/20. Five days later, the patient complained of sore throat and palpitations. These symptoms progressed and she was evaluated in an urgent care on 12/31/20 where she was found to have tachycardia. Infectious work-up, including PCR for COVID-19, was negative and she was sent home. She took ibuprofen with some improvement of her symptoms. The following day she went to the ED; she was found to have a heart rate in the 130s with sinus tachycardia on EKG. Thyroid function testing was done which revealed TSH &lt;0.01, fT4 4.58, fT3 11.8. Her TPO antibody was &lt;28 and inflammatory markers were elevated including sed rate of 62. The patient was prescribed prednisone 40mg daily and propranolol 20mg as needed for symptoms. She reports rapid improvement of symptoms with prednisone. On 1/21/20, thyroid function showed TSH &lt;0.01, fT4 down to 3.2, tT3 normal at 135. Thyroglobulin was elevated at 140.8 with negative thyroglobulin antibody, TRAb and TSI. Her inflammatory markers had decreased with sed rate of 26 and normal C-reactive protein. She had improved symptoms.
Discussion: Cases of subacute thyroiditis are most commonly associated with upper respiratory viruses but cases have been reported with traditional inactivated viral vaccines or live-attenuated vaccines such as those for annual influenza. We present the case of a 42-year-old female who has presented with a classic case of subacute thyroiditis which occurred in the time frame after receiving the Pfizer mRNA vaccine for COVID-19. Research has been ongoing for decades regarding development of mRNA vaccines but the mRNA vaccines for the SARS-CoV-2 virus have been the first to be widely distributed to the general population. Thyroiditis has not been reported as a common side effect but the cross recognition between the coronavirus spike protein targeted with the mRNA vaccine and healthy thyroid cell antigens exists as evidenced by this case.
Sources: 1. Prummel M, Strieder T, Wiersinga WM. The environment and autoimmune thyroid diseases. Eur J Endocrinol. 2004;150:605-618. Altay FA, Guz G, Altay M. 2. Subacute thyroiditis following seasonal influenza vaccination. Hum Vaccin Immunother. 2016;12(4):1033-1034.
Subacute Thyroiditis Associated With Liraglutide
Authors: Erturk Banu , Dagdelen Selcuk 
Published: May 2021

Abstract
Objective: Incretins are expressed in thyroid tissue but without clearly-known clinical significance in human. The long-term effect of GLP-1 receptor activation on the thyroid is unknown. In the literature, liragludite-related thyroiditis has not been reported yet and here we wanted to draw attention to this association. Case Summary: A 52-year-old woman with type 2 diabetes mellitus presented with thyroid tenderness, tremor and fever. Her lab results were as follows: undetectable TSH, free T4 (FT4) = 2,4 ng/dl (0.93-1.7), free T3 (FT3) = 4.4 pg/mL (2-4.4). Erythrocyte sedimentation rate (ESR) was 60 mm/hour, C-reactive protein (CRP) was 80 mg/L. Thyroid autoantibodies were negative. USG revealed that thyroid gland was in normal localization and the right lobe was 24x22x46 mm and the left lobe was 20x21x45 mm, isthmus thickness was 5 mm. The parenchyma was heterogeneous, coarsely granular, with bilateral patchy hypoechoic areas. All these findings suggested that the patient had subacute thyroiditis. When we examine the etiological factors of subacute thyroiditis in the patient, there was no history of trauma, no previous viral or bacterial illness, contrast agent exposure. But, she had only been using liraglutide for a week. Firstly liraglutide therapy was ceased and than 20 mg prednisolone and 40 mg beta-blocker therapy was initiated. At the 8 weeks’ of cessation, patient had no symptoms. Also thyroid function tests and other laboratory values were all in normal limits. Conclusions: It has been proven by previous studies that liraglutide has several effects on the thyroid gland. Liraglutide therapy might be related to subacute thyroiditis, as well.
Superior Sagittal Vein Thrombosis in the Setting of Thyroid Storm
Authors: Moran Heberth , Sosa-Pagan Max 
Published: May 2021

Abstract
A 25-year-old female with a two-month history of left lower quadrant pain, found to have an ovarian cyst and recently started on OCPs, presented to an outside medical center after a witnessed seizure with fever, tachycardia, and altered mental status. Her husband reported that she had been lethargic, complained of headaches, and had brief intermittent episodes of staring into space or stopping mid-task four days prior to the current event.
On physical exam, she was hypertensive to 170/90s, tachycardic to 120s, febrile to 101, with hyperreflexia and altered mental status without focal deficits. Burch Wartofsky scale was calculated to be 50, suggestive of thyroid storm. Initial labs showed a suppressed TSH (&lt;0.01 uIU/mL) and an elevated free T4 (7.27 ng/dL). Blood cultures and a lumbar puncture demonstrated no evidence of infection. A non-contrast brain CT showed no acute intracranial findings. She was started on propylthiouracil (PTU), propranolol, hydrocortisone, and Lugol’s solution. Thyrotropin Receptor Antibody and Thyroid Stimulating Immunoglobulin levels were elevated, confirming the diagnosis of Grave’s disease.
After the initial management, her vital signs normalized and free T4 decreased to 4.2 (ng/dL), but she had no mental status improvement. Although she had no further seizure activity, she continued to have waxing and waning levels of consciousness. She then developed left sided focal deficits and was transferred to our hospital for the management of a possible cerebrovascular event. MRI and MRV of the brain were performed and demonstrated a thrombus within the superior sagittal sinus. She was started on heparin and bridged on warfarin prior to discharge. Her anti-thyroid regimen was down titrated, steroids tapered and discontinued, PTU changed to methimazole, and propranolol changed to metoprolol. Her mental status and focal deficits improved prior to discharge.
Patients who present with hyperthyroidism and new-onset neurological symptoms, especially in the setting of OCP use or other risk factors for a hypercoagulable state, should be evaluated for possible cerebral venous thrombosis. The association between overt hyperthyroidism and acute venous thrombosis, especially at cerebral sites, has been documented in numerous case reports.