scholarly journals Low-Dose Prednisone Therapy is Efficacious in Treating Painful Subacute Thyroiditis

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A940-A940
Author(s):  
Mohamed K M Shakir ◽  
Robert D Leimbach ◽  
Rinsha P V Sherin ◽  
Michael I Orestes ◽  
Vinh Q Mai ◽  
...  

Abstract Subacute thyroiditis (SAT) usually presents with neck pain, radiating to ears and is often associated with hyperthyroidism. Currently the available treatment involves administration of NSAID or in more symptomatic patients prednisone 40mg daily tapered over 6 weeks or longer. We report successful treatment of 3 patients (Pts) with SAT with low-dose prednisone therapy (20mg/day) (LDP20) initially and tapered over 4 weeks. Patient 1: A 32-year-old female presented with severe neck pain radiating to both ears and low- grade fever of 2-weeks duration. Two weeks prior, patient had cold-like symptoms lasting for 3 days. Physical examination: HR 110bpm, tremors of fingers noted, tenderness of the anterior neck present, thyroid 30-gms in size. Labs: ESR 92 mm/hr, CRP 3.2 mg/dL, TSH <0.005 uIU/mL, free T4 2.71 ng/dL, total T3 168 ng/mL. Thyroid scan and uptake showed a 24-hrs uptake <1%, thyroid gland not visualized, consistent with SAT. Patient was treated with atenolol and LDP20 tapered over 4 weeks. Pain significantly improved after 2 days of treatment. Six weeks later TSH was 0.9 uIU/mL with a free T4 1.4 ng/dL and ESR 8 mm/hr. Patient 2: A 19-year-old female presented with left-ear pain, anterior neck pain, fever, and extreme fatigue. PE: HR 111bpm, heat shield present, tender-to-palpation thyroid, brisk DTR. Lab: CBC normal, ESR 98 mm/hr, CRP 9.9 mg/dL, TSH <0.01 uIU/mL, free T4 3.8 ng/dL, total T3 210 ng/mL. Thyroid scan and uptake: uptake <1%, no thyroid gland visualized and SAT was diagnosed. Patient was started on LDP20 and atenolol. Four days following prednisone therapy her symptoms completely resolved and prednisone was tapered off over 4 weeks. Thyroid functions were normal by the seventh week. Patient 3: A 38-year-old male presented with fever, fatigue, severe neck pain, palpitation and a weight loss of 8 pounds. PE: HR 120 bpm, thyroid severely tender on palpation, brisk DTR. Lab: normal CBC, ESR 128 mm/hr, CRP 11.9 mg/dL, TSH <0.001 uIU/mL, free T4 4.2 ng/dL, total T3 201 ng/mL. Thyroid scan: thyroid gland not visualized and uptake was < 1%. SAT was diagnosed and patient was treated with propranolol and LDP20. After 5 days the dose of prednisone was reduced to 15mg/day and the prednisone was tapered over five weeks. Patient had resolution of symptoms in 70 hours and remained asymptomatic for the next 12 months of follow-up. Thyroid function normalized by the eighth week. Conclusion: SAT is a painful disabling thyroid disorder apparently caused by a viral infection; and NSAID or high-dose steroid treatment remains the standard of care. We have treated 3 Pts with relatively lower doses of prednisone than previously recommended and attained remission successfully. Thus side effects can be avoided with lower prednisone dose.

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A946-A946
Author(s):  
Marvyn Allen G Chan ◽  
Bisrat T Teweldemedhin ◽  
Josemaria M Demigillo ◽  
Ma Pamella G Demigillo ◽  
Patrick Benjamin ◽  
...  

Abstract Background: Subacute thyroiditis is a self-limiting condition brought about by an inflammatory reaction often linked to a recent viral infection. SARS-COV2 (COVID-19), an RNA coronavirus that started a global pandemic in December 2019 has been linked mostly to severe acute respiratory distress syndrome. However, there have been increasing reports of its effect on other organ systems. We present a case of a 32-year-old female recovering from COVID-19, only to develop silent thyroiditis afterwards. Clinical Case: A 32-year-old female with anxiety disorder but otherwise in excellent health was diagnosed with COVID-19 via nasal swab RT-PCR after experiencing low grade fever and cough. She quarantined at home and was on her way to recovery when, a few weeks later, she began to experience increasing bouts of chest pain with no relation to activity, intermittent headaches and lower extremity edema. This prompted her to visit the emergency department. Work-up done at that time was unremarkable and her symptoms were attributed mostly to anxiety. She was advised to follow-up as an outpatient with a cardiologist. One month later, due to the persistence of her fatigue, low exercise tolerance and tremors, she decided to seek consult with a cardiologist. An electrocardiogram done during that visit showed normal sinus rhythm with poor-R wave progression and early repolarization changes. Both the echocardiogram and 24-hour Holter monitoring, which were subsequently done, were unremarkable. Blood work-up, however, revealed a significantly low thyroid stimulating hormone (TSH) level of 0.17 mU/L, for which she was referred to an endocrinologist. A month later, she sought consult with an endocrinologist. Thyroid gland was non-tender on palpation. Repeat blood work-up showed an elevated TSH level (23.50 mU/L) with a low Free T4 (0.42 ng/dL) and an elevated thyroid peroxidase antibody (TPO-Ab) level (900 mU/mL), indicative of subacute thyroiditis, but without associated neck pain. Thyroid sonography done showed diffusely heterogeneous thyroid lobes with no evidence of a dominant mass or nodule. A decision was made to start her on low dose levothyroxine. Two months into treatment, she underwent repeat thyroid hormone levels. Normal TSH and normal free T4 were observed. However, TPO-Ab was still elevated. It was decided to continue her therapy for one more month before gradually tapering her levothyroxine dose. She was told to follow-up in a month for further monitoring. Conclusion: Subacute thyroiditis associated with COVID-19 infection has become a more common occurrence as more cases of COVID-19 are noted worldwide. Our patient followed the usual course of subacute thyroiditis, initially presenting with a thyrotoxicosis phase which typically lasts 4-10 weeks, then subsequently developing hypothyroidism, inadvertently needing thyroid hormone replacement. What made this case more intriguing was that she did not have severe anterior neck pain, the classic clinical presentation of subacute thyroiditis. While there is a very strong association between COVID-19 and respiratory failure, there is paucity of evidence linking COVID-19 to dysfunction of other body systems. This case of thyroiditis presenting post COVID-19 illness, buttresses the versatility of COVID-19. Physicians should keep this in mind when evaluating a COVID-19 survivor who continue to present with persistent tachycardia or palpitations with or without anterior neck pain even after a month or two from infection. Routine follow-up TSH assay on COVID-19 survivors may be a valuable consideration.


1984 ◽  
Vol 27 (9) ◽  
pp. 1050-1052 ◽  
Author(s):  
Joseph E. Zerwekh ◽  
Ronald D. Emkey ◽  
E. D. Harris

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A957-A957
Author(s):  
Banu Erturk ◽  
Selcuk Dagdelen

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.


1989 ◽  
Vol 15 (3) ◽  
pp. 569-576
Author(s):  
William P. Docken

2020 ◽  
Vol 6 (6) ◽  
pp. e361-e364
Author(s):  
Mari Des J. San Juan ◽  
Mary Queen V. Florencio ◽  
Mark Henry Joven

Objective: Subacute thyroiditis (SAT) is an inflammatory disorder of the thyroid gland that causes destructive thyrotoxicosis and is attributed to a viral or post-viral response. SARS-CoV-2 is a novel coronavirus that caused a global pandemic in 2020. We present a case that suggests that there may be a relationship between SAT and corona-virus disease 2019 (COVID-19). Methods: We describe the clinical findings, thyroid function tests, and neck ultrasound of a patient presenting with anterior neck pain. Results: A 47-year-old, Filipino female presented with anterior neck pain associated with neck tenderness and goiter. She did not have fever or respiratory symptoms but had right lower lobe pneumonia on chest radiograph. Thyroid function tests were consistent with subclinical hyperthyroidism with thyroid-stimulating hormone of 0.05 μIU/mL (reference range is 0.47 to 4.68 μIU/mL), free thyroxine of 1.68 pg/mL (reference range is 0.78 to 2.19 pg/mL), and total triiodothyronine of 1.4 ng/mL (reference range is 0.97 to 1.69 ng/mL). Anti-thyroid peroxidase, anti-thyroglobulin, and thyroid-stimulating hormone receptor antibodies were negative. Neck ultrasound showed heterogenous thyroid tissues with normal vascularity. Reverse transcription-polymerase chain reaction for SARS-CoV-2 using nasopharyngeal and oropharyngeal swabs were positive. The patient was diagnosed as having SAT and was treated with mefenamic acid, which was later switched to celecoxib. Ceftriaxone and hydroxychloroquine were started for COVID-19 pneumonia. Complete resolution of symptoms and primary hypothyroidism occurred after 2 months. Conclusion: SAT may be a presenting symptom or a sequela of COVID-19. Histopathology studies and definitive documentation of the virus in thyroid tissues may be required to confirm the relationship between SAT and COVID-19.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A922-A922
Author(s):  
Francisco Javier López Maldonado ◽  
Rene Arturo Cota Arreola

Abstract Subacute thyroiditis is a transient inflammatory disease of the thyroid associated with anterior neck pain, and systemic symptoms. The diagnosis is generally reserved for a specific type of thyroiditis characterized by granulomatous inflammation and the presence of giant cells. We hereby present a case of a woman with a COVID-19 diagnosis, and a compatible biopsy result for subacute thyroiditis. On 06/03/2020, a 28 year old woman with previous history of ankylosing spondylitis managed with certolizumab pegmol, presented with fatigue, headache, odynophagia, and fever (38.1°C). 2 days later an oropharyngeal swab (PCR) for SARS-CoV-2 turned out positive. On the 4th day the fever spiked to 39°C with added malaise. Acetaminophen 1 gr PO TID was prescribed. The patient denied dyspnea, and thorax CT-Scan was normal. Complete remission was achieved in 3 weeks. On 08/01/20 she returned to work after a negative swab test. On 08/04/20, she presented with fever (38.7°C), malaise, distal tremors, anorexia, tachycardia, myalgias, arthralgias, and fatigue. 2 days later anterior neck pain that radiated to the jaw, and diffuse goiter was noticed. A thyroid function panel reported Total T4: 24 µg/dL (4.5-12.5), fT4 5.2 ng/dl (0.8-1.8), TSH: 0.001 mUI/L (0.37-4.7), thyroglobulin 135 ng/ml (3-42). TPO-Ab <35 IU/mL and TgAb <20 IU/mL. A neck US showed increased volume in the right lobe with multiple hypoechoic regions on both lobes, and diminished vascularization at color Doppler. I-131 scan showed no uptake. A biopsy of the right lobe reported fibrosis with inflammatory infiltrate composed of lymphocytes, plasma cells, histiocytes, and scarce neutrophils. Some cells with epithelioid appearance and a multinucleated giant cell were also found. Residual thyroid follicles showed colloid depletion and degenerative changes to the epithelium, which was consistent with a diagnosis of subacute thyroiditis. Treatment was initiated with prednisone 10 mg PO QD, propranolol 20 mg PO BID for 2 weeks, and acetaminophen 1 gr PO TID PRN. Fever and pain were intermittent for 6 weeks, but the rest of the symptoms subsided within 2 weeks. On 11/15/20, the patient attended a check-up with lab results that were consistent with hypothyroidism, negative IgM, and positive IgG SARS-CoV-2. Replacement therapy with levothyroxine 88 mcg per day was initiated. This case, which confirms the diagnosis of subacute thyroiditis via biopsy, among the others reported worldwide suggests that there’s an increased risk for women for subacute thyroiditis associated with COVID-19. Further research is needed to confirm risk factors for the development of the disease.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Simona Stefan ◽  
Whitlatch B Hillary

Abstract Introduction: Thyroid storm is a rare, potentially fatal condition, affecting 1% of individuals with thyrotoxicosis. Although it can theoretically be seen in any cause of thyrotoxicosis, the most likely underlying etiology is Graves’ disease. The rarity of thyroid storm due to thyroiditis makes the diagnosis challenging as the clinical and biochemical features overlap Grave’s disease. Here we describe a rare case of severe thyrotoxicosis in a woman due to subacute thyroiditis that developed after receiving an influenza vaccine. Case report: A 30 year-old Caucasian female with no known past medical history presented to the ED with worsening sore throat, odynophagia and anterior neck pain. Symptoms began 4 weeks ago prior to presentation, 1 day after receiving an influenza vaccine. Other symptoms included loss of appetite, chills, fever, fatigue, malaise, abdominal pain, diarrhea, palpitations, heat intolerance and 5lbs weight loss. She was treated by her primary care provider for suspected pharyngitis with a course of corticosteroids and antibiotics. Two weeks later, given worsening symptoms, was referred to the emergency room. On exam, she appeared anxious and was tachycardic (124 beats per minute) and tachypneic (28 breaths per minute). She had no lid lag, stare, thyromegaly or thyroid bruit. However, there was significant tenderness on palpation of the anterior neck. Laboratory evaluation was notable for TSH <0.01 uIU/mL (0.39 - 4.0.8), free T4 5.19 ng/dL (0.58 - 1.64), free T3 10 pg/ml (2.53-3.87), ESR 95 mm/hr (0-20) and CRP 9.339 mg/dl (0.0-0.9) consistent with thyrotoxicosis. Given Burh-Wartofsky score of 45, there was a concern for impending thyroid storm. She received hydrocortisone, methimazole and beta blockers and was admitted to the intensive care unit. She responded dramatically to treatment and was discharged within 24 hours on prednisone and metoprolol. The 24-hour radioactive iodine uptake (RAIU) was 2.7% 2 weeks post admission, consistent with a diagnosis of subacute thyroiditis. TSI was negative. Family history was negative for autoimmune disease. She continued on beta blockers with a steroid taper for 8 weeks. Thyroid function tests and inflammatory markers normalized within 3 months. Conclusion: Aside from the described patient, only three other cases of thyrotoxic crisis due to subacute thyroiditis have been reported in the literature. This case underscores the importance of thoroughly investigating the etiology of severe thyrotoxcosis, given the management and prognosis varies depending on underlying cause. Thyroiditis should be considering in the differential diagnosis of thyroid storm in patients who do not have a personal or family history of autoimmunity and present with neck tenderness in the setting of a precipitating event. Subacute thyroiditis is very uncommon after influenza vaccine, there have been 4 reported cases.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Mansur Assaad ◽  
Bisher Zuhdi ◽  
Jordan Groubert ◽  
Ahmad Al-Shoha

Abstract Introduction: Thyroid storm is a rare disorder with high mortality risk. It is often precipitated by an acute event in a patient with longstanding untreated hyperthyroidism. However, thyroid storm is rarely reported as a result of subacute thyroiditis (SAT). To the best of our knowledge, there are only three documented cases of thyroid storm caused by SAT. Herein we report the first patient with thyroid storm caused by SAT associated with methicillin-resistant Staphylococcus aureus (MRSA) septicemia and intravenous drug abuse (IVDA). Case: A 19-year old Caucasian woman with a history of IVDA presented with right upper extremity abscess. Symptoms included confusion, agitation, fever, chills, generalized pain, malaise, nausea, and vomiting. Heart rate was over 140, and she was found to have fever and leukocytosis. She was admitted with severe sepsis and acute encephalopathy. On exam, she had a diffusely enlarged and exquisitely tender thyroid gland without discrete nodules or bruit. Thyroid tests were consistent with primary thyrotoxicosis (TSH 0.026 IU/mL, free T3 16.90 pg/mL, and free T4 > 6.99 ng/dL). Burch-Wartofsky score was 75, highly suggestive of thyroid storm. In addition to treating her sepsis, the patient was started on a beta blocker, high dose hydrocortisone, and methimazole. Thyroid ultrasound showed a diffusely enlarged heterogeneous thyroid gland with decreased flow on color Doppler. Upon improvement, the patient admitted to symptoms of anterior neck pain, heat intolerance, palpitations, excessive sweating, and anxiety for two days prior to presentation. Blood cultures later grew MRSA. Methimazole was discontinued when the thyrotropin-receptor antibody result came back negative. The patient continued to improve clinically. Her thyroid tenderness improved, and her free T4 and T3 decreased over a 3-week period. Steroids were tapered off. Discussion: SAT usually causes mild to moderate thyrotoxicosis. It is unusual for SAT to cause thyroid storm. Identifying such a diagnosis in a patient with sepsis is complex. In a septic patient, it is crucial to obtain detailed history, perform a comprehensive physical exam (including neck exam), and have a high level of clinical suspicion for thyroid storm in order to reach the diagnosis early and institute appropriate interventions. Establishing the underlying etiology of the thyrotoxicosis would have long term implications regarding prognosis and treatment. References: Salih AM, Kakamad FH, Rawezh QS, et al. Subacute thyroiditis causing thyrotoxic crisis; a case report with literature review. Int J Surg Case Rep. 2017;33:112-114. Swinburne JL, Kreisman SH. A rare case of subacute thyroiditis causing thyroid storm. Thyroid. 2007;17(1):73-6. Sherman SI, Simonson L, Ladenson PW. Clinical and socioeconomic predispositions to complicated thyrotoxicosis: a predictable and preventable syndrome?. Am J Med. 1996;101(2):192-8.


Rheumatology ◽  
1992 ◽  
Vol 31 (2) ◽  
pp. 91-96 ◽  
Author(s):  
R. F. J. M. LAAN ◽  
P. L. C. M. VAN RIEL ◽  
L. J. TH. O. VAN ERNING ◽  
J. A. M. LEMMENS ◽  
S. H. J. RUIJS ◽  
...  

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