Cause Of Thyroiditis Research Articles

7504 A Case of Methicillin Sensitive Staphylococcus Aureus Thyroiditis

Abstract Disclosure: K. Patel: None. P. Kachhadia: None. S. Khan: None. F. Akanbi: None. A. Abu Limon: None. S.A. Aldasouqi: None. Introduction: Acute suppurative thyroiditis refers to bacterial infection of the thyroid gland. It is rare as the thyroid gland is typically protected from infection due to isolation of the gland from neighboring structures as well as its rich blood supply and adequate lymphatic drainage. It shares characteristics with subacute and autoimmune thyroiditis which make for difficult diagnosis. Here we present a case of acute suppurative thyroiditis in the setting of methicillin sensitive staphylococcus aureus (MSSA) bacteremia. Case Presentation: We have a 45 year old gentleman with a history of polysubstance abuse who was admitted after a drug overdose. He was being treated for rhabdomyolysis and approximately ten days after admission he became febrile with Tmax 103.3 Farenheit with a sore throat and dysphagia. Workup showed leukocytosis, ESR 86 mm/h [0-15], CRP 45.5 mg/dL [0-1], blood cultures with MSSA, negative viral upper respiratory panel, throat culture, Syphilis and HIV testing. He had a positive Hepatitis C antibody without a detectable viral load. Echocardiogram ruled out vegetations. He was treated with cefazolin. CT neck was obtained and showed thyroid enlargement. Subsequent ultrasound showed heterogeneous echotexture and increased color flow and a left inferior pole nodule 2.3 x 2.1 x 2.0 cm. Thyroid labs showed TSH 0.16 [0.35 - 4.01 u[IU]/mL,] Free T4 3.91 ng/dL [0.61 - 1.37], TPO <0.3. The nodule was biopsied and endocrinology was consulted. On exam thyroid was nontender. He was started on beta blockers and thyroid labs were monitored. TSI and TRAB were negative. TSH, Free T4 and Free T3 improved to normal range. Nodule biopsy results showed benign follicular cells with abundant acute inflammation suggestive of an abscess. Metronidazole was added after biopsy results. Post antibiotic therapy, CRP improved to 1.7 mg/dL. Discussion/Conclusion: Incidence of acute suppurative thyroiditis has been published as occurring <1% of all thyroid diseases. One systematic review found 200 cases reported from January 2000 to January 2020. Prior case reports have described acute suppurative thyroiditis in adult patients with prior thyroid gland pathology or an immunocompromised state and some demonstrated a correlation with intravenous drug users. The most common culprits include Staphylococcus spp, Streptococcus spp, Salmonella spp, Escherichia spp. Management includes antimicrobial therapy and/or needle aspiration. Non-responders can undergo incision and drainage of abscess or thyroidectomy. Mortality was reported in about 8% of the reported 200 cases. In our patient, his history of drug use and Hepatitis C likely made him prone to infection. Although there was no description of pus during biopsy, pathology suggested acute inflammation. This along with elevated inflammatory markers led to the diagnosis. This case highlights an uncommon but potential cause of thyroiditis. Presentation: 6/3/2024

7099 Severe Hypothyroidism from Potassium Iodide Supplements: A Case of Failure to Escape from Wolf- Chaikoff Effect

Abstract Disclosure: M.G. Hamilton: None. A. Kulkarni: None. P. Lekprasert: None. Introduction: The Wolf-Chaikoff effect (WCE) is a physiological response of the thyroid gland to supraphysiologic iodide levels. Failure to escape the WCE can lead to thyroid dysfunction, and we present such a case in a patient with Hashimoto’s thyroiditis taking high-dose potassium iodide (KI). Case Description: A 44-year-old female with hypothyroidism secondary to Hashimoto’s thyroiditis presented with 10-pound weight gain, extremity swelling, fatigue, and abnormal menstruation. She was prescribed Levothyroxine several years ago but stopped taking it shortly after as she felt no improvement. On physical exam, she was bradycardic with heart rate of 58 bpm. There is no goiter but dry skin and edematous lower extremities. Labs revealed TSH of 127 pg/mL (0.35-4.94), free T4 0.1ng/dL (0.8-1.8), TPO Ab 645 (<9) IU/mL in comparison to her labs 2 months ago of TSH 11 pg/mL and free T4 0.9 ng/dL. Suspicion for worsening hypothyroidism from Hashimoto’s was low given this dramatic change on labwork and clinically. On further questioning, she had been taking KI 130 mg/day (Iodine 100 mg, daily requirement 150 mcg/day) as advised by her homeopathic doctor. The supplements were stopped, and she was re-started on Levothyroxine. After 8 weeks, she reported improvement of symptoms and weight loss. TSH is normal at 3.54pg/ml and free T4 1.2 ng/dL. Discussion:The WCE serves as a protective mechanism to decrease thyroid hormone production in the setting of high iodide levels to prevent development of hyperthyroidism. WCE is explained by the formation of Iodopeptides inhibits thyroid peroxidase (TPO) mRNA and protein synthesis resulting in an inhibition of thyroglobulin iodination. WCE is temporary and expected to wane over a few days to weeks and is known as the Wolf-Chaikoff escape due to down regulation of the sodium iodine symporter (NIS) thereby decreasing the intrathyroidal inorganic iodine concentration and permitting normal TPO activity. Rarely, failure to escape WCE can lead to hypothyroidism due to continued suppression of thyroid hormone synthesis. Risk factors include underlying thyroid diseases i.e. Hashimoto’s or other causes of thyroiditis, use of Amiodarone, Lithium or Iodine-containing radiocontrast media and KI supplements. In our case, Hashimotos’ thyroiditis predisposed her to thyroid dysfunction and failure to escape from WCE after taking high-dose KI supplements causing severe hypothyroidism. Thus, this report highlights that in clinical practice, especially in patients with pre-existing thyroid dysfunction, a significant TSH increase, a high suspicion index is needed to investigate for other causes like concurrent use of iodine-containing food/drug leading to the failed escape from WCE apart from verifying compliance to thyroid replacement therapy. Presentation: 6/3/2024

8105 Radiation-Induced Hyperthyroidism in the Context of Palliative Radiation Therapy

Abstract Disclosure: A. Randhawa: None. G. Palaguachi: None. J.G. Karam: None. Introduction: Palliative radiotherapy, designed to alleviate focal symptoms in advanced, incurable cancer, aims to enhance quality of life with minimal treatment burden. The thyroid gland's susceptibility to neck radiation is known, primarily leading to hypothyroidism. However, hyperthyroidism is a much less frequently reported adverse effect that is poorly understood. This case report highlights an unusual instance of radiation-induced hyperthyroidism. Case Presentation:The patient is a 53 years-old woman with history of Ewing’s sarcoma of the sacrum diagnosed in August 2022, treated initially with chemotherapy (cyclophosphamide, vincristine, etoposide and ifosfamide), but diagnosed with leptomeningeal metastasis and T12/L1 mass in October 2023 when she presented with lower extremities weakness and urinary incontinence. She underwent T12-L1 laminectomy, resection of tumor and fusion, and was started on palliative intent radiation therapy for the brain and C-spine. A month later, she was admitted for altered mental status and was found to be persistently tachycardic at 140 bpm. Thyroid function testing was sent and revealed hyperthyroidism with TSH of 0.07 mIU/L (0.39-4.08), Free T4 of 1.74 ng/dl (0.58-1.64), T4 of 10.7ug/ml (4.4-9.5), T3 of 0.54 ng/ml (0.72-1.35), with undetectable Thyroid Peroxidase Antibodies and Thyroid Stimulating Immunoglobulin level. Thyroid Ultrasound showed a small and homogenous thyroid gland with no discrete nodules. Radioactive Iodine uptake and scan was not obtained because of exposure to iodized contrast during hospital stay. The patient had no available baseline thyroid function tests. She had no recent fever or viral illness. Unfortunately, her clinical condition deteriorated rapidly, and she passed away on the seventh day of admission. Conclusion: While hypothyroidism is a well-established consequence of high-dose irradiation, the mechanisms behind the rarer radiation-induced hyperthyroidism remain unclear. Speculation includes the release of autoantigens from damaged thyroid glands, triggering an immune response and potentially leading to Graves' hyperthyroidism. However, our case more likely represents a hyperthyroid phase in the triphasic sequence of destructive subacute thyroiditis, given the absence of elevated thyroid antibodies, thyroid nodules, and other causes of thyroiditis. Increasing awareness of radiation-induced hyperthyroidism, unraveling its mechanisms, and refining diagnostic strategies such as obtaining baseline and monitoring thyroid function testing are crucial, particularly in the context of palliative therapy, where striking the delicate balance between efficacy and minimizing toxicity is paramount. Presentation: 6/3/2024

Hypothyroid Patients Show Significant Association with Antithyroid Antibodies: A Cross Sectional Study in Khulna

Background and Objectives: A high prevalence of thyroid disorder is found worldwide and it is a serious public health problem. A community‑based investigations showed that; overall occurrence of thyroid disease was 20.43%, highest incidence of diffuse goiter (7.35%), followed by sub-clinical hypothyroidism (6.59%), hypothyroidism (4.97%), hyperthyroidism (0.86%) and sub-clinical hyperthyroidism (0.65%) in Khulna, Bangladesh. Antithyroid autoantibodies are one of the most important causes of thyroiditis resulting hypothyroidism. The aim of this study was to investigate the prevalence of antithyroid antibody to hypothyroid patients in Khulna region. Methods: This cross‑sectional study was done on Hypothyroid patients of Khulna Medical College Hospital and Institute of Nuclear Medicine and Allied Science (INMAS), Khulna, from July 2023 to December 2023. After having informed written consent of adult sixty hypothyroid patients, was interviewed and examined the blood sample for relevant information; data recorded in a preformed, semi-structured data collection sheet (Patient particulars form) and analyzed. Results: About 20 percent had positive family history of hypothyroidism, 27 percent patient was associated with other autoimmune diseases and about 80 percent was associated with anti-thyroid antibody. Out of the sixty hypothyroid patients about fifty percent was obese, eighty percent was female of 30-60 years age group. Ninety percent of them belongs to poor socioeconomic conditions and came from rural area of Khulna district. Conclusions: Most of the patients were rural female of low socioeconomic back ground of reproductive age groups. There was very significant association of anti-thyroid antibody with these patients. They also associated with chronic autoimmune diseases and poverty.

Subacute thyroiditis and rapidly developing goiter in a 16-year-old female: a case report

Subacute thyroiditis (SAT) is an inflammatory disease of the thyroid gland with multiple etiologies and clinical features, often challenging to recognize. The classic presentation is the painful, granulomatous thyroiditis (DeQuervain’s) characterized by diffuse swelling of the gland, usually preceded by an upper respiratory tract infection. A painless variant, also referred to as autoimmune subacute thyroiditis, has been documented and is strongly linked to postpartum state, reported following ~10% of pregnancies. It can be differentiated from the former by the presence of anti-thyroid antibodies, which classifies it as an autoimmune thyroiditis. Any spontaneous development of painful swelling of the thyroid gland warrants a complete work up that includes thyroid hormones, thyroid autoimmune panel, acute phase reactant titers, and, if available, imaging that may lead to the diagnosis of an inflammatory or infectious cause of thyroiditis.

Acute thyrotoxicosis-like graft-versus-host disease after cord blood transplantation

Reports of thyrotoxicosis and hypothyroidism occurring immediately after allogeneic stem cell transplantation are limited, and the detailed mechanisms remain unclear. Here, we present the case of a man in his 20s with thyrotoxicosis and hypothyroidism that occurred early after cord blood transplantation (CBT), with histopathology suggesting an immune reaction in the thyroid gland. The patient had acute myeloid leukemia and underwent a second CBT procedure. The patient developed thyrotoxicosis on day 43. The patient’s condition initially improved with increasing immunosuppressive drug doses; however, he later developed hypothyroidism and required thyroid hormone replacement therapy. Since conventional subacute thyroiditis, Graves’ disease, and Hashimoto’s thyroiditis were excluded due to the lack of histological evidence and autoantibodies, acute graft-versus-host disease (GVHD) was considered the main cause of thyroiditis. The possibility of even minor post-transplant thyroid function abnormalities is more common than expected and further studies are required.

ODP519 Thyroid Cyst Grows E. coli

Abstract Background Thyroid abscesses are extremely rare, representing less than 1% of all thyroiddiseases. The thyroid gland is very robust against infections due to its vastlymphatic drainage, dual blood supply, encapsulation, and iodine concentration. Immunocompromised patients are at greater risk of developing thyroid abscesses. 1 Case: A 51-year-old female presented to her primary care provider with acute onset ofpainful right neck mass with associated cough, hoarseness, fever, and fatigue. She was seen by an Otolaryngologist who aspirated 6 cc of brown purulentmaterial from a suspected thyroid mass. The thyroid fluid was sent for culture,and she was empirically started on Augmentin. CT neck demonstrated a cysticlesion of the right thyroid gland, retropharyngeal edema, and mass effect withleftward deviation of the larynx and trachea without airway obstruction. Due tothese findings, the patient was admitted to the hospital where initial two setsof blood cultures were negative but repeat blood cultures revealed 2 of 2positive for E. coli. Thyroid cyst fluid also grew E. coli. Urine culture hadno growth. She was found to have a suppressed TSH of 0.24 uIU/mL, elevated free T4 of 1.80 ng/dL, and suppressed total T3 of 0.52 ng/mL. Previous TSH was within normal limits, 0.82 uIU/mL. The suppressed TSH and suppressed T3 were thought to be secondary to euthyroid sick syndrome. She was maintained onCeftriaxone while admitted and discharged on Ciprofloxacin. Pathology from theright thyroid cyst revealed acute inflammatory cells only consistent with anabscess, negative for malignancy. The patient elected to undergo a righthemithyroidectomy with isthmusectomy. Discussion Thyroiditis is defined as inflammation of the thyroid gland and has a variety ofetiologies. Suppurative thyroiditis, which includes thyroid abscess as in thiscase we have described, is an infrequent cause of thyroiditis. It is usuallycaused by hematogenous spread or direct inoculation of a pathogen. Treatmentincludes systemic antibiotics targeting the causative organism; although thegold standard remains surgical drainage. Surgical management is the mainstay ofmanaging patients with thyroid abscesses. 2

Abstract #1003850: Case of COVID-19 Related Thyroiditis

The severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) is a novel enveloped RNA beta-coronavirus responsible for the Coronavirus disease-19 (COVID-19) ranging from asymptomatic cases to severe respiratory involvement. The SARS-CoV-2 pandemic has spread rapidly worldwide. Few cases and case series have been published reporting COVID-19 related subacute thyroiditis. We report a case of COVID-19 related thyroiditis. 73-year-old female presented to the hospital with complaint of shortness of breath, fever and weakness. She was diagnosed with COVID-19 pneumonia and treated with dexamethasone and convalescent plasma. Patient was discharged home after 10 days. Two days after discharge, she presented with complaint of generalized weakness. She was noted to have thyrotoxicosis. Patient was not taking lithium or amiodarone and she did not receive iodinated contrast. She had no sign or symptoms of thyrotoxicosis. She denied neck pain or difficulty swallowing. On laboratory evaluation, SARS Coronavirus 2 RNA was positive. RSV, Influenza A and Influenza B by PCR were negative. TSH was low at 0.182 uIU/mL (0.450-5.330 uIU/mL), free T4 elevated at 3.00 ng/dL (0.58-1.64 ng/dL), free T3 elevated at 5.24 pg/mL (2.20-4.10 pg/mL). Her TSH 3 weeks ago was normal at 0.723 uIU/mL. Thyroid stimulating immunoglobulin negative < 0.10 (< =0.54 IU/L). Thyroid ultrasound showed normal sized gland, few sub centimeter nodules bilaterally. NM thyroid uptake and scan showed low uptake and no focal hot or cold nodule. Her workup was consistent with thyroiditis. Correlating with the diagnosis of COVID-19, this could be most likely COVID-19 related thyroiditis. Repeat labs in a week showed normal TSH 1.138 uIU/mL, normal free T4 1.28 ng/dL and low free T3 1.93 pg/mL. The patient likely had thyroiditis during early course of COVID-19 infection and was caught during the late phase and hence, improvement of thyroid function within a week of biochemical diagnosis. Subacute thyroiditis is a self-limited inflammatory disorder, characterized by neck pain, general symptoms and thyroid dysfunction. It has been linked to viral infection like mumps virus, coxsackievirus, adenovirus, Epstein-Barr virus, rubella and cytomegalovirus. In our patient, SARS-CoV-2 was the likely cause of thyroiditis. A single center retrospective study done in 287 patients hospitalized with COVID-19 in Milan, Italy reported 20% of patients with thyrotoxicosis, 5% with hypothyroidism and 74% with normal thyroid function test. We report this case to alert clinicians that thyroiditis and resultant thyrotoxicosis should always be considered as a differential diagnosis in patients with COVID-19.

Cytomegalovirus-mononucleosis-induced thyroiditis in an immunocompetent patient.

Enteroviruses, including coxsackieviruses and Echovirus, are well known pathogens responsible for the development of thyroiditis. We describe the case of a 49-year-old woman with no personal or family history of thyroid disease who presented to the emergency room with a two-week history of daily fevers up to 39°C, a sore throat, occasional palpitations and diaphoresis, decreased appetite and an unintentional 10 kg weight loss over the same time course Physical examination revealed mild tachycardia, an intention tremor and a normal-sized, nontender thyroid gland without palpable nodules. The remainder of the physical examination was unremarkable and without stigmata of Graves’ disease. Her initial blood tests revealed overt thyrotoxicosis, elevated liver enzymes, an elevated C-reactive protein, a negative monospot and a positive CMV IgM antibody. Thyroid sonography revealed areas of hypoechogenicity and relatively low vascularity. Fine-needle biopsy showed a lymphocytic infiltrate. The patient was treated symptomatically with propranolol. On follow-up, the patient became euthyroid, and her liver enzymes normalised. Previous cases of CMV-induced thyroiditis occurred in immunosuppressed patients. This is the first reported case of a CMV-mononucleosis-induced thyroiditis in an immunocompetent adult patient and serves as a reminder that viral illnesses are a common cause of thyroiditis with abnormal liver enzymes.Learning points:The differential diagnosis of thyrotoxicosis with abnormal liver enzymes includes severe hyperthyroidism and thyroid storm caused by Graves’ disease as well as the thyrotoxic phase of a thyroiditis, usually caused by a virus such as coxsackievirus or, in this case, cytomegalovirus.Cytomegalovirus appears to be a recently recognized causal agent for thyroiditis, both in immunosuppressed and immunocompetent patients.Careful follow-up of thyroid function tests in patients with thyroiditis allows clinicians to determine if patients’ thyroid hormone secretion normalizes or if they remain hypothyroid.

A clinico-pathological study of Thyroiditis

Thyroiditis is the inflammation of the thyroid gland due to various causes like autoimmune disorders, infections, drugs, exposure to physical agents, radiation and without any apparent predisposing factors. This leads to progressive inflammation and replacement of thegland by fibrous tissue, if it is chronic. Hence the patient might have initial thyrotoxic phase followed by progressive hypothyroidism. Hence this study was conducted to describe the common causes of thyroiditis in day to day practice. Hashimoto thyroiditis was the most common cause followed by lymphocytic thyroiditis. It was commonly seen in young females. The commonest complaint was swelling, followed by pain. The thyroid was enlarged and tender on palpation in majority of the cases. At the time of presentation, 4 had recurrent laryngeal nerve palsy and 1 had dyspnoea. On investigating, 4 patients had Hashi-thyrotoxicosis. Hashimoto patients had hypothyroidism. Those with intractable pain, pressure symptoms, cosmetic reason and lymphoma underwent thyroidectomy. Most common post-operative complications were recurrent laryngeal nerve palsy and hypocalcaemia.

Thyroiditis in children.

Thyroiditis ranks with diabetes as the most common of the endocrine disorders of childhood. The term encompasses all forms of thyroid gland inflammation and infection, although chronic lymphocytic thynoiditis is overwhelmingly the most frequent. Thyroiditis may appear as a mass in the neck of an asymptomatic child or it may be a painful, erythematous goiter in a sick child. The affected thyroid gland may be small on large, with varying degrees of dysfunction. Most commonly, thyroiditis causes euthyroid function, although the disease process can result in transient or permanent thyroid dysfunction. The causes of thyroiditis in childhood, as well as the less common thyroid disorders in the differential diagnosis of goiter, are listed in Table 1. Thyroid physiology and pathophysiology will be discussed briefly to explain the rationale for diagnostic studies and treatment strategies. The more recent diagnostic techniques and therapeutic controversies regarding thyroiditis will be included. The goal is to provide the clinician with renewed awareness of this most common pediatric problem. THYROID PHYSIOLOGY Thyroid hormone production is regulated by a classical negative feedback system (Fig 1). Hypothalamic thyrotropin-releasing hormone (TRH) stimulates the synthesis and secretion of thyroid-stimulating hormone (TSH) from the pituitary. TSH, in turn, stimulates production and release of thyroxine (T4) and triiodothyronine (T3).

Thyroiditis in Children

Thyroiditis ranks with diabetes as the most common of the endocrine disorders of childhood. The term encompasses all forms of thyroid gland inflammation and infection, although chronic lymphocytic thynoiditis is overwhelmingly the most frequent. Thyroiditis may appear as a mass in the neck of an asymptomatic child or it may be a painful, erythematous goiter in a sick child. The affected thyroid gland may be small on large, with varying degrees of dysfunction. Most commonly, thyroiditis causes euthyroid function, although the disease process can result in transient or permanent thyroid dysfunction. The causes of thyroiditis in childhood, as well as the less common thyroid disorders in the differential diagnosis of goiter, are listed in Table 1. Thyroid physiology and pathophysiology will be discussed briefly to explain the rationale for diagnostic studies and treatment strategies. The more recent diagnostic techniques and therapeutic controversies regarding thyroiditis will be included. The goal is to provide the clinician with renewed awareness of this most common pediatric problem. THYROID PHYSIOLOGY Thyroid hormone production is regulated by a classical negative feedback system (Fig 1). Hypothalamic thyrotropin-releasing hormone (TRH) stimulates the synthesis and secretion of thyroid-stimulating hormone (TSH) from the pituitary. TSH, in turn, stimulates production and release of thyroxine (T4) and triiodothyronine (T3).