Silent Thyroiditis as a Complication of Severe Acute Respiratory Syndrome Coronavirus 2 Vaccine

Introduction: Silent autoimmune thyroiditis, a type of chronic autoimmune thyroiditis, as an adverse effect of Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination is infrequently reported in the literature. We hereby describe a case of silent thyroiditis followed by Grave's orbitopathy after vaccination against SARS-CoV2. Case Description: An 84-year-old male presented to clinic with a 10-pound weight loss with no other symptoms of hyperthyroidism, no personal history of thyroid illnesses, or recent viral infections. He had normal thyroid function 3 months prior to presentation. He had received 3 doses of SARS-CoV2 Pfizer-BioNTech vaccine with the last dose 5 months prior to presentation. Thyroid exam was normal. Laboratory testing revealed thyroid stimulating hormone (TSH) level of 0.005 IU/ml (0.45-4.5 IU/ml), total T4 14.4 g/dl (4.5-12.1 g/dl), and total T3 1.22 nmol/l (0.6-1.81 nmol/l). Thyroid Ultrasound revealed a heterogeneous atrophic thyroid gland with no nodules or hypervascularity. He was started on Methimazole by primary care provider. Four months later, he was seen in the Endocrinology clinic and reported no hyperthyroidism symptoms. His TSH level at that time was 65.9 IU/ml, free T4 0.47 ng/dl (normal: 0.82-1.77 ng/dl), total T3 level 75 ng/dl (normal: 71-180 ng/dl), thyroid stimulating immunoglobulin 2.05 IU/l (0-0.55 IU/L), thyrotropin receptor antibody level 2.8 (0-1.75). Methimazole was discontinued. At 6 months after initial presentation laboratory testing showed TSH 5.010 IU/ml, free T4 1.2 ng/dl, thyroid peroxidase antibody of 148 IU/ml (normal 0-34 IU/ml), thyroglobulin antibody 131.6 IU/ml (normal 0.0-0.9 IU/ml). He was diagnosed with silent autoimmune thyroiditis. A few weeks later, the patient presented to an ophthalmologist with bilateral eye bulging and impaired vision. He was diagnosed with acute Graves' orbitopathy and started on pulse-dose of intravenous Methylprednisolone 250 mg twice daily and urgently referred to a tertiary ophthalmology center for teprotumumab infusion. His thyroid function tests were normal at that time on no thyroid medications. Discussion(s): The underlying mechanisms of thyroid impairment following SARS-CoV2 vaccination are not completely understood. There is a role of molecular mimicry between SARS-CoV2 antigens and thyroid antigens that may help to hasten the emergence of autoimmunity in vulnerable individuals. Our patient developed multiple thyroid-related antibodies following vaccination. Silent painless thyroiditis is a self-limiting condition, characterized by temporary thyrotoxicosis, followed by a brief period of hypothyroidism and then a complete return to normal thyroid function. A radioactive iodine uptake scan can help differentiate between the different causes of thyrotoxicosis in the acute thyrotoxic phase. Development of severe Graves orbitopathy following silent autoimmune thyroiditis after SARS COV2 vaccination has not been previously reported.Copyright © 2023

Thyroid dysfunction reflects severity of COVID-19 pneumonia in hospitalized patients

Introduction: Coronavirus disease 2019 COVID-19 is clearly the pandemic of the new millennium. COVID-19 determines multi organ dysfunction including the inflammatory immune responses of thyroid gland. Objective(s): To determine whether the involvement of the thyroid gland by COVID-19 manifests as thyroid hormonal changes and development of thyroid disorders. Method(s): We studied prospectively 60 patients with COVID-19 pneumonia,without previous known history of thyroid disease nor pre-existing endocrine disorders, hospitalized between May and July 2021, and we performed serum thyroid hormonal analysis within the first 24 hours after admission, including TSH, Free T3, Free T4 and their antithyroglobulin antibodies (Anti-TG and Anti-TPO), and correlate them with clinical and laboratory data. Result(s): Samples were collected from 60 patients (31 males, 51.7%). 32 out of 60 (53.3%) showed significantly lower values of TSH (0,29 +- 0,07 mIU/mL) with decreased Free T3 serum levels (2,07 +- 0,131 pmol/L) and the thyroid autoantibodies (both Anti-TG and Anti-TPO) were positive. These 32 patients (27 males) demonstrated moderate to critical illness and they needed high oxygen flow. The other 28 patients with no evidence of thyroid abnormalities showed mild to moderate COVID-19 pneumonia and none needed high oxygen flows. Conclusion(s): In our study, 32/60 (53.3%) patients with moderate to severe COPVID-19 pneumonia were diagnosed with thyroid abnormalities. Thus, the development and the progression of respiratory failure due to SARS-COV-2 may affect the thyroid function.

A case of subacute thyroiditis after influenza vaccination

A 40-year-old Japanese woman presented to the outpatient clinic with fever and palpitations 2 days after receiving the influenza vaccine (Influenza HA Vaccine 'KMB') following the second dose of coronavirus disease 2019 (COVID-19) vaccine (COVID-19 vaccine Moderna intramuscular injection). At the first visit, the patient presented with a swollen thyroid gland with mild tenderness, and she was diagnosed with subacute thyroiditis (SAT) based on the presence of thyrotoxicosis (free T3: 5.42 pg/mL;free T4: 2.34 ng/dL;and thyroid-stimulating hormone (TSH): <0.01 muIU/mL), a high C-reactive protein level (5.77 mg/dL), a negative TSH receptor antibody, and characteristic ultrasound findings. The patient's human leukocyte antigen types were A2, A11, B35, B51, DR4, and DR1403. Prednisolone (15 mg/day) was given as an initial dose, after which the fever subsided, and the dose was tapered and discontinued after 6 weeks. The patient was thought to have developed SAT due to influenza vaccination. SAT after influenza vaccination may be overlooked. For patients with SAT, it is necessary to obtain information regarding their vaccination history.Copyright © 2023 The authors.

Spectrum of Thyroid Illness in COVID-19

Background: De novo thyroid dysfunction can occur as a result of COVID-1. Patients have diverse manifestations of thyroid illness, ranging from asymptomatic hyperthyroidism to secondary hyperthyroidism. Aim: To evaluate various thyroid diseases and compare them to mortality and clinicopathological features. Methods: After approval from the institutional ethical review board, this observational cross sectional study was carried out at a private sector hospital in Karachi. Patients diagnosed with COVID-19 admitted between December 2020 to May 2021 were recruited using consecutive sampling. Patients who did not give informed consent and had known thyroid disorders or history of thyroidectomy were excluded. To analyse the relationship between thyroid laboratory reports, and clinicopathological features, the Chi-square test and “Fischer's exact test” were utilised. SPSS version 21 was used for statistical analysis. A statistically significant P value of 0.05 was used. Results: Majority of the patients 105(72.9%) had higher FT3 levels and none of them reported with the decreased levels. 88(61.1%) came up with the higher FT4 levels while 9(6.3%) reported with decreased FT4. 9(6.3%) and 6(4.2%) were positive for the anti-thyroperoxidase and anti-thyroglobulin antibodies. The results showed statistical significance for free FT4 (p value 0.018), anti-TG (p-value 0.001) and anti-TP antibodies (p value 0.005). Conclusion: COVID-19 patients had a high frequency of thyroid abnormalities. Thyroid dysfunction appears to fluctuate over time and to recover slowly and naturally.

A Case of Hashimoto's Encephalopathy Presenting with Cognitive Impairment and Visual Hallucinations

Introduction: Hashimoto's encephalopathy (HE) is a rare immune–mediated complication of Hashimoto thyroiditis. It is presented as subacute onset of altered mental status with confusion, seizures and myoclonus. It is a diagnosis of exclusion and requires that all other possible causes of cognitive impairment are excluded with a response to steroid therapy and evidence of thyroid autoimmunity in a patient. Here, we present a case of HE in a patient who presented with altered mental status and visual hallucinations despite no history or symptoms of thyroid disorder. Case Description: A 77 year old male with past medical history of hypertension presented with altered mental status, lethargy, and visual hallucinations. Per patient’s wife, patient started to get somnolent and was having memory problems six weeks prior to presentation. His mental status gradually deteriorated, and he started to have visual hallucinations. He was somnolent and noted to have myoclonus and twitching on admission. Magnetic resonance imaging (MRI) of the brain with gadolinium showed chronic microvascular changes with no acute intracranial pathology or masses. Electroencephalogram (EEG) showed no signs of epileptiform activity. Infectious disease work up, including complete blood count, urinalysis, sexually transmitted diseases, and cerebrospinal fluid (CSF) analysis, was negative. Blood glucose levels, serum electrolytes, liver function tests, blood urea nitrogen, and creatinine were normal. Coronavirus disease 2019 (COVID-19) was negative. CSF analysis for autoimmune encephalopathy and Creutzfeldt-Jakob disease was negative. Thyroid function tests were normal. Thyroid peroxidase antibody (TPOAb) was negative (8.6 IU/mL [reference range (RR): < 9.0 IU/mL]) and TgAb was positive (8.2 ng/ mL [RR: < 4 IU/ mL]). With suspicion of Hashimoto's encephalopathy, he was started on intravenous Solu-Medrol 1 g for five days. He was then switched to oral prednisone 60 mg daily, which he received for ten days. His mental status improved upon day 14 of admission. On day 17 of admission, he was discharged on oral prednisone 40 mg daily with taper for five weeks. He was evaluated in the clinic few months after discharge. His mental status had improved significantly, and he was back to his baseline in about two months after discharge as per his wife. Repeat thyroid function tests, TPOAb, and TgAb were negative. Discussion: The incidence of Hashimoto’s encephalopathy (HE) is 2.1 per 100,000 individuals in the general population, and is more common in women than men. This case highlights that HE should be considered in patients with subacute presentation of neurological problems, which cannot be explained with other possible diagnosis, despite no symptoms of thyroid disease such as the patient in this case study. Therefore, HE should be evaluated for in patients with cognitive impairment for prompt diagnosis and treatment with steroid therapy in order to improve the prognosis in these patients.

Hashimoto's encephalopathy in a patient with severe hypothyroidism

Introduction: Hashimoto's encephalopathy (HE) manifests itself with neuro-psychiatric disorders, which can reach coma;HE usually occurs in euthyroid, being less frequent states of thyroid dysfunction. We present the case of a patient with HE and severe hypothyroidism. Case Description: A 71-year-old woman;history of rheumatoid arthritis, hypertension and cerebral infarction without sequelae. The family referred a 3-week history of illness characterized by disorientation and "jerking" movements, she progressed to drowsiness with left hemiparesis, focal epileptic seizures and myoclonus. The brain CT showed atrophy and left frontal malacia;diagnosed status epilepticus and cerebral infarction, indicating phenytoin. During hospitalization she was added valproic acid and levetiracetam, without improvement. Brain MRI showed cerebral atrophy and periventricular leukoaraiosis. The study of the CSF: hyperproteinorraquia;EEG: diffuse slowing and periodic lateralized discharges in the right hemisphere. They request an endocrinology evaluation for TSH: > 75uIU/ml, Free T4: 0.31ng/dl, we expand with Anti-TPO > 1000 and Anti-thyroglobulin > 3000, and we indicate treatment for severe hypothyroidism with levothyroxine for nasogastric tube and intravenous hydrocortisone for 5 days and with minimal recovery from sensory disorder. After the withdrawal of hydrocortisone, she developed drowsiness and intensified myoclonus despite an improvement in the blood concentration of thyroid hormones. Having excluded infectious, metabolic and paraneoplastic etiology of encephalopathy, with the presence of elevated antithyroid antibodies in blood and CSF, the diagnosis of Hashimoto's encephalopathy was raised, receiving methylprednisolone (1 g/day for 5 days), then human immunoglobulin (25g for 5 days) Faced with poor response, she received 5 sessions of plasmapheresis with favorable clinical and paraclinical evolution. After overcoming hospital infection by COVID-19, she was discharged at 3 months. In the follow-up, cognitive deterioration, partial dependence, without epileptic seizures or myoclonus were reported. Discussion: HE is rare, with variable clinical presentation. HE has a good response to corticosteroids, although it sometimes requires other interventions. The alteration of thyroid function itself can be confusing at the time of diagnosis. Severe hypothyroidism can present neurological complications such as seizures, dementia, or psychosis;but it differs from HE in that manifestations improve when thyroxine is replaced.

Thyroiditis: A Potential Complication of COVID-19 Infection

Introduction: SARS-CoV-2 causes COVID-19 disease which can affect multiple organs including the lungs, heart, gastrointestinal tract, kidneys, central nervous system, and the endocrine system. Subacute thyroiditis is commonly caused by viral etiologies and is emerging as a potential complication of COVID-19. We report herein a case of subacute thyroiditis following COVID 19 infection. Case Description: A 57-year-old gentleman known to have hypertension, hyperlipidemia, and reactive airway disease, presented to the Emergency Department (ED) 10 days after testing positive for SARS-CoV-2. He reported worsening shortness of breath, chest pain, increasing cough, generalized weakness, exercise intolerance, and decreased appetite. In the ED, he was hypoxemic (SpO2=93%), afebrile (T=36.9ºC) and hemodynamically stable (BP=120/76 mmHg, HR=88bpm). Otherwise, the rest of his physical exam was unremarkable. Chest X-Ray revealed COVID-19 associated pneumonia and his COVID PCR test was positive. He had elevated liver function tests (AST 588 U/L;ALT 933 U/L;AlkPhos 819 U/L) and electrolytes imbalance were noted. The patient was admitted and treated with a course of antibiotics and steroids. Labs also exhibited suppressed TSH at 0.164 mcUnits/mL (0.350 - 5.000 mcUnits/mL), elevated free T3 at 4.3 pg/mL (2.2 - 4.0 pg/mL) and free T4 at 2.2 ng/dL (0.8 - 1.5 ng/dL), and negative anti-thyroid peroxidase antibodies, anti-thyroglobulin and TSH receptor antibodies. Upon further investigation, he reported heat intolerance, excessive sweating, and occasional tremors. He denied any personal or family history of thyroid disease as well as any amiodarone consumption. Subacute thyroiditis was diagnosed. The home medication of Beta-blocker (metoprolol) was continued and cholestyramine 4g twice daily was added to his regimen. Symptoms and free T3 and T4 levels improved and were back to normal upon discharge. Four months later, in the outpatient setting, thyroid function tests remained normal. Discussion: COVID-19 can cause simultaneous inflammatory multi-organ damage. Our patient had COVID-19 associated pneumonia, liver injury and subacute thyroiditis. Non-thyroidal illness and steroid use may affect thyroid functions and lead to suppressed TSH. In such instances, we would expect the free T3 to be low, unlike our patient’s data. Due to the wide range of organ involvement and presenting symptoms associated with COVID-19, it is not uncommon to neglect some emerging conditions while focusing and treating the more life-threatening ones. Subacute thyroiditis is a commonly overlooked complication associated with COVID-19. Its presentation can range from being asymptomatic to a full-blown thyroid storm. Untreated hyperthyroidism can cause worsening hemodynamics in COVID-19 patients. Therefore, recognizing subacute thyroiditis in such patients may prevent more severe and serious sequelae.

Subacute thyroiditis post COVID-9 vaccinations

Background: Subacute thyroiditis is being frequently seen after Covid infection as the cases of many other viral infections. Patients classically complain of symptoms of thyrotoxicosis mainly palpitations and sweating but with associated tenderness in neck with or without fever. Subacute thyroiditis has seldom been seen after viral vaccinations. We present a case series of subacute thyroiditis which presented after administration of the COVID-19 vaccine. Material(s) and Method(s): Case 1: A 28-year-old female without previous medical problems, presented to the clinic for sore throat, palpitations and dizziness . No recent history of any upper respiratory tract infection or pregnancy. The patient received her second dose of Pfizer/BioNTech mRNA vaccine for COVID-19 2 weeks earlier. Thyroid function testing was done and revealed TSH 0.001, fT4 3.29, fT3 6.8. Her TPO antibody, thyroglobulin antibodies and Trab were negative. Technetium-99m pertechnetate scan revealed diffuse thyroiditis. The patient was prescribed prednisone 20 mg daily. She reports rapid improvement of her symptoms and prednisone treatment was given for 3 weeks then stopped. Repeated tests showed normal TSH 10 days after stopping steroids. Case 2: A 49-year-old female with the history of V Leiden mutation and repetitive abortions presented to the clinics on May 25, 2021 for the complaint of unintentional weight loss of 6 kg in 20 days and palpitations, preceded by fever and neck pain at the end of April. The patient noted that she was vaccinated with her second dose of Sinopharm vaccine on the 6th of April 2021. Thyroid function test revealed a thyrotoxic profile TSH 0.005, fT4: 42, fT3 9,02. With negative thyroglobulin antibody, TRAb. CRP 60 , . Thyroid Ultrasound showed a diffuse heterogenous echtexture of the thyroid. A fever work up was done to rule out other infectious causes including Salmonella and Brucella, all were negative. The patient was prescribed prednisone 40 mg daily and propranolol 10 three times daily, gradually tapered over one months. Her Symptoms resolved and her follow up tests showed normal tsh and CRP Result(s): Discussion: Subacute thyroiditis is usually associated with upper respiratory tract infections including Covid -19 infection. This can be explained by T cells cross reacting between the virus and the thyroid cells. Moreover, De Quervain thyroiditis following viral vaccines has been reported influenza vaccines. Thyroiditis has not been described until now as a frequent side effect of Covid vaccine. So we presented the cases of a 28 and 49- year-old females who has presented with cases of subacute thyroiditis after receiving respectively the Pfizer mRNA vaccine and Sinopharm vaccine for COVID-19. Conclusion(s): Conclusion: Subacute thyroiditis after Covid-19 vaccine is rare but may be underreported. Further investigations are required to evaluate predisposing factors to De Quervain thyroiditis following Covid-19 vaccine.

Hypovitaminosisd on an adult female: From autoimmune conditions to pandemic days

Objective: COVID-19 pandemic was associated with increased risk of hypovitaminosis D due to lockdown regulations and limited outdoor activities, while young adult patients with autoimmune conditions may associated decreased values of 25-hydroxyvitamin D due to copresence of celiac disease, glucocorticoid exposure, malabsorption, overtreatment of autoimmune hypothyroidism, etc. (1-5).We aim to introduce a female case known with autoimmune conditions who was admitted for vitaminD deficiency related symptoms during pandemic. Case report: A 41-year-old, nonsmoker female is admitted for nonspecific muscle cramps, and joints pain, asthenia which is persistent for the last several months in addition to chronic low back pain (which required chronic use of nonsteroid anti-inflammatory medication). Her personal medical background reveals a diagnosis of HLA-B27-positive ankylosing spondylitis that was established seven years before current admission. She is also known with autoimmune thyroiditis with negative antibodies, a diagnostic that was based on suggestive ultrasound features with highly hypoechoic pattern of relative small thyroid gland (and normal thyroid function). She is also confirmed with thrombophilia. She has a negative personal history of confirmed COVID-19 infection and she followed the lockdown restrictions for several weeks. The family medical history is irrelevant. On admission, clinical examination of the thyroid is within normal limits on amenstruated normal weighted female. Biochemistry data points out normal total calcium of 9.45 mg/dL (normal: 8.4-10.3 mg/dL). Endocrine panel shows TSH=1.28 μUI/mL (normal: 0.5-4.5 μUI/mL), free levothyroxine=11.65 pmol/L (normal: 9-19 pmol/L), anti-thyroperoxidase antibodies=10.88 UI/mL (normal: 0-35), anti-thyroglobulin antibodies=10 UI/mL (normal: 0-115 UI/mL). 25-hydroxyvitamin D=10 ng/mL (normal >30 ng/mL) with increased PTH levels and negative antibodies for celiac disease. Supplementation with daily 2000 UI of vitamin D for 12 weeks followed by daily 1000 UI was recommended. Conclusion: The association thrombophilia-hypovitaminosis D has been reported in some patients, but it is rather incidental. Chronic use of antiinflammatory medication may cause malabsorption, and also the potential of a second autoimmune disease at intestinal level may cause this deficiency, but the current pandemic reality has become a new cause of it.