Thyroiditis Post COVID-19 mRNA Booster Dose Vaccination

Introduction: SARS-CoV-2 vaccines have been associated with thyroid dysfunction including thyroiditis and Graves' disease. We report a patient who developed thyrotoxicosis secondary to thyroiditis after COVID-19 mRNA booster dose vaccination. Case Description: A 74-year-old man with no known personal or family history of thyroid disorders went to his primary care physician with symptoms of palpitations. Of note, he had the first booster (third dose) of the Pfizer/BioNTech vaccine about 1 week before. He did not recall any similar symptoms after the first two doses of the same vaccine. There were no other symptoms of thyrotoxicosis such as hand tremors, weight loss or mood change. There was no family history of thyroid disorders. He was not on any medications such as amiodarone and was not taking any herbal supplements. He did not have any symptoms of upper respiratory tract infection. There was no neck pain. Physical examination was unremarkable with no goiter or thyroid eye manifestations. Thyroid function: free T4 elevated at 46.7 pmol/L (11.5-22.7) and TSH suppressed at 0.01 mIU/L (0.5-4.5). Thyroid stimulating immunoglobulin was positive at 200% (50-179). He was initially started on carbimazole 15mg daily. However, the patient became rapidly hypothyroid despite dose reduction and subsequent discontinuation of carbimazole with free T4 of 8 pmol/L and TSH of 36.4 mIU/L. An ultrasound of the thyroid gland showed vascularity with no discrete nodules. No thyroid uptake scan was done. The diagnosis was revised to thyroiditis post vaccination. Hypothyroidism persisted despite discontinuation of carbimazole before recovery 8 months later. Patient was well and did not require any thyroxine supplementation. Discussion(s): It is postulated that COVID-19 vaccines triggered thyroiditis via an autoimmune inflammatory syndrome caused by the vaccine adjuvants. A high index of suspicion is necessary and a thyroid uptake scan may be useful in making the diagnosis. Thyroiditis is a self-limiting condition and recognising it is important as no specific thyroid treatment is necessary in most patients. Patients should not be deterred from subsequent vaccination as COVID-19 infection has higher mortality risk than thyroiditis.Copyright © 2023

SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 (SARSCoV- 2) VACCINE-INDUCED THYROID DYSFUNCTION: A TALE OF TWO PATIENTS

Introduction SARS-CoV-2 vaccine has been the main pillar in battling the coronavirus disease 2019 (COVID-19) pandemic. However, the current vast scale of SARS-CoV-2 vaccination programme has led to inevitable reports of various adverse reactions, one of which include thyroid dysfunction. CASES We describe two patients who manifested hyperthyroidism following BNT162b2 mRNA-based COVID-19 vaccine boosters. Patient 1, a previously euthyroid 46-year-old female, has an eight-year history of type 1 diabetes mellitus. She developed palpitations of increasing severity about two weeks after her COVID-19 booster vaccine on 20th January 2022. She had weight loss of 4 kg and experienced menstrual irregularities in the subsequent three months. Examination revealed tachycardia (112 beats per minute, regular) and bilateral fine tremors of the hands. There was no goitre or neck tenderness. Blood investigations showed overt hyperthyroidism with positive thyroid autoantibodies, consistent with Graves' disease. Treatment with carbimazole led to marked symptomatic improvement. Patient 2, a 38-year-old female with a six-year history of Hashimoto thyroiditis, was clinically and biochemically euthyroid while taking levothyroxine 100 mcg daily prior to her COVID-19 booster vaccine on 5th January 2022. Five weeks following the vaccine, her thyroid function test during her endocrine clinic appointment showed overt hyperthyroidism, which was confirmed by a second blood sample ten days later. There was neither a change in levothyroxine dose nor any additional supplement intake. She was otherwise asymptomatic. Levothyroxine was then withheld. She regained her baseline hypothyroid state two weeks later, during which levothyroxine was resumed. Conclusion SARS-CoV-2 vaccine-induced thyroid dysfunction can affect both euthyroid and hypothyroid patients. A history of recent COVID-19 vaccination should be included in the clinical evaluation of a newly diagnosed hyperthyroid patient or unexplained hyperthyroidism in a long-standing hypothyroid patient.

NEW ONSET GRAVES' DISEASE AFTER SARS-CoV-2 VACCINATION

Introduction There is an increasing number of reports of thyroid dysfunction after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination. We would like to report a case of new onset Graves' disease following vaccination with the adenovirus-vectored Vaxzevria (Oxford-AstraZeneca). METHODOLOGY A 29-year-old female with no prior history of endocrine or autoimmune diseases, presented with a week of palpitations, heat intolerance and excessive sweating three days after her second dose of Vaxzevria. She did not experience these symptoms after her first dose which she received two months earlier. Her father and sister have Graves' disease. She had a diffuse goiter with no orbitopathy. Thyroid Stimulating Hormone (TSH) was <0.01 mIU/L (normal range: 0.27-4.2) with a markedly elevated free T4 of >100 pmol/L (normal range: 12-22). TSH receptor antibody was positive at >40.00 IU/L (Normal range: <1.75). Ultrasonography revealed a hypervascular, diffusely enlarged goiter. She was started on oral carbimazole and propranolol. Five months later, her free T4 had normalized at 18 pmol/L though her TSH was still undetectable. To date, she remains hesitant for her booster dose. Results SARS-CoV-2 infection and vaccination have been associated with subacute thyroiditis and autoimmune thyroid disease. While there are reports of new onset Graves' disease after mRNA and adenovirus-vectored vaccines, it has not been associated with inactivated virus vaccines. The current prevailing theory is that the adjuvants in the vaccines can trigger an autoimmune event, also called 'autoimmune/ inflammatory syndrome induced by adjuvants' (ASIA). Conclusion Physicians need to be aware of thyroid dysfunction after SARS-CoV-2 vaccination, especially in those with a strong family history of autoimmune disease. Nevertheless, it is also important to note that the benefit of vaccination far outweighs this uncommon potential risk. More studies are required to establish a causal relationship.

GLASSY LUNGS, DRUGS AND MELENIC RUNS, A CASE REPORT

CASE: A 73-year-old male with a history of prostate cancer, hypertension and hyperthyroidism presented with one week of worsening dyspnea, productive cough and pleurisy. He also endorsed new orthopnea and melena over the last three days. Home medications included abiraterone, prednisone, methimazole and amlodipine. On admission, vitals were notable for tachycardia, tachypnea and hypoxia (82% on room air and 90% on 3L by nasal canula (NC)). Initials labs showed WBC count 17.4, Hemoglobin 7.1, proBNP 256, two negative COVID-19 PCR tests, negative respiratory virus panel and normal TSH and PSA. CTPE was negative for pulmonary embolism but showed new diffuse ground glass opacities. The patient was started on broad spectrum antibiotics and IV diuretics for possible pneumonia and new heart failure. However, the patient's respiratory status continued to decline, now requiring 6L by NC. Hemoglobin also continued to drop precipitously. A broad rheumatologic and infectious workup was largely negative with findings notable for a positive ANA, CRP 74, LDH 359 and an undetectable haptoglobin. A urinalysis was positive for protein and blood. At this time, empiric treatment for pneumocystis pneumonia was initiated with a plan for bronchoscopy. The bronchoscopy with bronchoalveolar lavage (BAL) revealed diffuse alveolar hemorrhage (DAH) with studies negative for infection or malignancy. An upper endoscopy did not reveal any gastrointestinal source of bleeding but rather favored a pulmonary source due to some red blood in the esophagus and coffee ground material in the stomach. Given these findings, a diagnosis of “Methimazole induced vasculitis with DAH” was made, a diagnosis of exclusion. The patient was started on pulse steroids for three days and his methimazole was held. By day four, the patient reported improvement and his oxygen was decreased to 2L. He was subsequently discharged on a steroid taper. At his two-week follow-up, the patient had improving respiratory status and repeat labs showed an improved and stable hemoglobin, and normal haptoglobin. IMPACT/DISCUSSION: This case illustrates a rare but life-threatening complication of methimazole use. Common offenders of drug-induced DAH include propylthiouracil, carbimazole and hydralazine. This complication is reported in 15-37% of patients on propylthiouracil but only 0-3% of patients on methimazole. A third of patients with DAH do not present with hemoptysis making this diagnosis challenging. Lab findings can also be largely nonspecific making a thorough history, imaging and interdisciplinary collaboration key in identifying this adverse effect early on to prevent mortality. CONCLUSION: Include drug-induced DAH on the differential for patients presenting with respiratory failure in the setting of new anemia, melena or hemoptysis. Stopping the offending drug and initiating steroids is the treatment of choice. Consider empiric PCP treatment and BAL for patients with severe hypoxia, ground glass opacities and immunosuppression.

A Patient with Thyroid Storm Precipitated by COVID-19 Vaccine

Introduction: SARS-COV-2, causing the COVID-19 pandemic, had a disease spectrum affecting multiple organs since its emergence in 2019. There is an association between COVID-19 and thyroid disease. Multiple vaccines had been approved for SARS-COV-2. Despite their safety profile, adverse effects have been reported. An association between thyrotoxicosis after the vaccine has been reported. But COVID-19 vaccine is very rare to precipitate a thyroid storm. Case Description: 29-year-old gentleman, presented to Emergency Department (ED) complaining of shortness of breath for 5 days, increasing in severity. He had a cough with whitish sputum, no fever or chest pain. He had palpitations and 10 kg weight loss, for 6 months. Five days prior to the presentation he received the second dose of the BNT162b2 vaccine (Pfizer-BioNTech COVID -19 vaccine) Physical examination: the vital signs showed tachycardia 175 beat/minute with an irregular pulse, otherwise unremarkable, he was conscious alert and oriented to time place and person, there was bilateral mild exophthalmos and diffuse soft goiter. Chest exam showed bilateral coarse basal crackles. He has bilateral pitting edema of the lower limbs. Blood investigation was remarkable for TSH < 0.01 (0.3-4.5 mIU/L), FT3 12.6 (3.6-7.4 pmol/L), FT4 48.5 (11-23.5 pmol/L) and TSH receptor antibodies (TRAB) 34, Positive > 1.75 IU/L. Electrocardiography showed atrial fibrillation with a rapid ventricular response. Echocardiography showed reduced ejection fraction (40%) with moderate global hypokinesia. The patient was admitted under MICU care as thyroid storm (Bursh-Wartosfsky score 50/140) secondary to Graves’s disease and precipitated by COVID 19 vaccine. He was started on Propylthiouracil 200 mg every 4 hours, hydrocortisone 100 mg every 8 hours, Lugol’s solution 10 drops every 8 hours, cholestyramine 4 gm every 6 hours, and metoprolol 12.5 mg every 12 hours, the dose of metoprolol increased gradually to avoid worsening of heart failure. The patient’s condition was improving, he was switched from propylthiouracil to carbimazole 20 mg twice daily, and after a few days, he was stable and discharged home on carbimazole and metoprolol. The patient didn’t attend the endocrine clinic for follow-up as he traveled back to his home country. Discussion: The association between thyrotoxicosis and the COVID-19 vaccine is reported in the literature. Very rarely COVID-19 vaccine can precipitate thyroid storm in a patient with Graves’s disease. The immune system activation after the vaccine possibly leads to a decompensated state in this patient with existing hyperthyroidism.