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COVID-19 is a severe immunosuppressive disease that can cause changes in the clinical course of autoimmune diseases. Autoimmune thyroiditis (AIT) is no exception. It is relevant to study the features of the clinical course of existing AIT in the post-COVID-19 period. The work aims to study the changes in the structure and function of the thyroid in patients with AIT with subclinical and manifest compensated hypothyroidism who had moderate COVID-19. A total of 123 patients aged 21-49 with AIT with subclinical hypothyroidism - 43 (group 1, 12 of whom had moderate COVID-19) and manifest hypothyroidism in the stage of medical compensation - 80 (group 2, 32 of whom had moderate COVID-19). The duration of AIT ranged from 4 to 13 years. In all cases, upon inclusion in the study and 2 and 6 months after it, changes in the structure of the thyroid gland were studied according to ultrasound data, as well as its functional capacity and the degree of compensation of hypothyroidism according to the thyroid-stimulating hormone indicator. In all patients with AIT, COVID-19 caused the progression of structural changes in the thyroid within one of two variants of the ultrasound picture of thyroiditis - hypoechoic heterogeneous or pseudo micronodular. The hormone-producing function also changed: in 7 out of 12 patients of group 1 of the main subgroup, hypothyroidism changed from subclinical to manifest hypothyroidism in the postoperative period, and in all patients of group 2 of the main subgroup, a further decrease in hormone synthesis was noted. In the post-COVID-19 period, patients with AIT undergo a progression of structural changes in the thyroid gland and a decrease in the synthesis of thyroid hormones.Copyright © 2023 The Authors.
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Since the outbreak of coronavirus disease 2019 (COVID-19), a number of COVID-19 related thyroid disorders have been reported, including subacute thyroiditis, autoimmune thyroid disease, non-thyroidal illness syndrome and some unexplained thyroid dysfunction. This review aimed to summarize clinical characteristics of COVID-19 related thyroid disorders and to discuss some possible mechanisms.Copyright © 2022, Peking Union Medical College Hospital. All rights reserved.
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Introduction: there are reports of autoimmune disease related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) such neurological syndromes and hematological syndromes, and more recently autoimmune thyroid dysfunctions have been described. These reports suggest that SARS-CoV-2 acts as a probable trigger for triggering the autoimmunity process. Aim: to evaluate structural similarity between thyroid peroxidase [Homo sapiens] (TPO) and SARS-CoV-2 spike glycoprotein (COVID-19), and to propose this similarity as a likely trigger for autoimmune thyroiditis. Methodology: using bioinformatics tools, we compare the amino acids (AA) sequences between protein structure of TPO and chain A COVID-19, chain B COVID-19, and chain C COVID-19, accessible in the National Center for Biotechnology Information database, by Basic Local Alignment Search Tool in order to locate the homologous regions between the sequences of AA. Results: the homology sequence between the TPO and COVID-19 ranged from 27.0 % (10 identical residues out of 37 AA in the sequence) to 56.0% (5 identical residues out of 9 AA in the sequence). The similar alignments demonstrated relatively high E values in function of short alignment. Conclusion: data suggest a possible pathological link between TPO and COVID-19. The structural similarity of AA sequences between TPO and COVID-19 may present a molecular mimicry suggesting the possibility of antigen crossover between TPO and COVID-19 that might represent an immunological basis for autoimmune thyroiditis associated with COVID-19.
Introdução: há relatos de doenças autoimunes relacionadas à síndrome respiratória aguda grave por coronavírus 2 (SARS-CoV-2), tais como síndromes neurológicas e hematológicas, e mais recentemente disfunções autoimunes da tireoide foram descritas. Esses relatos sugerem que o SARS-CoV-2 atue como um provável gatilho para desencadear o processo de autoimunidade. Objetivo: avaliar a similaridade estrutural entre a peroxidase tireoidiana [Homo sapiens] (TPO) e a glicoproteína de superfície SARS-CoV-2 (COVID-19) e propor essa similaridade como provável gatilho para o desencadeamento da tireoidite autoimune. Metodologia: utilizando ferramentas de bioinformática, comparamos as sequências de aminoácidos (AA) entre a estrutura da TPO e a estrutura da cadeia A do COVID-19, a cadeia B do COVID-19 e a cadeia C do COVID-19, acessível no banco de dados do National Center for Biotechnology Information, através da Ferramenta Básica de Pesquisa de Alinhamento Local para localizar as regiões homólogas entre as sequências de AA. Resultados: a sequência de homologia entre o TPO e COVID-19 variou de 27,0% (10 resíduos idênticos em 37 AA nas sequências) a 56,0% (5 resíduos idênticos em 9 AA nas sequências). Os alinhamentos semelhantes demonstraram valores E relativamente altos em função do alinhamento curto. Conclusão: os dados sugerem uma possível ligação patológica entre TPO e COVID-19. A similaridade estrutural das sequências de AA entre TPO e COVID-19 pode apresentar um mimetismo molecular sugerindo a possibilidade de cruzamento de antígeno entre TPO e COVID-19 que podem representar uma base imunológica para tireoidite autoimune associada a COVID-19.
Subject(s)
Humans , Male , Female , Thyroiditis, Autoimmune , Peroxidase , Molecular Mimicry , Severe Acute Respiratory Syndrome , SARS-CoV-2ABSTRACT
Background: The coronavirus disease-19 (COVID-19) pandemic has significantly affected healthcare systems. Down syndrome (DS) is a chronic disease caused by trisomy of chromosome 21 which is associated with a variety of medical problems such as autoimmune thyroid disease (AITD) that necessitate comprehensive routine treatment. During the COVID-19 pandemic, there was an increasing an unavailability, which became an impediment to chronic disease patients' drug consumption. Objective(s): The purpose of this study was to examine the barriers to medication adherence faced by DS patients during the COVID-19 pandemic. Method(s): An observational analytic study was conducted from January to July 2021 among parents of DS patients who registered in the pediatric endocrinology outpatient clinic of Dr. Soetomo General Hospital. Inclusion criteria include: The parents of DS with AITD patients aged 1-18 years who came to the pediatric endocrinology polyclinic, routinely took oral medication before March 2020, can fill out questionnaire forms independently, and signed the informed consent. Exclusion criteria were parents of DS patients who did not take regular medication, or started treatment after March 2020. Data were collected and analyzed using the Wilcoxon comparison test Results: There are 31 DS patients responded and completed the questionnaires. Adherence to hospital visits in DS with AITD patients before and during the COVID-19 pandemic showed significant differences (P = 0.001). The main barriers to follow-up visits during the pandemic were lockdown protocol which made travel difficult (28%). The compliance for taking medication was still high although 13 (41.9%) obtained the medicine without a prescription. Conclusion(s): Changes in terms of medication adherence during the pandemic have highlighted the importance of improving DS patient's access to healthcare. Shifting medication counseling to the nearest primary health care provider with supervision from a tertiary referral specialist appears to be a reasonable and potentially cost-effective strategy in improving treatment adherence especially in a pandemic setting.Copyright © 2023, Author(s).
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Background. There are numerous reports indicating increased risk of diabetic ketoacidosis (DKA) in new-onset type 1 diabetes (T1D) in childhood during COVID-19 pandemic. Delayed diagnosis, reduced access to immediate health care and psychological effects of pandemic have been suggested as possible reasons. Method(s): We conducted cross sectional, single-center study at Department of Pediatrics, University Hospital Center Zagreb, Croatia, evaluating severity of DKA in patients diagnosed during COVID-19 pandemic as compared to pre-pandemic period. Besides COVID-19 pandemic, Croatia suffered two severe earthquakes, adding psychological burden and difficulties to health care organization. The data collected for the period March 2012 - March 2022 included: age, sex, laboratory parameters at presentation (pH, HCO3, HbA1c), association of celiac and autoimmune thyroid disease and frequency of positive pancreatic antibodies. The pandemic group (PG) included patients diagnosed form March 2020 to March 2022 while previously diagnosed patients comprised control group (CG). Result(s): There were 107 patients in pandemic group (57M/50F) as compared to 337 controls (191M/146F). No significant difference was found between PG and CG regarding age (9.2/ 8.9 years), sex, DKA frequency (44.9/40.4%) or severity (mild: 15.2/13.8%;moderate 15.2/13.5%;severe: 13.3/12.3%), HbA1c at diagnosis (11.5/ 11.2%) and frequency of admission to intensive care unit. There was no difference regarding frequency of celiac (5.6/ 3.0%) and autoimmune thyroid disease (15.0/22.0%) at presentation, or negative pancreatic antibodies (6.8%/4.5%). We found significantly higher frequency of new-onset diabetes in children < 5 years during pandemic (32.7% vs. 20.5%, p=0.009). Particularly increased frequency during pandemic was noted in children < 2 years (12.1% vs. 6.2%, p=0.045). The age distribution was as following in PG/CG: <2 yrs 12.1/6.2%, 2-5 yrs 20.6/14.2%, 5-11 yrs 26.2/41.8%, 11-18 yrs 41.1/37.7%. No difference in DKA frequency or severity between PG and CG was noted among age groups. When comparing 1st and 2nd pandemic year, there was no difference regarding age, sex, frequency and severity of DKA. Conclusion(s): Despite adversities experienced during COVID- 19 pandemic and post-earthquake recovery, we did not find increased frequency or severity of DKA in new-diagnosed T1D. However, we found increased percentage of new-onset T1D among patients <5 years during pandemic, particularly < 2 years, but we did not find increased DKA presentation in any age group. Further studies are necessary to elucidate the effect of COVID-19 pandemic on presentation and related complications of T1D and to determine if the shift toward the younger age at presentation will be abiding.
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Background. Type 1 Diabetes (T1D) is a chronic disease resulting from autoimmune destruction of insulin-secreting pancreatic beta cells. Viruses are known to play a role in the pathogenesis of T1D. There is no consistent evidence that SARS-CoV-2 induces T1D in children or adults. Nevertheless, evidence suggests that the SARSCoV- 2 affects beta cell function, suggesting a role for the virus in the pathogenesis of the disease. It is thus plausible that the effects of the SARS-CoV-2 on beta cells and the environmental alterations caused by the COVID-19 pandemic affected the clinical and immunological characteristics of new-onset T1D. Objective(s): To find the clinical and immunological signatures of the COVID-19 pandemic on children diagnosed with T1D. Method(s): A single-center, retrospective observational study comparing the clinical and immunological characteristics of children diagnosed with T1D at our clinic the year before and during the first two years of the COVID-19 pandemic. Data were extracted from the medical records of the children at the time of diabetes diagnosis, including clinical and demographic parameters, COVID-19 PCR results, and the presence of anti-islet, thyroid, and celiac-related autoantibodies. Also obtained from the medical records were a family history of T1D, celiac disease, and autoimmune thyroid disease in a first-degree family member. Result(s): 376 children were diagnosed with T1D at our diabetes clinic during the study period. 132, 121, and 123 children were diagnosed during the pre-COVID-19 era, the first and second pandemic years, respectively. The rate of diabetic ketoacidosis at presentation was slightly higher during the COVID-19 era than in the pre-COVID-19 era (not reaching statistical significance) and comparable between the first and second pandemic years. Multiple antibodies were significantly higher among patients diagnosed in the pre-COVID-19 era than those diagnosed in the first two years of the pandemic (72% vs.61%, p=0.03). Islet-cell autoantibodies (ICA) levels were higher among children diagnosed during the COVID-19 era compared to pre-COVID-19 era (1341.34+1786.36U/ml vs.968.02+1495.66U/ml, p=0.042). GADantibodies levels were higher in children diagnosed with COVID- 19 before the diagnosis of T1D than in children without COVID-19 (614.86+793.90U/ml vs.317.08+611.45U/ml, p=0.027). Tissue Transglutaminase antibodies were more common among children diagnosed during the COVID-19 era compared to the pre- COVID-19 era (17% vs. 8%, p=0.024). Conclusion(s): Our findings suggest that SARS-CoV-2 and the environmental alterations caused by the pandemic affected the immunological profile of children diagnosed with T1D. Thus, it appears that the virus plays a role in the autoimmune process causing T1D.
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The coronavirus disease-19 (COVID-19) is an infectious disease caused by the enveloped RNA beta-severe acute respiratory syndromecoronavirus-2 (SARS-CoV-2). The COVID-19 may have a variable presentation, from an asymptomatic disease to acute respiratory distress syndrome (ARDS) and multi-organ failure. Impairment of endocrine systems may also occur in COVID-19 patients and thyroid gland involvement was reported in a not negligible number of patients, as documented in several studies since the pandemic outbreak. Abnormal thyroid function tests (TSH and/or thyroid hormones) are frequently reported in COVID-19 patients with variable prevalence and mild to moderate severity in available studies. Keys for understanding this dilemmaare introduced in this overview. Copyright © 2022, Anka Publishers. All rights reserved.
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Background: Vitamin D is classified as an immunomodulatory hormone that is synthesized because of skin exposure to sunlight. It is known to come into play during the regulation of hormone secretion, immune functions, cell proliferation, and differentiation. Its deficiency can cause many diseases and their associated pleiotropic effects. In addition, in relation to its eminent function as regards adaptive immune response and innate immune response, vitamin D level is associated with immune tolerance. Method(s): Literature search prior to May 2021 was conducted through selected websites, including the MEDLINE, Embase, Web of Science, Cochrane Central, www.ClinicalTrials.gov, PubMed, Science Direct, Google Scholar, and EFSA. Result(s): Vitamin D is found effective for the regulation of hormone secretion, immune functions, and cell proliferation along with differentiation. Its role as an immune modulator is based on the presence of receptors on many immune cells and the synthesis of its active metabolite from these cells. Vitamin D, an immune system modulator, inhibits cell proliferation and stimulates cell differentiation. A fair number of immune system diseases, encompassing autoimmune disorders alongside infectious diseases, can occur because of low serum vitamin D levels. Supplementation of vitamin D has positive effects in lessening the severity nature of disease activity;there exists no consensus on the dose to be used. Conclusion(s): It is figured out that a higher number of randomized controlled trials are essential to evaluate efficacy pertaining to clinical cases, treatment duration, type, and dose of supplementation and pathophysiology of diseases, immune system functioning, and the effect of vitamin D to be administered. Copyright © 2022, The Author(s).
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Background: Immune hemolytic anemia (AIHA) and thrombocytopenia (ITP) may rarely coexist with autoimmune disorders. Primary IHA and ITP usually respond to steroids and intravenous immunoglobulins. However, IHA+ITP may be difficult to treat when associated with autoimmune disorders. Aim(s): We report a case of a 57-year- old man diagnosed with AIHA and ITP and also found to have thyroiditis. Method(s): A retrospective review of the patient's medical history was performed. Result(s): A 57-year- old- woman with bruises, weakness, fatigue, and dizziness was admitted to the hematology center. This time CBC test was revealed hyperchromic macrocytic anemia with anisocytosis, thrombocytopenia, lymphocytosis and high level of ESR. Coomb's reactions were positive. The patient had been on autoimmune thyroiditis for about 5 years and was receiving 50 mg of L-thyroxin. Laboratory testing revealed only slightly elevated LDH level in serum and no other significant abnormalities. Instrumental examination were also normal. Our differential diagnosis included TTP, Evans and marrow infiltrative disorders. Direct antiglobulin test positive (IgG, IgG + C3d). We made a diagnosis of immune hemolytic anemia and thrombocytopenia and started treatment with Prednisolone 65mg per day. In about six months Duplex scan showed acute thrombosis of right external iliac vein. October 2021. The patient was diagnosed with COVID-19, Bilateral interstitial pneumnonia. On the way home ischemic stroke occurred. Thrombectomy -within 12 h Conclusion(s): ITP can rarely coexist with thyroiditis and Thrombosis episode. In such cases, we involuntarily deviate from the contraindications of standard anticoagulant therapy, and, regardless of the low platelet count, administer anticoagulant therapy and combine it with steroid medication. The clinical case is evidence that the treatment of concomitant immune system disorders improves the course of treatment for all pathologies but poses a thrombotic complication.
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The 100th anniversary of the discovery of vitamin D3 (VitD3) coincides with significant recent advances in understanding its mechanism of action along with accumulating knowledge concerning its genomic and nongenomic activities. A close relationship between VitD3 and the immune system, including both types of immunity, innate and adaptive, has been newly identified, while low levels of VitD3 have been implicated in the development of autoimmune thyroiditis (AIT). Active 1,25(OH)2 D3 is generated in immune cells via 1-α-hydroxylase, subsequently interacting with the VitD3 receptor to promote transcriptional and epigenomic responses in the same or adjacent cells. Despite considerable progress in deciphering the role of VitD3 in autoimmunity, its exact pathogenetic involvement remains to be elucidated. Finally, in the era of coronavirus disease 2019 (COVID-19), brief mention is made of the possible links between VitD3 deficiency and risks for severe COVID-19 disease. This review aims to commemorate the centennial of the discovery of VitD3 by updating our understanding of this important nutrient and by drawing up a framework of guidance for VitD3 supplementation, while emphasizing the necessity for personalized treatment in patients with autoimmune thyroid disease. A tailored approach based on the specific mechanisms underlying VitD3 deficiency in different diseases is recommended.
Subject(s)
COVID-19 , Hashimoto Disease , Thyroiditis, Autoimmune , Vitamin D Deficiency , Humans , Vitamin D , Vitamins , Cholecalciferol , InflammationABSTRACT
Background: Multimorbidity in patients with rheumatoid arthritis (RA) has been described as the coexistence of two or more chronic diseases and is the most common cause of death in this population. Objectives: To describe the prevalence of multimorbidity and mortality trends in a well-characterized cohort of patients with RA. Methods: A retrospective cohort study of patients with RA (1987 ACR criteria) was conducted. Each patient was evaluated and followed by a rheuma-tologist in a single outpatient private center in Bogotá, Colombia, from 2014 to 2021. Categorical variables were expressed in frequency and percentage and quantitative variables in mean and standard deviation or median with interquartile range, depending on the distribution of the data. Statistical package: SPSS 25. Results: A total of 783 patients were included. 11% of patients with RA present multimorbidity. Baseline characteristics were as follows: female gender 81.6%, mean age 51.8±11 years, mean disease duration 8 (IQR 3-15) years, RF positive 80.1%, ACPA positive 58.2%, and erosions 24.9%. Most patients have received glucocorticoids (89.8%), and conventional synthetic DMARDs (97.8%), being prednisone and methotrexate the most frequently prescribed. Hypertension was prevalent in 27.7%, osteoporosis 19.3%, malignancies in 5.5% and principal infection was urinary infection 14.3%. Polyautoimmunity was present in 5.7% most frequently Autoimmune thyroid diseases 10.6% and Sjögren syndrome 9%. After a median of 73 months of follow-up, the mortality rate was 1% of the entire cohort, being cardiovascular disease and COVID-19 infection the main causes. Conclusion: Patients with RA have an important multimorbidity burden and this increased risk of adverse outcomes and mortality.
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Background: Primary Sjögren's syndrome (pSS) is a chronic and progressive multisystem autoimmune disease which rarely onset in children and adolescents. Diagnostic delay in large part of patients are common due to the non-specifc and variable symptoms and the slow progression of disease. Objectives: To analyse demographic data, specifc extraglandular, salivary and ocular manifestations, laboratory parameters and therapy of pSS with juvenile onset. Methods: Retrospective study of all patients (pts) with pSS in single center. Results: pSS was verifed in 15 pts (6.7% were boys), which amounted to 23.8% of all pts with SS in our pediatric rheumatologic department. The median age of pSS onset was 8.0 y.o. [IQR 7.0;10.2]. The median of disease duration at the time of pSS verifcation was 2.75 years [2.2;5.6]. All patients had systemic manifestations at onset: constitutional abnormalities-33.3%, nonerosive polyarthritis-64.3%, polyarthralgias-26.7%, lymphadenopathy-73.3%, cutaneous involvement-53.3% (2-xerosis, 2-annular erythema, 1-erythema nodo-sum, 2-Raynaud phenomenon, 2-nonspecifc spotty rashes, 1-hemorrhagic rash). At the time of diagnosis 7 pts (46.7%) had isolated involvement of salivary glands, 8 pts (53.3%)-combined with involvement of lacrimal glands. The decrease in salivary gland function was recorded in 80% of cases, hypolacrimia-in 46.7%, 1 patient had isolated hypolacrimia. Recurrent parotitis was present in 6 pts (40.0%). At time of diagnosis pulmonary involvement had 20.0% of pts, 1 patient had renal tubular acidosis. 8 pts (53.3%) had various hematological disorders: anemia-in 3 pts (20.0%), leukopenia-in 6 (40.0%). ANA Hep-2 were detected in 100% pts (in titer 1/640-4, 1/1280-7, 1/2560-3, 1/20480-1, with mixed patterns in all pts: speckled + homogeneous-9 pts, speckled + homogeneous+cytoplasmic-6 pts), anti-Ro-in 12 pts (80.0%), anti-La-in 8 pts (53.3%), RF+-in 9 pts (60.0%). 6 pts (40.0%) had polyclonal hypergammaglob-ulinemia, max 42%. 2 pts (13.3%) had concomitant autoimmune non-rheumatic disease;1-cutaneous psoriasis, 1-autoimmune thyroiditis. The treatment of each patient was justifed by the main individual manifestations: 93.3% received glucocorticoids, 26.7%-methotrexate, 33.3%-hydroxychloroquine, 6.7%-mycophenolate mofetil. Treatment with biologics (B) was received by 13 (93.3%) pts (7-rituximab (RTM), 6-abatacept (ABA)) with a good response in 10 pts, including improvement in the function of the salivary and lacrimal glands in 7 pts. 1 patient received 2B-RTM and ABA sequentially due to the development of MAS 7 days after 1st RTM infusion. B was discontinued in 3 pts: 1 due to development of hemorrhagic vasculitis 2 days after the 1st RTM infusion, 1-COVID-19 with lung involvement (CT 3-4) 2 weeks after the 1st RTM infusion, 1-inefficiency of ABA during 15 months. Conclusion: In our pediatric rheumatologic department pts with pSS made up less than a quarter of all pts with SS. The diagnosis was verifed delayed in all pts, which can be explained by a wide range of nonspecifc manifestations at the onset. However, the manifestations of SS that were present at the time of diagnosis were brought under control on the background of complex therapy, including the prescription of B, with a good efficacy and safety profile of therapy.
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There are several interactions between a SARS-CoV2 infection and the thyroid, bidirectionally in both directions. In severe COVID-19 infection, changes in thyroid hormone levels are a marker for poorer prognosis. SARS-CoV2 appears to interact directly with thyrocytes as well as modulate the immune system and trigger autoimmune thyroid disease. As early as 2020, SARS-CoV2 associated thyroiditis was described in patients with COVID-19, which is similar to subacute thyroiditis but typically painless. There are now a wide variety of reports on the occurrence of chronic autoimmune thyroiditis and Graves' disease following both viral infection and vaccination. Existing thyroid disease does not appear to be associated with either a higher risk of SARS-CoV2 infection or a more severe disease course. The present paper summarizes the current knowledge regarding the thyroid gland and SARS-CoV2.
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Introduction The relationship between autoimmunity and SARS-CoV-2 vaccine has explained how thyroid dysfunction developed following vaccination but the onset of thyroid eye disease (TED) is scarcely described. We report a case of Graves' disease (GD) who developed TED after three weeks of BNT162B2 SARS-CoV-2 vaccine (Pfizer-BioNTech) injection. CASE A 54-year-old non-smoking male presented with newonset bilateral eyes redness, proptosis, and diplopia three weeks after receiving the second dose of mRNA BNT162B2 SARS-CoV-2 vaccine. He was diagnosed with GD without TED in 2003 and underwent radioactive iodine ablation in 2020. He subsequently developed hypothyroidism and was started on levothyroxine with stable thyroid function test throughout clinic visits. There were no recent stressful events including COVID-19 infection. On examination, he has bilateral exophthalmos, chemosis, conjunctival injection, swollen eyelids and caruncles, with intact vision. Blood tests revealed normal TSH, free T4, and T3, but elevated TSH-receptor antibodies of 3.60 IU/L (<1.75) and antithyroid peroxidase (TPO) antibodies of >600 IU/ml (0-34). MRI orbit showed bilateral extraocular muscle enlargement and proptosis. Intravenous methylprednisolone was given weekly for 12 weeks. There was significant improvement concerning congestive symptoms and diplopia after the third dose of methylprednisolone. Thyroid eye disease is the extrathyroidal manifestation of GD resulting from the autoimmune and inflammatory process. The temporal relationship of the onset of TED after mRNA SARS-CoV-2 vaccination in our case was suggestive, and there were no other inciting events identified. The postulated mechanisms include immune reactivation, molecular mimicry between the SARS-CoV-2 spike proteins and thyroid proteins, and the autoimmune/ inflammatory syndrome induced by adjuvants present in the mRNA vaccine. Conclusion Patients with autoimmune thyroiditis should be monitored closely after SARS-CoV-2 vaccine as they may develop TED and require treatment.
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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.
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PURPOSE: SARS-CoV-2 infection can be associated with destructive thyroiditis and triggers thyroid autoimmunity. More recent evidence suggests that SARS-CoV-2 vaccines may also be associated with permanent or transient thyroid dysfunction in susceptible individuals. METHODS: We observed three patients who developed/exacerbated autoimmune thyroid diseases (AITDs) shortly after receiving mRNA-based vaccines against SARS-CoV2. Clinical histories are reported, and relevant literature in the field is summarized. RESULTS: Our case series gives a description of the full spectrum of autoimmune disorders that may occur after SARS-CoV-2 vaccines administration, ranging from a case of new-onset Graves' disease to autoimmune hypothyroidism in two patients with pre-existing AITDs. Our three patients had a personal and/or family history of autoimmune disorders, suggesting that genetic predisposition is an important risk factor for the development of AITDs following vaccination. Moreover, our real-life experience demonstrates that persistent hypothyroidism may occur in the long run and should be overlooked; subjects with a previous AITDs are at risk of developing it. Reviewing the pertinent literature up to date Graves' disease is the most common vaccine-related AITDs with up to 51 cases reported in the literature, occurring mainly in female patients with no personal history of AIDTs, while only a case of autoimmune hypothyroidism has been reported so far. CONCLUSIONS: SARS-CoV-2 vaccines can trigger autoimmune reactions and the present case series contributes to make clinicians aware of full spectrum of AITDs that may occur following vaccination. Thyroid function monitoring is recommended, mainly in subjects with a personal/family history of AITDs.
Subject(s)
Autoimmune Diseases , COVID-19 Vaccines , COVID-19 , Graves Disease , Hypothyroidism , Female , Humans , Autoimmunity , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , RNA, Viral , SARS-CoV-2ABSTRACT
Since the Covid-19 pandemic emerged in 2019, several adenoviral-vectored, mRNA-based and inactivated whole-virus vaccines have been developed. A massive vaccination campaign has been undertaken around the world, and an increasing number of SARS-CoV-2 vaccine-induced thyroid diseases have been described in the literature. Subacute thyroiditis has been reported in 52 patients, mean age 45.5 ± 1.8 years, mainly in women (n = 39). Graves' disease is more frequent in women (n = 22) than in men (n = 10), mean age 46.2 ± 2.6 years, reported as new onset, recurrent or exacerbation of well-controlled hyperthyroidism. The mean time to symptoms onset is 9.0 ± 0.8 days in subacute thyroiditis, and 15.1 ± 2.6 days in Graves' patients. Rare patients (n = 6) present silent or painless autoimmune thyroiditis. Thyroid function and autoimmune tests, inflammatory markers, thyroid echography with colour flow Doppler, radio-activity uptake on thyroid scan, medical treatment and follow-up are described and compared in patients with SARS-CoV-2 vaccine-induced thyroid diseases. The underlying pathogenic mechanisms of vaccine-induced thyroid diseases, molecular mimicry (various SARS-CoV-2 proteins sharing a genetic homology with a large heptapeptide human protein) or autoimmune/inflammatory syndrome induced by adjuvants (ASIA) are discussed in the context of predisposition or genetic susceptibility. The benefits of SARS-CoV-2 vaccination far outweigh the potential vaccine-induced adverse effects, but clinicians should be aware of possible autoimmune and inflammatory thyroid diseases, and can advise patients to seek medical assistance when experiencing anterior neck pain, fever or palpitations following SARS-CoV-2 vaccines. Further studies are warranted to investigate the etiopathogenesis and to clarify the factors which predispose patients to SARS-CoV-2 vaccine-induced thyroid diseases.
Subject(s)
COVID-19 , Graves Disease , Thyroiditis, Subacute , Thyroiditis , Male , Humans , Female , Adult , Middle Aged , COVID-19 Vaccines/adverse effects , Thyroiditis, Subacute/etiology , Pandemics , SARS-CoV-2 , COVID-19/prevention & control , Graves Disease/diagnosis , Vaccination/adverse effectsABSTRACT
Introduction: There have been few reported cases of post-vaccination thyroiditis and Grave's disease. Here, we present a unique case of post vaccination thyroiditis associated with thyrotoxic myopathy after COVID-19 vaccination. Case Description: A 39-year-old man with no significant past medical history presented to the ED complaining of diffuse muscle pain, joint pain and stiffness for 2 days. He was unable to stand without support. On examination, he had normal deep tendon reflexes but decreased power on the right arm and leg. Admission labs revealed TSH of 0.008 (0.55- 4.7 uIU/mL), Free T4 2.49 (0.89 - 1.76 ng/dl) and FT3 7.4 (2.3-4.2 ng/dl), low potassium of 3.0 L (3.6 - 5.1 mmol/L) and normal CPK 135 (49 – 397 IU/L). MRI of the brain and cervical spine did not show any pathology. Muscle weakness was assessed to be from hypokalemia related to thyrotoxicosis. After potassium replacement, his symptoms improved but did not resolve completely. He was discharged home on methimazole and propranolol. During out-patient follow up 2 months later, his TFTs did not improve (FT4 2.90 ng/dl and TSH of 0.008 uIU/mL) with persistent muscle weakness and muscle aches despite normal potassium of 4.4 (3.6 - 5.1 mmol/L). TSI and TPO antibodies came back negative. Thyroid uptake and scan revealed decreased 4-hour (3.4%) and 24-hour (4%) uptake. Additional history revealed that he received his second dose of COVID-19 vaccine 6 days prior to onset of symptoms. At this point, a diagnosis of post COVID vaccination thyrotoxic myopathy was made. Methimazole was stopped and he was treated with a tapering dose of prednisone. His symptoms resolved completely with normalization of TFTs after a month (Free T4 1.28 ng/dl, TSH 2.993 uIU/mL). Discussion: Autoimmune thyroid disease including thyroiditis and Grave‘s disease have been reported after receiving COVID-19 vaccine. One of the mechanisms for this complication is thought to be autoimmune/inflammatory syndrome induced by vaccine adjuvants. This case illustrates the importance of keeping broad differentials in mind in patients who recently received COVID-19 vaccine especially as the pandemic persists and more people are being vaccinated.
ABSTRACT
Background: This is the first study, that aimed: a) to compare immune response, namely the kinetics of neutralizing antibodies (Nabs), after vaccination with BNT162b2 mRNA vaccine (Comirnaty, Pfizer/BioNTech) between patients with autoimmune thyroiditis and controls, and b) to investigate changes in thyroid function in healthy subjects with no history of thyroid dysfunction before and after vaccination with BNT162b2 mRNA vaccine (Comirnaty, Pfizer/BioNTech). Methods: The entire study consisted of two sub-studies. In the first sub-study, NAbs levels after BNT162b2 mRNA vaccination were compared between 56 patients with autoimmune thyroiditis and 56 age and gender-matched healthy controls from the day of the first dose until a period of up to three months after the second dose. In the second sub-study, thyroid hormones (T3, T4, TSH) and thyroid auto-antibodies levels (anti-TG, anti-TPO) of 72 healthy subjects with no history of thyroid disease were examined before (D1) and one month after completion of the second dose (D50). Results: Among patients with autoimmune thyroiditis, the median neutralizing inhibition on D22, immediately before second dose, was 62.5%. One month later (D50), values increased to 96.7%, while three months after the second dose NAbs titers remained almost the same (94.5%). In the healthy group, median NAbs levels at D22 were 53.6%. On D50 the median inhibition values increased to 95.1%, while after three months they were 89.2%. The statistical analysis did not show significant differences between two groups (p-values 0.164, 0.390, 0.105 for D22, D50 and three months). Regarding changes in thyroid function, the mean value for T4 before vaccination was 89.797 nmol/L and one month after the second dose was 89.11 nmol/L (p-value=0.649). On D1 the mean T3 value was 1.464 nmol/L, which dropped to 1.389 nmol/L on D50 (p-value = 0.004). For TSH, mean levels were 2.064 mIU/ml on D1 and fell to 1.840 mIU/ml one month after the second dose (p-value=0.037). Despite decrease, all thyroid hormone levels remained within the normal range. No changes were found for anti-TPO or anti-TG. Conclusions: This study provided evidence that patients with autoimmune thyroiditis present similar immunological response to COVID-19 BNT162b2 mRNA vaccine (Comirnaty, Pfizer/BioNTech) with healthy subjects, while vaccination may affect thyroid function.