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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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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
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
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Background: Urticarial reactions following Covid-19 vaccine were rarely reported and have a short self-limited resolution. However only one case of chronic spontaneous urticaria (CSU) after mRNA vaccine was observed (1). Herein, we describe an original case series of patients who exhibited a CSU after Sars-Cov- 2 vaccination. Method(s): It was a retrospective case series of patients referred to the department of Clinical pharmacology of the University of Monastir for exploration of urticaria after Covid-19 vaccination., between January 2021 and January 2022. Result(s): Eight patients (8 F /5M) were included in this study. The median patient age was 36.5 years. None of them had a medical history of CSU. Urticaria was reported in 4 patients following mRNA vaccine (BNT162b2 and Moderna). Viral vector vaccine (Oxford/ AstraZeneca) was offended in 2 cases and inactivated virus vaccine (Sinovac, CoronaVac) was reported in 2 others cases. The mean time interval between vaccination and the onset of urticaria was 28.5 hours. The first shot of vaccine was the mostly offended dose (n = 6). Urticaria was associated with angioedema in 5 patients after Oxford/AstraZenecavaccine (n = 2) and following mRNA vaccine (n = 2). One case of urticaria was associated with angioedema and dyspnea after the CoronaVac administration. Blood tests showed polynuclear leucocytosis in 37% of patients. Positive anti-thyroperoxidase antibodies, and elevated polyclonal hypergammaglobulinemia were present in one patient 3 months after receiving BNT162b2 vaccine. Total serum IgE were high in 25% of patients following BNT162b2 and CoronaVac. All patients required antihistamines and 4 cases required intravenous betametasone. The median time to symptom resolution was 3 days but urticaria rapidly reccured throughout the entire body inspite the regular use of full dose of antihistamine. Intradermal test for the vaccine excipient as well as the offended Covid-19 vaccine was carried out in 5 patients, and were negative in all of them.Currently, all patients still has the pruritic rash daily. Conclusion(s): These cutaneous reactions seem to be particularly prolonged despite the use of symptomatic drugs, as compared with of drug induced-urticaria. Consequently, careful monitoring of urticaria over an extended period of time is needed.
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Allergic and hypersensitivity reactions induced by COVID-19 vaccines are increasingly reported and some patients may develop prolonged urticarial reactions following COVID-19 vaccination. Herein, we investigated the risk factors and immune mechanisms for patients with COVID-19 vaccines-induced immediate allergy and chronic urticaria (CU). We prospectively recruited and analyzed 129 patients with COVID-19 vaccine-induced immediate allergic and urticarial reactions as well as 115 COVID-19 vaccines-tolerant individuals from multiple medical centers during 2021-2022. The clinical manifestations included acute urticaria, anaphylaxis, and delayed to chronic urticaria developed after COVID-19 vaccinations. The serum levels of histamine, IL-2, IL-4, IL-6, IL-8, IL-17A, TARC, and PARC were significantly elevated in allergic patients comparing to tolerant subjects (P-values=4.5x10-5-0.039). Ex vivo basophil revealed that basophils from allergic patients could be significantly activated by COVID-19 vaccine excipients (polyethylene glycol 2000 and polysorbate 80) or spike protein (P-values from 3.5x10-4 to 0.043). Further BAT study stimulated by patients' autoserum showed positive in 81.3% of patients with CU induced by COVID-19 vaccination (P=4.2x10-13), and the reactions could be attenuated by anti-IgE antibody. Autoantibodies screening also identified the significantly increased of IgE-anti-IL-24, IgG-anti-FceRI, IgG-anti-TPO, and IgG-anti-thyroid-related proteins in COVID-19 vaccines-induced CU patients comparing to SARS-COV-2 vaccines-tolerant controls (P-values= 4.6x10-10-0.048). Patients with COVID-19 vaccines-induced recalcitrant CU patients could be successfully treated with anti-IgE therapy. In conclusion, our results revealed that multiple vaccine components, inflammatory cytokines, and autoreactive IgG/IgE antibodies contribute to COVID-19 vaccine-induced immediate allergic and autoimmune urticarial reactions (Minor revision in Journal of Autoimmunity [IF=14.551]).Copyright © 2023
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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.
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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.
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Background and Aims: There has been a considerable impact of the COVID-19 pandemic on healthcare services and the management of type 1 diabetes (T1D) at onset. The aim is to describe the clinical characteristics of children with T1D onset in Kuwait during the two years of the COVID-19 pandemic in comparison to the previous years (2017-2019) Methods: Children aged 14 years or less diagnosed with T1D onset between the years (2017-2022) were included. Children were categorized according to the diagnosis year and during (Feb 24th- Feb 23rd,the following year) Results: A significant increase in DKA rates was observed during the first & second years of the pandemic compared to the previous years (2020, 53.3%, 2021, 55.8% vs 2019, 39.4%, 2018,35.5%, 2017,39.1%,p-value=>0.001respectively);as well as ICU admission (26.4% in 2020,27.6% in 2021,13.9% in 2019,15.0% in 2018, and 19.7% in 2017, p-value = 0.002 respectively). Frequency of TTG-IgA antibodies was slightly higher in the second year compared to the previous years (12.4% in 2021,9.3% in 2020,8.8% in 2019,9.8% in 2018, and 6.0% in 2017,p-value = 0.06 respectively). Frequency of TPO antibodies didn't differ across the years (20.0% in 2021, 22.6% in 2020,14.8% in 2019,12.7% in 2018, and 16.0% in 2017,p-value = 0.06 respectively, p-value = 0.10, respectively) Conclusion(s): DKA & ICU admission rates continue to rise in the second year of the pandemic. In 2021,celiac screening positivity was slightly higher at onset. To better understand the longterm effects of the pandemic on the clinical course of children with T1D, it is essential to evaluate further clinical presentation, autoimmune involvement & outcomes over long periods of time.
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Introduction: Thyroid dysfunctions associated with SARS-CoV-2 acute infection have been extensively described since the beginning of COVID-19 pandemics. Conversely, few data are available on the occurrence of thyroid autoimmunity after COVID-19 resolution. We assessed the prevalence of autoimmune thyroid disease (ATD) and thyroid dysfunctions in COVID-19 survivors three months after hospital admission. Design and methods: Single-center, prospective, observational, cohort study performed at ASST Papa Giovanni XXIII Hospital, Bergamo, Italy. 599 COVID-19 survivors were prospectively evaluated for thyroid function and autoimmunity thyroperoxidase antibodies (TPOAb), thyroglobulin antibodies (TgAb). When a positive antibody concentration was detected, thyroid ultrasound was performed. Multiple logistic regression model was used to estimate the association between autoimmunity and demographic characteristics, respiratory support, and comorbidities. Autoimmunity results were compared to a cohort of 498 controls referred to our Institution for non-thyroid diseases before the pandemic onset. A sensitivity analysis comparing 330 COVID-19 patients with 330 age and sex-matched controls was performed. Results: Univariate and multivariate analysis found that female sex was positively associated (OR 2.01, SE 0.48, p = 0.003), and type 2 diabetes (T2DM) was negatively associated (OR 0.36, SE 0.16, p = 0.025) with thyroid autoimmunity; hospitalization, ICU admission, respiratory support, or COVID-19 treatment were not associated with thyroid autoimmunity (p > 0.05). TPOAb prevalence was greater in COVID-19 survivors than in controls: 15.7% vs 7.7%, p = 0.002. Ultrasonographic features of thyroiditis were present in 94.9% of the evaluated patients with positive antibodies. TSH was within the normal range in 95% of patients. Conclusions: Autoimmune thyroid disease prevalence in COVID-19 survivors was doubled as compared to age and sex-matched controls, suggesting a role of SARS-CoV-2 in eliciting thyroid autoimmunity.
Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Hashimoto Disease , Thyroiditis, Autoimmune , Humans , Female , Prospective Studies , Iodide Peroxidase , Cohort Studies , Prevalence , COVID-19 Drug Treatment , COVID-19/epidemiology , SARS-CoV-2ABSTRACT
A 51-year-old male had a history of well-controlled Graves' disease (GD) under regular follow-up, and thyroid eye disease (TED) with post bilateral orbital decompression. However, after COVID-19 vaccination, recrudescence of GD and moderate-to-severe TED were diagnosed by increased thyroxine levels and decreased thyrotropin levels in serum, and positive results of thyrotropin receptor antibody and thyroid peroxidase antibody. Weekly intravenous methylprednisolone was prescribed. Symptoms gradually improved accompanied with reduction in proptosis: 1.5 mm of the OD and 2.5 mm of the OS. Possible pathophysiological mechanisms discussed included molecular mimicry theory, autoimmune/inflammatory syndrome induced by adjuvants, and certain genetic predisposition of human leukocyte antigen. Physicians should remind patients to seek treatment if the symptoms and signs of TED recur following COVID-19 vaccination.
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Background: Coronavirus Disease-19 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is characterized by a wide range of clinical manifestations 1. Although COVID-19 was initially considered a respiratory infection, it was shortly recognized as a multisystemic disorder associated with heightened infammatory responses, including autoimmune phenomena 1. The presence of autoantibodies (AAbs) has been described in COVID-19 patients, highlighting the state of immune dysregulation in COVID-19 1. The clinical signifcance of AAbs, however, is still elusive. Objectives: To assess the prevalence of AAbs in critically ill, mechanically ventilated COVID-19 patients admitted to the intensive care unit (ICU) and investigate whether AAbs influence the clinical outcome of these patients. Methods: The current study evaluated prospectively from March 8th, 2021 to May 10th, 2021 the presence of AAbs against nuclear antigens (ANA), extracta-ble nuclear antigens (ENA), neutrophil cytoplasmic antigens (ANCA), cyclic cit-rullinated peptides (anti-CCP), double stranded-DNA (anti-dsDNA), cardiolipin (anti-CL), β2-glycoprotein-I (anti-β2-GPI), thyroid peroxidase (anti-TPO), and thyroglobulin (anti-TG) in critically ill COVID-19 patients upon admission in the ICU (n=217). Samples from 60 COVID-19 patients that were available 15 days after ICU admission were further analyzed for the evaluation of de novo AAbs production. Serum samples of age and sex matched healthy individuals before the COVID-19 pandemic were used as a control group (n=117). Results: COVID-19 patients treated in ICU had more commonly at least one AAb compared to age and sex matched controls (174/217, 80.2% vs 73/217, 62,4%, p< 0,001). More specifcally, COVID-19 patients expressed more frequently ANAs (48.4% vs 21.4%, p<0.001), anti-dsDNA (5.1% vs 0%, p=0.01), anti-CCP (8.3% vs 1.7%, p=0.014) and anti-CL IgM AAbs (21.7% vs 9.4%, p=0.005) than controls. The majority of critical COVID-19 patients who were positive for AAbs (144, 82.8%) expressed reactivity in up to three autoantigens with the most prominent being ANA, anti-phospholipid, ANCA and anti-TPO AAbs. AAbs-positive patients demonstrated more robust anti-SARS-CoV-2 humoral responses compared to AAbs-negative patients [detectable anti-SARS-CoV-2 S1-protein IgG antibodies: 150 (86.2%) vs 28 (65.1%), p=0.001;adequate neutralizing activity: 159 (91.4%) vs. 33 (76.7%), p=0.007]. The two groups, however, did not differ in terms of clinicoepidemiologic characteristics or the incidence of death in the ICU. Convalescent COVID-19 patients (n=111) compared to those who died (n=106), did not differ in the prevalence of serum AAbs or antibody responses against SARS-CoV-2. Differences were only shown in clinicolaboratory parameters including patients' age, comorbidities, O2 saturation, infammatory markers, and in-hospi-tal prognostic scores as expected. Paired samples testing (n=60) revealed that 45 patients had at least one newly induced AAb, 28 patients lost at least one reactivity and only 6 patients didn't show any seroconversion. The most common new-onset AAb reactivity was against anti-CL (IgG isotype) (n=21) followed by ANA (n=20), anti-β2-GPI (IgG isotype) (n=11), myositis-related antigens (n=13) and ENAs (n=9);nevertheless, no associations with clinicoepidemiologic features or COVID-19 outcome were revealed. Conclusion: Patients with severe COVID-19 express AAbs more commonly than age and sex matched controls, suggesting that SARS-COV-2 infection may induce a hitherto unknown B-cell autoreactivity. The presence of autoantibodies does not play a role in the outcome of SARS-COV-2 infection. However, further studies are needed to defne their role in future development of systemic autoimmune disorders or the long-COVID syndrome.
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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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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.
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Objective: We aim to discuss a case of COVID-19-related Hashimoto's and VGKC Encephalitis Background: COVID-19 has been associated with many common neurological sequalae. However, autoimmune encephalitis has been reported only 6 times in the literature. Design/Methods: Retrospective Case Review Results: A 67-year-old male presented to the ED for dyspnea, tested positive for COVID-19, and was treated accordingly. He began to have frequent anger outbreaks and disorientation. His neurological examination was unremarkable. EEG, MRI brain and CSF studies did not reveal abnormalities. While CSF autoimmune panels were pending (which eventually returned negative), he was administered IVIG and improved somewhat. He was readmitted to the hospital for worsening of his neuropsychiatric condition in 1 month. He was verbally abusive, engaged in impulsive behaviors such as purchasing farm animals and riding motorcycles naked. An MRI brain did not reveal any acute changes. He was started on a course of IVIG. He was advised further workup, but he left against medical advice. He was then admitted again for mania. Serum workup revealed elevated anti-thyroid peroxidase antibodies (71 IU/mL). He was therefore considered as a Hashimoto's Encephalitis and was given pulse steroids. He had remarkable improvement in both his neuropsychiatric symptoms, with anti-TPO normalization. He then presented to the ED with dyspnea 8 months later and diagnosed again with COVID-19. Subsequently he had increased disorientation and mania. Repeat anti-TPO antibodies were negative. CSF Autoimmune encephalitis panel revealed VGCC N-type antibody (62), AChR Gangionic antibody (112) and VGKC antibody (85). Therefore, this admission he was considered as a COVID-19-related VGKC encephalitis and given pulse steroids with significant improvement. He was discharged home in good condition and was tapered off steroids in the outpatient setting Conclusions: Per our literature search, this is the only case of both Hashimoto's and VGKC related encephalitis found in a single patient post-COVID-19.
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Objective: We present three patients with insidious onset of high-frequency atypical seizures, in association with atypical autoantibodies, with significant improvement with immunotherapy. Background: Autoimmune epilepsy (AE) is a relatively newly discovered epilepsy etiology. Although, It was described to present as New-Onset Refractory Status Epilepticus (NORSE). Our understanding of the clinical presentations and autoantibodies linked to AE is still sparse. Design/Methods: Case Series Case 1: A 44-year-old man presented with more than 10 years of recurrent episodes of mild confusion. Patient presented to our ER during one of these episodes where EEG revealed right temporal lobe status epilepticus. He had suboptimal response to multiple Antiepileptic Drugs (AEDs). MRI brain showed T2/FLAIR hyperintensities in the right frontal, parietal, and temporal lobes consistent with postictal effect. CSF was positive Neuronal Intermediate Filament (NIF) heavy chain antibodies Treatment with plasmapheresis (PLEX) and intravenous immunoglobulin (IVIG) with a good response. Case 2: A 73-year-old woman presented with daily episodes of mild confusion and falls over few months. EEG was consistent with frontal lobe seizures. MRI brain and CSF were unremarkable. She was treated with multiple AEDs, without adequate control. Serum paraneoplastic panel was positive for voltage-gated potassium channel antibodies. Seizures were controlled with PLEX. Case 3: A 22-year-old woman presented with daily episodes of behavioral arrest and confusion few weeks after COVID-19 vaccination. EEG showed bitemporal seizures, refractory to AEDs, requiring pentobarbital induced coma. CSF and MRI brain were unremarkable. Thyroid peroxidase and anti-thyrotropin antibodies were highly elevated. Treatment with IVIG and PLEX for AE, with a prolonged recovery. Conclusions: Seizures associated with AE appear to be trivial;however, it can have an aggressive course. Among antibodies have been reported in AE, NIF antibodies has not been reported. AE should be considered in patients with High-frequency of atypical seizures. Early initiation of immunotherapy is the key for disease control.
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Background: Sanjad Sakati Syndrome (SSS) is an autosomal recessive multisystem disorder characterized by congenital hypoparathyroidism, prenatal and postnatal growth and mental delay, dysmorphic features, and hypocalcemia seizures. It has not been linked with autoimmune disorders such as Type 1 Diabetes (T1D). Viral infections may play a role in triggering the development of T1D. Contracting SARS-CoV-2 virus may induce an autoimmune response by damaging the pancreatic β cells and accelerate the onset of T1D. To the best of our knowledge, no case studies of SSS has been reported to develop T1D were reported. Aim: To present a child with SSS who was newly diagnosed with T1D and SARS-CoV-2 infection (COVID-19). Method: Data on the patient were extracted from the Childhood Onset Diabetes electronic Registry (CODeR) in Kuwait. Results: The child was diagnosed early in life with SSS by tubulin-specific chaperone E (TBCE) gene mutation. The child is under multidisciplinary care and managed by alphacalcidol treatment. In May 2021, she presented with a history of fever, cough, polyuria, polydipsia, and poor appetite which lasted for 6 days. On investigations, random blood sugar level was 22 mmol/l and HbA1c level was 10%. There was no evidence of diabetic ketoacidosis. Autoantibodies to glutamic acid decarboxylase (GAD) and thyroperoxidase antibodies (TPO) were positive, with normal thyroid function results. Serum insulin and c-peptide levels were low (0.93 miu/ml, 28 pmol/l respectively). Thus, T1D diagnosis was made, and insulin therapy was started. No family history of diabetes was reported. On admission, the child tested positive for SARS-CoV-2 PCR and had positive contacts with family members with COVID-19 infection. As per WHO COVID-19 infection severity criteria, the child’s condition was classified as mild. She was discharged home with no short-term sequelae of COVID-19 infection;diabetes and dietary education was provided. Discussion: To the best of our knowledge, this is the first case reported in literature of a patient with SSS who presented with T1D onset along with COVID-19 infection. Viral infections such as SARS-CoV-2 virus may trigger the development of autoimmune diseases such as T1D. Exploring the relationship between COVID-19 infection and T1D onset is needed for better understand the effect of COVID-19 infection and outcome on pediatric patients with comorbidities. Further explorations are also needed to study the relationship of SSS and autoimmune disorders as well;to fully appreciate the impact on such patients.
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Background: ASIA syndrome is an entity that incorporates diverse autoimmune conditions after exposure to various adjuvants in vaccines. There is limited literature available regarding development of thyroid disorders after covid 19 vaccination. Aims and Objectives: Retrospective case series of patients diagnosed with thyroid disease within 2 months of covid-19 vaccination. History, examination, relationship with covid infection and vaccination, onset of symptoms, thyroid function tests, TRAb, Anti-TPO, ESR, CRP, Tc99-thyroid scan were recorded for each of the patient. Results: We observed 9 subjects (females 5, males 4;age range 22-63 yrs) with thyrotoxicosis. The onset of symptoms after vaccination ranged from 2 days to 60 days. Six subjects had Graves' disease (GD) while 3 had subacute thyroiditis (SAT). Two subjects had acute onset of thyroid associated opthalmopathy;one patient needed glucocorticoids (GC). All subjects with GD were treated with antithyroid drugs while subjects with SAT were treated with NSAIDS;none required GC. Conclusions: SAT and GD may develop as a manifestation of ASIA syndrome after covid 19 vaccine. Long-term multicentric observational studies are needed to establish the natural history of ASIA syndrome following covid vaccination.
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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.
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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.
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Introduction: Non-cardiogenic pleural involvement in hyperthyroidism is rare, with unilateral involvement being rarer still. We present the case of a patient with Graves’ disease (GD) with thyroid storm criteria who presented right pleural effusion compatible with exudate. Case Description: A 40-year-old female patient, with a history of hyperthyroidism for 3 years without treatment for severe rash to thiamazole on two occasions. She was admitted to the emergency room of a private clinic due to dyspnea that progressed to respiratory failure, a massive right pleural effusion was found for which they performed evacuatory thoracentesis, prescribed lugol, bisoprolol and dexamethasone, and she was transferred to our hospital with a total of 45 points on the Burch-Wartofsky’s scale, had respiratory failure and jaundice. The analysis showed: Hemogram: Leukocytes 9700, Hemoglobin: 10.8 g/dl;CRP: 0.43 mg/dl;Glucose 157 mg/dl;Creatinine: 0.29 mg/dl, TSH: < 0.004 uIU/ml, Free T4: > 7.77 ng/ml;Free T3: > 16 pg/ml, Anti-thyroperoxidase: > 1000 IU/ml;Total bilirubins: 5.52 mg/dL;Direct bilirubin: 3.79 mg/dL. COVID infection was ruled out, the analysis of the pleural fluid was compatible with exudate, an echocardiogram showed LVEF: 60% and mild pulmonary hypertension. Thyroid ultrasound revealed diffuse hypervascularized goiter;thyroid scintigraphy showed diffuse hyper-uptake goiter. Dexamethasone with lithium carbonate was indicated with gradual improvement in thyroid function tests and cholestatic pattern. Once compensated she received 20mCi of 131I. She was discharged with an improvement in her symptoms. Her X-ray and her control chest ultrasound did not show the presence of pleural effusion. Discussion: GD is a pathology that presents with a variety of symptoms and signs due to its multisystemic involvement, which can become life-threatening, such as a thyroid storm, if it is not treated properly and in a timely manner. The fact of presenting unilateral massive pleural effusion is a rare presentation of hyperthyroidism reported in other cases.