Editorial collaboration
Medical &
COVID-19 has caused the disease in nearly 500 million people worldwide, according to the World Health Organization. Although airlines are their number one target, SARS-CoV-2 can enter many organs via angiotensin-converting enzyme 2 (ACE). -2) Protein. ACE-2 is highly expressed in thyroid cells and COVID-19 has been reported to cause thyroid disorders and after SARS-CoV-2 infection. Autoimmune manifestations of the thyroid similar to those of COVID-19 come with Graves’ disease and thyroid. eye disease (PDD), although COVID-19 can lead to many other thyroid disorders.
The Times of India recently reported on a dramatic development: referrals of patients with new PDDs to a primary chain of Indian eye hospitals increased by as much as 25% in the first two years of the COVID-19 pandemic. This raises compelling questions: Is there a link between COVID-19 and -19, thyroid autoimmunity, and your headaches (including PDD)?Could COVID-19 vaccination and thyroid autoimmunity be related?Could they be influenced by COVID-19 public fitness measures and delays in seeking care?Fortuitous and unrelated to the COVID-19 pandemic?
To answer those questions, we want to review our understanding of how Graves’ disease and PDD arise. Graves’ disease is an autoimmune disease of the thyroid caused by thyroid-stimulating hormone receptor-stimulating antibodies, leading to hyperthyroidism. Graves’ disease is the ultimate disease. A common cause of hyperthyroidism and > 1% of the U. S. populationIn the U. S. PDD is the most common complication of Graves’ disease that occurs outside the thyroid gland. PDD causes a variety of eye symptoms and symptoms that can negatively affect patients. quality of life, disfigurement and, in rare cases, threaten vision.
The precise occasions that cause thyroid autoimmunity are unknown; However, we know that there is a complex interplay between genetic and environmental sites, including:
Genetics: Genes with polymorphisms that predispose to Graves’ disease come with human leukocyte antigens (HLA), elegance II genes for HLA-DR; TSHR; CLTA-4; CD40; and PTPN22.
Age: Graves’ disease has a low incidence in children and then expands to about age 50, after which the incidence stabilizes or decreases slightly.
Gender: Women are about five times more likely to develop Graves’ disease than men.
Race: Black people and probably Asians or Pacific Islanders have higher rates of Graves’ disease, at least in the United States.
Smoking: Smoking is a clear environmental threat to the progression of Graves’ disease and PDD.
Two other conceivable triggers of Graves’ disease are stress and infection.
Stress has been implicated as a cause of Graves’ disease since 1825. That year, as reported by Dr. Ralph W. Major in Classic Descriptions of Disease, 21-year-old Elizabeth S. developed symptoms of hyperthyroidism, goiter, and eye symptoms. Shortly after being thrown out of her wheelchair while running down the hill.
It has also been warned that other autoimmune diseases pose a greater threat after tense events. One theory that stress can cause Graves’ disease in vulnerable Americans is the release of hormones, including catecholamines and cortisol, that change the immune reaction to the production of pathognomonic diseases. antibodies against Graves. La mental strain imposed by a global pandemic is a potential (though unproven) cause of Graves’ disease and PDD.
It has also been proposed that infection with bacteria such as Yersinia enterocolitica and Helicobacter pylori and viruses, parvoviruses, Epstein-Barr viruses, and hepatitis C viruses are the causes of Graves’ disease.
In the last 2 years, several case reports have emerged describing the onset of hyperthyroidism (with and without ocular involvement) shortly after COVID-19 (Tomer & Davies; Jiménez-Blanco et al; Lanzolla et al; Mateu-Salat et al; Harris and Al Mushref; one speculation about this link is that the COVID-19-related hyperinflammatory disease state triggers a series of immune responses in genetically predisposed Americans, leading to the activation (or reactivation) of Graves’ disease and PDD. Some cases have occurred in middle-aged women, the main demographic at risk of developing Graves’ disease. The smoking prestige of those Americans has not been reported.
Thyroid autoimmune phenomena have been reported after mRNA and inactivated COVID-19 vaccines (Vera-Lastra et al; Rubinstein; Zettinig and Krebs; Lui et al). Cases of Graves’ disease and/or PDD have been reported days or weeks after receiving the first dose of vaccine.
The researchers wondered if those reactions might simply constitute an adjuvant-induced autoimmune/inflammatory syndrome (ASIA). Adjuvants in vaccines are used for the immune reaction by employing a reduced amount of antigen, creating a prolonged and long-lasting immune reaction. Potential mechanisms The methods by which adjuvants disrupt the host’s “immune balance” are accompanied by molecular mimicry (similarities between foreign antigens and oneself), excessive production of cytokines (which promote inflammation), and faulty immune regulation (through regulatory T cells).
Association does not necessarily mean causation. Given the huge number of people diagnosed with COVID-19 around the world every day, it is inevitable that some patients seeking medical attention for respiratory symptoms (or other headaches caused by COVID-19) may have pre-existing Graves’ disease. disease and/or PDD.
Similarly, more than 11 billion vaccine doses have been administered internationally (including more than 700 million doses in the United States); one would expect new cases of Graves’ disease and PDD to occur in a small subset of a much larger population that is being vaccinated. It is reassuring that cases of post-vaccination ASIA leading to thyroid autoimmunity appear to be incredibly rare, although there is a threat of underreporting of cases or lack of awareness by clinicians.
COVID-19 restrictions, lockdowns, and stay-at-home orders have also led to a delay in care-seeking behaviors. This has been observed in a wide spectrum of diseases, in addition to medical emergencies (e. g. e. g. , acute coronary syndrome) (Bansal et al; Dreyer et al) and surgical emergencies (e. g. e. g. , acute appendicitis) and in cancer care. Abnormal thyroid is associated with more severe PDD. Any delay in diagnosing Graves’ disease and initiating antithyroid treatment will undoubtedly contribute to worsening of the disease at presentation.
COVID-19 has presented the world with many challenges, in addition to deciphering causation and association. However, the pandemic also gives us the opportunity to ask questions and learn more about disease processes in many organs. Anecdotal knowledge from India related to recent TED presentations is an example of this. With more high-quality knowledge, we will be able to definitively address the role of stress, infection, in all likelihood vaccination, and behavioral adaptations to public health responses in the progression and presentation of Graves’ disease and PDD. .
Follow Medscape on Facebook, Twitter, Instagram and YouTube
Credits: Feature photo: Dreamstime Image 1: Margaret Whillier – Diabetes CNC (Clinical Nurse Consultant), Royal Women’s and Brisbane Hospital Image 2: Courtesy of Royal Brisbane and Women’s Hospital
© 2022 WebMD, LLC
endocrinology researcher; Personnel Specialist, Royal Brisbane
Senior Specialist, Department of Endocrinology and Diabetes, Royal Brisbane
You’ve Decided on My Alerts
Click on the topic below to receive emails when new parts are available.