Thyroid damage has been associated with acute conditions and several viral infections, among which hepatitis C virus (HCV) occupies an important place. Substitution therapy is recommended in overt disease. In the general population, subclinical hypothyroidism has a prevalence of 4.3–8.5%, while overt disease is found in 0.3–0.4% it is commonly associated with environmental iodine deficiency and autoimmune thyroid diseases.
In this regard, a study published in 2021 including 122 patients without previous thyroid conditions found an increase in antithyroid peroxidase antibodies during COVID-19 and convalescence. One interesting article reported a temporal correlation between COVID-19 and thyroid damage: the first to develop is subacute thyroiditis, followed by Hashimoto’s disease (in patients with pre-existing autoimmunity), Graves’ disease (peak incidence at 4 weeks after infection), and painless thyroiditis in patients with pre-existing autoimmunity. Cases of autoimmune hypothyroidism have been described, but there were no indicators that the condition developed before or during SARS-CoV-2 infection. Ī recent meta-analysis has found an association between SARS-CoV-2 infection and the triggering of Graves’ disease, as well as subacute thyroiditis. The presence of SARS-CoV-2 virus in the thyroid tissue obtained by autopsy after death due to COVID-19 suggests a possible direct infection of the thyroid and may provide an explanation for the thyroid dysfunction in these patients. Furthermore, due to the abundance of ACE2 and TMPRSS2 receptors in the thyroid, required for internalization of the virus, it seems likely that SARS-CoV-2 can affect the thyroid directly, as well as in the context of an increased systemic inflammatory response. It appears that COVID-19 can directly affect the cardiovascular, gastrointestinal (including the liver and the pancreas), renal, nervous, and musculoskeletal systems. As time progresses, more and more studies are published reflecting the systemic impact of what was originally thought to be a respiratory infection. The COVID-19 pandemic has proven an important test of the ability of the scientific medical world to effectively understand, describe, and manage pathophysiology processes when dealing with epidemics of newly-emerged pathogens.
Keywords: ACE2 Protein, Human, Hepatitis C, Chronic, Thyroid Diseases Thyroid function tests may be considered as part of the laboratory work-up in patients with COVID-19. At 3-month follow-up, levels of ATPO were decreased in all patient groups and the levels of thyroid hormones increased to normal values.ĬONCLUSIONS: This study supports previous reports of an association between SARS-CoV-2 infection and thyroid dysfunction associated with thyroid autoantibodies. Also, levels of TSH, fT3, and fT4 were significantly decreased. RESULTS: One-month follow-up showed that both patients with autoimmune thyroiditis as well as patients without antibodies had increased ATPO levels.
Evaluation at 1 and 3 months after SARS-CoV-2 infection included serum determination of antithyroid antibodies (anti-thyroglobulin and antithyroid peroxidase ), thyroid-stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), and evaluation of thyroid medication, with dose adjustment if required. MATERIAL AND METHODS: From April 2020 to October 2020, we performed a prospective observational study of patients with cured hepatitis C virus (HCV) infection and documented thyroid disease who became infected with SARS-CoV-2 (confirmed by SARS-CoV-2 RNA detection via reverse-transcription polymerase chain reaction from the upper respiratory tract, both nasal and pharyngeal swabs). Therefore, we performed this prospective observational study of 42 patients with COVID-19 infection and a history of hepatitis C virus infection and thyroid disease with follow-up thyroid function and autoantibody testing. There have been reports of an association between SARS-CoV-2 infection and the onset or re-activation of autoimmune hypothyroidism. BACKGROUND: Thyroiditis is an important extrahepatic association in chronic hepatitis C virus (HCV) infection.