Hashimoto’s thyroiditis following SARS-CoV-2 infection
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A 33-year-old female patient came from the city of Santana de Parnaíba, São Paulo. The patient was infected with SARS-CoV-2, demonstrated by real-time PCR test using a nasopharyngeal swab sample on 1 November 2020. Twenty days later, the patient sought healthcare service, reporting fatigue and severe hair loss. Laboratory tests for thyroid function were ordered, as well as thyroid ultrasound.

The test results elucidated altered TSH levels of 8 mIU/mL (upper limit of the normal range of 4.3 mIU/mL); free T4 of 0.5 ng/dL (normal range 0.7–1.8 ng/dL) and antibodies, anti-Tg of 252?IU/mL and anti-TOP of 115 IU/mL. Ultrasonographic examination of the thyroid showed the presence of diffusely hypoechoic and heterogeneous glands.

She was prescribed to start pharmacological management with levothyroxine sodium (Levoid) 25 µg. After 8 weeks, the patient was instructed to undergo thyroid function laboratory tests again, which showed TSH of 6.4 mIU/mL, free T4 of 0.9 ng/dL and anti-TOP reduced to 55 IU/mL; in addition to laboratory parameters, the patient reported improvement in fatigue symptoms. Management remained, but with increased dosage of Levoid to 38 µg.

Eight weeks later, new laboratory tests were again collected, which showed a TSH of 2.2 mIU/mL, free T4 1.2 ng/dL, negative anti-TOP antibody and persistent improvement of clinical symptoms, elucidating the stabilisation of thyroiditis. In January 2021, the patient performed a genetic test, which assesses the genotyping of markers, observing a predisposition to exacerbation of proinflammatory cytokines, supported by polymorphisms in the tumour necrosis factor (TNF) alpha and interleukin (IL)-6 genes, where the patient’s alleles can be seen.

Learning points:
- To describe the case of a patient who developed Hashimoto’s thyroiditis after COVID-19 infection and was treated pharmacologically with levothyroxine, with a good clinical response.

- To describe the possible influence of genetic polymorphisms in proinflammatory genes, favouring chronic inflammatory signalling and the trigger for autoimmune diseases.

- To describe the possible pathophysiology of Hashimoto’s thyroiditis after SARS-CoV-2 infection, caused by an alteration in the sirtuin pathway, favouring the activation of autoimmune conditions.

Source: https://casereports.bmj.com/content/14/8/e244909?rss=1
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