Autoimmune thyroid diseases (ATD) are the most common organspecific autoimmune diseases with complex pathogenesis including the interaction between environmental, genetic, and immunological factors. 1 ATD comprise two main entities; Hashimoto's thyroiditis (HT) and Graves' disease (GD) which are considered the most common forms of ATD. Although, GD and HT usually have opposing clinical manifestations; hyperthyroidism and hypothyroidism, respectively, however, in line with a more flexible view of ATD, HT and GD can cause both hyperthyroidism and hypothyroidism, even alternating between one form and the other. 2 The hallmark of HT is the high rate of positivity of thyroglobulin and thyroid peroxidase antibodies (anti-TPO). 3 Moreover, high anti-TSH receptor antibody (TRAb) level is the mainstay in GD diagnosis. 4 The human microbiome consist of 100 trillion bacteria, protozoa, fungi, and viruses. It is of paramount importance in

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel RNA coronavirus responsible for the coronavirus disease-19 (COVID-19) pandemic. The clinical manifestations of COVID-19 are variable, ranging from asymptomatic cases to severe respiratory affection, and were found to cause thyroid dysfunction in some cases. Our case series aim to shed the light on the effect of SARS-COV-2 infection on thyroid function, thyroid gland size, and treatment of thyroid dysfunction. We demonstrated three cases indicating that COVID-19 infection can accentuate thyrotoxic state and Graves' ophthalmopathy, aggravate hypothyroidism, increase thyroid gland volume, and in euthyroid individuals can induce some sort of thyroiditis, characterized by hyperthyroidism followed by hypothyroidism which is eventually followed by euthyroidism. Furthermore, treatment of thyroid disease was found to be affected by COVID-19 infection.The novel coronavirus (SARS-COV-2) was first discovered at the end of the year 2019 in Wuhan, China. After which, it rapidly spread, causing an epidemic throughout China, which then spread across the entire world, resulting in coronavirus pandemic. In February 2020, the World Health Organization (WHO) designated the disease COVID-19, which stands for coronavirus disease 2019. 1 SARS-CoV-2-specific antibodies and cell-mediated responses are induced following infection. Preliminary evidence suggests that some of these responses are protective, but this remains to be definitively verified. Moreover, it is unknown whether all infected patients develop a protective immune response and how long a protective effect might last. 2 Data about the effect of SARS-COV-2 on the thyroid function are scarce; however, one study addressed this effect and demonstrated that, out of 287 patients with confirmed SARS-COV-2, 58 patients had hyperthyroidism and 15 patients had hypothyroidism. 3 Our case series aim to shed the light on the effect of SARS-COV-2 infection on thyroid function, which will ultimately influence thyroid disease sequelae and management in patients with COVID-19.

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Background: Hashimoto’s thyroiditis (HT) is a common autoimmune disorder that causes significant morbidity. Interleukin (IL)-17 was identified as a major contributing factor in the pathogenesis of HT. Blastocystis hominis (BH) is a very common infection and has been shown to be associated with several diseases. Our aim was to determine serum IL-17 level in HT patients with and without BH infection and the effect of eradicating BH in patients with HT. Methods: A prospective cohort study was conducted on 20 HT patients not infected with BH (group I), 20 HT patients infected with BH (group II), and 20 healthy patients (group III). Serum free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH), thyroid peroxidase antibodies (anti-TPO), and IL-17 were performed by ELISA method and were repeated in group II after 6 weeks of eradication of BH. Results: Patients with HT showed a significantly higher serum IL-17 compared with controls. IL-17 was significantly higher in HT patients infected with BH compared with HT patients not BH infected (mean 6.93 ± 2.83 pg/ml versus 3.25 ± 1.55 pg/ml, p = 0.003). After BH eradication TSH, anti-TPO, and IL-17 were significantly decreased (mean 14.76 ± 11.11 µIU/ml versus 9.39 ± 7.11 µIU/ml, p < 0.001; mean 308 ± 175.6 IU/ml versus 295.4 ± 167.1 IU/ml, p = 0.006; and mean 6.93 ± 2.83 pg/ml versus 6.45 ± 2.48 pg/ml, p < 0.001), respectively. Multivariate analysis after treating BH infection showed that IL-17 was significantly negatively correlated with FT3 (adjusted p = 0.002) and significantly positively correlated with anti-TPO (adjusted p = 0.045). Conclusion: Treatment of BH infection ameliorates HT through reduction in IL-17, anti-TPO, and TSH. Clinical trial registration number: PACTR201909495111649

Remdesivir can precipitate fatal acute necrotizing pancreatitis especially in patients who previously suffer from hypertriglyceridemia.