Coronavirus disease 2019 (COVID-19) is often associated with interstitial pneumonia. However, there is insufficient knowledge on the presence of autoimmune serological markers in patients with COVID-19. We analyzed the presence and role of autoantibodies in patients with COVID-19-associated pneumonia. We prospectively studied 33 consecutive patients with COVID-19, 31 (94%) of whom had interstitial pneumonia, and 25 age-and sex-matched patients with fever and/or pneumonia with etiologies other than COVID-19 as the pathological control group. All patients were tested for the presence of antinuclear antibodies (ANAs), antiantiphospholipid antibodies (APLs), and anti-cytoplasmic neutrophil antibodies (ANCAs). Clinical, biochemical, and radiological parameters were also collected. Fifteen of 33 (45%) patients tested positive for at least one autoantibody, including 11 who tested positive for ANAs (33%), 8 who tested positive for anti-cardiolipin antibodies (IgG and/or IgM) (24%), and 3 who tested positive for anti-β2-glycoprotein antibodies (IgG and/or IgM) (9%). ANCA reactivity was not detected in any patient. Patients that tested positive for autoantibodies had a significantly more severe prognosis than other patients did: 6 of 15 (40%) patients with autoantibodies died due to COVID-19 complications during hospitalization, whereas only 1 of 18 (5.5%) patients who did not have autoantibodies died (p = 0.03). Patients with poor prognosis (death due to COVID-19 complications) had a significantly higher respiratory rate at admission (23 breaths per minute vs. 17 breaths per minute; p = 0.03) and a higher frequency of autoantibodies (86% vs. 27%; p = 0.008). In conclusion, autoantibodies are frequently detected in patients with COVID-19 possibly reflecting a pathogenetic role of immune dysregulation. However, given the small number of patients, the association of autoantibodies with an unfavorable prognosis requires further multicenter studies.

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A subset of patients with idiopathic chronic urticaria (CU) has been recently classified as autoimmune on the basis of two main findings: association with thyroid autoimmunity and with anti-IgE and/or anti-IgE receptor antibodies. The association of CU with thyroid autoimmunity has been known since 1983, but its frequency varies in different reports. The objective of the present study was to verify the prevalence of thyroid antibodies (anti-thyroid peroxidase, TPO; thyroglobulin, TG; TSH-receptor, TSH-R) in two distinct series of CU: of known cause (70 cases, group A) and idiopathic (52 cases, group B). Twenty-three patients (M/F:7/16) of group A (33%) and 12 (M/F:4/8) of group B (23%) tested positive for at least one type of thyroid antibody. The difference was not statistically significant. Thyroid disease or altered serum TSH levels (requiring treatment) were present in 39% of group A and 42% of group B seropositive patients. In conclusion, the present study shows that CU, either of known cause or idiopathic, is more common in females than in males and is significantly associated with thyroid autoimmunity. These results were not expected on the assumption that autoimmune phenomena are a specific pattern of idiopathic CU. Thus, screening for thyroid autoimmunity and function is advisable in all patients with CU for the early identification of patients requiring either treatment of underlying thyroid dysfunction or follow-up.

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