The third patient was a non-smoking 69-year-old woman, fully vaccinated against SARS-CoV-2. The disease history started 6 months before her referral, when she complained of coughing and dyspnoea. At disease onset, she was diagnosed with COVID-19 because of CT scan presentation with peribronchovascular and subpleural consolidation, although PCR for SARS-CoV-2 was negative. The symptoms remained, leading to a diagnosis of post-COVID-19 ILD. A few months later, breathlessness increased, and a new CT scan showed extension of GGOs, peribronchovascular consolidation and traction bronchiectasis (Fig. 1D). At her referral, physical examination revealed crackles bilaterally, periungual erythema, and mechanic's hands. Pulmonary function testing revealed a forced vital capacity of 50% of predicted and diffusion capacity of carbon monoxide of 30% of predicted. Blood tests showed lymphopenia and anaemia, and muscle enzymes were normal. Autoimmune tests revealed anti-PL7 and anti-Ro52 positivity. Electromyography showed no muscle involvement. The patient had respiratory failure and received pulses of methylprednisolone, followed by oral prednisolone in combination with i.v. CYC, with partial improvement.
We describe three patients with anti-synthetase syndrome, positive for anti-PL7, who were referred for post-COVID-19 ILD. Misdiagnosis between post-COVID-19 ILD and anti-synthetase syndrome is not surprising, because the CT pattern combining GGOs and consolidation is highly suggestive of COVID-19, but can be observed in many other conditions, including myopathies. There are data about myositis-associated lung abnormalities mimicking acute COVID-19. In fact, several pathological features of COVID-19, such as epithelial and endothelial alterations, are common to autoimmune ILD.
Apart from the well-known similarity of CT features in CTD-related ILD and COVID-19-related lesions, it has been described how we could differentiate between CTD-related ILD and COVID-19. Consolidations in a round shape and GGOs are proposed to be suggestive of COVID-19 in the absence of typical fibrotic abnormalities. Subpleural sparing, absence of parenchymal consolidation and fibrosis inside GGOs might suggest a diagnosis of CTD-related ILD.
New-onset autoimmune disease after COVID-19 has also been described, including nine patients diagnosed with myositis after COVID-19, but none was characterized by anti-PL7 positivity. However, causality between SARS-CoV-2 infection and autoimmune disease development should be attributed with caution.
These cases illustrate that even during a pandemic, it is essential to apply rigorous diagnostic algorithms when evaluating patients with ILD. Post-COVID-19 ILD should not be a dustbin diagnosis. Worsening of symptoms should lead to consideration of an alternative diagnosis. Autoimmune screening, including myositis-associated autoantibodies, should be performed in patients with persistent ILD in a post-COVID-19 context.
 Funding: Eirini Vasarmidi was funded by European Respiratory Society, Fellowship ID number: LTRF202101-00863.
 Disclosure statement: The authors have declared no conflicts of interest.
 Consent: Informed patient consent was obtained for the publication of this paper.