Introduction: Post-COVID-19 sarcoidosis is an intriguing clinical phenomenon in which SARS-CoV-2 infection may act as a potential immunological trigger. In predisposed individuals, the systemic inflammatory response to the virus may induce the formation of non-caseating granulomas. Unlike classic idiopathic sarcoidosis, these cases exhibit a temporal relationship (typically within months) between COVID-19 pneumonia and granuloma onset. Diagnosis is often delayed due to the overlap of symptoms—notably the triad of fatigue, dyspnoea, and cough—with Long COVID syndrome.

Clinical Case Description: We present a case series of seven patients (mean age 51 years), all with RT-PCR–confirmed SARS-CoV-2 infection preceding respiratory symptoms. Clinically, the predominant features were fatigue, persistent cough, and progressive dyspnea. At diagnosis, all patients were classified as Scadding Stage II, exhibiting imaging patterns of consolidation, architectural distortion, and hilar lymphadenopathy, notably lacking the typical perilymphatic micronodular distribution. Diagnosis was histologically confirmed (non-caseating granulomatous inflammation) via transbronchial biopsies and/or EBUS-TBNA. Bronchoalveolar lavage revealed marked lymphocytosis with elevated CD4/CD8 ratios (up to 10.06).
Baseline pulmonary function tests showed a mild-to-moderate restrictive pattern and impaired diffusion. Two patients progressed to Stage IV with fibrotic features.

Therapeutic management required stepwise escalation: while all initiated corticosteroid therapy, clinical, functional, or radiological worsening necessitated methotrexate in five cases. Two patients remained refractory, requiring biologic therapy with infliximab, both achieving functional stability at six months.

Conclusions: In conclusion, we describe a form of sarcoidosis possibly triggered by COVID-19, characterized by challenging clinical control and frequent need for therapeutic escalation. CT findings often include parenchymal consolidations mimicking post-COVID organizing pneumonia, complicating the distinction between viral sequelae and active granulomatous infiltration. This phenotype appears more resistant to corticosteroid monotherapy, with cases requiring early introduction of steroid-sparing agents or biologics.