Loading
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis / Lung Cancer Diagnosis and Treatment / Medical Imaging and Pathology Studies · Journal article
Frontiers in Immunology · September 8, 2026
Early or partial results. Treat as a signal, not a conclusion.
This case report documents misdiagnosis of invasive mucinous adenocarcinoma as interstitial pneumonia with autoimmune features in a 78-year-old female patient. The patient presented with compatible imaging and autoantibody positivity but was found at biopsy to have lung cancer; the report highlights the need to exclude malignancy before attributing ILD to autoimmune etiology, and cautions against initiating immunosuppression on autoantibody and imaging findings alone.
Retrospective single case report with literature review. 78-year-old female patient presenting with cough and sputum production lasting two months, with chest CT showing diffuse bilateral high-density opacities and septal thickening, positive autoantibodies, and moderate diffusion impairment on pulmonary function testing.. Intervention: Empirical methylprednisolone 40 mg/d initiated; mycophenolate mofetil and nintedanib added after one week..
78-year-old female with bilateral high-density opacities, positive ANA (1:100, cytoplasmic granular pattern), AMA-M2 (161.75 U/mL), RF (78.2 IU/mL), and anti-CCP antibody (300 U/mL) All systemic inflammatory markers (ESR, CRP, and six cytokines) were normal despite clinical presentation BALF and liquid-based cytology showed no malignant cells; CT-guided biopsy confirmed invasive mucinous adenocarcinoma with immunophenotype CK7+, focal CK20+, TTF-1−, Napsin A−
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
Clinicians should recognize that invasive mucinous adenocarcinoma can mimic autoimmune interstitial pneumonia and that autoantibody positivity combined with compatible imaging does not establish autoimmune etiology. Normal inflammatory markers alongside autoantibody positivity and resistance to initial immunosuppression should prompt urgent re-evaluation for malignancy before continuing immunosuppressive therapy.
A single case report describing diagnostic misidentification of lung cancer as autoimmune interstitial pneumonia; raises awareness of a pitfall but provides no comparative data or outcome measures to support clinical decision-making.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should recognize that invasive mucinous adenocarcinoma can mimic autoimmune interstitial pneumonia and that autoantibody positivity combined with compatible imaging does not establish autoimmune etiology. Normal inflammatory markers alongside autoantibody positivity and resistance to initial immunosuppression should prompt urgent re-evaluation for malignancy before continuing immunosuppressive therapy.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background Interstitial pneumonia with autoimmune features (IPAF) is an exclusionary diagnosis that requires the exclusion of alternative etiologies, including malignancy. Invasive mucinous adenocarcinoma (IMA) of the lung can radiologically and clinically mimic interstitial lung disease (ILD), and some lung cancer patients may present with non-specific autoantibody positivity, creating a diagnostic trap that may lead to misdiagnosis as IPAF. Methods We retrospectively analyzed the clinical data, serology, imaging, bronchoalveolar lavage fluid (BALF) cytology, and pathology of a 78-year-old female patient, combined with a literature review. Results The patient presented with cough and sputum production lasting two months. Chest CT showed diffuse bilateral high-density opacities with septal thickening. Pulmonary function tests revealed moderate diffusion impairment, and Velcro crackles were present on auscultation. Autoantibodies were positive for ANA (1:100, cytoplasmic granular pattern), AMA-M2 (161.75 U/mL), RF (78.2 IU/mL), and anti-CCP antibody (300 U/mL). Notably, all systemic inflammatory markers (ESR, CRP, and six cytokines) were normal. BALF and liquid-based cytology revealed no malignant cells. Rheumatology consultation favored a diagnosis of IPAF, and empirical methylprednisolone 40 mg/d was initiated. After one week, chest CT showed no resolution; mycophenolate mofetil and nintedanib were added. Despite standard anti-infective and immunosuppressive therapy, imaging remained unchanged and tumor markers remained persistently elevated. CT-guided percutaneous lung biopsy was performed, and histopathological examination confirmed invasive mucinous adenocarcinoma (CK7+, focal CK20+, TTF-1−, Napsin A−). Conclusion In patients with suspected IPAF, the combination of normal inflammatory markers with other atypical features should prompt re-evaluation of the autoimmune etiology. The lepidic growth pattern of IMA can lead to false-negative BALF cytology; a negative result does not exclude malignancy. As an exclusionary diagnosis, IPAF must be established only after thorough exclusion of infection, malignancy, and other causes. Immunosuppressive therapy should not be initiated based solely on autoantibody positivity and ILD imaging.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.