Invasive mucinous adenocarcinoma (IMA) is an uncommon histological subtype of lung adenocarcinoma accounting for 3-10% of pulmonary adenocarcinomas. A case study details a lifelong never-smoking woman in her late 60s presenting with persistent bilateral pulmonary consolidations, cavitation, and traction fibrosis that initially simulated an atypical infection or granulomatous disease.
In Plain English: The Clinical Takeaway
- Uncommon Presentation: Lung cancers like invasive mucinous adenocarcinoma (IMA) can sometimes mimic pneumonia, showing up as patchy lung consolidations rather than a neat, solid tumor mass.
- The Diagnostic Hurdle: When standard breathing tests, blood work, and washings fail to find an infection, persistent shadows on chest imaging require a direct tissue biopsy to rule out malignancy.
Uncovering a Rare Malignancy Behind Mimicked Pneumonia
The patient presented to the Accident and Emergency Department with a one-day history of dull, non-radiating retrosternal chest tightness, an intermittent productive cough with white sputum lasting several weeks, and approximately 4 stones (approximately 25 kg) of unintentional weight loss over the preceding seven months. Her medical history included hypothyroidism and bilateral hip replacement, alongside two recently treated community chest infections. She had never smoked tobacco, had no passive smoke exposure, and reported no occupational lung exposures.
Initial blood work revealed a markedly elevated C-reactive protein (CRP) level of 155 mg/L, while her white cell count, neutrophil count, and procalcitonin remained entirely normal. A chest radiograph demonstrated diffuse parenchymal nodular changes predominantly in a perihilar distribution. Subsequent contrast-enhanced computed tomography (CT) of the thorax, abdomen, and pelvis revealed widespread bilateral, multilobar patchy consolidations paired with internal cavitary changes and tractional architectural distortion.
| Diagnostic Parameter | Patient Initial Value | Clinical Reference Range |
|---|---|---|
| C-Reactive Protein (CRP) | 155 mg/L | 0–5 mg/L |
| White Blood Cell Count | 5.49 x 10⁹/L | 4.00–11.0 x 10⁹/L |
| Troponin | 4.7 ng/L | <11.6 ng/L |
| Serum Angiotensin-Converting Enzyme (ACE) | 30 IU/L | 16–85 IU/L |
Navigating Negative Scans and Extended Differential Diagnoses
Because the initial radiological pattern featured cavitation and traction bronchiectasis alongside consolidations, the clinical team initially suspected granulomatous diseases such as sarcoidosis or tuberculosis, as well as atypical fungal infections. Extensive evaluations—including serum angiotensin-converting enzyme levels, vasculitis panels, autoimmune screens, T-SPOT.TB assays, and beta-D-glucan tests—yielded largely unremarkable results. Although a p-ANCA test was positive, myeloperoxidase (MPO) and proteinase 3 (PR3) antibodies were negative, failing to support an ANCA-associated vasculitis diagnosis.
Bronchial wash and bronchoalveolar lavage (BAL) samples displayed no microbiological evidence of bacterial, mycobacterial, or fungal pathogens on microscopy and cultures. Because the initial non-invasive testing and bronchoscopic sampling remained unrevealing while radiological abnormalities persisted, clinicians performed a CT-guided tissue biopsy of the lung. Histopathological analysis confirmed the diagnosis of IMA, supported by immunohistochemistry indicating a primary pulmonary origin.
Molecular Profiling and Chemotherapy Initiation
Invasive mucinous adenocarcinoma possesses a unique pathology, characterized by goblet or columnar tumor cells packed with abundant cytoplasmic mucin and a lepidic growth pattern featuring microscopic skip lesions.
