A 55-year-old Caucasian female with an active smoking history of 25 pack-years was referred to our pulmonology department due to complaints of chronic intermittent rhinitis and for vigilance of a 6 mm nodule on the chest CT scan in the right upper lobe. Imaging surveillance was maintained but 12 months after the initial chest CT scan, in addition to a stable 6 mm nodule on the right upper lobe, a heterogeneous and irregular 36 mm mass, with a central hypodense zone (RHS), was diagnosed on the apico-posterior region of the left upper lobe (Fig. 1)
The patient had no respiratory or constitutional symptoms and denied complaints suggestive of connective tissue disease. Her husband had been treated, 6 months earlier, for PT but her contact screening was negative. She had no prior relevant medical history and was being treated for her rhinitis with budesonide nasal spray 100 mcg and levocetirizine 5 mg.
The general examination was unremarkable, except for a pale nasal mucosa.
Laboratory analysis showed an increase in haemoglobin levels, 16.2 g/dl (normal 12-15 g/dl), probably due to the patient's smoking history, with no other relevant changes, particularly regarding inflammatory markers, which were normal. Due to her smoking history, a panel of tumour markers was requested (CEA, CA 19.9, CA 15.3, CA 125, CYFRA-21, NSE and SCC) which were also normal. Serologic tests for hepatitis B, C and HIV were negative and autoimmune antibodies (anti-CCP, ANAs and ANCAs) were within normal values. Pulmonary function tests revealed small airway obstruction with a normal diffusing capacity for carbon monoxide.
The case was discussed in a multidisciplinary team meeting. Given the lack of symptoms, the appearance of a relatively large mass over a short period of time (which made the diagnosis of cancer less likely) and the presence of the RHS on the chest CT scan, OP was considered the most likely diagnosis and initiation of corticotherapy was suggested.
Before starting corticotherapy, in order to rule out alternative causes and confirm the diagnosis, a bronchofibroscopy with bronchoalveolar lavage (BAL) and a percutaneous CT-guided transthoracic needle biopsy of the lung were performed. Pathological analysis of the lung biopsy revealed necrotic tissue. The BAL findings were nonspecific: a total of 63 ml (out of 150 ml) of opaque fluid was recovered with a total cell count of 494 cells/mcl with a macrophage predominance (94%). Microbiological and cytological analyses of the BAL fluid were negative for infectious or neoplastic disease. However, bronchial secretions collected during the bronchofibroscopy showed Mycobacterium tuberculosis (MT), susceptible to all first-line drugs (isoniazid, rifampin, pyrazinamide and ethambutol).
The patient had the final diagnosis of PT and not OP, as initially suspected.
She was referred to a specialised tuberculosis center and the recommended treatment for drug-susceptible PT was initiated. The patient completed a 2-month intensive phase with 4 drugs (isoniazid 300 mg/day, rifampin 600 mg/day, pyrazinamide 1,500 mg/day and ethambutol 1,200 mg/day) and is now completing the 4-month continuation phase with: isoniazid 300 mg/day and rifampin 600 mg/day. She remains clinically stable, asymptomatic and without adverse effects arising from the medication. A re-evaluation chest CT scan was performed and showed imagiological improvement, confirming the diagnosis of PT.