A 49-year-old male bus driver presented with a five-month history of dyspnea on exertion of insidious onset associated with easy fatiguability and non-radiating central chest pain with associated palpitations. The dyspnea waxed and waned but never completely resolved. He had no history of chronic cough. On examination, he was stable, with blood pressure of 132/87mmHg, pulse 99b/min, temperature 36.2 C, and blood oxygen saturation on room air of 96%. On chest examination, air entry was reduced bilaterally, but breath sounds were normal. The cardiovascular system exam disclosed an apex beat located in the left 5th intercostal space, anterior axillary line; heart sounds were normal with no murmurs. A diagnosis of respiratory tract infection was made. The initial plan was to do a full blood count, urine routine exam, renal and liver function tests, lipid profile, chest X-ray, and an electrocardiogram (ECG). He presented the next day with the lab (Table 1), ECG, and chest X-ray results. Chest X-ray showed diffuse bilateral reticulonodular infiltrates without bilateral hilar lymphadenopathy (Figure 1(a)) with differentials of pulmonary tuberculosis with fibrosis, sarcoidosis, and pneumoconiosis.
The electrocardiogram showed sinus rhythm and no abnormalities. Subsequently, the plan was to request a gene expert for acid-fast bacilli. He presented a day after with a negative gene expert for Mycobacterium tuberculosis.
A computerized tomography (CT) scan of the chest disclosed, diffuse bilateral reticulonodular, predominantly reticular opacities with multiple left lung calcifications. In a focus, the nodules coalesced to form a macronodule with central calcification. There was no associated traction bronchiectasis, and the hilar was normal. The trachea was central with normal caliber. Other significant findings included cardiomegaly and a dilated pulmonary trunk (Figure 1(b)). Suggested differential diagnoses included idiopathic pulmonary fibrosis with pulmonary hypertension, lymphangitis, carcinomatosis, and stage 3 sarcoidosis. A CT-guided tru-cut biopsy of the lung lesion was done.
At the histopathology lab, two tru-cut tissue cores were examined, measuring 20 mm on average. Hematoxylin and eosin-stained slides showed effacement of lung architecture by multiple naked noncaseating granulomata, a few associated with Langhans' giant cells (Figures 2(a)-2(d)) The features were suggestive of a noncaseating granulomatous inflammation with differentials of sarcoidosis, foreign body inhalation, and parasitic infection.
Serum calcium and angiotensin-converting enzyme (ACE) levels were suggested, and if high, to favor a diagnosis of sarcoidosis. A clinical-radiologic correlation was recommended.
Further history taken revealed no prior history of penile rashes or ulcers, no history of terminal hematuria, and no recent close contact with a cat. Lung spirometry revealed severe restriction with no significant bronchodilator response. The test result showed elevated serum calcium and ACE level (Table 1).
A diagnosis of stage 3 pulmonary sarcoidosis was made due to the presence of granulomata microscopically, the presence of pulmonary reticulonodular infiltrates without bilateral hilar lymphadenopathy, and scant to absent fibrosis on chest imaging. He was commenced on prednisolone at 60 mg daily to be continued in tapering doses for a period of 1 year. He reported 2 months after starting medication and is doing well.