A 57-year-old man presented with a history of shortness of breath and dry cough for 2 weeks in duration. His respiratory symptoms were of sudden onset, gradually progressive, and not associated with chest pain or palpitations. In addition, his shortness of breath was not associated with any diurnal variation. There was no history of hemoptysis, pyrexia, or weight changes. There was no history of contact with the COVID-19-positive case or tuberculosis patient. The patient took the first dose of the AstraZeneca/Covishield vaccine in February 2021; 2 weeks prior to the onset of his symptoms.
He is known to have hypertension, hyperlipidemia, diabetes mellitus type 2, and hidradenitis suppurativa diagnosed in 2006 on biological therapy for 1 year in duration.
There was no history of recent travel or exposure to industrial chemicals or gases.
There is no history of similar symptoms among family members.
On admission, the patient was normotensive with a blood pressure of 136/80 mmHg and mildly tachypneic with a respiratory rate of 20 breaths per minute and oxygen saturation of 98% on room air. Upon auscultation of his chest reduced air entry bilaterally with bibasal crepitations. The patient was not pale nor cyanosed with no signs of icterus or clubbing. All other systemic examinations were unremarkable.
On admission, routine investigations revealed a hemoglobin of 12.3 g/dL, a total count of 5440 with 59.7% neutrophils, 19.1% lymphocytes, 5.0% eosinophils, 13.8% monocytes, and a platelet count of 225,000. His erythrocyte sedimentation rate was 68 mm/h. He has normal urea and creatinine. The liver function test revealed total bilirubin of 5.5 mumol/L, alanine transaminase 18.3 IU/L, aspartate aminotransferase 16 IU/L, alkaline phosphatase 80 IU/L, total protein 72.9 g/L, albumin 37.2 g/L, and globulin 35.7 g/L (Table 1).
Chest X-ray (Fig. 1) revealed patchy bilateral infiltration. A CT pulmonary angiography (Fig. 2) revealed bilateral diffuse patchy consolidation with no pulmonary embolus and few mediastinal reactive lymph nodes. Bronchoscopy was done, which revealed mild bilateral inflammation mainly in the right upper lobe lingula and the right middle lobe with no endobronchial lesion or mucous secretion. TB PCR Gene Expert of bronchial washing came positive for mycobacterium tuberculosis. Hence, the patient was started on Ethambutol 1200 mg OD PO, Isoniazid 300 mg OD PO, Pyrazinamide 1500 mg OD PO and Rifampicin 600 mg OD PO.
A month later, the patient presented with similar symptoms as the previous admission with non-specific chest pain that is poorly localized and non-radiating in nature. A repeated chest X-ray (Fig. 3) was performed, which showed worsening of the patchy infiltration bilaterally. Hence, a high-resolution computed tomography of the chest (HRCT) (Fig. 4) was carried out, which revealed patchy bilateral areas of consolidation and ground-glass opacities with early changes of fibrosis and enlarged mediastinal and hilar lymph nodes. A repeated bronchoscopy was done secondary to non-resolving findings in computed tomography of the chest with a primary impression of sarcoidosis. A bronchial biopsy (Fig. 5) was done which showed a non-caseating granuloma with minimal inflammatory cell infiltrate compatible with sarcoidosis (H&E stain).
We noticed the appearance of a chronic skin lesion during the patient's second admission after the chest symptoms. The patient was referred to dermatology for biopsied chronic skin lesions and the pathology report showed granulomatous dermatitis in keeping with sarcoidosis. Microscopic examination of the skin biopsy showed multiple granulomas in the upper dermis composed of epithelioid cells with few lymphocytes and occasional giant cells. The stain for acid-fast bacilli is negative.
After confirmation of sarcoidosis, prednisolone treatment started (30 mg OD PO) and it was tapered gradually with every subsequent monthly follow-up visit to the clinic. Treatment was given for a total of 6 months from the onset of detection of sarcoidosis.
The patient was later discharged on antimycobacterial therapy alongside corticosteroid treatment on prednisolone 30 mg OD PO. The patient was advised for repeated HRCT of the chest after two months. An extended duration of antimycobacterial treatment was recommended for a total of 9 months from initiation and tapering down the dose of prednisolone.
A pulmonary function test was carried out as an out-patient prior to the commencement of steroid therapy once the diagnosis of sarcoidosis has been established which showed an FVC of 3.36 (74% predicted), an FEV1 of 2.81 (78% predicted) and a TLC of 4.12 (57% predicted). Three months later, a repeated pulmonary function test was carried out which showed an FVC of 3.68 (81% predicted), an FEV1 of 2.92 (82% predicted), and a TLC of 3.68 (81% predicted) (Table 2).
Repeated HRCT of the chest (Fig. 6), revealed the total subside of the previously noted diffuse pulmonary ground-glass opacities with patchy para-hilar consolidations. Currently, only residual fibrotic changes are pointed out at the interstitial level surrounding the para-hilar segmental and sub-segmental bronchi on both sides with associated traction bronchiectasis. Relative left-side pulmonary volume loss is noted due to the underlying fibrosis with obvious upward traction of the left upper bronchus and mid-portion downward kink of the left oblique fissure due to the underlying fibrotic changes.
Upon subsequent follow-ups in the clinic, the patient symptomatically improved.
A repeated high-resolution computed tomography of the chest revealed the total subside of the previously noted diffuse pulmonary ground-glass opacities with patchy para-hilar consolidations.