A 57-year-old male with a personal history of well-controlled intrinsic asthma treated with β-2 agonists and inhaled steroids.
She was diagnosed with chronic hepatitis C (type 1b) in 1991.
The infection was probably acquired after a blood transfusion during childhood.
In 2004, treatment with pegylated interferon and ribavirin was initiated due to the presence of a high viral load and secondary necrotization (moderate anaemia in liver biopsy, but treatment had to be discontinued due to side effects).
Although viral RNA persisted in plasma, there was a biochemical response with normalization of liver function tests.
In February 2009, a slight increase in transaminases and viral load of 8,218,400 IU/ml was detected.
Transient elastography (Fibroscan®) showed liver stiffness of 10.4 kPa (F3), so treatment with pegylated interferon 2b (100 mcgr/1000mg) was started.
Twelve weeks after starting treatment, the patient came to the emergency department with progressive dyspnea on exertion.
Vital signs on arrival to the emergency room were as follows: blood pressure 120/70 mmHg, respiratory rate 16, heart rate 80 and axillary temperature 36.7 or C. Physical examination was normal.
Basal oxygen saturation was 96%.
Complete blood count and biochemistry showed no abnormalities except mild anemia (hemoglobin 9.6 g/dl, hematocrit 31.3% and mean corpuscular volume 112).
Basal arterial gas showed the following results: pH 7.55, PO2 103 mmHg and PCO2 24 mmHg.
The chest X-ray was normal.
Oxygen saturation was recorded at baseline after the patient performed a moderate effort (bladder closure), showing marked desaturation (up to 90%).
Treatment with interferon and ribavirin was discontinued.
Twenty-four hours later, a high-resolution chest CT scan showed bilateral multifocal ground glass infiltrates of peripheral location.
Respiratory function tests showed no restriction or obstruction and decreased diffusion capacity was observed.
Bronchoalveolar lavage was performed.
Gram results and staining for acid-alcohol resistant bacilli and cultures for bacteria, mycobacteria and viruses were negative and pleural fluid cytology was negative for malignant cells.
After discontinuation of treatment, the patient showed progressive improvement in dyspnea, and after eight weeks the symptoms disappeared completely with progressive normalization of pulmonary function tests.
