As a result, in young adult patients receiving bronchodilator therapy with diagnosis of bronchitis, methemoglobinemia should be considered as the reason of cyanosis and hypoxemia. None declared. “
“There are a number of etiologies associated with interstitial lung disease (ILD).1 ILD has been recognized as an early presentation of polymyositis-dermatomyositis (PM-DM) with frequency as high as 65%.2 ILD in PM-DM is associated with a high rate of morbidity and mortality.2 We report a case of a patient with dyspnea, cough, and intermittent fever in the setting of positive anti-Jo-1 antibodies, who was subsequently documented to have ILD

on lung biopsy. A 52 year-old man who was previously healthy and a non-smoker presented

to an outside facility with cough, progressive dyspnea this website and fevers. He was empirically treated for suspected community acquired pneumonia with intravenous Ceftriaxone and Levofloxacin. A diagnostic bronchoscopy with bronchioalveolar lavage sampling was unrevealing. Because of poor therapeutic response, progression of shortness of breath, and hypoxemia, the patient was transferred to our institution for further evaluation and management. The patient’s social history included a recent business trip to Bangkok and Tokyo, but he denied any specific environmental or infectious exposures. He denied weight loss, previous pulmonary symptoms, muscle weakness, joints swelling and rashes. Initial vital signs revealed that he was Bay 11-7085 febrile to 38.8 °C, blood pressure of 170/72 mmHg, Natural Product Library datasheet and hypoxic with oxygen saturation in the low 80 s on 3 liters per minute (LPM) of oxygen by nasal cannula. Physical examination was remarkable for bilateral inspiratory crackles and otherwise unrevealing.

Laboratory evaluation was remarkable for leukocytosis of 9.3 × 103/mm3 with an elevated fraction of eosinophils 0.85% (normal 0.05–0.5%), an elevated sedimentation rate of 43 mm/1 h (normal 0–22 mm/1 h), an elevated C-reactive protein of 21.8 mg/L (normal ≤ 8.0 mg/L) and creatinine kinase of 740 U/L (normal 52–336). Urine analysis was normal; no myoglobin was seen. Spirometry was consistent with a restrictive pattern (FVC 38% predicted). Repeat chest computed tomography (CT) demonstrated a progressive and bilateral scattered consolidative appearing infiltrates (Fig. 1). Given the recent travel and eosinophilia, an extensive infectious disease evaluation was performed, which was unrevealing. A subsequent video-assisted thoracic surgery (VATS) lung biopsy showed patchy organizing pneumonia and diffuse mixed inflammatory infiltrates involving interstitial septa and alveolar spaces (Fig. 2). Subsequent serologies revealed slight increase in antinuclear antibody to 2.2 (normal < 1.0 units) with increased anti-Jo-1 antibody of 2.2 (normal < 1.0 units); other extractable nuclear antibodies, rheumatoid factor, and anti-neutrophil cytoplasmic antibodies were not detected.