Abstract
Invasive pulmonary aspergillosis is a serious threat that primarily affects immunocompromised patients, those who are severely neutropenic under cancer chemotherapy or bone-marrow transplantation, or those with acquired immunodeficiency syndrome (AIDS) (Kristan et al., 2002; Aliff et al., 2003). Also, immunocompetent patients with chronic obstructive pulmonary disease (COPD), especially those under corticosteroid therapy, have recently been implicated in the appearance of invasive aspergillosis. However, early diagnosis of invasive pulmonary aspergillosis is very difficult (Kristan et al., 2002).
Here we describe a patient with COPD who developed rapidly progressive respiratory failure and died after short-term corticosteroid treatment, in whom poor laboratory findings overwhelmed the clinical suspicion of invasive pulmonary invasive aspergillosis, which was confirmed only at post-mortem.
An 83-year-old man with a long history of COPD was admitted because of worsening dyspnoea and productive cough. He had been treated with an anticholinergic inhalation of oxitropium bromide and had repeated respiratory exacerbations resulting from bronchitis, which had improved every time with both short-term intravenous corticosteroid and antimicrobial therapy. On admission, severe wheezes were heard bilaterally. A chest radiograph was unremarkable, with pleural thickening as a sequela to tuberculosis of youth and emphysematous change. Arterial blood gases whilst breathing room air showed pH 7.41; pCO2, 33 mmHg; pO2, 44 mmHg; and HCO-3, 17 mmol l-1. His leukocyte count was 6500 µl-1 and C-reactive protein was 3.2 mg dl-1. Left nephrectomy had been done in his youth and the remaining kidney had a 20-year history of diabetic nephropathy. His blood urea nitrogen was 38.1 mg dl-1, serum creatinine was 1.6 mg dl-1 and creatinine clearance was 20 ml min-1; these values reflect his history.
Therapy with methylprednisolone (80 mg day-1) and cefmetazole (2 g day-1) was initiated, but his bronchospasm and dyspnoea continued. On day 7, he experienced an acute dyspnoea attack with blood-tinged sputum. A bolus of hydrocortisone (300 mg) was administered and methylprednisolone was increased to 240 mg per culture. Repeated sputum culture yielded only methicillin-resistant Staphylococcus aureus (MRSA), which was not likely to be the pathogen responsible. Blood-stained sputum raised the suspicion of aspergillosis, but serological evidence was poor [(13)-ß-D-glucan at 15 pg ml-1 and the latex agglutination test for galactomannan was negative]. As empiric itraconazole seemed to be ineffective during treatment with an H2-receptor blocker, fluconazole was initiated instead (Fig. 1). Intensification of therapy did not improve his respiratory failure. Methylprednisolone was decreased gradually, as the increase did not seem to improve the patient's condition.