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* From the Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Health Sciences Center, Denver, CO.
Correspondence to: Marvin I. Schwarz, MD, FCCP, University of Colorado Health Sciences Center, Division of Pulmonary Sciences and Critical Care Medicine, Campus Box C272, 4200 East Ninth Ave, Denver, CO 80262; e-mail: MarvinSchwarz{at}UCHSC.edu
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Abstract |
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Key Words: acute eosinophilic pneumonia • AIDS • interstitial lung disease
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Introduction |
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Case Report |
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A physical examination revealed a young man in moderate respiratory distress. His temperature was 38.2°C, BP was 130/70 mm Hg, pulse was 120 beats/min, and respiration was 24 breaths/min. The results of a head and neck examination were normal. Auscultation of the lungs revealed scattered rhonchi and diffuse crackles. A cardiac examination indicated tachycardia but was otherwise normal. The abdomen was without disease, and without masses or hepatosplenomegaly. The results of extremity and neurologic examinations were normal. Arterial blood gas measurements with the patient breathing room air revealed the following: pH, 7.43; PaCO2, 32 mm Hg; PaO2, 46 mm Hg; and oxygen saturation, 82%. The initial results of laboratory tests, liver function tests, and urinalysis were within normal limits. His WBC count was 9,100 cells/µL with 85% polymorphonuclear cells, 8% lymphocytes, and 2% eosinophils. The hemoglobin level was 14.2 g, and the platelet count was 199,000 cells/µL. The results of initial sputum and blood cultures, sputum stains for acid-fast bacteria, and direct fluorescent antibody tests for P carinii were negative. A chest radiograph is shown (Fig 1 ). The patient underwent endotracheal intubation 1 day after hospital admission because of deteriorating blood gas levels and increasing respiratory distress. The following day, he underwent bronchoscopy with BAL. Bronchoscopy revealed healthy airways. Stains for P carinii, fungal organisms, and acid-fast bacteria, as were Gram’s stain. Cultures for acid-fast bacteria, fungus, bacteria, and viruses (ie, influenza, parainfluenza, respiratory syncytial virus, adenovirus, cytomegalovirus, herpes virus, and varicella) were negative. Cultures for Mycoplasma and Legionella were negative. Trimethoprim-sulfamethoxazole therapy was reduced to a prophylactic dosage, and the corticosteroid medications were discontinued. The patient continued to worsen over the next 48 h, requiring positive end-expiratory pressure of 10 cm H2O and a 75% fraction of inspired oxygen to maintain an oxygen saturation of 90%. A thoracoscopic lung biopsy was performed and revealed changes that were consistent with AEP (Fig 2 ). The results of all stains for infectious pathogens were negative. His WBC differential count eventually indicated 8% eosinophils with a total WBC count of 10,200 cells/µL. The patient subsequently began receiving methylprednisolone therapy, 1 g daily for 3 days, followed by a rapid taper. He was extubated 72 h later and was discharged from the hospital without supplemental oxygen on the 10th day of his hospital stay. There was marked radiographic improvement at that time (Fig 3 ).
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Discussion |
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The present case meets the clinical definition of AEP as proposed by Pope-Harman et al.11 This definition includes an onset of < 7 days, fever, bilateral infiltrates, severe hypoxemia, lung eosinophilia (ie, a BAL differential count of > 25% eosinophils or predominance of eosinophils shown in open-lung biopsy specimen). Moreover, there can be no history of hypersensitivity to drugs, no historical or laboratory evidence for infection, and no other known causes of acute eosinophilic lung disease. In addition, the histologic appearance of interstitial and alveolar eosinophils that was found in the patient in this case, in the face of acute and organizing diffuse alveolar damage, meets the criteria of Tazelaar et al12 for AEP. It is important to note that neither the above definition nor our case featured peripheral eosinophilia. This is frequently the case in patients with AEP, although the patient in the present case eventually developed peripheral eosinophilia while in the hospital. This delay in peripheral eosinophilia also has been recognized previously.13 The BAL WBC differential counts were not performed in the present case since the diagnosis was not suspected at the time of bronchoscopy. In retrospect, BAL differential cell counts may have established the diagnosis prior to the open-lung biopsy and should be considered when performing bronchoscopy on HIV-positive patients with diffuse pulmonary infiltrates.
Although trazodone is reported to cause AEP,14 we do not believe that this was the case here since the medication was not discontinued during the course of his illness, he still improved, and he still receives this drug without recurrence of his lung disease. Likewise, the fluoxetine and trimethoprim-sulfamethoxazole therapy15 16 were continued throughout the patient’s illness and after hospital discharge and are, thus, unlikely candidates. Ibuprofen has been associated with pulmonary infiltrates with eosinophilia syndrome.17 However, life-threatening AEP has not been associated with the use of nonsteroidal anti-inflammatory medications. In addition, this patient was only intermittently receiving ibuprofen and continued to do so after hospital discharge without a recurrence of his pulmonary illness.
The present patient represents the first biopsy-proven case of AEP in an AIDS patient. We believe that this is important because a number of infections common to AIDS patients (most notably PCP, aspergillus, and coccidioidomycosis) are known to cause BAL eosinophilia and are not always detectable in the BAL fluid.18 19 This patient also demonstrated a failure to respond to 80 mg prednisone daily followed by rapid improvement on higher dosages of IV methylprednisolone. The optimal corticosteroid dosage for the treatment of AEP not associated with AIDS is unknown, but 60 mg prednisone daily is reported to be successful.12 Given that lower doses of prednisone can be effective in treating AEP, and that most hospitalized AIDS patients with suspected PCP are treated with a corticosteroid preparation, one could speculate that the incidence of AEP might be higher than previously thought and is masked by the attendant corticosteroid therapy for PCP.
The finding of eosinophilic lung disease in a patient with HIV is not surprising as patients frequently have peripheral blood eosinophilia, especially when the CD4 count is low.20 21 22 In addition, eosinophilic pustular folliculitis and hypereosinophilic syndrome are well-described in HIV-infected patients. The mechanism of eosinophilia and eosinophil-related disease is unknown but may be related to the predominantly Th2 phenotype seen in patients with advancing HIV infection.23 Th2 lymphocytes produce interleukin (IL)-4, IL-5, IL-6, and IL-10. IL-5 is the primary cytokine responsible for eosinophil growth, differentiation, release from bone marrow, and survival.24 IL-5 production does not appear to be impaired in AIDS patients despite low CD4 counts.25 Other possible pathophysiologic explanations include the well-described production of IL-5 or eotaxin (a potent mediator of eosinophil accumulation in tissue) by lung epithelial cells or fibroblasts.26 27
Other ILDs that are known to complicate AIDS include NSIP, LIP, BOOP, and secondary alveolar proteinosis. NSIP is most common in adults. Suffredini et al1 reported that 32% of all clinical episodes of pneumonitis were caused by NSIP. In a more recent study, Sattler et al2 reported on 354 AIDS patients who were admitted to the hospital with a presumptive diagnosis of PCP. Of these, 67 patients (19%) did not have P carinii present, as determined by either BAL or transbronchial biopsy. In 15 of the 67 patients (23%), NSIP was present in lung biopsy specimens. Moreover, an additional 40% of patients had nondiagnostic results of transbronchial biopsies, a finding that frequently occurs in patients who subsequently receive diagnoses of NSIP on open-lung biopsy. Although LIP is the most common ILD in children with AIDS, and is considered to be an AIDS-defining illness in that population, it is less common in adult AIDS patients.3 28 29 Idiopathic BOOP is another uncommon interstitial reaction in this population.5 30 However, the appearance of organizing pneumonia in the face of infection is not unusual. There also have been reports of the appearance of alveolar proteinosis in the lungs of AIDS patients, but this is associated with PCP or tuberculous infection.4 31
Here we have reported on an adult AIDS patient with AEP. This extends the spectrum of ILDs in AIDS patients. A diagnosis of AEP should be considered in an AIDS patient who presents with acute respiratory failure and bilateral infiltrates that are unresponsive to antibiotic therapy. Differential bronchoalveolar cell counts indicating significant eosinophilia point to this diagnosis.
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Footnotes |
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Supported by Specialized Center of Research (SCOR) grant No. HL-27353 from the National Heart, Lung, and Blood Institute.
Received for publication December 4, 2000. Accepted for publication May 22, 2001.
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References |
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TH2 switch is a critical step in the etiology of HIV infection. Immunol Today 14,107-110[CrossRef][ISI][Medline]
This article has been cited by other articles:
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  M. I. Schwarz and R. K. Albert "Imitators" of the ARDS: Implications for Diagnosis and Treatment Chest, April 1, 2004; 125(4): 1530 - 1535. [Full Text] [PDF]
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