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Case Report |
1
Department of Radiology, S072A, Stanford University Medical Center, Stanford,
CA 94305-5105.
2
Department of Pathology, Stanford University Medical Center, Stanford, CA
94305-5105.
3
Division of Infectious Diseases, Stanford University Medical Center, Stanford,
CA 94305-5105.
4
Division of Pulmonary and Critical Care, Stanford University Medical Center,
Stanford, CA 94305-5105.
5
Division of Oncology, Stanford University Medical Center, Stanford, CA
94305-5105.
Received April 19, 2000;
accepted after revision July 3, 2000.
Address correspondence to A. N. Leung.
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Four days after the infusion of paclitaxel, the patient developed fevers and chills as well as a nonpruritic truncal and abdominal rash, which resolved spontaneously after 4 days. One week after paclitaxel therapy, she developed a dry cough and was increasingly short of breath. A complete blood count revealed a WBC of 4.7x103/mL and no peripheral eosinophilia. The chest radiograph showed interval development of a bilateral, reticulonodular pattern predominating in the upper lung zones (Fig. 1A). CT of the chest revealed diffuse, bilateral patchy areas of increased parenchymal attenuation predominantly in the upper lobes, although all lobes were affected (Fig. 1B).
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Empiric antibiotic therapy consisting of trimethoprim-sulfamethoxazole and levofloxacin was initiated to cover Pneumocystis carinii and community-acquired pneumonias. The patient continued to have intermittent fevers, a dry unproductive cough, and moderate dyspnea with an arterial oxygen saturation of 88% on room air. To determine the cause of her pneumonitis, we performed a bronchoscopy with bronchoalveolar lavage and transbronchial biopsies. Lavage specimens sent for cytologic evaluation; Gomori's methenamine silver stain; and bacterial, viral, and fungal cultures were negative. Serologic test results were not consistent with an acute infection caused by Mycoplasma or Chlamydia species. Test findings for Legionella urinary antigen were negative. Transbronchial biopsies taken in the right upper and lower lobes showed cellular interstitial pneumonitis composed of mononuclear inflammatory cells in association with poorly formed granulomas and focal air-space collections of loose fibromyxoid plugs (Fig. 1C). No infectious changes were identified in the slides prepared for bacterial, fungal, or acid-fast organisms. Because the patient had no history of significant inhalational exposure, the findings were interpreted as drug-induced hypersensitivity pneumonitis.
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The patient's fevers and pulmonary symptoms abated after 6-7 days, oxygen saturation on room air returned to 98%, and a repeated chest radiograph obtained 18 days after paclitaxel infusion showed resolution of abnormalities shown on the previous radiographs. When the biopsy results became available after the resolution of symptoms, the patient was treated with a 10-day course of steroid therapy. Because of the risk of a recurrent hypersensitivity reaction, the patient was not re-challenged with paclitaxel and instead was switched to another taxoid, doxetaxel (Taxotere; Rhone-Poulenc Rorer, Collegeville, PA), that is believed to be less allergenic. Administered in conjunction with a premedication regimen consisting of steroids and histamine1 and histamine2 antagonists, five cycles of doxetaxel were tolerated by the patient without complications.
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Hypersensitivity reactions are a well-recognized complication of paclitaxel therapy and typically occur with the first or second dose [3]. These reactions are characterized by dyspnea, hypotension, bronchospasm, urticaria, and erythematous rashes. Respiratory symptoms may develop hours to weeks after paclitaxel administration. Severity of these symptoms ranges from mild dyspnea to respiratory failure requiring mechanical ventilation [3,4]. The mechanism of paclitaxel-induced hypersensitivity reactions remains unclear. It may be mediated by release of histamine or other vasoactive substances similar to anaphylactoid reactions encountered with IV contrast agents [3], or it may result from a delayed hypersensitivity response [5], which is what is likely to have occurred in this patient.
Of the possible hypersensitivity reactions to paclitaxel, interstitial pneumonitis that results in abnormalities shown on radiography is a rare phenomenon [6, 7]. To our knowledge, our case is unique in that we present the radiographic and CT findings of paclitaxel-induced pneumonitis in a patient who had alternate diagnoses excluded by bronchoalveolar lavage and transbronchial biopsies. Histologic features of the biopsied lung specimens revealed a cellular mononuclear-cell interstitial pneumonitis associated with poorly formed granulomas. These two features are characteristic of hypersensitivity pneumonitis and are similar to histologic findings previously reported in paclitaxel-induced pneumonitis [5]. As seen in this patient, paclitaxel-induced hypersensitivity pneumonitis most frequently manifests radiographically as a bilateral interstitial pattern consisting of reticular or reticulonodular opacities [3,4,5,6,7], although a focal consolidative form [6] has also been described. On CT, parenchymal findings consisted of bilateral patchy areas of increased attenuation predominating in the upper lobes.
Paclitaxel-induced hypersensitivity pneumonitis responds rapidly to steroid therapy. In some patients, symptoms and abnormalities seen on radiographs are self-limited and can undergo spontaneous regression [6]. Although a premedication regimen consisting of dexamethasone, diphenhydramine, and a histamine2 receptor antagonist is commonly administered as prophylaxis for paclitaxel-induced hypersensitivity reactions, the true efficacy of this regimen is unknown [3], and severe hypersensitivity reactions have been reported despite premedication, just as we observed in our patient [7].
In summary, hypersensitivity pneumonitis is a rare complication of paclitaxel therapy. The diagnosis of paclitaxel-induced interstitial pneumonitis should be considered in any patient who, hours to weeks after infusion of paclitaxel, develops nonspecific respiratory symptoms and a diffuse bilateral interstitial pattern on chest radiography.
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