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Abstract
Background: Cyclophosphamide (CYC) is an immunosuppressive medication used to treat life threatening complications of various rheumatic diseases like vasculitis and systemic lupus erythematosus. 1% of patients on this medication develop pneumonitis. When considering CYC induced lung toxicity, other etiologies such as opportunistic infections and diffuse alveolar hemorrhage should be ruled out.
Case presentation: The patient is an 83-year-old woman with a past medical history of microscopic polyangiitis, and hypothyroidism who presented with progressive dyspnea at rest, exacerbated on exertion, associated with orthopnea. The patient was admitted due to acute on chronic hypoxemic respiratory failure with multifactorial etiology and heart failure exacerbation with preserved ejection fraction of 65%. Three months prior to this admission, the patient was diagnosed with ANCA-positive pauci immune crescentic and necrotizing glomerulonephritis; she was started on CY, as well as prednisone. On admission, her pulse oximetry was 88% on room air, with a systolic murmur at the right upper parasternal border, and bibasilar inspiratory crackles. Initial workup showed pancytopenia. Echocardiogram revealed severe aortic stenosis, and a right systolic ventricular pressure of 65mmHg, suggestive of pulmonary hypertension-likely group 2. Medical management was recommended since the patient was a poor candidate for procedures. CT Chest showed worsening bilateral ground-glass densities and inter and intralobular septal thickening, not present on CT performed three months ago. Empiric coverage for opportunistic infections with clindamycin, primaquine, and azithromycin was started. Bronchoscopy ruled out diffuse alveolar hemorrhage, and bronchoalveolar lavage was negative for Coccidioides, Histoplasma, acid-fast bacilli, Pneumocystis jiroveci, and Aspergillus, same for the viral respiratory panel. Antibiotics were de-escalated. The patient was discharged home on oxygen, CYC was discontinued given significant detrimental adverse effects and prednisone tapering with a close follow-up of renal function.
Conclusion: Patient presented with progressive shortness of breath, and respiratory failure, CYC-induced pneumonitis was diagnosed after ruling out other causes. The patient's symptoms started within six months of ANCA therapy use, which placed the patient in the early-onset type with more favorable outcomes. Pulmonary toxicity associated with CYC is underscored by the low prevalence rates in patients with ANCA-associated vasculitis, so it is essential to have a high rate of suspicion.
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Poster
Recommended Citation
Bartl, Mery; Ng-Wong, Yilen Karen; Alexander, Blesset; Rodriguez-Paez, Josenny L.; Gomez Casanovas, Jose G.; Loftis, Christine; and Suarez Parraga, Andres, "It is not PCP; it is Cyclophosphamide Induced toxicity" (2024). Research Colloquium. 48.
https://scholarworks.utrgv.edu/colloquium/2023/posters/48
Included in
It is not PCP; it is Cyclophosphamide Induced toxicity
Background: Cyclophosphamide (CYC) is an immunosuppressive medication used to treat life threatening complications of various rheumatic diseases like vasculitis and systemic lupus erythematosus. 1% of patients on this medication develop pneumonitis. When considering CYC induced lung toxicity, other etiologies such as opportunistic infections and diffuse alveolar hemorrhage should be ruled out.
Case presentation: The patient is an 83-year-old woman with a past medical history of microscopic polyangiitis, and hypothyroidism who presented with progressive dyspnea at rest, exacerbated on exertion, associated with orthopnea. The patient was admitted due to acute on chronic hypoxemic respiratory failure with multifactorial etiology and heart failure exacerbation with preserved ejection fraction of 65%. Three months prior to this admission, the patient was diagnosed with ANCA-positive pauci immune crescentic and necrotizing glomerulonephritis; she was started on CY, as well as prednisone. On admission, her pulse oximetry was 88% on room air, with a systolic murmur at the right upper parasternal border, and bibasilar inspiratory crackles. Initial workup showed pancytopenia. Echocardiogram revealed severe aortic stenosis, and a right systolic ventricular pressure of 65mmHg, suggestive of pulmonary hypertension-likely group 2. Medical management was recommended since the patient was a poor candidate for procedures. CT Chest showed worsening bilateral ground-glass densities and inter and intralobular septal thickening, not present on CT performed three months ago. Empiric coverage for opportunistic infections with clindamycin, primaquine, and azithromycin was started. Bronchoscopy ruled out diffuse alveolar hemorrhage, and bronchoalveolar lavage was negative for Coccidioides, Histoplasma, acid-fast bacilli, Pneumocystis jiroveci, and Aspergillus, same for the viral respiratory panel. Antibiotics were de-escalated. The patient was discharged home on oxygen, CYC was discontinued given significant detrimental adverse effects and prednisone tapering with a close follow-up of renal function.
Conclusion: Patient presented with progressive shortness of breath, and respiratory failure, CYC-induced pneumonitis was diagnosed after ruling out other causes. The patient's symptoms started within six months of ANCA therapy use, which placed the patient in the early-onset type with more favorable outcomes. Pulmonary toxicity associated with CYC is underscored by the low prevalence rates in patients with ANCA-associated vasculitis, so it is essential to have a high rate of suspicion.