ABSTRACT
BACKGROUND: Acute rejection of lung allografts is an important contributor to morbidity and mortality in the transplant patient population, resulting in the dysfunction and destruction of the graft by the host's immune system via cellular or antibody-mediated mechanisms. Acute cellular rejection (ACR) is more common and better characterized than antibody-mediated rejection, which to date lacks any widely agreed upon, standardized set of diagnostic criteria. We present a case of AMR attributable to a rare phenomenon, non-human leukocyte antigen (HLA) antibodies. CASE REPORT: A 50-year-old male underwent an uneventful single lung transplant for pulmonary sarcoidosis. Donor and recipient blood type was A positive. No pretransplant donor-specific antibodies were identified. Flow cytometric crossmatch was negative. The postoperative course was significant for a single-unit transfusion of packed red blood cells on postoperative day (POD) 1 and persistent asymptomatic Serratia marcescens in bronchial washes despite ongoing levofloxacin treatment. A surveillance biopsy (POD 34) showed no evidence of rejection. One week later (on POD 41), the patient presented with fever, shortness of breath, and imaging abnormalities of the grafted lung. Inpatient antibiotic escalation to cefepime, ertapenem, and meropenem resolved the positive cultures and fever, but the patient's respiratory function continued to decline, requiring intubation and extracorporeal membrane oxygenation. High-dose steroids and therapeutic plasma exchanges were initiated for suspected acute rejection. During the workup, a newly developed anti-A1 red blood cell antibody was identified. Despite supportive efforts, the patient died on POD 55, 14 days after symptomatic presentation. CONCLUSION: This case highlights the clinical significance of AMR in lung allografts, as well as the need to investigate both HLA and non-HLA antibody sources in pulmonary transplant rejection refractory to treatment.
ABSTRACT
Bronchiolitis obliterans with organizing pneumonia (BOOP) is characterized by excessive proliferation of granulation tissue within small airways (proliferative bronchiolitis) and alveolar ducts associated with chronic inflammation in the surrounding alveoli. It is generally idiopathic but may occur during the resolution of viral or mycoplasmic pneumonia. It is also associated with a variety of systemic illnesses and clinical settings. Complete resolution occurs in 65-85% of patients treated with corticosteroid therapy, and recurrence is not uncommon. Although rapidly fatal BOOP is rare, respiratory failure leading to death may occur in up to 5% of patients. We describe a fatal case of BOOP suspicious for pneumonia in a patient with rheumatoid arthritis.
