Abstract Introduction We report a case of rapidly progressive fibrocavitary Mycobacterium avium complex pulmonary disease in a 74-year-old woman with longstanding seropositive rheumatoid arthritis. Her clinical course was complicated by delayed diagnosis and treatment-limiting toxicity. This case highlights the diagnostic complexity and poor prognosis of fibrocavitary MAC in patients with autoimmune/structural lung disease. Case Presentation 74-year-old woman with seropositive rheumatoid arthritis presenting for progressive dyspnea. Her RA had been treated with rituximab and prednisone, with her last infusion over a year prior to admission. Several months before admission, she was hospitalized at an OSH for AMS secondary to bacteremia. At that time, sputum cultures grew MAC, which was considered colonization and not treated. Shortly after, she followed up with Rheumatology, where rituximab was held due to positive Hepatitis B serology, but daily prednisone was continued. Months later, she presented with severe arthralgias and hypoxia. CT imaging showed extensive fibrosis, honeycombing, bronchiectasis, and multiple cavitary lesions in the right upper and middle lobes. She was treated with intravenous steroids for presumed ILD exacerbation, later transitioned to oral prednisone. Bronchoscopy with BAL and cryobiopsy was performed. Cultures were pending at discharge. BAL cultures grew acid-fast bacilli, and she started RIPE therapy plus azithromycin as an outpatient. She returned within a week of RIPE initiation with worsening respiratory symptoms, and repeat imaging demonstrated enlarging cavitary lesions and new ground-glass opacities. Final cultures confirmed MAC, resistant to several antibiotics, but sensitive to clarithromycin. Her course was complicated by drug-induced liver injury and biliary pancreatitis. Despite these interventions, she developed progressive hypoxic respiratory failure requiring intubation. Her condition, unfortunately, deteriorated and she expired in the ICU. Discussion This case illustrates the diagnostic and therapeutic complexity of MAC infection. While fibrocavitary MAC typically occurs in elderly male smokers with COPD or prior tuberculosis, our patient had no smoking history but had suspected RA-associated ILD, a known predisposing factor for NTM infection. Her clinical trajectory highlights the need for suspicion of NTM in RA patients with cavitary lung lesions, even in the absence of immunosuppression. Once diagnosed, treatment is difficult with prolonged multidrug therapy, frequent adverse effects, and drug-drug interactions, making early initiation critical. Conclusions Fibrocavitary MAC should be considered in patients with suspected autoimmune ILD with cavitary features regardless of lack of typical risk factors. Prompt recognition and tailored treatment are essential to improving outcomes in this increasingly recognized population at risk for disseminated NTM infections. This abstract is funded by: None
Pappas et al. (Fri,) studied this question.