Abstract Introduction Sarcoidosis is a chronic granulomatous disorder of unclear etiology often treated with corticosteroids. However, long-term immunosuppression increases the risk of opportunistic infections, including endemic fungal diseases such as coccidioidomycosis (Valley Fever). Distinguishing infection-related granulomatous inflammation from sarcoid activity presents a significant diagnostic dilemma, especially when both coexist. Case Presentation A 66-year-old female with a 20-year history of biopsy-proven sarcoidosis presented with progressive shortness of breath and chest tightness. Her medical history included hypertension, paroxysmal atrial fibrillation on apixaban, and a remote COVID-19 infection. She had been on prolonged corticosteroid therapy—prednisone 40 mg daily for years, recently transitioned to dexamethasone 6 mg twice daily—for sarcoidosis control. The patient denied smoking or prior oxygen use. She had been diagnosed with coccidioidomycosis several months earlier in Texas and was started on fluconazole 200 mg twice daily but discontinued it prematurely. On admission, chest CT revealed multiple calcified pulmonary nodules, calcified thoracic lymphadenopathy, and linear scarring consistent with granulomatous disease. Laboratory evaluation showed normal angiotensin-converting enzyme (ACE) and vitamin D levels. Fungal studies demonstrated positive β-D-glucan (500 pg/mL) and positive coccidioidal antibody (titer 1:16), with negative cryptococcal and Aspergillus antigens. These findings suggested persistent or recrudescent coccidioidomycosis rather than isolated sarcoid activity. Discussion This case highlights the complex interplay between chronic steroid therapy and opportunistic fungal infections. Long-term corticosteroid use likely impaired the patient’s cell-mediated immunity, hindering fungal clearance and promoting persistence of coccidioidal infection. Differentiating sarcoid flare from active fungal disease is challenging because both can manifest with overlapping radiographic and clinical findings. The normal ACE level and presence of fungal biomarkers favored an infectious etiology. Management required balancing immunosuppression control while providing prolonged antifungal therapy. The Infectious Diseases team recommended resumption and continuation of fluconazole suppression, while careful tapering of corticosteroids was advised to prevent further immunosuppression. Conclusion Patients with sarcoidosis on chronic corticosteroid therapy are at increased risk of opportunistic fungal infections, including persistent or reactivated coccidioidomycosis. This case underscores the need for high clinical suspicion, comprehensive diagnostic evaluation, and multidisciplinary coordination between pulmonology and infectious disease specialists. Long-term antifungal suppression with cautious immunosuppression tapering may be necessary to achieve clinical stability and prevent relapse. This abstract is funded by: None
Patel et al. (Fri,) studied this question.
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