Frontiers in immunology · 2026
Rapid-onset massive immune-mediated pericardial effusion in a patient with anti-IFN-γ autoantibodies syndrome.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Chen Fushou, Ning Yan, Liang Hanlin, Qin Jiaqi, Liang Siqiao, Huang Xuemei, Liang Xiaona, Tan Feixiang, Chen Ni, Wu Siyao, Hong Limei, He Zhiyi, Feng Tao
Аннотация
BACKGROUND: Anti-interferon-gamma (IFN-γ) autoantibodies (AIGAs) syndrome is an emerging adult-onset immunodeficiency (AOID) associated with opportunistic infections and immune dysregulation. Pericardial effusion as a direct manifestation of this syndrome is rarely reported.
CASE PRESENTATION: A 46-year-old man with a history of Talaromyces marneffei (TM) infection and clinically suspected pulmonary nontuberculous mycobacterial (NTM) disease presented with rapid-onset massive pericardial effusion. The NTM diagnosis was not microbiologically confirmed, as the patient declined bronchoscopy. Pericardial fluid analysis revealed a high inflammatory cell count and an anti-IFN-γ autoantibody titer of 1:2500, identical to serum, despite a negative microbiological workup and no definitive evidence of malignancy on available cytological evaluation. The patient responded well to corticosteroids and anti-NTM therapy, with complete resolution of effusion.
CONCLUSION: This case highlights pericardial effusion as a potential immune-mediated complication of AIGAs syndrome. Clinicians should consider this diagnosis in patients with unexplained serositis and a history of opportunistic infections.
CASE PRESENTATION: A 46-year-old man with a history of Talaromyces marneffei (TM) infection and clinically suspected pulmonary nontuberculous mycobacterial (NTM) disease presented with rapid-onset massive pericardial effusion. The NTM diagnosis was not microbiologically confirmed, as the patient declined bronchoscopy. Pericardial fluid analysis revealed a high inflammatory cell count and an anti-IFN-γ autoantibody titer of 1:2500, identical to serum, despite a negative microbiological workup and no definitive evidence of malignancy on available cytological evaluation. The patient responded well to corticosteroids and anti-NTM therapy, with complete resolution of effusion.
CONCLUSION: This case highlights pericardial effusion as a potential immune-mediated complication of AIGAs syndrome. Clinicians should consider this diagnosis in patients with unexplained serositis and a history of opportunistic infections.