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Published on: May 31, 2018
A rare trigger for macrophage activation syndrome
Shikhar Agarwal1, Jayavani Moodley, Gati Ajani Goel
1Department of Internal Medicine, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA. dr.shikhar.agarwal@gmail.com
Abstract:
Macrophage activation syndrome (MAS) is a disorder characterized by increased activation of mononuclear cells leading to phagocytosis of blood cell precursors in the bone marrow. We describe a case of MAS triggered by disseminated histoplasmosis occurring in a patient with Still's disease on long-term treatment with adalimumab.
Insights
Macrophage activation syndrome (MAS) is a severe condition where immune cells attack blood cell precursors. This case highlights MAS triggered by disseminated histoplasmosis in a patient with Still’s disease on adalimumab therapy.
Area of Science:
- Immunology
- Hematology
- Infectious Diseases
Background:
- Macrophage activation syndrome (MAS) is a life-threatening hyperinflammatory condition.
- It involves the overactivation of macrophages and T-cells, leading to cytokine storm and hemophagocytosis.
- MAS can be primary or secondary to various conditions, including infections and autoimmune diseases.
Observation:
- A patient with Still's disease, treated with adalimumab, presented with disseminated histoplasmosis.
- The patient subsequently developed MAS.
- This suggests a potential link between adalimumab, histoplasmosis, and MAS development.
Findings:
- Disseminated histoplasmosis can precipitate MAS in immunocompromised patients.
- Adalimumab, a TNF-alpha inhibitor, may increase the risk of opportunistic infections like histoplasmosis, potentially triggering MAS.
- This case underscores the importance of considering MAS in patients with underlying inflammatory conditions and new infections.
Implications:
- Clinicians should maintain a high index of suspicion for MAS in patients with Still's disease on TNF-alpha inhibitors who develop disseminated infections.
- Early diagnosis and prompt treatment of both the underlying infection and MAS are crucial for patient survival.
- Further research is warranted to elucidate the precise mechanisms linking TNF-alpha inhibition, opportunistic infections, and MAS pathogenesis.
