A 41-year-old woman with rheumatoid arthritis treated with etanercept presents with productive cough, fever (38.9°C), and dyspnea. Vital signs show BP 128/82, HR 102, RR 22, SpO2 92% on room air. Chest X-ray reveals bilateral lower lobe infiltrates. Sputum culture grows acid-fast bacilli; tuberculin skin test is negative. She denies night sweats. Which mechanism best explains her increased susceptibility to this infection despite appropriate TNF-alpha inhibitor dosing?
- A)Loss of TNF-alpha-mediated Th1 differentiation and granuloma maintenance impairing mycobacterial controlGABARITO
- B)Inhibition of B cell maturation preventing antibody production
- C)Complement pathway inhibition reducing opsonization of mycobacteria
- D)Blocking of IL-4 signaling reducing Th2 cell differentiation
- E)Direct antibody-mediated destruction of alveolar macrophages by etanercept
Explicação
TNF-alpha is critical for Th1 differentiation and granuloma formation essential for controlling intracellular mycobacteria. TNF-inhibitors impair the Th1 response and destabilize granulomas, allowing latent TB to reactivate. This is a well-established risk wit... Ver explicação completa e trilha adaptativa →