The use of tumor necrosis factor (TNF) inhibitors (anti-TNF) has expanded treatment options for autoimmune diseases such as rheumatoid arthritis (RA). However, these agents increase the risk of reactivation of latent infections, particularly tuberculosis (TB). Although TB is more commonly associated with infliximab, other anti-TNFs, such as certolizumab, are also implicated. A 73-year-old woman with RA, on certolizumab for approximately three years, with negative tuberculin tests prior to therapy, presented with a 6-month history of anorexia, 20-kg weight loss, asthenia, and mucoid cough with throat clearing, without fever. She progressively developed functional decline and limited oral intake to soft foods and liquids. Extensive outpatient evaluation for neoplasia was performed due to mediastinal and retroperitoneal lymphadenopathy. On hospital admission, she had desaturation and required 3 L/min supplemental oxygen. Sputum smear microscopy revealed acid-fast bacilli arranged in globi, and rapid molecular testing (TRM) detected Mycobacterium tuberculosis. Chest CT showed multiple small randomly distributed pulmonary nodules consistent with miliary pattern, as well as nodules and coalescent masses, some cavitary, in the upper lobes, up to 6.2 cm in the apical/posterior segment of the right upper lobe. Disseminated (miliary) and pulmonary tuberculosis was diagnosed. Standard RIPE therapy (rifampicin, isoniazid, pyrazinamide, and ethambutol) was started. After two days, she experienced respiratory worsening and required high-flow oxygen mask. Prednisone 25 mg/day was initiated. Anti-TNF therapy was suspended during hospitalization. She evolved favorably, with clinical improvement and hospital discharge after one month. Patients on anti-TNF have an increased risk of TB reactivation due to suppression of TNF-α–mediated immune responses. Early diagnosis and suspension of immunosuppressive therapy, along with appropriate treatment, are essential for favorable outcomes. This case highlights the importance of rigorous TB monitoring in patients receiving anti-TNF therapy, even with negative pre-treatment tuberculin tests, and the need for high clinical suspicion for disseminated TB in immunosuppressed patients.
Nascimento et al. (Sun,) studied this question.