Rare primary bone tuberculosis associated with ruxolitinib therapy: A case report and literature review
Liang-Yan Jin, Ping Yu, Fan Huo, Ya-Hui Cui, Bao-Liang Wu, Ting LiRationale:
Ruxolitinib, a Janus kinase (JAK) inhibitor, may increase the risk of tuberculosis infection by suppressing cellular immunity. Tuberculosis associated with ruxolitinib has generally been reported as disseminated or multisystem disease. However, no previous cases of primary bone tuberculosis secondary to ruxolitinib have been reported.
Patient concerns:
A 68-year-old female patient had been taking ruxolitinib for over 2 years for primary thrombocythaemia and developed recurrent high fever without other localizing symptoms.
Diagnoses:
Imaging studies revealed multiple areas of bone destruction with increased metabolic activity throughout the skeleton (sacroiliac joints, humeral heads), necessitating differential diagnosis from malignant tumors. Following exclusion of hematological malignancies via bone marrow aspiration, Xpert MTB/RIF (X-pert) testing of the bone lesion tissue confirmed
Interventions:
Standard four-drug antituberculosis therapy was administered once daily: isoniazid 200 mg, rifampicin 450 mg, pyrazinamide 1125 mg, and ethambutol 625 mg, while ruxolitinib was continued for the underlying myeloproliferative disorder.
Outcomes:
Follow-up MRI examinations of the right humeral head and sacroiliac joints at 4 and 5 months post-tuberculosis treatment revealed a marked reduction in lesion size and decreased edema at both sites, consistent with an effective therapeutic response..
Lessons:
This case shows that ruxolitinib-associated tuberculosis can present as an isolated skeletal infection. It may occur without any pulmonary or systemic involvement. Latent tuberculosis screening should be performed before initiating ruxolitinib. Vigilance for extrapulmonary tuberculosis should be maintained throughout therapy. Unexplained bone lesions in JAK-inhibitor users warrant multidisciplinary evaluation. Empirical fluoroquinolone use before diagnosis may transiently mask the disease and delay recognition. Finally, CYP3A4-mediated interactions should be anticipated when rifampicin-based therapy is combined with ruxolitinib.