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Tuberculosis complicating imatinib treatment for chronic myeloid leukaemia

Depts of ¹ Pulmonary Diseases, and ² Haematology, VU University Medical Centre, Amsterdam, and ³ Dept of Tuberculosis, University Medical Centre, Groningen, The Netherlands.

CORRESPONDENCE: J. M. A. Daniels, Dept of Pulmonary Diseases, Medisch Centrum Alkmaar, Wilhelminalaan 12, Alkmaar, Noord-Holland, 1815 JD, The Netherlands. Fax: 31 725482167. E-mail: j.m.a.daniels{at}mca.nl

Keywords: Chronic myeloid leukaemia, imatinib, immunity, infection, T-cell receptor, tuberculosis

Received: February 18, 2008
Accepted May 25, 2008

Although imatinib is not considered a predisposing factor for tuberculosis (TB), the present case report describes three patients in whom imatinib treatment for chronic myeloid leukaemia was complicated by TB. This raises the question of whether imatinib increases susceptibility to TB.

There are several reports suggesting that imatinib might impair the immune system, leading to a variety of infections, including varicella zoster and hepatitis B. Control of TB in healthy individuals is achieved through acquired immunity, in which antigen-specific T-cells and macrophages arrest growth of Mycobacterium tuberculosis bacilli and maintain control over persistent bacilli. In the chronic stage of the infection, CD8+ T-cells assist macrophages in controlling intracellular mycobacteria. The T-cell receptor orchestrates this process.

The fact that tyrosine kinases play an important role in T-cell receptor signal transduction and that imatinib has been shown to affect T-cell receptor signal transduction, presents a mechanism by which imatinib might impair control of Mycobacterium tuberculosis; thereby leaving the host susceptible to reactivation of tuberculosis.