RISK-FACTORS FOR PULMONARY TUBERCULOSIS IN BONE-MARROW TRANSPLANT RECIPIENTS

Citation
Msm. Ip et al., RISK-FACTORS FOR PULMONARY TUBERCULOSIS IN BONE-MARROW TRANSPLANT RECIPIENTS, American journal of respiratory and critical care medicine, 158(4), 1998, pp. 1173-1177
Citations number
22
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
158
Issue
4
Year of publication
1998
Pages
1173 - 1177
Database
ISI
SICI code
1073-449X(1998)158:4<1173:RFPTIB>2.0.ZU;2-7
Abstract
Little is known about the profile of infection with Mycobacterium tube rculosis in bone marrow transplant (BMT) recipients. Of five BMT serie s with a total of more than 5,000 patients, only 10 cases of M. tuberc ulosis infection were described, with an overall incidence of 0.19%. W e have conducted a prospective evaluation of 183 consecutive BMT recip ients, and 10 patients were found to develop pulmonary tuberculosis po st-BMT, yielding an incidence of 5.5%. We described the clinical featu res of these 10 patients, and analyzed the risk factors for developmen t of tuberculosis using age- and sex-matched case control subjects who did not develop the disease. The median age of the 10 patients who de veloped tuberculosis was 29 yr (range, 17 to 40 yr). The median time f or onset of symptoms was 150 d (range, 23 to 550 d), mainly presenting with fever and cough, with infiltrates on chest radiograph. Respirato ry tract specimens, mostly sputum, yielded positive smears for acid-fa st bacilli in three and positive M. tuberculosis culture in eight, whe reas lung tissue histology was the first diagnostic test in two patien ts. Treatment with standard antituberculosis drugs for a longer durati on was highly effective, with no excessive side effects. Risk factors identified for development of tuberculosis included allogeneic BMT (p < 0.05, relative risk [RR] = 23.7), total body irradiation (p < 0.05, RR = 4.9), and chronic graft-versus-host disease (GVHD) (p < 0.05, RR = 3.6). It is postulated that chronic GVHD predisposed to development of tuberculosis mainly via disruption of host reconstitution of immune defenses against M. tuberculosis.