TUBERCULOSIS IN HEART-TRANSPLANT RECIPIENTS

Citation
Mm. Korner et al., TUBERCULOSIS IN HEART-TRANSPLANT RECIPIENTS, Chest, 111(2), 1997, pp. 365-369
Citations number
11
Categorie Soggetti
Respiratory System
Journal title
ChestACNP
ISSN journal
00123692
Volume
111
Issue
2
Year of publication
1997
Pages
365 - 369
Database
ISI
SICI code
0012-3692(1997)111:2<365:TIHR>2.0.ZU;2-P
Abstract
Study objectives: To clarify the prevalence and factors associated wit h tuberculosis, as well as patient survival in heart transplant recipi ents. Design: A retrospective review of case records of all heart tran splant recipients from March 1989 to February 1996 during a 7-year per iod. Setting and patients: During the period reviewed, 727 orthotopic heart transplantations were performed in 716 patients at the Heart Cen ter Northrhine-Westphalia, Germany. Results: Tuberculosis was proved i n seven (1%) patients (four men/three women; age, 33 to 71 years; two miliary lesions, three pulmonary lesions, and two urogenital lesions), None of them had primary history of tuberculosis, Tuberculin skin tes ts were not performed before transplantation because there were no les ions indicating primary infection of tuberculosis. The immunosuppressi ve regimen was based on double-drug (cyclosporine + azathioprine) ther apy, Immunosuppression had been intensified by methylprednisolone puls es at least three times in those seven patients, and prednisone had be en used orally in six of seven patients. Tuberculosis developed from 2 .5 to 41 months after transplantation. Tuberculosis was found by routi ne examinations in four of seven patients. Diagnoses were made with bo th direct microscopy and cultures in six patients, and by histologic s tudy in one. Treatment consisted of isoniazid, rifampicin, ethambutol, and pyrazinamide. Two patients with miliary lesions were treated with four drugs, and the others were treated with three drugs. Isoniazid w as used in all patients. Rifampicin, which decreases cyclosporine seru m levels, was not used from the beginning in one patient and treatment with it was stopped halfway in another patient because low cyclospori ne level had induced rejection. Six of the seven patients are doing we ll while receiving antituberculous therapy. One patient died with mili ary tuberculosis as a cause of death. Conclusions: The prevalence of t uberculosis in heart transplant recipients was higher than that in the general population. We recommend that a high degree of clinical suspi cion is maintained for tuberculosis in heart transplant recipients wit h meticulous follow-up, and that the treatment of tuberculosis has to be with meticulous care, especially during the use of rifampicin.